2013, Number 5
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Med Int Mex 2013; 29 (5)
Mitochondrial Dysfunction as an Explanation for the Multiple Organic Dysfunction in Sepsis Syndrome
Duarte-Mote J, Domínguez HI, Vega HC, Lee Eng CV, Romero FS, Espinosa LR, Sánchez RG
Language: Spanish
References: 45
Page: 504-512
PDF size: 231.32 Kb.
ABSTRACT
Sepsis is still the leading cause of death in intensive care
units. New therapeutic approach based on goals achieved
to reduce the mortality rate, however continues to be high.
During the evolution of the septic process, the systemic
inflammatory response and metabolic response to trauma
form the two main responses of compensatory type with
which the organism is faced with sepsis. The different phases
of the metabolic response to trauma denote different stages
of organic adaptation, which often first evolves to a phase
of multiple organ dysfunction and then a multiple organic
failure. Basal energy expenditure in patients with sepsis is
greatly diminished at the stage corresponding to multiple
organ dysfunction. At this stage, the functional alterations
that are observed are secondary to disoxia and decrease in the
production of energy at the mitochondrial level. This phase of
dysfunction is thought to be an adaptive phase of the body
with the purpose of preserving the organic cell structure. In
this article, we reviewed the mitochondrial alterations that
are observed during the phase of multiple organ dysfunctions,
its relationship with the therapeutic approach and the
importance in mortality of these patients.
REFERENCES
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; 29:1303-10.
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368-77.
Dellinger RP, Levy MM, et al. Surviving Sepsis Campaign: International Guidelines for management of Severe Sepsis and Septic Shock: 2012. Crit Care Med 2013; 41:580-637.
Ait-Oufella H. The endothelium: physiological functions and role in microcirculatory failure during severe sepsis - Intensive Care Med 2010; 36(8):1286-98.
Namas R, Zamora R. Sepsis: Something old, something new, and a systems view. J Crit Care 2012;27:314. e1–314.e11
Fink MP. Cytopathic hypoxia: mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis. Crit Care Clin 2001;17:219-237.
Lavery GG, Glover P. The metabolic and nutritional response to critical illness. Curr Opin Crit Care 2000;6:233- 238.
Balestra GM. Microcirculation and mitochondria in sepsis: getting out of breath. Curr Opin Anaesthesiol 2009;22:184-90.
Hotchkiss RS, Karl IE. Reevaluation of the role of cellular hypoxia and bioenergetics failure in sepsis. JAMA 1992;267:1503-1510.
Brealey D, Karyampudi S, Jacques TS, et al. Mitochondrial dysfunction in a long term rodent model of sepsis and organ failure. Am J Phys 2004;286:R491-497.
Lopez LC, Escames G, Ortiz F, et al. Melatonin restores the mitochondrial production of ATP in septic mice. Neuro Endocrinol Lett 2006;27: 623-630.
Shapiro NI, Howell MD, Bates DW et al. The association of sepsis syndrome and organ dysfunction with mortality in emergency department patients with suspected infection. Ann Emerg Med 2006; 48: 583-90.
Reinhart K, Meisner M, Hartog C. Diagnosis of sepsis: Novel and conventional parameters. Adv Sepsis 2001; 1: 42-48.
Lemieux C, Maliba R, Favier J et al. Angiopoietins can directly activate endothelial cells and neutrophils to promote proinflammatory responses. Blood 2005; 105: 1523-1530.
Rangel-Frausto M. The natural history of the systemic inflammatory response syndrome (SRIS): a prospective study. JAMA 1995; 273: 117-23.
Hennein HA, Ebba H, Rodríguez JL et al. Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization. J Thorac Cardiovasc Surg 1994; 108: 626-35.
Casey LC. Role of cytokines in the pathogenesis of cardiopulmonary induced multisystem organ failure. Ann Thorac Surg 1993; 56: S92-S96.
Marrie TJ, Lau CY, Wheeler SL et al. A controlled trial of a critical pathway for treatment of community-acquired pneumonia. JAMA 2000; 283: 749-755.
Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med 2001; 344: 699-709.
Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004; 32: 1637-1642.
