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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
PubMed1990

[Syndrome of multiple organ failure].

The multiple organ failure syndrome (MOF) is a relatively new entity defined as the successive occurrence of respiratory (ARDS), hepatic, renal, myocardial, gastro-intestinal or neurological failure in patients with hyperkinetic haemodynamic and hypermetabolic states. The etiologies are: infection, septic and non-septic shock, burns and multiple injuries. The MOF syndrome is considered to be a generalised "inflammatory reaction" to tissue aggression involving a cascade of mediatory factors (TNF, interleukines...) of macrophagic, lymphocytic origin, causing multiple organ failure. The treatment depends on early correction of cellular hypoxia related to circulatory disturbances, nutritional support, anti-infective therapy and, in the near future, "control of mediator activity" (immunotherapy).

Antibodies, Monoclonal↗
PubMed1990

[Continuous hemofiltration in the treatment of acute kidney failure in multiple organ failure].

Twenty-nine patients with acute renal failure and multiple organ failure were treated with continuous arterio-venous or veno-venous haemofiltration for a period of 6 +/- 5 days. Sixteen of these patients were improved and haemofiltration was withdrawn, but secondary worsening occurred in 8 cases. The method is well tolerated by the cardiovascular system and provides a satisfactory metabolic control. The low patient's survival rate (27 percent) is due to the severity of the disease. In the absence of controlled studies, it is difficult to assert that continuous haemofiltration is better than conventional haemodialysis.

Acute Kidney Injury↗
PubMed1990

[Clinical patterns and stages of multiple organ failure in the elderly].

Multiple organ failure in the elderly (MOFE) is a new clinical syndrome different from multiple organ failure (MOF) caused by trauma occurring most often in young and mid-aged persons. The authors retrospectively analysed 158 cases of MOFE hospitalized in the past 12 years and commented on its definition, diagnostic criteria, clinical patterns and stages. The suggested definition of MOFE is the sequential 2 or more organs failure within a short period in the elderly patients (greater than or equal to 60 years old) with multiple organ chronic diseases in the presence of aging of organs and age-related malfunction. The most common precipitating factors are pulmonary infections and acute attack of chronic cardiac, cerebral and renal diseases. The interval between failures of various organs is mostly less than 10 days and seldom longer than 1 month. MOFE has 3 different patterns: rapid pattern with single phase; delayed pattern with two phases and recurrent pattern with multiple phase. In the last pattern the patients suffer from multiple attacks of multiple organ failure. It is only seen in MOFE, but not in MOF. The presentation of this particular pattern is related to the following facts: (1). A few organs or only the heart and lungs are involved. (2) Kidney, brain and hemopoietic system etc. usually with poor prognosis are not involved. (3) The age of patients are relatively younger. (4) More resuscitation experiences have been accumulated and better resuscitation measures are available. The clinical course of MOFE can be divided into 3 stages: prefailure stage (stage I), failure compensations stage (stage II) and decompensation stage (stage III).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

[Liver failure as part of multiple organ failure following polytrauma].

In the last few years there has been increasing evidence that adult respiratory distress syndrome is only part of a much more complex syndrome called multiorgan failure (MOF). Since renal and lung failure have become rare because of our increased understanding of the pathomechanisms involved and the treatment changes, liver dysfunction has been noted more often. In a clinical trial with 38 patients with severe trauma, we investigated liver function using ordinary parameters like the transaminases, bilirubin, etc. To define one group with MOF and one without we used the Goris MOF Score. In both groups glutamate dehydrogenase (GLDH) was increased initially up to 14 U/l, indicating hypoxia of the liver cells right after trauma. From day 6 on, a second increase up to 12 U/l of GLDH in the MOF group was evidence of liver cell dysfunction. The glutamine oxalacetic transaminase (GOT) level remained normal in both groups after an initial increase of up to 60 U/l in both groups. As 30% of serum GOT is released by muscle cells, the initial peak values could be due to direct muscle trauma, because an initial increase was noted even in the creatinine kinase. A decrease in clotting factor V down to 30% on day 8 in the MOF group indicated that the metabolic synthesis activity of the liver was lower. Bilirubin increased in the MOF group from day 5 on up to 240 mumol/l on the day 14. As this increase was not parallel to the gamma glutamyl transferase (Gamma BT) level, the reason for the bilirubin increase may be dysfunction of the liver cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Clinical feature and laboratory findings of multiple organ failure].

The pathology of multiple organ failure consists of tissue-cell damage (disruption of energy metabolism) and severe infections (host exhaustion). The impairment of the TCA cycle was mild in two-organ disease but was nearly arrested in three-organ disease, and the cells are considered to have been in lactic acidosis with a shift of the glycolytic system from pyruvate to lactate. Significant differences were observed also in the number and the function of lymphocytes between two-organ and three-organ diseases. Therefore, in multiple organ failure, infections are considered to worsen as the ability of antigen recognition is impaired and differentiation of B cells into antibody-producing cells is inhibited with a decrease in lymphocytes. The phagocytic activity of neutrophils did not decrease unless leukocytes were reduced.

Citric Acid Cycle↗
PubMed1990

Clinical features of multiple organ failure in the elderly.

