PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Multiple Organ Failure”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

[The role of elective hemofiltration in the management of sepsis and multiple organ failure].

Septic shock and the multiple organ dysfunction syndrome carries a very high risk of mortality. The exact pathomechanism of the development of multiorgan dysfunction is yet to be revealed and its treatment remains the biggest challenge in intensive care. In order to prevent the development of multiple organ dysfunction new therapeutic modalities have been investigated over the last years. One promising intervention is the exchange of large volumes of ultrafiltrate during haemofiltration termed as "elective" haemofiltration. By removing several middle molecular weight inflammatory mediators from the circulation, currently thought to be responsible for a number of complications due to sepsis, it as been suggested, that it might improve survival in theses patients.

Female↗

[Kidney failure during acute pancreatitis. A unique aspect of multiple organ failure].

Eighty-two patients with acute pancreatis observed in the last seven years were included in prospective trial of monitoring protocol comprising: multiple organ failure and non invasive imaging of pancreatic lesion. One organ failure noted in the 60.9%, M.O.F. with three organ failure represented in the 21.9%. Renal failure was confirmed in 18.9%, trough nine clinical and biological index, become with shock in 73% and with extensive necrosis in 53%. ARF appeared with functional picture and normal diuresis in 73.3% and with organic failure in 26.7%. Index of specific mortality was 33.3%, while the comprehensive index of mortality in the study group was 12.9%, with a significant incidence in the half of deaths.

Acute Disease↗

MOF, MODS, and SIRS: what is in a name or an acronym?

The most prominent contributions to multiple organ failure, multiple organ dysfunction syndrome, and systemic inflammatory response syndrome are described in this article. However, it is quite possible that there are others that have been missed. The problem of organ failure continues to perplex clinicians and scientists, and it contributes to fatal outcomes for patients with illnesses, infections, and injuries after operations. Although we know a fair bit about these problems, we frequently can do little about it. The best approach remains support to prevent failure.

Humans↗

[Reactive haemophagocytic syndrome and multiple organ failure in intensive care unit patients].

The incidence of the haemophagocytic syndrome in the ICU patients with multiple organ failure seems to be high. The haemophagocytic syndrome can be considered as the consequence of the initial aggression leading to multiple organ failure. On the contrary the haemophagocytic syndrome could be the cause of multiple organ failure. A case of haemophagocytic syndrome is presented which led to rapidly fatal multiple organ failure.

Critical Care↗

Nutrition support in patients with multiple organ failure.

The problem with any attempt to feed patients in multiple organ failure is that, because of an ongoing inflammatory process, the conventional techniques of supplying energy and protein do not maintain lean tissue mass. In addition, the conventional markers of nutritional status, both anthropometric (body mass and composition, arm circumference, etc.) and visceral protein (albumin, prealbumin) as well as immunological markers (delayed reactive skin hypersenstivity to common antigens and lymphocyte counts) are confounded by fluid retention (5-15 l) and the metabolic response to the illness. Recent research has focussed on the nature and origin of this inflammatory response, the problems of trying to feed an individual undergoing such a response, the details of the protein breakdown observed in sepsis and multiple organ failure and methods of modifying the response favourably.

Animals↗

Septic patients in multiple organ failure can oxidize infused glucose, but non-oxidative disposal (storage) is impaired.

