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PubMed2006

Use of growth-hormone-releasing peptide-6 (GHRP-6) for the prevention of multiple organ failure.

Novel therapies for the treatment of MOF (multiple organ failure) are required. In the present study, we examined the effect of synthetic GHRP-6 (growth hormone-releasing peptide-6) on cell migration and proliferation using rat intestinal epithelial (IEC-6) and human colonic cancer (HT29) cells as in vitro models of injury. In addition, we examined its efficacy when given alone and in combination with the potent protective factor EGF (epidermal growth factor) in an in vivo model of MOF (using two hepatic vessel ischaemia/reperfusion protocols; 45 min of ischaemia and 45 min of reperfusion or 90 min of ischaemia and 120 min of reperfusion). In vitro studies showed that GHRP-6 directly influenced gut epithelial function as its addition caused a 3-fold increase in the rate of cell migration of IEC-6 and HT29 cells (P<0.01), but did not increase proliferation ([3H]thymidine incorporation). In vivo studies showed that, compared with baseline values, ischaemia/reperfusion caused marked hepatic and intestinal damage (histological scoring), neutrophilic infiltration (myeloperoxidase assay; 5-fold increase) and lipid peroxidation (malondialdehyde assay; 4-fold increase). Pre-treatment with GHRP-6 (120 microg/kg of body weight, intraperitoneally) alone truncated these effects by 50-85% (all P<0.05) and an additional benefit was seen when GHRP-6 was used in combination with EGF (1 mg/kg of body weight, intraperitoneally). Lung and renal injuries were also reduced by these pre-treatments. In conclusion, administration of GHRP-6, given alone or in combination with EGF to enhance its effects, may provide a novel simple approach for the prevention and treatment of MOF and other injuries of the gastrointestinal tract. In view of these findings, further studies appear justified.

Animals↗
PubMed1991

[Multiple organ failure. Reflection of generalized cell damage of all organs following severe trauma].

Multiple organ failure (MOF) is presently recognized as the most severe, and often lethal, complication after multiple trauma. Causal factors and pathomechanisms remain unclear, however. Generalized inflammatory cell tissue injury with a subsequent increase in permeability in all organs has been suggested. For this reason, 38 polytraumatized patients were examined in a prospective study. Organ function was analyzed, and specific clinical and histological studies were performed to check for generalized cell tissue damage and increased respiratory permeability. In all organs we found signs of tissue damage immediately after trauma. Disturbances of organ function were seen consistently, starting precisely from day 4. It was not possible to confirm an influence of blunt organ trauma on organ function during follow-up. The severity of injury (especially intrathoracic and intraabdominal) and massive bleeding increases the risk of MOF. MOF was not always associated with the onset of sepsis, and no temporal dependence could be shown. Histological studies demonstrated an inflammatory change in organ tissues, which is probably the result of toxic substances (endotoxin, TNF, oxygen radicals, proteases and eicanosoids) released into the blood circulation after trauma. Insufficient neutralization of these toxic metabolites leads to generalized permeability damage and consequently to progressive organ failure. Therefore, even with optimized initial treatment of multiple trauma patients, MOV and mortality can only be reduced with a causal approach to therapy.

Adolescent↗
PubMed2001

Multiple organ failure still a major cause of morbidity but not mortality in blunt multiple trauma.

