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At least 19 recordsLinked to original sources

PubMed1994

Multiple organ failure, multiple organ dysfunction syndrome, and the systemic inflammatory response syndrome-where do we stand?

Multiple organ failure, multiple organ dysfunction syndrome, and the systemic inflammatory response syndrome are problems of medical progress and intensive care units (ICUs) and require prevention of organ failure through excellent patient care. New concepts in prevention include: 1) the need to improve microcirculatory blood flow (Mbf) early after injury or illness, 2) stopping or controlling injury or infection by early definitive operation when necessary, 3) a zero defect operation is necessary, 4) necrotic tissue and an overwhelming inflammatory burden are problems and should be lessened when possible, 5) adequate resuscitation to improve Do2, Vo2, and organ blood flow is necessary, 6) supporting metabolism and the GI tract may decrease complications of injury and sepsis, 7) support of host defense and/or immunomodulation to decrease the incidence of sepsis, and 8) treating the patient and the illness or injury, not just the mediators. Experimental evidence in animals and human volunteers for concepts, mechanisms, and treatment of injury or illness can be substantial and persuasive, but it may be difficult to demonstrate efficacy in sick patients. Clinical situations are variable and complex. It is difficult to dissect out, identify, and control or block a single factor or mediator. All biologic processes require a level of activity that can be hazardous in excess but dangerous if decreased or eliminated. Stimulation of our natural defense or control mechanisms of inflammation, replacement of lost or decreased factors, and better understanding of the interrelationships and mechanisms of inflammation will contribute to therapy. Whether blockade of mediators or treatment of the manifestations of diseases or injuries will have substantial impact remains to be learned. A single magic bullet for complex and diverse illnesses is not likely to appear or to be successful. In this review it was not possible to describe many of the observations and recommendations in this immense and complex field. I apologize to those whose work I have inadvertently not included.

Humans↗

PubMed1997

Multiple organ failure, multiple organ dysfunction syndrome, and systemic inflammatory response syndrome. Why no magic bullets?

The concept of multiple organ failure and related abnormalities was first developed in the 1970s. Multiple organ failure became evident when the support systems in intensive care units were able to keep patients alive long enough for multiple organ problems to develop in them. The high mortality of patients with multiple organ failure provided a focus for the problems that ultimately led to death for many patients in the intensive care unit. The frequency of infection, sepsis, or inflammation in producing multiple organ failure led to clinical trials of so-called magic bullets for the treatment of patients with sepsis. These trials have had either limited success or negative results, despite considerable evidence for efficacy or protection by such agents in experimental animals and in studies of normal human volunteers. I believe a major reason for these negative results has been the use of general entry criteria for the trials rather than the treatment of specific diseases or injuries.

Humans↗

PubMed1993

Multiple organ failure.

Multiple organ failure remains a leading cause of death in surgical intensive care units. This review of multiple organ failure focuses on recent (1990 to 1992) laboratory and clinical advances related to diagnosis, prognosis, and therapy of multiple organ failure and is divided into three parts. First, it recasts multiple organ failure into the currently accepted terminology, ie, the multiple organ dysfunction syndrome. Second, it examines the strengths and weaknesses of three mechanistic hypotheses proposed for the clinical syndrome. The three hypotheses focus on the gut, molecular mediators, and the microvasculature. Third, it synthesizes those three mechanisms into a single paradigm; this unifying paradigm can serve as a framework in which to interpret subsequent laboratory and clinical advances.

Bacterial Toxins↗

PubMed1992

[Multiple trauma: definition, shock, multiple organ failure].

Multiple organ failure (MOF) following major trauma occurs in response to perfusion deficits, a persistent inflammatory focus, or a persistent focus of dead and/or injured tissue. Several pathophysiologic aspects are considered relevant to current clinical practice. Their application in settings of trauma and surgical sepsis reduces overall mortality and incidence of multiple organ failure. With regard to the pathophysiologic background (I) microcirculatory resuscitation, (II) source control, and (III) metabolic support appear to be important therapeutic principles. (I) Microcirculatory Resuscitation: Since time is a critical factor in damage control, resuscitation and restoration of microvascular perfusion needs to occur as soon as possible if multiple system organ failure is to be avoided during the later time course. (II) Source control: The best treatment for multiorgan failure appears to be prevention. With early, aggressive control or removal of risk factors for multiple organ failure, namely early surgical intervention for control of hemorrhage, control of potential septic sources, decompression, and early fracture stabilization reductions in the incidence and mortality of MOF have been observed. Metabolic support: Malnutrition appears to be an important cofactor in morbidity and mortality. (III) Metabolic support needs to be started early and prior to the phenomenon of nitrogen retention during the hypermetabolic state of multiple organ failure.