1. Patients suffering trauma and sepsis are insulin resistant, but no studies have specifically been made of patients suffering multiple organ failure. 2. We have studied exogenous glucose utilization in multiple organ failure using a combination of the hyperglycaemic glucose clamp and indirect calorimetry to quantify glucose utilization in multiple organ failure, partitioning it into oxidative and nonoxidative disposal (storage). 3. Fourteen septic patients with multiple organ failure were studied. APACHE II (Acute Physiological and Chronic Health Evaluation Mark II) scores on the day of the study ranged from 11 to 31 (median 16). Twenty percent D-glucose was infused and blood glucose was clamped at 12 mmol/l for 3 h. The results were compared with those obtained on seven healthy control subjects. 4. Glucose utilization and energy expenditure were similar in the two groups for the first 90 min of the clamp, after which glucose utilization and energy expenditure increased steadily in the control subjects but did not change in the patients. Respiratory exchange ratio rose in both groups; considered over the whole of the clamp period, respiratory exchange ratio was slightly lower in the patients than in the control subjects (P < 0.05) but not at any specific time point. Glucose oxidation rose in both groups but non-oxidative glucose disposal (storage) rose only in the control subjects. Glucose oxidation was slightly lower in the patients (P < 0.05) but not at any specific time point and there was no difference between the groups in the amount by which glucose oxidation increased. Non-oxidative disposal in the patients fell significantly (P < 0.01) over the course of the clamp and was significantly lower than in the control subjects (P < 0.01). 5. Growth hormone increased in response to glucose infusion in the patients but not in the control subjects. 6. Like patients suffering uncomplicated sepsis or trauma, patients with multiple organ failure are also insulin resistant. The defect appears to lie in an impairment of the ability to store glucose rather than oxidize it, and this may be due in part to the increase in growth hormone in patients with multiple organ failure.

Adolescent↗

Multiple organ failure in patients with thermal injury.

OBJECTIVE: To assess the frequency and significance of multiple organ failure in patients with burn injuries. DESIGN: Retrospective review and prospective assessment of patients with acute burns. SETTING: University hospital burn center. PATIENTS AND METHODS: We reviewed 529 patients admitted for acute burn treatment whose lengths of stay exceeded 72 hrs. A new scoring system, the Thermal Injury Organ Failure Score, was used to assign scores from 0 (normal) to 6 (severe dysfunction) to each of 6 organ systems, which were then totaled to compile the overall score. This system was also used for prospective assessment of 83 adult burn patients, and compared with the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system during the first week of treatment. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: For 496 survivors, mean organ failure score was 3.28, compared with 23.1 in 33 nonsurvivors (p < .0001). All nonsurvivors but one had scores of > or = 15, indicating dysfunction of at least three organs. Scores and mortality rate increased with age and burn size. Pulmonary dysfunction was the most frequent form of organ failure seen, but correlated less with outcome than did cardiovascular or neurologic scores. Sepsis was present in 22 of 33 patients who died. In the prospective study, organ failure scores correlated with outcome more closely than did APACHE II scores. Weekly evaluation of these patients demonstrated progressive divergence in scores between survivors and nonsurvivors. CONCLUSIONS: Multiple organ failure was almost invariably present in burn patients who died > 72 hrs after injury. Burn victims, who have been excluded from reviews of multiple organ failure, appear to manifest organ failure in a manner similar to that of other surgical populations. The scoring system reported here may prove useful in evaluating organ failure in thermally injured patients.

Adolescent↗

[Treatment of 10 cases of multiple organ failure].

From 1985 to 1987, 10 cases of multiple organ failure (MOF) caused by severe infection, major surgery, and trauma were treated in our hospital. The sequence of the organs that came to a failure varied with different diseases. The diagnosis was made on the objective index and numbers of the failed organs. All patients were monitored and treated with modern medical equipment including hemodialysis, plasma-exchanging technique, and artificial heart-lung machine. It was found that the increase of curative rate lay on the intensive care and comprehensive treatment. Five patients in this group survived, and the diagnosis of MOF was finally confirmed by autopsy (heart, lung, liver, kidney, brain, and GI tract) in three cases. Based on the pathological findings, the authors suggested that patients with MOF could only be cured when the disease was on its first, second, or early third stage.

Adult↗

Plasma concentrations of cytokines, their soluble receptors, and antioxidant vitamins can predict the development of multiple organ failure in patients at risk.