BACKGROUND: Multiple organ failure (OF/MOF) was found to be the major complication after blunt multiple trauma during the last 25 years and was correlated with a high mortality rate. Recently, several publications reported a decreased ARDS-related mortality, but there is little information about mortality rates from posttraumatic MOF. The purpose of this study was to describe the development of MOF-related death after blunt multiple trauma during the last 25 years. METHODS: Blunt multiple trauma patients with an Injury Severity Score (ISS) > 15 points were included in this evaluation. According to the year of trauma, the population was divided into five groups: years 1975-1980 (n = 317), years 1981-1985 (n = 308), years 1986-1990 (n = 246), years 1991-1997 (n = 368), and years 1998-1999 (n = 122). Main outcome measurements were death, cause of death, and length of ICU stay. Patients dying within the first 24 hours after trauma were excluded. All data indicated in the Results section are presented as mean +/- SEM. Continuous variables were compared by ANOVA. Ordinal variables were analyzed by chi2 contingency table analysis and, if significant, subsequently by Fisher's exact test (two-tailed test, p < 0.05). RESULTS: Mean ISS remained unchanged between 1975-1980 (ISS 29 +/- 1) and 1998-1999 (ISS 31 +/- 1) (p = 0.56). During the observation period, the mean age increased from 33 +/- 1 years (1975-1980) to 40 +/- 2 years (1998-1999) (p = 0.03). The overall incidence of OF/MOF slightly increased from 25.6% (1975-1980) to 33.6% (1998-1999) (p = 0.1). Length of ICU stay was not different between 1975-1980 (LOS: 14 +/- 1 d) and 1998-1999 (LOS: 19 +/- 2 d) (p = 1.0). The overall mortality decreased significantly, from 28.7% (1975-1980) to 13.9% (1998-1999) (p < 0.001). While the mortality due to severe head injuries remained unchanged (1975-1980, 8.2%; 1998-1999, 9.0%) (p = 0.85), mortality due to OF/MOF decreased significantly (p < 0.001), from 18.0% (1975-1980) to 4.1% (1998-1999). The age of patients dying from OF/MOF increased significantly (p = 0.04) during the observation period, from 44 +/- 3 years (1975-1980) to 63 +/- 6 years (1998-1999). CONCLUSION: Although MOF incidence remains unchanged, there is a significant fall in MOF-related mortality in patients with severe trauma, and death from single organ failure is virtually absent. Severe brain injury is now the leading cause of death in patients with severe multiple injuries admitted to the ICU.

Adult↗
PubMed1990

Multiple organ failure: inflammatory priming and activation sequences promote autologous tissue injury.

Systemic inflammation promotes multiple organ failure through the induction of diffuse microvascular leak. Inflammatory cells such as neutrophils propagate this process. Tissue injury by neutrophils may be viewed as a normal process, inflammation, that has become uncontrolled and generalized. Multiple inflammatory stimuli synergistically promote neutrophil-mediated tissue injury in priming and activation sequences. In some settings, cellular priming is mediated by platelet-activating factor and can be prevented by platelet-activating factor antagonists. Inhibiting cellular priming could be efficacious in the therapy of multiple organ failure.

Animals↗
PubMed1989

[Role of the liver in septic encephalopathy. A disorder associated with multiple organ failure caused by sepsis].

The appearance of jaundice during a septic process is usually associated to multiple organ failure and a high mortality rate. Among 17 septic patients followed prospectively, we found 11 with hepatic dysfunction. Abnormal levels of bilirubin and alanine-aminotransferase were found. Glutamine concentration in spinal fluid was 26 +/- 19.4 mg/dl vs 9.43 +/- 2.41 in patients without liver failure (p less than 0.05). Significant correlations were found among levels of bilirubin and glutamine (r = 0.83), creatinine (r = 0.708), number of platelets (r = 0.778) and between glutamine and creatinine (r = 0.708). Patients with liver failure presented a higher rate of renal failure and thrombocytopenia (p less than 0.01) and a higher mortality rate. These findings confirm that liver failure is associated to multiple organ failure and thrombocytopenia. It may be related to small vessel occlusion.

Acute Kidney Injury↗
PubMed1989

[A study of refractory pneumonia complicated by multiple organ failure in the elderly].

