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2002, Número 6

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Cir Cir 2002; 70 (6)


Inflamación-endotelio-coagulación en sepsis. Conceptos actuales

Carrillo-Esper R, González-Salazar JA

Idioma: Español
Referencias bibliográficas: 69
Paginas: 433-441
Archivo PDF: 67.09 Kb.


RESUMEN

Objetivo: revisar los conceptos actuales de la interrelación fisiopatológica entre infección, inflamación y coagulación que se presentan en la sepsis grave. Material y métodos: se llevó a cabo una revisión en medline de los estudios recientes y relevantes en los que se discute la patogénesis de la sepsis grave. Resultados: la sepsis grave es una de las principales causas de ingreso a la Unidad de Terapia Intensiva y se asocia a una elevada morbilidad y mortalidad. Las exotoxinas y endotoxinas bacterianas activan al sistema inmune, el cual sintetiza citocinas proinflamatorias como son el factor de necrosis tumoral y una serie de interleucinas, que desencadenan una reacción denominada respuesta inflamatoria sistémica que tiene como finalidad limitar y erradicar el proceso infeccioso. De no controlarse por la respuesta inflamatoria sistémica compensadora la amplificación de la respuesta inflamatoria lesiona el endotelio y activa la coagulación a través de la expresión del factor tisular, consumo de trombomodulina y disminución de los niveles de proteína C activada. Lo que evoluciona a trombosis microvascular, hipoxia e isquemia tisular y disfunción orgánica múltiple. La sepsis grave se caracteriza por una compleja interacción entre la infección, coagulación e inflamación que de no controlarse evoluciona a trombosis microvascular y disfunción orgánica múltiple.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Balk RA. Severe sepsis and septic shock. Definitions, epidemiology and clinical manifestations. Crit Care Clin 2000;16:179-192.

  2. Bone RC, Balk RA, Cerra FB, et al. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 1992;101:1644-1655.

  3. Derek CA, Walter TL, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001;29:1303-1310.

  4. Sands KE, Bates DW, Lanken PN, et al. Epidemiology of sepsis syndrome in 8 academic medical centers. JAMA 1997;278:234-240.

  5. Bone RC, Grodzin CJ, Balk RA. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest 1997;112:235-243.

  6. Brandtzaeg P, Kerrulf P, Gaustad P, et al. Plasma endotoxin as a predictor of multiple organ failure and death in systemic menigococcal disease. J Infect Dis 1989;159:195-204.

  7. Deitch EA, Goodman ER. Prevention of multiple organ failure. Surg Clin N Am 1999;79:1471-1488.

  8. Gross PL, Aird WC. The endothelium and thrombosis. Semin Thromb Hemost 2000;26:463-478.

  9. Balk RA. Pathogenesis and management of multiple organ dysfunction or failure in severe sepsis and septic shock. Crit Care Clin 2000;16:337-352.

  10. Bistrian BR. Acute phase proteins and the systemic inflammatory response syndrome. Crit Care Med 1999;27:452-453.

  11. Rangel-Frausto MS, Pittet D, Costigan M, et al. The natural history of the systemic inflammatory response syndrome (SIRS): a prospective study. JAMA 1995;273:117-123.

  12. Murphy K, Haudek SB, Thompson M, et al. Molecular biology of septic shock. New Horiz 1998;6:181-193.

  13. Heumann D, Glauser MP, Calandra T. Molecular basis of host-pathogen interaction in septic shock. Curr Opin Microbiol 1998:149-155.

  14. Van der Poll T, Levi M, Hack CE, et al. Elimination of interleukin 6 attenuates coagulation activation in experimental endotoxemia in chimpanzees. J Exp Med 1994;179:1253-1259.

  15. Pajkrt D, Van der Poll T, Levi M, et al. Interleukin-10 inhibits activation of coagulation and fibrinolysis during human endotoxemia. Blood 1997;89:2701-2705.

  16. Matot I, Sprung CL. Definition of sepsis. Intensive Care Med 2001;27 (Suppl):3-9.

  17. Nustrom PO. The systemic inflammatory response syndrome: definitions and etiology. J Antimicrob Chemother 1998;41(Suppl A):1-7.

  18. Vincent JL. Dear SIRS, I’m sorry to say that I don’t like you. Crit Care Med 1997;25:372-374.

  19. Werra I, Jaccard C, Corradin SB, et al. Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations: comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia. Crit Care Med 1997;25:607-613.

  20. Van der Poll T, Van Deventer JH. Cytokines and anticytokines in the pathogenesis of sepsis. Infect Dis Clin North Am 1999;13:413-426.

