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 235 records · Page 13Linked to original sources

PubMed1989

[Changes of plasma amino acid on the course of septic multiple organ failure].

The changes of plasma amino acid (AA) pattern on the course of septic multiple organ failure (SMOF), and the effect of branched chain amino acid enriched solution (BCAA-S) on the AA pattern were evaluated in thirteen patients who died of SMOF in ICU. The course of ICU was divided into the following three stages. Stage I was a few days after the admission in ICU. Stage II was severe infected state. Stage III was terminal state. Following results were obtained: 1) Total AA value (TAA) of each stage was 2,693 n.mol/ml, 6,666 n.mol/ml and 19,480 n.mol/ml. 2) BCAA/aromatic AA (B/A) of each stage was 1.4, 1.03 and 1.05. Above values were lower than those of normal one (2.44). 3) Most kinds of AA in stage III were exhibited significantly higher than those of stage I as evaluated in absolute value. 4) In the BCAA-S administered group, B/A exhibited higher values than those of control, but, there was no sign of amelioration for SMOF condition in the former group. In severe infected or septic shock state, AA metabolism is deeply deteriorated. So, we can not decide whether BCAA-S given in this condition plays beneficial effect on the course of SMOF or not.

Adult↗

PubMed1994

The role of phagocyte proteinases and proteinase inhibitors in multiple organ failure.

Although numerous other inflammatory mediators are important, the following review of our research and that of other authors reveals a prominent role for the phagocyte proteinases, polymorphonuclear (PMN) elastase and cathepsin B, in the development of multiple organ failure. The release of these enzymes in relation to the severity of trauma- and/or infection-induced inflammation was clearly verified in a variety of clinical studies. The amounts of the extracellularly discharged phagocyte proteinases were highly predictive of forthcoming organ failure and ultimate patient outcome. Moreover, the consumption of important proteinase inhibitors (e.g., alpha 1-proteinase inhibitor, antithrombin III) and other plasma proteins (e.g., fibrinogen), which are highly susceptible to proteolytic degradation, coincided with the occurrence of proteolytic activity, especially that of PMN elastase. Therefore, the therapeutic use of specific PMN elastase and/or thrombin inhibitors should prevent multiple organ failure or at least reduce severe signs of inflammation.

Animals↗

PubMed2000

[Survival and quality of life of patients with multiple organ failure one year after leaving an intensive care unit].

BACKGROUND: The patients' mortality with multiple organ failure (MOF) is very high and patients who consume the most resources are those with uncertain prognosis. In order to use the limited resources adequately, it is necessary to know the cost-benefit relationship of their treatment and in this study cost, mortality, quality of life (QOL) of survivors who developed MOF has been investigated. PATIENTS AND METHODS: Mortality in the Intensive Care Unit (ICU) and mortality QOL (with modified EuroQOL Instrument) one year after discharge were studied in 239 admitted patients who developed MOF. Cost was estimated from administrative dats of cost patients-day. To determine mortality independent predicting factors, a logistic regression model was used. RESULTS: Of the 239 patients studied, 144 (60%) died in ICU and 29 (12%) died after discharge. The independent predicting factors of mortality one year after discharge from ICU were: age (p < 0.1, odds ratio [OR] = 1.02), cardiac surgery (p < 0.0000, OR = 0.1899) and trauma (p < 0.05, OR = 0.2287). Of the 66 surviving patients, 18% were severely discapacitated. Forty one percent recovered their previous QOL, 18% improved it and 39% got worse. Patients with MOF consumed 64% of ICU total resources and of these, 77% was consumed by patients who died and by severely discapacitated. CONCLUSION: A high proportion of resources were used by MOF patients, but patients who died and who remained with worst QOL consumed the highest part. Although the mortality after one year was high (72%), 80% of the survivors achieved an acceptable QOL and for this reason, treatment of these patients should not be limited if survival and QOL predictions are not 100% correct.

Cost-Benefit Analysis↗

PubMed1997

Multiple organ failure following zymosan-induced peritonitis is mediated by nitric oxide.