Humans↗

PubMed2002

Adenosine: a potential mediator of immunosuppression in multiple organ failure.

Multiple organ failure following a variety of insults, including, trauma, shock and pancreatitis, is the cause of 50-80% of all deaths in surgical intensive care units. In most patients, infections secondary to a general immunosuppressive state serve to trigger the development of multiple organ failure. This immunosuppressive state may be a consequence of excessive release of adenosine into the extracellular space, as adenosine has multiple immunosuppressive effects. Activation of adenosine receptors on immune cells inhibits the production of proinflammatory cytokines such as tumor necrosis factor alpha and interleukin (IL)-12, and increases the production of the anti-inflammatory cytokine IL-10. In addition, adenosine receptor activation appears to suppress cellular immunity by decreasing T helper cell (Th)1 and increasing Th2 responses. A deeper understanding of the role of adenosine in multiple organ failure may facilitate the development of adenosine-based therapeutic strategies.

Adenosine↗

PubMed1996

Prevention and therapy of multiple organ failure.

Multiple organ failure (MOF) stems from a complex interaction between the host's immune response and inadequate tissue perfusion. Prevention of MOF therefore addresses these two components. The risk of inflammation is reduced through treatment of any infection and early stabilization of traumatized regions. Adequate respiratory and cardiocirculatory resuscitation is achieved to restore and maintain tissue perfusion. Although a supranormal cardiac output is often indicated, it is difficult to define precise endpoints for hemodynamic stabilization. Instead of increasing the oxygen supply to supranormal values in all patients, it is probably safer and more effective to increase it only in those patients for whom persistent ischemia is suspected. Provision of adequate nutritional support is important, and whenever possible the enteral route is preferred. Once MOF has developed, treatment turns to support of individual organs. Unfortunately, there is no single treatment for MOF that seems to reverse the associated trend of high mortality. Survival is more likely when the cause of MOF can be found and eliminated.

Combined Modality Therapy↗

PubMed1992

Superoxide dismutase and catalase in an experimental model of multiple organ failure.

Multiple organ failure (MOF) can be induced by sterile intraperitoneal injection of zymosan in the rat. This results in a typical triphasic illness with maximal clinical signs at Days 2 and 12. In this model, superoxide production and lipid peroxidation closely correlate with the triphasic clinical illness. In the present experiment we studied the effect of albumin conjugated superoxide dismutase (SOD) and catalase (CAT) on lipid peroxidation and organ damage in the acute phase (Days 1 and 2). Lipid peroxidation in plasma was significantly decreased by SOD and CAT but clinical condition, mortality, and organ damage did not improve. We conclude that oxygen radical damage is not a key factor in the pathogenesis of the acute phase of multiple organ failure.

Animals↗

PubMedDate not supplied

Levels of soluble adhesion molecules and cytokines in patients with septic multiple organ failure.

Multiple organ failure (MOF) is a common complication of sepsis or septic shock. In this condition, it is believed that activated neutrophils adhere to the vascular endothelium and induce various mediators and tissue damage, leading to organ damage. We investigated the plasma levels of inflammatory cytokine activating neutrophils, soluble adhesive molecules, and endotoxin in 8 patients with septic MOF, 15 patients with sepsis but without MOF, and in 5 patients with MOF unrelated infection. The soluble intercellular adhesion molecule-1 (sICAM-1) concentration in sepsis-complicated groups was significantly higher than that in the multiple organ failure (MOF) group without infection. Of sepsis-complicated groups, the sICAM-1 value in the MOF group was significantly higher than that in the sepsis group without MOF. In sepsis-complicated groups, both soluble endothelial-leukocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) concentrations were significantly higher than those in the MOF group without infection. However, there was no significant difference between the septic MOF group and the sepsis group without MOF. In patients showing high levels of soluble adhesion molecule, prognosis was poor, and the concentration of soluble adhesion molecules rapidly decreased during recovery from MOF. It is speculated that endotoxin and inflammatory cytokines damage vascular endothelium as well as various other cells and produce, a large number of adhesion molecule, especially in patients with septic MOF, causing leakage of adhesion molecules into blood.

Adult↗

PubMed1994

Splanchnic ischaemia and its role in multiple organ failure.

Multiple organ failure remains the leading cause of death in the intensive care unit. Increasing numbers of investigators have focused their attention on the role of gastrointestinal tract in the pathogenesis of this syndrome. Their data indicate that inadequate gut perfusion leads to a measurable imbalance between oxygen delivery and the needs of the tissues, i.e., ischaemia. Gut ischaemia of sufficient duration impairs gastrointestinal tract barrier function, facilitating the passage of enteric bacterial endotoxin into the circulation. It has been hypothesized that production of tumor necrosis factor alpha, and other biologic mediators by endotoxin-stimulated macrophages, triggers a generalized and uncontrolled inflammatory response that ultimately leads to multiple organ failure. Preliminary evidence suggests that survival can be improved significantly if gut ischaemia is promptly identified and aggressively treated by administration of fluids and inotropic drugs, using gastric intramucosal pH as the therapeutic endpoint. Future studies are needed to determine whether additional treatment modalities can improve outcome once the inflammatory response has fully developed.