  21. Dinarello CA. Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. Chest 1997;112: 321S-329S.

  22. Bone RC. Sir Isaac Newton, sepsis, SIRS, and CARS. Crit Care Med 1996;24:1125-1129.

  23. Cines DB, Pollak ES, Buck CA, et al. Endothelial cells in physiology and in the pathophysiology of vascular disorders. Blood 1998;91:3527-3561.

  24. Mavrommatis AC, Theodoridis T, Orfanidoui A, et al. Coagulation system and platelets are fully activated in uncomplicated sepsis. Crit Care Med 2000;28:451-457.

  25. Boldt J, Papsdorf M, Rothe A, et al. Changes of the hemostatic network in critically ill patients: is there a difference between sepsis, trauma, and neurosurgery patients? Crit Care Med 2000;28:445-450.

  26. Cerik H, Sacha Z. The endothelium in sepsis: source of and a target for inflammation. Crit Care Med 2001;29:S21-S27.

  27. Tschaikowsky K, Sagner S, Lehnert N, et al. Endothelin in septic patients: effects on cardiovascular and renal function and its relationship to proinflammatory cytokines. Crit Care Med 2000;28:1854-1860.

  28. Bombeli T, Mueller M, Haeberli A. Anticoagulant properties of the vascular endothelium. Thromb Haemost 1997;77:408-423.

  29. Young JS, Headrick JP, Berne RM. Endothelial-dependent and -independent responses in the thoracic aorta during endotoxic shock. Circ Shock 1991;35:25-30.

  30. Reidy MA, Bowyer DE. Scanning electron microscopy: morphology of aortic endothelium following injury by endotoxin and during subsequent repair. Atherosclerosis 1997;26:319-328.

  31. Mantovani A, Bussolino F, Introna M. Cytokine regulation of endothelial cell function: from molecular level to the bedside. Immunol Today 1997;18:231-240.

  32. Wang P, Wood TJ, Zhou M, et al. Inhibition of the biological activity of tumor necrosis factor maintains vascular endothelial cell function during hyperdynamic sepsis. J Trauma 1996;40:694-701.

  33. Sugano M, Tsuchida K, Makino N. High-density lipoproteins protect endothelial cells from tumor necrosis factor-alpha-induced apoptosis. Biochem Biophys Res Commun 2000;272:872-876.

  34. De Jonge E, Levi M, Van der Poll T. Coagulation abnormalities in sepsis: relation with inflammatory responses. Curr Op Crit Care 2000;6:317-322.

  35. López-Aguirre Y, Páramo JA. Endothelial cell and hemostatic activation in relation to cytokines in patients with sepsis. Thromb Res 1999;94:95-101.

  36. Nieuwland R, Berckmans RJ, McGregor S, et al. Cellular origin and procoagulant properties of microparticles in meningococcal sepsis. Blood 2000;95:930-935.

  37. Van Deventer SJ, Buller HR, Ten Cate JW, et al. Experimental endotoxemia in humans: analysis of cytokine release and coagulation, fibrinolytic, and complement pathways. Blood 1990;76:2520-2526.

  38. Schleef RR, Bevilacqua MP, Sawdey M, et al. Cytokine activation of vascular endothelium. Effects on tissue-type plasminogen activator and type 1 plasminogen activator inhibitor. J Biol Chem 1988;263: 5797-5803.

  39. Pralong G, Calandra T, Glauser MP, et al. Plasminogen activator inhibitor 1: a new prognostic marker in septic shock. Thromb Haemost 1989;61:459-462.

  40. Kidokoro A, Iba T, Fukuraga M, et al. Alterations in coagulation and fibrinolysis during sepsis. Shock 1996;5:223-228.

  41. Stefanec T. Endothelial apoptosis: could it have a role in the pathogenesis and treatment of disease? Chest 2000;117:841-854.

  42. Leclerc J, Pu Q, Corseaux D, et al. A single endotoxin injection in the rabbit causes prolonged blood vessel dysfunction and a procoagulant state. Crit Care Med 2000;28:3672-3678.

  43. Sessler C, Windsor A, Schwartz M. Circulating ICAM-1 is increased in septic shock. Am J Respir Crit Care Med 1995;151:1420-1427.

  44. Xu H, Gonzalo JA, St Pierre Y, et al. Leukocytosis and resistance to septic shock in intercellular adhesion molecule 1-deficient mice. J Exp Med 1994;180:95-109.