A retrospective study of refractory pneumonia (n = 54), who were randomly selected from total of 657 cases of pneumonia in the elderly, was performed. These were divided into the following two groups in terms of complications. The group with multiple organ failure (MOF group; n = 30), complicated by multiple organ failure during their clinical course of refractory pneumonia, was compared with refractory pneumonia without multiple organ failure (non-MOF group; n = 24). Among 57% of cases of the MOF group, respiratory failure developed prior to MOF and among 37% of the cases respiratory failure occurred simultaneously with MOF. The respiratory failure in the MOF group was closely related to coagulopathy. Histopathological studies of the MOF group revealed remarkable congestion and edema. From these observations, respiratory management is considered the most important to avoid concomitant multiple organ failure.

Aged↗
PubMed2002

Effects of calpain inhibitor I on multiple organ failure induced by zymosan in the rat.

OBJECTIVE: Zymosan enhances the formation of reactive oxygen species, which contributes to the pathophysiology of multiple organ failure. We investigated the effects of calpain inhibitor I (5, 10, or 20 mg/kg) on the multiple organ failure caused by zymosan (500 mg/kg, administered intraperitoneally as a suspension in saline) in rats. SETTING: University research laboratory. SUBJECTS: Male Sprague-Dawley rats.INTERVENTIONS Multiple organ failure in rats was assessed 18 hrs after administration of zymosan and/or calpain inhibitor I and was monitored for 12 days (for loss of body weight and mortality rate). MEASUREMENT AND MAIN RESULTS: Treatment of rats with calpain inhibitor I (5, 10, or 20 mg/kg intraperitoneally, 1 and 6 hrs after zymosan) attenuated the peritoneal exudation and the migration of polymorphonuclear cells caused by zymosan in a dose-dependent fashion. Calpain inhibitor I also attenuated the lung, liver, and intestinal injury (histology) as well as the increase in myeloperoxidase activity and malondialdehyde concentrations caused by zymosan in the lung, liver, and intestine. Immunohistochemical analysis for nitrotyrosine and for poly(adenosine-disphosphate-ribose) revealed positive staining in lung, liver, and intestine from zymosan-treated rats. The degree of staining for nitrotyrosine and poly(adenosine-disphosphate-ribose) was reduced markedly in tissue sections obtained from zymosan-treated rats administered calpain inhibitor I (20 mg/kg intraperitoneally). Furthermore, treatment of rats with calpain inhibitor I significantly reduced the expression of inducible nitric oxide synthase and cyclooxygenase-2 in lung, liver, and intestine. CONCLUSION: This study provides the first evidence that calpain inhibitor I attenuates the degree of zymosan-induced multiple organ failure in the rat.

Animals↗
PubMed1995

Kupffer cells in multiple organ failure--their activation as revealed by immunohistochemistry for lysozyme, alpha 1-antichymotrypsin, and lectins.

It has been recently suggested that multiple organ failure (MOF) is caused by activation of inflammatory cells and subsequent release soluble factors from these cells. However, morphologic data to support this hypothesis is lacking. Thus, the present study was conducted to evaluate the activation of Kupffer cells in multiple organ failure by applying immunohistochemical techniques to formalin-fixed, paraffin-embedded autopsy materials. Eleven liver samples of multiple organ failure were stained for lysozyme, alpha 1-antichymotrypsin, and by lectins, such as ConA, RCA-I, WGA and PNA. Normal livers and diseased livers of miscellaneous origins were also stained and compared. In normal livers, Kupffer cells were generally negative or weakly positive for lysozyme, alpha 1-antichymotrypsin, ConA, RCA-I, and PNA, while they were positive for WGA. In multiple organ failure, by contrast, Kupffer cells showed stronger staining for alpha 1-antichymotrypsin, lysozyme, ConA, RCA-I, WGA, and PNA, indicating activation of Kupffer cells. Increased reaction to WGA and RCA-I was also observed in diseased livers of miscellaneous origins. These results are in agreement with the current hypothesis that activation of Kupfer cells is involved in the pathogenesis of MOF. Our findings also indicate, however, that activation of Kupffer cells is not a phenomenon unique to MOF.

Carbohydrates↗
PubMed2003

Severe falciparum malaria: an important cause of multiple organ failure in Indian intensive care unit patients.