In the present study we tested the hypothesis that nitric oxide may play a role in the pathogenesis of multiple organ failure induced by peritoneal injection of zymosan in the rat. A severe inflammatory response characterized by peritoneal exudation, high plasma and peritoneal levels of nitrate/ nitrite (breakdown products of nitric oxide), prostaglandin E2 and leukocyte infiltration into peritoneal exudate was induced by zymosan administration. This inflammatory process started within 3 h of administration and onset occurred at 18 h, coinciding with damage of lung, small intestine and liver, as assessed by histological examination and by increase of myeloperoxidase activity, indicative of neutrophil infiltration. Furthermore, at 18 h after zymosan-induced peritonitis, expression of inducible nitric oxide synthase enzyme was found mainly in the macrophages of inflamed lungs. Subcutaneously administration of a nonisoform selective nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, reduced formation of peritoneal exudate fluid, blocked plasma and peritoneal nitrate/nitrite accumulation, and attenuated the elevated release of peritoneal prostaglandin E2. In addition, nitric oxide synthase inhibition was effective in preventing the development of organ failure since tissue injury and neutrophil infiltration, by myeloperoxidase evaluation, was reduced in lung, small intestine, and liver. In conclusion, major findings of our study are that nitric oxide exerts a proinflammatory role in the development of multiple organ failure and nitric oxide synthase inhibition is an effective antiinflammatory therapeutic tool, since inhibits not only nitric oxide but also prostaglandin production and cellular infiltration in inflamed organs.

Acute Disease↗

PubMed2003

[Increasing activity of the intestinal mucosal mast cells in rats with multiple organ failure].

OBJECTIVE: To investigate changes in activities of the intestinal mucosal mast cells (IMMC) in multiple organ failure(MOF). METHODS: MOF model in rat was established by injection of zymosan. The concentrations of histamine and tumor necrosis factor-alpha(TNF-alpha) in plasma and intestine tissue were examined. Both the function and the pathological alterations of vital organs including intestine, liver, kidneys and lungs were measured or visualized under light microscope. Furthermore, the ultrastructure of the IMMC was observed with a transmission electronic microscope. RESULTS: The injection of zymosan resulted in obvious inflammatory response in multiple organs, as well as significantly impaired function. Compared with the normal rats, the histamine levels in the intestinal tissue from rats with MOF remarkably decreased [(11.63+/-1.97) ng/g vs.(8.67+/-1.16) ng/g], while the plasma histamine levels did not show any significant changes. For TNF-alpha, apparently increasing levels in both intestinal tissue and plasma were observed in MOF rats. Meanwhile, the increasing number and degranulation of IMMC during MOF were impressive. CONCLUSION: The histamine and TNF-alpha released from activated IMMC may play an important role in the development of MOF.

Animals↗

PubMed1993

[Multiple organ failure related to disseminated intravascular coagulation].

This paper describes the main pathophysiological events leading to multiple organ failure (MOF) related to disseminated intravascular coagulation (DIC), caused by circulatory failure or infection. The main mechanisms responsible for the development of MOF in DIC are discussed, as are both the organ ischemia due to stasis and/or obstruction and the close interrelated reactions between inflammatory reaction, immune system and coagulation systems, especially focused on the close connection between the endothelium and superimposed mediators.

Capillary Permeability↗

PubMed1992

Multiple organ failure in patients with fulminant hepatitis and in post-operative patients with liver cirrhosis.

Multiple organ failure (MOF) appeared during the course of nine cases with fulminant hepatitis, and it was compared with that of seven cirrhotic patients with post-operative hepatic failure. The number of organs failed was 4.9 and 3.6 on average in fulminant hepatitis and post-operative cirrhosis, respectively. All the patients died in less than nine days following the occurrence of MOF. Gastrointestinal bleeding was more frequently observed in fulminant hepatitis cases than in cirrhotic patients. In post-operative cirrhotics, hepatic failure occurred later and the elevation of serum total bilirubin was mild and slow. Renal failure and/or gastrointestinal bleeding was observed prior to death in fulminant hepatitis cases, and cardiac failure and hepatic failure in post-operative cirrhotics. These organ failures resulted in death, although extensive and multimodal treatments were carried out in both groups of patients.

Adult↗

PubMed1995

[The multiple-organ failure syndrome in acute pancreatitis. Its pathogenesis and treatment].

