2015, Number 2
PDF size: 200.16 Kb.
ABSTRACTBackground: Elevated concentrations of C3a, has been found in patients with severe sepsis and septic shock. Objective: To investigate the value of C3 in survivors and non-survivors patients with diagnosis of septic shock and survival at 28 days.
Material and methods: Prospective, longitudinal, observational and comparative study, we included 14 patients with septic shock.
Results: 43% men and 57% women. Among survivors and non survivors patients the mortality for APACHE II was 40% in survivors and 55% non-survivors (p = 0.01), serum C3 was 69 mg/dL and 30 mg/dL in survivors and non-survivors respectively (p = 0.0001), lactate levels was 2 mmol/L and 4.1 mmol/L in survivors and non-survivors respectively (p = 0.03), finally the SvcO2 was 72 and 65% in survivors and non-survivors patients respectively (p = 0.04). Lactate levels among patients with C3 greater than 30 mg/dL was 1.9 and 4.1 (p = 0.05), SvcO2 was 74 and 56% (p = 0.03) among survivors and non-survivors respectively. All patients with C3 values less than 30 mg/dL died.
Conclusions: There is a high consumption of C3 in patients with septic shock in both groups being much higher in the latter group. C3 levels less than 30 mg/dL are presented in non-survivors patients.
Carrillo ER. El reto en sepsis. Cir Ciruj. 2005;73:77-78.
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;101:1644-1655.
Sands KE, Bates DW, Lanken PN, et al. Epidemiology of sepsis syndrome in 8 academic medical centers. JAMA. 1997;278:234-240.
Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated cost of care. Crit Care Med. 2001;29(7):1303-1310.
Annane B, Bellisant E, Cavaillon JM. Septic shock. Lancet. 2005;365:63-78.
Meakins JL, Pietsch JB, Bubenick O, et al. Delayed hypersensitivity: indicator of acquired failure of host defenses in sepsis and trauma. Ann Surg. 1977;186:241-249.
Ledere JA, Rodrick ML, Mannick JA. The effects of injury on the adaptative immune response. Shock. 1999;11:153-159.
Oberholzer A, Oberholzer C, Moldawer LL. Sepsis syndromes: understanding the role of innate and acquired immunity. Shock. 2001;16:83-96.
Nodlin RL, Brightbill HD, Godowski PJ. The toll of innate immunity on microbial pathogens. N Engl J Med. 1999;340:1834-1835.
Brown MA, Jones WK. NF-kappa B action in sepsis: the innate immune system and the heart. Front Biosci. 2004;9:1201-1217.
Abbas AK, Murphy KM, Sher A. Functional diversity of helper T lymphocytes. Nature. 1996;383:787-793.
Hotchkiss RS, Tinsley KW, Swanson PE, et al. Sepsis-induced apoptosis causes progressive profound depletion of B and CD4+ T lymphocytes in humans. J Immunol. 2001;166:6952-6963.
Ertel W, Kremer JP, Kenney J. Downregulation of proinflammatory cytokine release in whole blood from septic patients. Blood. 1995;85:1341-1347.
Leibovici L, Shraga I, Drucker M, Konigsberger H, Samra Z, Pitlik SD. The benefit of appropriate empirical antibiotic in patients with bloodstream infection. J Intern Med. 1998;244:379-386.
Ranieri VM, Suter PM, Tortorella C, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1999;282:54-61.
Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med. 2003;348:138-150.
Creasey AA, Reinhart K. Tissue factor pathway inhibitor activity in severe sepsis. Crit Care Med. 2001;29 Suppl. 7:S126-S129.
Liaw PC, Esmon CT, Kahnamoui K, et al. Patients with severe sepsis vary markedly in their ability to generate activated protein C. Blood. 2004;104:3958-3964.
Dellinger PR, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41:580-637.
Rivers E, Nguyen B, Haystad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-1377.
Reinhart K, Meisner M, Brunkhorst FM. Markers for sepsis diagnosis: what is useful? Crit Care Clin. 2006;22:503-519.
Haeney MR. The role of the complement cascade in sepsis. J Antimicrobe Chemother. 1998;41:41-46.
Walport MJ. Complement first of two parts. N Engl J Med. 2001;344:1058-1066.
Ortega MA, Membreño JP, Poblano MM, Aguirre J, Martínez J. Es útil el BNP como factor pronóstico en pacientes sépticos. Rev Asoc Mex Med Crit y Ter Int. 2008;22(2):66-73.
Monneret G, Venet F, Pachot A, Lepape A. Monitoring immune dysfunctions in the septic patient: a new skin for old ceremony. I Mol Med. 2008;14:64-78.
Selberg O, Hecker H, Martin M, Klos A, Bautsch W, Köhl J. Discrimination of sepsis and systemic inflammatory response syndrome by determination of circulating plasma concentrations of procalcitonin, protein complement C3, and interleukin-6. Crit Care Med. 2000;28:2793-2798.
Stove S, Welte T, Wagner TO, et al. Circulating complement proteins in patients with sepsis or systemic inflammatory response syndrome. Clin Diagn Lab Inmunol. 1996;3:175-183.
Charchaflieh J, Wel J, Labaze G, et al. The role of complement system in septic shock. Clin Dev Inmunol. 2012;23:1-8.