  45. Hack CE. Tissue factor pathway of coagulation in sepsis. Crit Care Med 2000;28:S25-S30.

  46. Zimmerman GA, Prescott SM, McIntyre TM. Endothelial cell interactions with granulocytes: tethering and signaling molecules. Immunol Today 1992;13:93-100.

  47. Kyriakides C, Austen WG Jr, Wang Y, et al. Neutrophil mediated remote organ injury after lower torso ischemia and reperfusion is selectin and complement dependent. J Trauma 2000;48:32-38.

  48. Lauw FN, Simpson AJU, Hack CE, et al. Soluble granzymes are released during human endotoxemia and in patients with severe infection due to Gram-negative bacteria. J Infect Dis 2000;182:206-213.

  49. Spaeny-Dekking EH, Hanna WL, Wolbink AM, et al. Extracellular granzymes A and B in humans: detection of native species during CTL responses in vitro and in vivo. J Immunol 1998;160:3610-3616.

  50. Tihomir Stefanec MD. Endothelial apoptosis. Chest 2000;117:841-854.

  51. Kyriakides C, Woodcock SA, Wang Y, et al. Soluble P-selectin moderated complement-dependent reperfusion injury of ischemic skeletal muscle. Am J Physiol 2000;279:C520-C528.

  52. Kyriakides C, Austen W Jr, et al. Skeletal muscle reperfusion injury is mediated by neutrophils and the complement membrane attack complex. Am J Physiol 1999;277:C1263-C1268.

  53. Seekamp A, Till GO, Mulligan MS, et al. Role of selectins in local and remote tissue injury following ischemia and reperfusion. Am J Pathol 1994;144:592-598.

  54. Wolbink GJ, Bossink AW, Groeneveld AB, et al. Complement activation in patients with sepsis is in part mediated by C-reactive protein. J Infect Dis 1998;177:81-87.

  55. Hack CE, Nuijens JH, Felt-Bersma RJ, et al. Elevated plasma levels of the anaphylatoxins C3a and C4a are associated with a fatal outcome in sepsis. Am J Med 1989;86:20-26.

  56. Hack CE, Wolbink GJ, Schalkwijk CT, et al. A role for secretory phospholipase A2 and C-reactive protein in the removal of injured cells. Immunol Today 1997;18:111-115.

  57. Lagrand WK, Visser CA, Hermens WT, et al. C-reactive protein as a cardiovascular risk factor. More than an epiphenomenon? Circulation 1999;100:96-102.

  58. Corrigan JJ, Ray WL, May N. Changes in the blood coagulation system associated with septicemia. N Engl J Med 1968;279:851-856.

  59. Vervloet MC, Thijs LG, Hack CE. Derangements of coagulation and fibrinolysis in critically ill patients with sepsis and septic shock. Semin Thromb Haemost 1998;24:33-44.

  60. McGilvray ID, Rotstein OD. Role of the coagulation system in the local and systemic inflammatory response. World J Surg 1998;22:179-186.

  61. Levi M, van der Poll T, Ten Cate H, et al. The cytokine-mediated imbalance between coagulant and anticoagulant mechanisms in sepsis and endotoxaemia. Eur J Clin Invest 1997;27:3-9.

  62. Vincent JL. Microvascular endothelial dysfunction: a renewed appreciation of sepsis pathophysiology. Crit Care 2001;5:S1-S5.

  63. Grinnell WB, Joyce D. Recombinant human activated protein C: a system modulator of vascular function for treatment of severe sepsis. Crit Care Med 2001;29:S53-S61.

  64. Esmon TC. The normal role of activated protein C in maintaining homeostasis and its relevance to critical illness. Crit Care Med 2001;5:S5-S12.

  65. Faust NS, Heyderman SR, Levin M. Coagulation in severe sepsis: a central role for thrombomodulin and activated protein C. Crit Care Med 2001;29:S62-S68.

  66. Yan SB, Dhainaut JF. Activated protein C versus protein C in severe sepsis. Crit Care Med 2001;29:S69-S74.

  67. Gordon B, Artigas A, Dellinger P, Esmon TC, et al. Clinical expert round table discussion at the Margaux Conference on Critical Illness: the role of activated protein C in severe sepsis. Crit Care Med 2001;29:S75-S77.

  68. Fisher JC, Yan BS. Protein C levels as a prognostic indicator of outcome in sepsis and related diseases. Crit Care Med 2000;28: S49-S56.

  69. Kanji S, Devlin WJ, Piekos AK, et al. Recombinant human activated protein C, drotrecogin alfa (activated): a novel therapy for severe sepsis. Pharmacotherapy 2001;21:1389-1402.




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