OBJECTIVE: To study the incidence and severity of multiple organ dysfunction in severe falciparum malaria. DESIGN: Prospective, observational study. SETTING: Intensive care unit of a tertiary care university hospital. PATIENTS: Three hundred one consecutive patients with severe falciparum malaria admitted during the 30-month study period. INTERVENTIONS: Daily assessment of clinical and biochemical variables required for calculating the Sequential Organ Failure Assessment (SOFA) score. MEASUREMENTS AND MAIN RESULTS: Central nervous system failure was present in 121 patients (53 deaths). Renal failure occurred in 91 patients (48 deaths), and 33 required dialysis. Severe thrombocytopenia occurred in 114 patients (seven required platelet transfusion), and 19 patients had thrombocytopenia and disseminated intravascular coagulation; all required component therapy; 229 patients received blood transfusion for severe hemolytic anemia. Hepatic failure occurred in 77 patients (38 deaths). Respiratory failure developed in 79 patients and carried the worst outcome (70 deaths). It occurred later in the course of the illness (mean, 3.1 days; p <.001) compared with cerebral, renal, and coagulation failure (mean, 1.3-2.3 days). Regardless of the organ system involved, only 11 of 172 patients with one or no organ failure died (6.8%), whereas mortality rate increased to 48.8% in 129 patients with multiple organ failure. Other abnormalities associated with poor outcome included seizures in 54 patients (56% mortality rate), metabolic acidosis in 167 (40% mortality rate), hypoglycemia in 88 (39% mortality rate), and hemoglobinuria in 190 (33% mortality rate). Sixty patients had quinine toxicity requiring dosage reduction. Bacterial sepsis occurred in 39 patients (35 deaths) and accounted for 85% of deaths occurring after day 7. Twenty-three pregnant women had no significant difference in outcomes. Overall mortality rate was 24.6% (301 patients, 74 deaths). CONCLUSIONS: Malaria is an important cause of multiple organ failure in India. Mortality rate is 6.4% when one or fewer organs fail but increases to 48.8% with failure of two or more organs. However, outcomes are better than for similar degrees of organ failure in sepsis.

APACHE↗
PubMed2001

Improved outcome prediction for patients with multiple organ failure undergoing continuous hemodiafiltration.

A number of patients with multiple organ failure (MOF) regardless of accompanying acute renal failure have been treated with continuous hemodiafiltration (CHDF). However, despite its high cost, the costs/benefits of CHDF for MOF patients still need to be evaluated. Although many scoring systems were established to predict the outcome of MOF, their predictive powers were not estimated in MOF patients undergoing CHDF. Therefore, using 52 Japanese patients with MOF treated with CHDF for more than 1 week, we estimated the predictive powers of multiple organ dysfunction (MOD) scores and acute physiology and chronic health evaluation (APACHE) III scores, retrospectively. The patients were divided into 2 groups according to outcome at Day 28 after the initiation of CHDF. In both scoring systems, the median values at Day 0 were not significantly different between the survival (n = 19) and the nonsurvival (n = 33) groups. In contrast, at Day 3, the median values of MOD scores was 4 (0-14) in the survival group and 9 (1-12) in the nonsurvival group (p = 0.0035). The median value of APACHE III scores were 37 (19-97) and 87 (16-150) at Day 3, respectively (p < 0.0001). In the survival group, APACHE III scores significantly decreased from the median value of 64 (32-89) to 37 (p = 0.0269), and in the nonsurvival group, it increased significantly from the median value of 70 (29-103) to 87 (p = 0.0116). In contrast, no significant changes were observed in the MOD scores. In conclusion, the MOD score and the APACHE III score systems had less power to predict the outcome of MOF patients undergoing CHDF at Day 0. However, rescoring at Day 3 of each index was much more powerful to accurately predict the outcome of such patients.

APACHE↗
PubMed2005

Prolonged use for at least 10 days of intraaortic balloon pumping (IABP) for heart failure.