OBJECTIVES: The aims of this study were: a) to evaluate plasma concentrations of cytokines and their soluble receptors, as well as antioxidant substances in patients at high risk of developing multiple organ failure; b) to investigate early change: and c) to examine the possible prognostic value of these elements. DESIGN: Prospective analysis. SETTING: Surgical intensive care unit (ICU) of a university hospital. PATIENTS: sixteen patients at risk for multiple organ failure. MEASUREMENTS AND MAIN RESULTS: Ten patients developed multiple organ failure and five of them died. Whereas tumor necrosis factor-alpha (TNF-alpha) plasma concentrations were only borderline higher in patients developing multiple organ failure, TNF-soluble receptors 55 and 75 were significantly increased during all ICU days compared with patients not going into organ failure. Interleukin-6 plasma concentrations were higher in patients developing multiple organ failure during the first 2 days after ICU admission. The antioxidant vitamin C was significantly decreased in patients going into multiple organ failure during all ICU days. Other biochemical markers of antioxidant activity, such as vitamin E, copper, and zinc plasma concentrations, did not differ between the two groups. CONCLUSIONS: Our data suggest that there is a marked increase in anti-TNF activity and a decrease of antioxidant defense in patients at risk of developing multiple organ failure. The predictive value of plasma concentrations of circulating TNF-soluble receptors and vitamin C in this type of patient needs further evaluation.

Adult↗

[Plasma contents of cytokines (TNF-alpha, IL-1 beta, IL-6) and their clearance during continuous hemofiltration in patients with sepsis and multiple organ failure].

The total-systems inflammatory response was assessed in patients with sepsis and multiple organ failure by measuring plasma cytokines TNF-alpha, IL-1 beta, and IL-6 and their clearance and total elimination in the course of permanent hemofiltration (PHF). Sepsis and multiple organ failure were found to involve a stable circulation of numerous cytokines, their levels reaching the peaks in some cases. No correlation between the content of individual cytokines in the plasma were detected. Appreciable amounts of TNF-alpha and IL-1 beta were eliminated during PHF, their clearance being approximately 15 ml/min, whereas elimination of IL-6 was negligible. Hence, PHF affects the mediator component in the pathogenesis of sepsis and the multiple organ failure syndrome.

Adolescent↗

Retinopathy of pancreatitis indicates multiple-organ failure and poor prognosis in severe acute pancreatitis.

During hospitalization for severe acute necrotizing pancreatitis, a connection between the onset of retinopathy of pancreatitis and multiple-organ failure was studied. Ophthalmoscopy was repeated every second day and continuous staging for multiple-organ failure was performed in 38 patients. Typical retinopathy of pancreatitis developed in 7 of 10 patients with multiple-organ failure and only in 4 of the 28 patients without multiple-organ failure. Retinopathy of pancreatitis was observed in 7 of the 18 cases leading to lethal outcome and only in 4 of the 20 surviving patients. No correlation was observed between the development of retinopathy of pancreatitis and hemodialysis, pre-existing diabetes mellitus, abnormal platelet count, result of hemoculture, c reactive protein value, fraction of inspired oxygen and adult respiratory distress syndrome. In the 21 control patients in grave general state but without acute pancreatitis, retinopathy of pancreatitis was never observed. In our prospective study the onset of retinopathy of pancreatitis had clinical prognostic value and indicated multiple-organ failure and poor prognosis in severe acute necrotizing pancreatitis.

Acute Disease↗

[The pathogenetic and treatment problems of multiple organ failure in patients with severe combined trauma and massive blood loss in the early postresuscitation period].

Analysis of the results of treatment of 583 patients with grave and terminal stages of shock resultant from severe combined injuries and blood loss, hospitalized in resuscitation wards, showed visceral involvement and development of pyoinflammatory complications in the early postresuscitation period (days 5-10 of treatment) in 43.6% cases. Prolonged mixed type hypoxia and persistence of impaired tissue perfusion, shown by rheovasography, play an important role in the mechanisms of development of complications. Early onset (6-8, 10-12 h after the beginning of treatment) and long standing of disseminated intravascular coagulation (DIC) contributes to the pathogenesis of polyorgan failure. A protocol of pathogenetically validated measures for the prevention and treatment of DIC is presented as one of approaches to the prevention and treatment of polyorgan failure.

Combined Modality Therapy↗

[Reappraisal of clinical pictures of multiple organ failure].