Multiple organ system failure (MOSF) is a severe clinical process that causes progressive renal and liver failure. Acute pancreatitis (AP) can cause MOSF. Several series document high mortality rate from necrotizing forms is associated with MOSF. The authors observed 199 cases of acute necrotizing pancreatitis in 10 years, with a mortality rate of 14.1%. MOSF occurred in 14 cases, resulting in death in 100% of affected patients. In AP, MOSF follows hemodynamic abnormalities suspected to be secondary to activation of kinins system and other vasoactive peptides that are responsible for pathogenetic mechanism of disease. Similar hemodynamic abnormalities can be observed in septic shock. Then many authors suppose causes of MOSF in AP are local (abscess, infection of pancreatic necrosis) and systemic septic complications or translocation of enteric bacteria or their endotoxins from the gut lumen. So it is important to provide prophylactic use of antibiotics that are effective against expected bacteria and also achieve a therapeutic concentration in pancreatic tissue and juice. Fluid replacement, nutritional support and other therapeutic strategies must be employed to prevent MOSF. When the MOSF is clearly developed, medical and surgical measures are unuseful and the mortality rate is very high also in an intensive care unit.

Acute Disease↗

PubMed1994

A study on acid-base disturbance in patients with post-traumatic multiple organ failure.

In order to diagnose accurately the type of acid-base disturbance (ABD) in patients with post-traumatic multiple organ failure (PMOF), arterial blood gases and electrolytes were determined 645 times on 112 patients with PMOF and the data were analyzed with the pre-estimated compensatory formula of ABD and the calculations of anion gap, potential bicarbonate, and blood chlorides. Simple ABD was found in 381 times of determinations and double ABD in 239 when only the formula was used in the analysis, while 264 times of simple ABD, 260 times of double ABD and 96 times of triple ABD were found when the formula was employed in combination with the calculations of anion gap, potential bicarbonate and blood chloride. The mixed types of ABD were increased by 49% (117 times) from 239 to 356 times and triple ABD was increased from 0 to 96 times. The findings indicate that the employment of the combined formula and the calculations of anion gap, potential bicarbonate and blood chloride is of great significance to assess ABD especially its mixed and complicate types in patients with PMOF. It is emphasized that along with the monitoring of blood gases, the determination of blood electrolytes and the calculation of anion gap and potential bicarbonate should be performed to determine the correct type of ABD.

Acid-Base Equilibrium↗

PubMedDate not supplied

[Bacterial translocation. Its role in the etiology of sepsis and multiple organ failure].

Under certain conditions or diseases the microorganisms that normally inhabited in the gastrointestinal tract reach the mesenteric lymph nodes, the portal circulation, the intra and extraperitoneal organs and the systemic circulation creating the possibility of infection, sepsis and multiple organ failure. This phenomenon has been termed bacterial translocation and although was described few decades ago, today it has regain critical importance due to the association to the multiple organ failure syndrome in critical and severely injured patients. In this review a series of pathologies where the translocation of bacteria has been demonstrated are described as well as the possible therapeutics maneuvers.

Bacteria↗

PubMed1992

[The comparison of postoperative multiple organ failure with arterial disease to that with gastrointestinal cancer].

The clinical features of 22 postoperative multiple organ failure (MOF) patients, comprised of 8 with arterial disease (A-MOF) and 14 with gastrointestinal cancer (G-MOF), were investigated. Differences in the operative time, blood loss, and mortality were not significant. The initial organ impaired was the lungs in 78.6% of G-MOF patients and the heart or kidneys in all A-MOF patients. Infection developed in over 80% of both groups. In many A-MOF patients, the pneumonia or septicemia developed secondary to organ failure, while intraabdominal infection triggered respiratory failure in many G-MOF patients. Our organisms in infected specimens and their antibiotic sensitivities was valuable for the early administration of effective antibiotics. Upper gastrointestinal tract bleeding was important in the prognosis of both groups and occurred more frequently in A-MOF than in G-MOF patients. Consumption coagulopathy in A-MOF patients and DIC induced by infection in G-MOF patients mainly caused such bleeding. Preoperative administration of heparin was effective in improving coagulopathy. Furthermore, measurement of intramural pH with tonometer in the stomach and gastric irrigation with oxygenated perfluorochemicals were effective in the prediction and prevention of gastrointestinal bleeding.

Aged↗

PubMed1994

A clinical analysis of multiple organ failure following elective surgery.