Intraaortic balloon pumping (IABP) is a useful therapy for refractory heart failure. However, the safe duration of this therapy and possible complications due to long-term IABP support remain unclear. In this study, we reviewed retrospectively patients requiring the long-term use of IABP, defined here as 10 days or more, to estimate the background and prognosis of patients undergoing long-term use of IABP. The characteristics and perioperative status were compared between survivors and nonsurvivors. A total of 18 patients including 12 males and 6 females required long-term IABP use. IABP was induced in 13 patients (72%) following cardiac surgery and in 5 without cardiac surgery. The mean duration of IABP support was 17 +/- 7 days. Seven patients survived and 11 died of heart failure and/or associated other organ failure. Multiple organ failure (MOF) was recognized in 10 patients, and the incidence of MOF was significantly (P = 0.005) lower in the survivors (14%) compared to the nonsurvivors (82%). The percentage of postcardiac surgery patients was also significantly (P = 0.027) higher in nonsurvivors (91%) than in survivors (43%). Logistic regression analysis identified MOF and cardiac surgery as independent predictors for death. Femoral arterial-venous fistula was the only IABP-related complication. In patients receiving long-term IABP, attention should be paid to other organ complications associated with heart failure, and the use of other circulatory supports such as PCPS or VAD to avoid MOF should be considered if necessary.

Aged↗
PubMed2000

Hemophagocytic lymphohistiocytic syndrome: Unrecognized cause of multiple organ failure.

OBJECTIVE: To describe an often-unrecognized clinical picture of multiple organ failure in hemophagocytic lymphohistiocytic syndrome (HLS). DESIGN: Retrospective chart review. SETTING: A ten-bed pediatric intensive care unit (PICU) in a tertiary children's university hospital. PATIENTS: A total of 11 children (age, 5 months to 13 yrs) who fulfilled the criteria for the diagnosis of familial- or infectious-associated hemophagocytic lymphohistiocytosis and who required intensive care support for organ failure. INTERVENTION: None. MAIN RESULTS: During a 10-yr period, 5,439 children were hospitalized in our PICU. A total of 11 children were diagnosed as suffering with HLS. Of these 11 patients, three (27%) had the familial form and eight had the infectious-associated form. After admission to the PICU, seven patients (63%) were diagnosed as suffering with HLS and each had one or more organ failures (patients 3-7, 9, and 10). All presented with fever, hepatomegaly, and splenomegaly; in addition, all had at least two of the following: anemia, neutropenia, or thrombocytopenia. All 11 had lymphohistiocytic accumulation in bone marrow (n = 10), lymph node (n = 2), lung (n = 2), and/or liver (n = 1). Organ failure was noted most often in the respiratory system (n = 7) attributable to severe, acute respiratory distress syndrome and pleural effusion. Of the 11 patients, six had cardiovascular involvement that manifested as shock in three and as capillary leak syndrome in three. Renal failure occurred in four patients. Of these, two required hemodiafiltration and one required peritoneal dialysis. Liver failure occurred in three and central nervous system involvement and coma in three. Most of the patients required massive therapeutic intervention, including assisted ventilation (n = 6), inotropic support (n = 3), and hemofiltration (n = 3). A total of seven patients (63%) died. CONCLUSIONS: Hemophagocytic lymphohistiocytic syndrome in the pediatric population may have a dramatic clinical picture, with multiple organ failure as a presenting symptom or early in the disease course, mandating intensive support in the PICU.

Journal Article↗
PubMed1998

Management of multiple organ failure: guidelines but no hard-and-fast rules.

Multiple organ failure is the commonest cause of death in the intensive care unit setting. There are numerous precipitating factors including sepsis, trauma and pancreatitis. The resulting tissue hypoxia, exaggerated inflammatory response and generation of free oxygen radicals leads to tissue damage and organ dysfunction. No definitive treatment exists despite considerable efforts to find a 'magic bullet'. Management still revolves around support of organ function and prevention of iatrogenic complications until recovery occurs. An increasing emphasis is being placed on prevention of organ dysfunction, including maintenance of tissue oxygenation, nutrition and infection control.

