2004, Número 6
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Rev Fac Med UNAM 2004; 47 (6)
Sepsis. Conceptos actuales (Primera de tres partes)
Carrillo ER, Carvajal RR
Idioma: Español
Referencias bibliográficas: 40
Paginas: 238-245
Archivo PDF: 109.54 Kb.
RESUMEN
La sepsis es la respuesta inflamatoria sistémica a la infección y es una de las principales causas de ingreso a las unidades de terapia intensiva. Se asocia a una elevada mortalidad. Es secundaria a la interacción de la respuesta inmune innata con microorganismos, lo que resulta en daño endotelial y coagulopatía que puede evolucionar a trombosis microvascular, hipoxia y disfunción orgánica múltiple. El diagnóstico temprano y oportuno es fundamental. El tratamiento está dirigido al control del disparador, al empleo racional de antibióticos, reanimación temprana y agresiva, control metabólico y otras medidas de sostén. La proteína C activada recombinante humana disminuye significativamente la mortalidad y está indicada en pacientes con sepsis grave que presenten APACHE II > 25 puntos, choque séptico y disfunción orgánica múltiple.
REFERENCIAS (EN ESTE ARTÍCULO)
Increase in National Hospital Discharge Survey rates for septicemia-United States, 1979-1987. MMWR Morb Mortal Wkly Rep. 1990; 39:31-34.
Angus DC, Wax RS. Epidemiology of sepsis: an update. Crit Care Med 2001; 29:109-116.
Angus DC, Linde-Zwirble WT, Lidicker J 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.
Bone RC. The sepsis syndrome: definition and general approach to management. Clin Chest med 1996; 17: 75-82.
Society of Critical Care Medicine Consensus Conference Committee. American Conference: definitions for sepsis and organ failure and guidelines of the use of innovative therapies in sepsis. Crit Care Med 1992; 20: 864-874.
Abraham E, Matthay MA, Dinarello CA et al. Consensus conference definitions for sepsis, septic shock, acute lung injury, and acute respiratory distress syndrome: time for a reevaluation. Crit Care Med 2000; 28: 232-235.
Levy MM, Fink MP, Marshall JC et al. 2001 SCCM/ESICM/ATS/SIS International Sepsis Definitions Conference. Crit Care Med 2003; 31: 1250-1256.
Vincent JL, Wendon J, Groeneveld J et al. The PIRO concept: O is for organ dysfunction. Crit Care Med 2003; 3: 260-264.
Opal M. Severe sepsis and septic shock: defining the clinical problem. Scand J Infect Dis 2003; 9: 529-534.
Carrillo ER, Nuñez FN. Systemic inflammatory response syndrome: new concepts. Gac Med Mex 2001; 137: 127-134.
Carrillo ER. Modulación genética de la respuesta inflamatoria sistémica en sepsis. Rev Asoc Mex Med Crit Int 2001; 15: 92-95.
Janeway JCA, Medzhitov R. Introduction: the role of innate immunity in the adaptive innate response. Semin Immunol 1998; 10: 349-350.
Carrillo ER, González JA. Inflamación–endotelio–coagulación en sepsis. Conceptos actuales. Cir Ciruj 2002; 70: 433-441.
Carrillo ER. Inmunidad innata, receptores Toll y sepsis. Cir Ciruj 2003; 71: 252-258.
Cines DB, Pollak ES, Buck CA et al. Endothelial cells in physiology and in the pathophysiology of vascular disorders. Blood 1998; 91: 3527-3561.
Cerik H, Sacha Z. The endothelium in sepsis: source of and a target for inflammation. Crit care med 2001; 29: S21-S27.
Mavrommatis AC, Theodoridis T, Orfanodoui A et al. Coagulation system and platelets are fully activated in uncomplicated sepsis. Crit Care Med 2000; 28: 451-457.
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.
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.
López-Aguirre Y, Páramo JA. Endothelial cell and hemostatic activation in relation to cytokines in patients with sepsis. Thromb Res 1999; 94: 95-101.
Vervloet MG, Thijs LG, Jack CE. Derangements of coagulation and fibrinolysis in critically ill patients with sepsis and septic shock. Semin Thromb Hemost 1998; 24: 33-44.
Marshall JC. Inflammation, coagulopathy, and the pathogenesis of multiple organ system. Crit Care Med 2001; 29: S99-S106.
Sessler C, Windsor A, Scwartz M. Circulating ICAM-1 is increased in septic shock. Am J Respir Crit Care med 1995; 151: 1420-1427.
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.
Zimmerman GA, Prescott SM, McIntyre TM. Endothelial cell interactions with granulocytes: tehtehring and signaling molecules. Immunol Today 1992; 13: 93-100.
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.
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.
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.
Corrigan JJ, Ray WL, May N. Changes in the blood coagulation system associated with septicemia. N Engl J Med 1968; 279: 851-856.
McGilvray ID, Rotstein OD. Role of the coagulation system in the local and systemic inflammatory response. World J Surg 1998; 22: 179-186.
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.
Yan SB, Dhainaut JF. Activated protein C versus protein C in severe sepsis. Crit Care Med 2001; 29: S69-S74.
Gordon B, Artigas A, Dellinger P 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.
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.
Balk RA. Pathogenesis and management of multiple organ dysfunction or failure in severe sepsis and septic shock. Crit Care Clin 2000; 16: 337-352.
Bistrian BR. Acute phase proteins and the systemic inflammatory response syndrome. Crit Care Med 1999; 27: 452-453.
Heumann D, Glauser MP, Calandra T. Molecular basis of host-pathogen interaction in septic shock. Curr Opin Microbiol 1998: 149-155.
Vincent JL, Bihari DJ, Suter PM et al. The prevalence of nosocomial infection in intensive care units in Europe. Results of the european prevalence of infection in intensive care (EPIC) study. EPIC International Advisory Commitee. JAMA 1995; 274: 639-644.
Vincent JL, Anaissie E, Bruining H et al. Epidemiology, diagnosis and treatment of systemic candida infection in surgical patients under intensive care. Int Care Med 1998; 24: 206-216.
Richards MJ, Edwards JR, Culver DH et al. National Nosocomials Infections Surveillance System: Nosocomial Infections in Medical Intensive Care Units In The United States. Crit Care Med 1999; 27: 887-892.