A retrospective analysis was made of 58 patients who unexpectedly developed multiple organ failure (MOF) following elective surgery, and the results were compared with those of 168 control patients who did not develop MOF. In 33 patients with liver cirrhosis, MOF was related to poor liver function, a low albumin level, excessive blood loss, many transfusions, and a high incidence of hypotension. MOF, rather than liver failure alone, was featured by postoperative bleeding and infection. In 15 patients with esophageal carcinoma, MOF was correlated with many transfusions, anastomotic leakage, and postoperative infection. In 10 patients who underwent surgery for an aortic aneurysm, poor renal function and extended anesthesia time were associated with MOF. These results indicate that to prevent MOF following elective surgery, it is important to: (1) Select patients for liver surgery according to their liver function, and minimize the risk of bleeding and infection, (2) avoid too many blood transfusions, and minimize the risk of leakage and infection in esophageal surgery, and (3) select patients for aortic surgery based on renal function and reduce the anesthesia time as much as possible.

Aortic Aneurysm↗

PubMed1998

Microvascular endothelial activation in the skeletal muscles of patients with multiple organ failure.

The relationship between microvascular damage and the presence of muscle fibre atrophy and necrosis has been investigated in skeletal muscle biopsies taken from 57 patients with multiple organ failure. Immunohistochemical studies showed no loss of capillaries and no luminal thrombosis, while neutrophil leucocytes were more prevalent in the patients' biopsies than in controls. Deposition of the complement membrane attack complex (C5-9MAC) in capillaries was observed in 41% of cases. Endothelial activation was suggested by an increased intensity of expression of ICAM-1, and by an increased proportion of capillaries expressing P selectin and E selectin, although this was not directly associated with neutrophil accumulation. Endothelial swelling was present in many biopsies with 38% of the biopsies having larger capillary profiles on immunohistochemical labelling for von Willebrand factor (vWF), thrombomodulin and CD34, and on Ulex europaeus agglutinin 1 binding. Endothelial swelling was confirmed by image analysis and morphometric evaluation of capillary ultrastructure, however, the capillary luminal area was not reduced as the capillaries were dilated. Increased vWF labelling was associated with C5-9MAC deposition and with fibre necrosis, but the vascular changes were not related to fibre atrophy nor to clinical indices of the severity of the patients' illness. The results suggest that microvascular damage and ischaemia may not be major factors in the pathogenesis of muscle fibre damage in multiple organ failure, but that endothelial activation is a common occurrence. The variability in the patterns of markers of endothelial activation, and the small proportion of capillaries affected, may reflect the complexity of the endothelial response to circulating or locally produced cytokines.

Adult↗

PubMed2002

Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure.

BACKGROUND: The abdominal compartment syndrome (ACS) has been implicated in the pathogenesis of postinjury multiple organ failure. The ACS is defined as intra-abdominal hypertension causing adverse physiologic response. This study was designed to determine the effects of IAH on the production of interleukin-1b (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and the effects on remote organ injury. METHODS: IAH was induced in Sprague-Dawley rats which were divided into 5 groups, 10 animals each. Intra-abdominal pressure (IAP) was increased to 20 mm Hg for 60 and 90 minutes in two different groups. In a third group following IAP of 20 mm Hg the abdomen was decompressed for 30 minutes before samples were collected. The other animals were used as controls. Hemodynamic response was monitored throughout the procedure. Cytokine levels were assessed in the plasma. Remote organ injury was assessed by histopathology and myeloperoxidase activity. RESULTS: IAH caused a significant decrease in MAP. After abdominal decompression MAP returned to baseline levels. A significant decrease in arterial pH was also noted. Increase in the levels of TNF-alpha and IL-6 was noted 30 minutes after abdominal decompression. Plasma concentration of IL-1b was elevated after 60 minutes of IAH. Abdominal decompression, however, did not cause a significant increase in the levels of this cytokine. Lung neutrophil accumulation was significantly elevated only after abdominal decompression. Histopathological findings showed intense pulmonary inflammatory infiltration including atelectasis and alveolar edema. CONCLUSIONS: IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF.

Abdominal Injuries↗

PubMed1994

[Multiple organ failure syndrome in fulminant hepatic failure].