Disseminated intravascular coagulation syndrome (DIC) and also multiple organ failure (MOF) still remain principal causes of death after major surgery or trauma. The author tried to reappraise the clinical features of MOF, especially with the special reference to DIC. One hundred and thirty three cases with MOF were collected from eight university hospitals. The results of analysis of these cases were as follows. 1. Criteria in the diagnosis MOF and also DIC remain controversial among each institute. 2. Severity in the impairment of organ functions also so different among various kinds of vital organs in the present conventional criteria in the diagnosis of MOF. 3. The author proposes a new criterion in the diagnosis of MOF, including serum total bilirubin level above 10 mg/dl or serum transaminase level above 200 K.U. as to the sign of impaired liver function, and BUN above 75 mg/dl or serum creatinin level above 5 mg/dl to indicate an impaired renal function. More precise and close relation between the numbers of impaired organs and the therapeutic results might to obtained by our new criterion. 4. Analysis of these collected cases with MOF also indicated that MOF associated with DIC might be considered to have more grave and serious prognosis, although 58 cases with MOF showed no sign and symptoms of DIC among 129 cases, diagnosed by Tamakuma 's criterion.

Adult↗

[The metabolic and immunological changes in appendiceal peritonitis in children complicated by multiple organ failure].

An investigation of 56 children with appendicular peritonitis complicated by multiple-organ failure has revealed typical, in the authors' opinion, metabolic and immunological changes such as the regulation of organism to minimization of the energy exchange with catabolism of the functionally important proteins and the formation of multiple-component secondary immunodeficient state. The data obtained facilitate earlier diagnosis of the multiple-organ failure and optimization of the management which resulted in 2 times less lethality among such patients.

Adolescent↗

The role of the gastrointestinal tract in postinjury multiple organ failure.

Despite intensive investigation, the pathogenesis of postinjury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly implicate that the gastrointestinal tract plays a pivotal role. Shock with resulting gut hypoperfusion appears to be one important inciting event. While early studies persuasively focused attention on bacterial translocation as a unifying mechanism to explain early and late sepsis syndromes that characterize postinjury MOF, subsequent studies suggest that other gut-specific mechanisms are operational. Based on our Trauma Research Center observations and those of others, we conclude that: 1) bacterial translocation may contribute to early refractory shock; 2) for patients who survive shock, the reperfused gut appears to be a source of proinflammatory mediators that may amplify the early systemic inflammatory response syndrome; and 3) early gut hypoperfusion sets the stage for progressive gut dysfunction such that the gut becomes a reservoir for pathogens and toxins that contribute to late MOF.

Bacterial Translocation↗

Sequential systemic platelet-activating factor and interleukin 8 primes neutrophils in patients with trauma at risk of multiple organ failure.

Plasma from 33 patients at risk of multiple organ failure (MOF) after major trauma was tested for a priming effect on neutrophils, and for the presence of platelet-activating factor (PAF) activity and interleukin (IL) 8. Plasma sampled at 3, 6, 12 and 24 h after injury significantly primed normal neutrophils to release mean(s.e.m.) 1.26(0.19), 1.33(0.26), 1.04(0.14) and 0.86(0.13) nmol superoxide per min per 1.3 x 10(6) neutrophils respectively (P < 0.05). Priming at 3 h after injury was inhibited by mean(s.e.m.) 63.8(7.0) per cent by the PAF antagonist, WEB 2170 (P < 0.01). Mean(s.e.m.) plasma IL-8 was raised at 6 and 12 h after injury to 785(183) and 836(175) pg/ml (P < 0.01). At 12 h after injury the plasma IL-8 level correlated directly with the number of units of red blood cells transfused (r = 0.64, P < 0.01), and was significantly higher in the group of six patients who developed MOF (P < 0.05). These data suggest that after trauma the mediators PAF and IL-8 appear sequentially in the circulation, are potential mechanisms of circulating neutrophil priming, and that IL-8 may also be an early biochemical marker predicting the onset of MOF.

Adolescent↗