World journal of surgery
-
World journal of surgery · May 1996
ReviewRole of the gut in multiple organ failure: bacterial translocation and permeability changes.
It is clear that increased gut permeability and bacterial translocation play a role in multiple organ failure (MOF). Failure of the gut barrier remains central to the hypothesis that toxins escaping from the gut lumen contribute to activation of the host's immune inflammatory defense mechanisms, subsequently leading to the autointoxication and tissue destruction seen in the septic response characteristic of MOF. However, the role of the gut is more than that of a sieve, which simply allows passage of bacteria and endotoxin from the gut lumen to the portal or systemic circulation. ⋯ A vicious cycle of increased intestinal permeability, leading to toxic mediator release, resulting in a further increase in gut permeability is generated. Additionally, the systemic and local inflammatory cells that become activated in the gut contribute to the systemic response characteristic of the sepsis syndrome and MOF. Thus even if the immune inflammatory system, rather than the gut, is the "motor of" MOF, the gut remains one of the major pistons that turns the motor.
-
Multiple organ failure (MOF) is considered to be the leading cause of death after severe trauma. Although there is extensive literature on MOF, little is known about the pattern, sequence, and onset of this clinical syndrome. The first goal of this clinical study was to define MOF; the second was to assess the typical onset, sequence, and pattern of MOF; and the third was to define certain risk factors for the development of MOF in 342 multiple trauma patients. ⋯ Significant renal failure and the need for dialysis decreased to < 5%; other signs of organ dysfunction (gastric, central nervous system) are difficult to verify. Typical risk factors for the development of MOF after severe trauma are the severity, type, and distribution of injury as well as the indicators of prolonged hemorrhagic shock (elevated lactate levels). The main therapeutic efforts, therefore, should be the effective treatment of traumatic hemorrhagic shock during the initial phase, adequate resuscitation, optimal oxygenation, and early surgical treatment.
-
World journal of surgery · May 1996
ReviewEarly risk factors for postinjury multiple organ failure.
Epidemiologic studies, based on retrospective data from heterogeneous populations with poor control of confounders, led early investigators to conclude that infection was the overriding risk factor for multiple organ failure (MOF). More recent studies have convincingly shown that MOF frequently occurs in the absence of infection. ⋯ Trauma also permits a clear distinction between the first insult and the outcome, both temporally and with respect to the definition criteria. In this review we discuss the background, rationale, and our initial attempts to use indicators of the first insult (i.e., tissue injury quantification and clinical signs of shock) and indicators of the host response (i.e., systemic inflammatory response syndrome) to predict MOF early after injury.
-
Mediators play a key role in the development of systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome, and multiple organ failure of vital organs. In this short review, we update our knowledge on these mediator networks. First, we summarize the stimuli that occur during severe trauma (intraoperative stress), including polymorphonuclear neutrophil-derived tissue-damaging substances, complement activation products, and adherence molecules such as selectins. ⋯ Second, we describe the mediators, including cytokines, nitric oxide, phospholipase A2, platelet-activating factor, and procoagulatory substances, that are released during sepsis. The release of mediators depends primarily on the severity of the trauma, shock, or sepsis and secondarily on the activation of the various cascades of mediators during posttraumatic/postoperative complications. The mediators are thus of decisive importance regarding the intensity of organ damage and the outcome.
-
Progress in the care of the critically ill patient with life-threatening infection has been hampered by inconsistent, often confusing terminology. The clinical syndrome of sepsis-familiar to all yet definable by none-describes a highly heterogeneous group of disorders with different causes and differing prognoses. The imminent availability of mediator-directed therapy has created a sense of urgency to develop better methods for delineating discrete clinical syndromes and to modulate the host response, which may bring both benefit and harm, depending on the clinical circumstances. ⋯ The development of cogent conceptual frameworks for classification of the septic response in critically ill patients is more than a question of linguistic pedantry. Optimal therapy presupposes identification of an homogeneous patient population with a characteristic disease process and a predictable response to an intervention. Although progress has been made in identifying such groups of critically ill patients, the disappointing results of clinical trials of agents that so clearly demonstrate efficacy in animal models indicates that considerable work remains.