BACKGROUND: in fulminant hepatic failure, different organs systems become involved and a multiple systems organic failure may ensure. AIM: to perform a retrospective analysis of patients with fulminant hepatic failure admitted to UC Hospital Intensive Care Unit. PATIENTS AND METHODS: the charts of fourteen patients (8 male) were analyzed. Multiple systems organic failure was defined as the presence of 2 or more organic dysfunctions. The evolution and mortality of these patients was analyzed. RESULTS: patient's ages ranged from 30 to 74 years. The etiology of hepatic failure was B hepatitis in 4, non A non B hepatitis in 5, acute fatty liver of pregnancy in 3 and use of halothane and HIN in 2. ICU stay ranged from 1 to 44 days and 2 patients survived (one with drug induced liver failure and one with acute fatty live of pregnancy). Mean prothrombin time was 19 +/- 9.5%, total bilirrubin was 24 +/- 8.9 mg/dl and 12 patients reached grade IV encephalopathy. Mean admission APACHE II score was 21.5 +/- 6. Twelve patients developed multiple systems organic failure, that appeared 1.5 days after or was already present at ICU admission; it lasted a mean of 2.5 days and all these 12 patients died. Neurologic involvement occurred in 13 patients, renal in 10, cardiovascular in 9, respiratory in 5 and hematological involvement in 1. CONCLUSIONS: multiple systems organic failure is frequent in fulminant hepatic failure and is associated with a high mortality.

Adult↗

PubMed1987

Acute renal failure and multiple organ system failure.

We treated 23 patients with acute renal failure who had multiple organ system failure. The patients ranged in age from 16 to 66 years (mean, 36 years). All patients underwent hemodialysis. Mortality increased with the number of organ systems involved, from 22% for patients with two systems involved to 100% for patients with four systems involved. The overall mortality was 47.8%. The association of ventilatory failure and sepsis resulted in the most deaths. Early resuscitation, eradication of the primary lesion, and hemodialysis are the most important points in the treatment and prevention of multiple organ system failure in patients with acute renal failure. Thus, the problems of single and multiple organ system failure in China are similar to those in other countries.

Acute Kidney Injury↗

PubMed2001

Post-injury multiple organ failure: the role of the gut.

Despite intensive investigation, the pathogenesis of post-injury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly suggests that the gastrointestinal tract (i.e., the gut) plays a pivotal pathogenic role. Since its inception in 1988, the Trauma Research Center (TRC) at the University of Texas-Houston Medical School (UTHMS) has focused its efforts on elucidating the role of the gut in post-injury MOF. On the basis of our observations and those of others, we believe that 1) shock with resulting gut hypoperfusion is an important inciting event, 2) the reperfused gut is a source of proinflammatory mediators that can amplify the early systemic inflammatory response syndrome (SIRS) and thus contribute to early MOF, 3) early gut hypoperfusion causes an ileus in both the stomach and small bowel that sets the stage for progressive gut dysfunction so that the proximal gut becomes a reservoir for pathogens and toxins that contribute to late sepsis-associated MOF, and 4) late infections cause further worsening of this gut dysfunction. Thus, the gut can be both an instigator and a victim of MOF. The purpose of this article is to provide the rationale behind these beliefs and to provide a brief overview of the ongoing research projects in the TRC at UTHMS.

Animals↗

PubMed1993

Role of serum endotoxin and antiendotoxin core antibody levels in predicting the development of multiple organ failure in acute pancreatitis.

It has been proposed that endotoxin contributes to the development of multiple organ failure (MOF) in acute pancreatitis. Endotoxaemia is transient and may not be detected by intermittent blood sampling. By contrast, not only can changes in the patient's endogenous antiendotoxin core antibody pool persist for many days, but depletion of this pool may be a key event in determining the physiological significance of endotoxaemia. A series of 33 patients with acute pancreatitis had daily measurement of Acute Physiology Score (APS) and levels of C-reactive protein, interleukin 6, endotoxin, immunoglobulin (Ig) G and IgM antiendotoxin core antibodies, and prospective documentation of complications. Endotoxin was detected in the serum of 13 patients, while a significant change in levels of endogenous antiendotoxin core antibodies was detected in all those with severe pancreatitis and in 28 overall. MOF developed in seven patients, five of whom died. The combination of a rising APS over the first 48 h of admission and a significant fall in endogenous IgG antibody level was observed in all patients who developed MOF (seven of seven), but in only one of 16 without MOF (P = 0.00003; overall predictive value 91 per cent). This study suggests that measuring the initial trend in APS and the concentration of endogenous IgG antiendotoxin core antibody provides a means of identifying patients with acute severe pancreatitis who are at high risk of developing MOF. This group might benefit from passive immunotherapy with antiendotoxin antibodies.

Acute Disease↗