Ruggieri AJ, Mitochondrial dysfunction and resuscitation in sepsis. Crit Care Clin 2010;26:567-575.
Elbers PW, Ince C. Bench-to-bedside review: mechanisms of critical illness classifying microcirculatory flow abnormalities in distributive shock. Crit Care Clin 2006;10: 221-227.
Fink MP. Bench-to-bedside review: cytopathic hypoxia. Crit Care Clin 2002; 6: 491-99.
Brealey D, Brand M, Hargreaves L, et al. Association between mitocondrial dysfunction and severity and outcome of septic shock. Lancet 2002;360:219-223.
Clementi E, Brown GC, Feelisch M, et al. Persistent inhibition of cell respiration by nitric oxide: crucial role of S-nitrosylation of mitochondrial complex I and protective action of glutathione. Proc Natl Acad Sci U S A 1998; 95: 7631-7636.
Verma R, Huang Z, Deutschman CS, et al. Caffeine restores myocardial cytochrome oxidase activity and improves cardiac function during sepsis. Crit Care Med 2009; 37: 1397-1402.
Zivadinovic D, Marjanovic M, Andjus RK. Some components of hibernation rhythms. Ann N Y Acad Sci 2005; 1048: 60-68.
Barcroft H, Allen WJ, Anderson DP, et al. Circulatory changes during fainting and coma caused by oxygen lack. J Physiol 1946; 104: 426-434.
Casserly B, Read R, Levy M. Hemodynamic monitoring in sepsis. Crit Care Clin 2009;25: 803-823.
Bauer P, Reinhart K, Bauer M. Significance of venous oximetry in the critically ill. Med Intensiva 2008; 32:134- 142.
Polonen P, Ruokonen E, Hippelaäinen M, et al. A prospective, randomized study of goal-oriented hemodynamic therapy in cardiac surgical patients. Anesth Analg 2000;90:1052-1059.
Kantrow SP, Tatro LG, PiantidosiCA. Oxidative stress and adenine nucleotide control of mitochondrial permeability transition. Free Radic Biol Med 2000; 28:251-260.
Levy RJ. Mitochondrial dysfunction, bioenergetic impairment, and metabolic down-regulation in sepsis. Shock 2007; 28: 24-28.
Hoffman DL, Brookes PS. Oxygen sensitivity of mitochondrial reactive oxygen species generation depends on metabolic conditions. J Biol Chem 2009;284:236-245.
Levy RJ, Vijayasarathy C, Raj NR, et al. Competitive and noncompetitive inhibition of myocardial cytochrome C oxidase in sepsis. Shock 2004; 21:110-114.
Fredriksson K, Hammarqvist F, Strigard K, et al. Derangements in mitochondrial metabolism in intercostal and leg muscle of critically ill patients with sepsis induced multiple organ failure. Am J Phys 2006; 291: E1044-45.
Kreymann G, Grosser S, Buggisch P, et al. Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock. Crit Care Med 1993;21:1012- 1019.
Zauner C, Schuster BI, Schneeweiss B. Similar metabolic responses to standardized total parenteral nutrition of septic and nonseptic critically ill patients. Am J Clin Nutr 2001; 74: 265-270.
Hoher JA, Zimermann Teixeira PJ, Hertz F, et al. A comparison between ventilation modes: how does activity level affect energy expenditure estimates? JPEN J Parenter Enteral Nutr 2008; 32: 176-183.
Van den Berghe G. Novel insights into the neuroendocrinology of critical illness. Eur J Endocrinol 2000; 143: 1-13.
Reid CL, Campbell IT, Little RA. Muscle wasting and energy balance in critical illness. Clin Nutr 2004; 23: 273-280.
Mongardon N. The evolutionary role of nutrition and metabolic support in critical illness. Crit Care Clin 2010;26: 443-450.
Brealey D, Brand M, Hargreaves I, et al. Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet 2002;360:219-223.
Hayes MA, Timmins AC, Yau EH, et al. Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 1994; 330: 1717-1722.
BayIr H, Kagan V. Bench-to-bedside review: Mitochondrial injury, oxidative stress and apoptosis-there is nothing more practical than a good theory. Critical Care 2008; 12:206-217.