Multiple organ failure (MOF) in the elderly is a new syndrome evolved from multiple organ chronic diseases on the basis of multiple organ dysfunction in the aged. Its characteristics are clinically different from those of MOF due to serious trauma. 122 cases of MOF were analysed retrospectively and their clinical features discussed. MOF with a long course is the natural presentation in many of the elderly before death. Its main precipitating factors are pulmonary infection, metastatic carcinoma, cardiac attack, etc. The sequence of a failure in organs is heart, lung, kidney, liver, etc. The mortality is similar to that of MOF due to trauma. However, those suffering from 4-organ failure can still survive, and instead, the renal failure can be mostly fatal. More attention should be paid to the prevention of MOF in the elderly so as to shorten its developing course.

Aged↗
PubMed1992

[Multiple organ failure after severe burns].

36 cases with multiple organ failure (MOF) in a group of 178 severe burn injury patients during 1969-1989 were observed in our department. The rate of occurrence of MOF in this group was 20.2% (36/178). 25 cases out of these 36 patients died, and the mortality rate was 69.5% (25/36). In 10 cases 2 organs were involved, and two patients died; 3 organs were involved in 13 cases and nine of them died; more than 4 organs were affected in 13 cases and all of them died. The relationship between MOF and shock, inhalation injury as well as septicemia was discussed. Although there were many factors which could induce postburn multiple organ failure (PBMOF), the severity of the injury was the most fundamental inducing factor. The severer the burn injury, the higher the morbidity and mortality of PBMOF. Both shock and inhalation injury were important inducing factors in early PBMOF. Wound sepsis and septicemia were major inducing factors in delayed PBMOF. Majority of the delayed PBMOF took place during septicemia. In consideration of the high mortality of PBMOF and lack of effective treatment at present, it is extremely important to prevent severe burn injury patients from developing PBMOF. The measures to prevent PBMOF included: to correct shock adequately as soon as possible, to select the optimal time and appropriate extent of escharotomy and skin grafting, to try our best to ensure complete or near complete take of skin grafts, and to strengthen systemic metabolic support.

Adolescent↗
PubMed1992

[The changes in serum angiotensin-converting enzyme and their relationships to pulmonary failure in experimental model of multiple organ failure].

The correlation of serum angiotensin-converting enzyme (SACE), PaO2 and pulmonary coefficient in rabbit model of multiple system organ failure (MOF). 16 rabbits were fed E coli (0.5-3.0 x 10(11)/kg B.W.) by gastrogavage, were induced hemorrhagic shock (5.33 kPa arterial pressure for an hour) and were rapidly reinfused with shed blood and dextran. According to the criteria of pulmonary failure, that is respiratory rates greater than 100/min, PaO2 less than 8.00 kPa, pulmonary coefficient greater than 6.0, 8 rabbits developed pulmonary failure. They showed a significantly low SACE values, decreased PaO2 values and increased pulmonary coefficients, while in other 8 control animals the values of SACE and PaO2 did not significantly change.

Animals↗
PubMed1992

Multiple organ failure. Pathophysiology and potential future therapy.

Multiple organ failure (MOF) has reached epidemic proportions in most intensive care units and is fast becoming the most common cause of death in the surgical intensive care unit. Furthermore, in spite of the development of successive generations of new and more powerful antibiotics and increasing sophisticated techniques of organ support, our ability to salvage patients once MOF has become established has not appreciably improved over the last two decades. Clearly, new therapeutic strategies aimed at preventing or limiting the development of the physiologic abnormalities that induce organ failure are needed to improve survival in these critically ill patients. Based on our rapidly increasing knowledge of the mechanisms of MOF and the fruits of molecular biology, a number of new therapeutic approaches are in various stages of development. To effectively use these new therapeutic options as they become available, it is necessary to have a clear understanding of the pathophysiology of MOF. Thus, the goals of this review are to integrate the vast amount of new information on the basic biology of MOF and to focus special attention on the potential therapeutic consequences of these recent advances in our understanding of this complex and perplexing syndrome.

Bacterial Infections↗
PubMed1992

Inflammatory mediators, infection, sepsis, and multiple organ failure after severe trauma.

The relation of (multiple) organ failure (OF) to the release of inflammatory mediators and the incidence of infection and sepsis was studied prospectively in 100 patients with multiple trauma (injury severity score = 37). Sixteen patients died of OF, 47 patients survived OF, and 37 patients had no OF. Fifteen (24%) of the patients with OF showed no signs of infection. In patients with early onset of OF (n=45), infection followed with a lag of 2 or more days. In 16 (44%) of these patients, infection led to a deterioration in organ function. With late onset of OF (n=18), infection preceded OF in nine patients. Polymorphonuclear leukocyte-elastase, neopterin, C-reactive protein, lactate, antithrombin III, and phospholipase A discriminated significantly among the three outcome groups. Of all factors, only polymorphonuclear leukocyte-elastase showed a difference between patients with and without infection or sepsis, respectively. These data indicate that infection might not play a crucial role in the pathogenesis of posttraumatic OF in a substantial portion of patients with trauma. Early OF, especially, seems to be mainly influenced by the direct sequelae of tissue damage and shock (eg, the release of inflammatory mediators). Since infection and sepsis did not lead to an augmented release of mediators in patients with trauma, the role of both entities remains unclear.

Adult↗