Cardiopulmonary Bypass↗

PubMed1996

Serum phospholipase A2 in patients with multiple organ failure.

Multiple organ failure (MOF) is the most common cause of death in the surgical intensive care unit. We studied the relation of MOF to changes in the concentration of group II phospholipase A2 (PLA2) in serum. Altogether, 215 surgical intensive care patients with multiple injuries, diffuse peritonitis, or sepsis and control patients, who were at a high risk for postoperative sepsis after various surgical interventions, were included in the present prospective study. The clinical performance of the MOF score and the concentrations of group II PLA2 and C-reactive protein (CRP) in serum were studied using receiver operating characteristic (ROC) curves. The group II PLA2 level was considerably above normal in all groups of patients during the first week of observation. There was a highly significant difference in group II PLA2 levels between patients with severe infections (peritonitis and sepsis) and the other patients studied (multiple injuries and elective surgery) (ROC 0.931, P < 0.0001). The concentration of group II PLA2 had a significant positive correlation to the CRP level and body temperature, which indicates that group II PLA2 is an acute phase reactant and that the determination of group II PLA2 is a useful measurement to diagnose severe infections. It was concluded that the concentration of group II PLA2 in serum effectively predicts lethal MOF in patients with multiple injuries after the second day (ROC 0.739, P < 0.01) and in patients with diffuse peritonitis after the fourth day (ROC 0.750, P < 0.02).

Adolescent↗

PubMed1989

[Respiratory insufficiency and its treatment in threatened multiple organ failure].

Multiple organ failure (MOF) is nowadays a frequent cause of death in the ICU. The pathophysiology is similar to that of ARDS: a generalized inflammatory reaction, a sepsis syndrome and a permeability disorder of the GI tract play major roles. Respiratory failure can cause or aggravate MOF, and pulmonary gas exchange must be improved and stabilized rapidly. However, ventilatory support may cause pulmonary problems able to trigger or maintain MOF, for instance bronchopulmonary superinfection or barotrauma. Side effects of positive pressure ventilation on other organ function must be avoided or treated. It seems clear today that MOF is associated with a systemic oxygen extraction defect. However, the beneficial effect of an artificial increase in oxygen transport has to be confirmed in these patients.

Combined Modality Therapy↗

PubMed2000

Advances in the understanding of multiple organ failure.

Multiple organ failure (MOF) is currently the most common cause of late death after injury and surgery. The pathogenesis of MOF remains incompletely understood but in all likelihood results from a combination of dysregulated balance between inflammatory response and immune function, maldistribution of microcirculatory blood flow, and ischemia/reperfusion injury. Advances in the understanding of the pathogenesis of MOF have been hampered by a lack of precise animal models, accurate definitions of disease, consistent means to qualitatively and quantitatively diagnose disease, and a definable at-risk group of patients for study. Several recent advances in critical care and proposed new therapies hold promise for improving the outcome of patients with multiple injuries who are at risk for MOF. However, as recent clinical trials have shown, studies demonstrating an improvement in outcome from use of these therapeutic agents are difficult to design. The purpose of this article is to discuss the evolution, clinical course, and pathogenesis of MOF, to attempt to better define and quantitate MOF, and to describe recent studies aimed at identifying an at-risk study population for improved treatment and prevention strategies for MOF.

Humans↗

PubMed1990

Mediators of multiple organ failure.

Multiple Organ Failure (MOF) has largely been attributed to bacterial sepsis, though conclusive evidence of an essential role for bacteria and/or their endotoxins is still lacking. On the other hand, MOF and the clinical syndrome of sepsis may be aseptically induced in germ-free animals. This paper reviews the evidence that excessive activation of endogenous humoral mediators and inflammatory cells may cause this highly lethal syndrome.

Complement Activation↗

PubMed1990

Hemodynamic aspects of multiple organ failure.

Multiple organ failure (MOF) secondary to sepsis is associated with a high mortality. A large body of evidence suggests that the disturbed relationship between oxygen supply and oxygen uptake plays an important role in the pathogenesis of MOF. The relationship between oxygen-supply dependency and MOF and the practical implications of the relationship are reviewed. It is concluded that, apart from the all-important eradication of the source of the sepsis, optimizing oxygen transport is the best method of preventing the development of MOF. Since the effects of hemodynamic and ventilatory treatments on oxygen uptake are often unpredictable, the impact of the treatments on oxygen uptake should be evaluated directly.