Anti-Bacterial Agents↗
PubMed1990

APACHE II score does not predict multiple organ failure or mortality in postoperative surgical patients.

A clinical study was undertaken to evaluate the ability of the APACHE (acute physiology and chronic health care) II system to predict the development of multiple organ failure syndrome and subsequent mortality. The study was conducted in a university general surgery intensive care unit using the admission APACHE II score. Over a 1-year period, 92 patients qualified for the study, 24 of whom survived, 69 of whom suffered multiple organ failure syndrome, and 68 of whom died. The APACHE II score did not predict the development of multiple organ failure syndrome or mortality with clinical utility and significantly underestimated the potential for the development of multiple organ failure syndrome. Factors that did predict the development of multiple organ failure syndrome and mortality were the time-dependent changes in the PaO2-to-fraction of inspired oxygen ratio and serum lactate, creatinine, and bilirubin levels. Better markers of cell injury are needed for use in decision making and quality assurance analysis in surgical patients.

Humans↗
PubMedDate not supplied

[Multiple organ failure (MOF) in tertian malaria. Report of a clinical case].

The authors describe a malignant malaria clinic case complicated by shock, disseminated intravascular coagulation (DIC) and multiple organ failure (renal, heart, lung failure): MOF. Early diagnosis and suitable therapy, with multiple organ failure intensive care allowed a good patient outcome.

Adult↗
PubMed1989

[Multiple organ failure following open heart surgery in adults].

The cases multiple organ failure (MOF) which occurred post-operatively following open heart surgery in adults were studied on a pre and post-operative hemodynamics. Post-operative low cardiac output syndrome (LOS) was thought to result in decreased renal and hepatic perfusion with subsequent ischemic damage to these organs. Therefore, to management MOF, we have to prevent post-operative LOS, for example, administration of cathecholamine and vasodilator, and early clinical application of IABP and ventricular assist device (VAD). In a post-operative hemodynamics, the cases of severe right ventricular failure tend to have more protracted MOF. It was though that MOF could be minimized with shortened cardiopulmonary bypass duration, and early application of assisted circulation.

Adult↗
PubMed1998

[Inflammatory mediator and organ dysfunction syndrome].

Inflammatory mediators include endotoxin (ETX), cytokines (interleukins [ILs], tumor necrosis factors [TNFs], and interferons), eicosanoids (prostaglandins and thromboxanes), reactive oxygen species (O2-, NO, and ONOO-), complements (C3 and C4), and stress hormones (catecholamine, cortisol, vasopressin, and growth hormone). These mediators work to maintain homeostasis under stressful conditions through a complex chain reaction or cascade that results in transient tissue damage known as the inflammatory response. The inflammatory response is decreased by a negative feedback system, which consists not only of the self-inhibitory action of ETX, TNF-alpha, IL-1, and IL-8, but also of the production of antiinflammatory mediators such as IL-4, -10, -11, and -13, TGF-beta, IL-Ra, and sTNFR. If excessive stress or a second attack of stress results in a higher level of inflammation-producing mediators than of inflammation-inhibiting mediators, tissue destruction occurs due to activation and infiltration of inflammatory cells or necrosis due to endothelial injury is seen, followed by disruption of homeostasis, organ dysfunction, and organ failure (multiple organ dysfunction syndrome [MODS] or multiple organ failure [MOF] induced by SIRS). In experimental liver dysfunction after 95% hepatectomy, massive apoptosis of hepatocytes is induced by prolonged hypercytokinemia, ONOO- production, decreased mitochondrial membrane potential of hepatocytes, and decreased Bc12 levels. On the other hand, if the antiinflammatory response is greater than the inflammatory response (CARS) a compromised state and refractory infection are seen, followed by progressive, irreversible organ dysfunction (MODS or MOF induced by CARS).

Animals↗