Fighting the multi organ failure

Abstract

Introduction: Multiple organ failure is the commonest cause of death in the intensive care unit setting. There are numerous precipitating factors including sepsis, trauma and pancreatitis. The resulting tissue hypoxia, exaggerated inflammatory response and generation of free oxygen radicals leads to tissue damage and organ dysfunction. No definitive treatment exists despite considerable efforts to find a 'magic bullet’. Management still revolves around support of organ function and prevention of iatrogenic complications until recovery occurs. An increasing emphasis is being placed on prevention of organ dysfunction, including maintenance of tissue oxygenation, nutrition and infection control. Multiple organ failure (MOF) is the commonest cause of death in the intensive care unit (ICU). A clinical assessment of a high likelihood of irreversible organ failure, particularly when multiple organs are involved, is the usual factor prompting a decision to withdraw treatment or not to add further therapy. Sepsis is one precipitating factor for MOF; numerous other causes of tissue damage are well recognized, e.g. trauma, burns and pancreatitis. No definitive treatment exists and controversy surrounds many aspects of the management of MOF. Problems include (i) a shortage of major multi-center, controlled studies in a well-defined patient population (other than immunotherapy trials which are often of flawed design), (ii) an inclination to use unproved interventions,(iii) over-extrapolation of data from laboratory studies,(iv) an often uncritical acceptance of simplified, schematic representations of inflammatory mechanisms, (v) variable disease syndrome definitions and (vi) diagnostic imprecision. The above contribute to the current lack of hardened-fast rules regarding patient management; instead, there are a number of generally accepted guidelines which still provide considerable scope for treatment variability. Examples of current grey areas include selective gut decontamination, extracorporeal respiratory support and prophylaxis against stressulcer-related bleeding. There is also the widespread, though as yet unproven and unlicensed, use of nitric oxide inhalation in acute lung injury, and the quest for a single ‘magic bullet’ to ameliorate the generalized, exaggerated inflammatory response associated with severe sepsis. In the case of the strongly promoted concept of ‘supranonnalizing’ hemodynamic parameters in the critically ill patient, whereby elevated values of cardiac output, oxygen delivery and oxygen consumption were striven for, it was several years before this approach was shown to be ineffective. Nevertheless, and despite the above caveats, there has been progress in several areas. A better, though still incomplete, insight is being gained into the pathophysiological mechanisms underlying the exaggerated inflammatory response that frequently underlies MOF. There is a greater appreciation of the need to prevent organ dysfunction by optimizing the circulation and avoidance or rapid correction of tissue hypoxia in high-risk patients. There is are cognition of the importance of standard definitions, for example sepsis, the systemic inflammatory response syndrome (SIRS), the multiple organ dysfunction syndrome (MODS) , the acute respiratory distress syndrome (ARDS) and acute lung injury. There is also a recognized need to improve the description of organ dysfunction. In addition, general advances and the increasing availability of intensive care, superior ‘whole body’ organ suppoit, appropriate infection control, nutrition and pressure area care, and avoidance of iatrogenic pulmonary barotrauma, have all contributed to improvements in outcome. Objective: To determine whether translocation of bacteria or endotoxin occurred into the thoracic duct in patients with multiple organ failure (M OF) is take active role in MOF. Methods: 1. Meta-analysis of 156 patients from retrospective - preview date base of patients in MOF. 2. The thoracic duct was drained for 5 days in patients with MOF caused either by generalized fecal peritonitis (n = 4) or by an event without clinical and microbiologic evidence of infection (n = 4). Patients without MOF who were undergoing a transthoracic esophageal resection served as controls. In lymph and blood, concentrations of endotoxin, proinflammatory cytokines, and anti-inflammtory cytokines were measured. Experimental data: Description - in heart of Mousses, was examined the function of heart (in vitro), in 3 state: 1. Normal without intervention. (Control group). 2. With lymph of MOF state. 3. With MOF state + thoracic duct ligation. Conclusion: This meta-analysis study provides evidence that translocation (especially of endotoxin) occurs into the thoracic duct. These data do support the concept that the thoracic duct is a major route of bacterial translocation in patients with MOF.