Hemodynamics↗

PubMed2001

Changes of cytokines in direct endotoxin adsorption treatment on postoperative multiple organ failure.

Multiple organ failure (MOF) is a serious condition that involves simultaneous or consecutive functional failure of several important organs. Furthermore, sepsis is known to play an important role in the occurrence of MOF. Hemoadsorption therapy with the endotoxin adsorption column containing polymyxin B immobilized fibers by direct hemoperfusion (PMX-DHP) is reportedly effective in the treatment of septic shock. This study examined the changes induced on cytokines upon PMX-DHP treatment in 25 patients who underwent emergency abdominal surgery and were immediately started on a postoperative regimen of continuous hemodiafiltration (CHDF) and PMX-DHP. Postoperative MOF was observed in these patients with a mean APACHE II SCORE of 25.5. Eighty percent of patients survived for more than 1 month. We were able to reduce the necessary dose of dopamine in 85.7% of patients because hemodynamic stability improved after administration of PMX-DHP. Interleukin 6 blood levels did not change significantly before or after PMX-DHP treatment in either the surviving or nonsurviving patients. Blood interleukin 1 receptor antagonist levels decreased in both groups. Intercellular adhesion molecular-1, NOx, and thrombomodulin did not change significantly during the course of treatment in either group. Decreased blood levels of PAI-1 levels were found in the surviving patients whereas increased levels of PAI-1 were found in the non-surviving patients. In conclusion, PMX-DHP treatment may be limited clinically in its ability to remove inflammatory cytokines and humoral mediators. However, PMX-DHP treatment is useful for hemodynamic stabilization, which prevents development of MOF.

APACHE↗

PubMed1990

Tissue oxygen extraction in patients with adult respiratory distress syndrome and multiple organ failure.

Multiple organ failure (MOF) associated with adult respiratory distress syndrome (ARDS) secondary to sepsis, trauma, etc., continues to be a syndrome with poor prognosis. It is generally accepted that tissue hypoxia is associated with the subsequent development of MOF. The purpose of this study was to find the relationship between the reduced tissue oxygen extraction and the severity of the syndrome. By correlating either the tissue oxygen extraction per unit volume of blood, CaO2-CvO2, or the oxygen extraction ratio, (CaO2-CvO2)/CaO2, with the intrapulmonary shunt, Qs/Qt, we found that there were significant inverse correlations between these two parameters of tissue oxygen extraction and the severity of the illness in patients with ARDS and MOF. The observed reduction in tissue extraction of oxygen may be related to the development of deranged metabolism in ARDS and MOF.

Adult↗

PubMed1989

Neutrophil function and lipid peroxidation in a rat model of multiple organ failure.

Multiple organ failure (MOF) was induced by sterile intraperitoneal inoculation of zymosan in the rat. This results in a typical triphasic illness with maximal clinical signs at Days 2 and 14. In this study, granulocyte superoxide production (unstimulated and phorbol myristic acid stimulated) was studied as well as lipid peroxidation (TBAR) in plasma, liver, and lung tissue. Mainly TBAR levels in liver and lung tissue closely correlated with the triphasic clinical illness, while bacteriological data did not. It is concluded that the severe inflammatory response in this experimental model probably is the result of excessive toxic oxygen radical production. The first phase of illness may mainly be due to oxygen radical formation by activated PMN, the third phase of illness to the production of lysosomal enzymes (proteinases) from PMN, and activated macrophages as indicated by elevated N-acetylglucosaminidase levels.

Alanine Transaminase↗

PubMed1999

Is the gut responsible for multiple organ failure?

Multiple organ failure is the consequence of many pathological processes, an acute reduction in oxygen supply being one of the most important. The splanchnic region is particularly susceptible to hypoxic injury, and the ischaemic gut mucosa may act as a neutrophil activating site. This is followed by leukocyte adhesion to endothelium and migration into the tissues where cytotoxic chemicals are released, producing tissue injury. This process is aggravated by multiple and sequential physiological insults, some of which may not be evident using basic clinical monitoring. The factors which precipitate cell injury and organ failures may be amenable to relatively simple preventative interventions, but once damage has occurred the process becomes increasingly complex and self-sustaining. Natural defence systems may become pathologically hyperactive, or suppressed, at different stages in critical illness, making it difficult to target therapies directed at the immunoinflammatory cascade with any degree of accuracy or safety, explaining in part the failure of immunotherapy for sepsis. There are significant genetic and constitutional components to susceptibility to critical illness, the most important of which affect cardiac reserve and the ability to maximise tissue oxygen supply. Whether the gut is the most important target organ for oxygen delivery in stress is still the subject of continued research.

Digestive System↗