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Multiorgan Dysfunction Syndrome (multiorgan + dysfunction_syndrome)
Selected AbstractsFunctional alterations of liver innate immunity of mice with aging in response to CpG-oligodeoxynucleotide,HEPATOLOGY, Issue 5 2008Toshinobu Kawabata Immune functions of liver natural killer T (NKT) cells induced by the synthetic ligand ,-galactosylceramide enhanced age-dependently; hepatic injury and multiorgan dysfunction syndrome (MODS) induced by ligand-activated NKT cells were also enhanced. This study investigated how aging affects liver innate immunity after common bacteria DNA stimulation. Young (6 weeks) and old (50-60 weeks) C57BL/6 mice were injected with CpG oligodeoxynucleotides (CpG-ODN), and the functions of liver leukocytes were assessed. A CpG-ODN injection into the old mice remarkably increased tumor necrosis factor (TNF) production in Kupffer cells, and MODS and lethal shock were induced, both of which are rarely seen in young mice. Old Kupffer cells showed increased Toll-like receptor-9 expression, and CpG-ODN challenge augmented TNF receptor and Fas-L expression in liver NKT cells. Experiments using mice depleted of natural killer (NK) cells by anti-asialoGM1 antibody (Ab), perforin knockout mice, and mice pretreated with neutralizing interferon (IFN)-, Ab demonstrated the important role of liver NK cells in antitumor immunity. The production capacities of old mice for IFN-,, IFN-,, and perforin were much lower than those of young mice, and the CpG-induced antitumor cytotoxicity of liver NK cells lessened. Lethal shock and MODS greatly decreased in old mice depleted/deficient in TNF, FasL, or NKT cells. However, depletion of NK cells also decreased serum TNF levels and FasL expression of NKT cells, which resulted in improved hepatic injury and survival, suggesting that NK cells are indirectly involved in MODS/lethal shock induced by NKT cells. Neutralization of TNF did not reduce the CpG-induced antitumor effect in the liver. Conclusion: Hepatic injury and MODS mediated by NKT cells via the TNF and FasL-mediated pathway after CpG injection increased, but the antitumor activity of liver NK cells decreased with aging. (HEPATOLOGY 2008.) [source] Severe blunt trauma in dogs: 235 cases (1997,2003)JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 6 2009Stephen A. Simpson DVM Abstract Objective , To evaluate population characteristics, injuries, emergency diagnostic testing, and outcome of dogs with blunt trauma requiring intensive care in an urban hospital. Design , Retrospective study 1997,2003. Setting , All data obtained from the University of Pennsylvania , Matthew J. Ryan Veterinary Hospital. Animals , Dogs admitted to the intensive care unit for treatment following blunt trauma. Interventions , None. Measurements and Main results , Of the 235 dogs that met inclusion criteria, 206 (88%) survived and 29 (12%) did not survive. Blunt vehicular trauma accounted for 91.1% of cases. Mild hyperglycemia and hyperlactatemia was common in both survivors and nonsurvivors. The chest was the most common region traumatized and the prevalence of polytrauma was 72.3%. Initial weight, vital signs, PCV, total plasma protein, BUN, glucose, lactate, acid-base status, and electrolytes did not differ between survivors and nonsurvivors. Nonsurvivors were significantly more likely to have had head trauma (P=0.008), cranium fractures (P<0.001), recumbency at admission (P<0.001), development of hematochezia (P<0.001), clinical suspicion of acute respiratory distress syndrome (P<0.001), disseminated intravascular coagulation (P<0.001), multiorgan dysfunction syndrome (P<0.001), development of pneumonia (P<0.001), positive-pressure ventilation (P<0.001), vasopressor use (P<0.001), and cardiopulmonary arrest (P<0.001). Conclusions , Outcome of severe blunt trauma in dogs treated with intensive care is very good. Despite the high survival rate, several features associated with poor outcome were identified. Neither admission lactate nor glucose was able to predict outcome. [source] Incidence and risk factors for the development of acute renal failure in patients with ventilator-associated pneumoniaNEPHROLOGY, Issue 3 2006GUL GURSEL SUMMARY: Aim: Infections are one of the most important risk factors for the development of acute renal failure (ARF) and ventilator-associated pneumonia (VAP) has been reported as one of the most frequent infection in intensive care units (ICU). Sepsis, shock, multiorgan dysfunction syndrome (MODS), use of nephrotoxic antibiotics and mechanical ventilation are potential risk factors for development of ARF during VAP. The objective of the study was to evaluate the incidence of ARF in patients with VAP and the role of VAP-related potential risk factors in the development of ARF. Methods: One hundred and eight patients who were admitted to the pulmonary ICU of a university hospital and developed VAP were included in this prospective observational cohort study. Only first episodes of VAP were studied. Diagnosis was based on microbiologically confirmed clinical findings. Potential outcome variables including responsible pathogens, recurrence, polymicrobial aetiology, bacteraemia, multidrug resistance of microorganisms, late/early VAP and sepsis and other known risk factors for development of ARF were evaluated. Risk factors were analysed by logistic regression analysis for significance. Results: Incidence of ARF was 38% (n = 41). Pneumonia with multidrug resistant pathogens (odds ratio, (OR) 5; 95% confidence interval (95%CI), 1.5,18; P = 0.011), sepsis (OR, 5.6; 95%CI, 1.7,18; P = 0.005) and severity of admission disease (Acute Physiology and Chronic Health Evaluation II score: OR, 1.1; 95%CI, 1.02,1.3; P = 0.017) were independent risk factors for the development of ARF during VAP episodes in multivariate analysis. Conclusion: These results showed that the incidence of ARF is high during the VAP episodes and that VAP developed with multidrug resistant pathogens and sepsis have an independent effect on the development of ARF. [source] Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2006R. Mofidi Background: Mortality in patients with acute pancreatitis is associated with the number of failing organs and the severity and reversibility of organ dysfunction. The aim of this study was to assess the significance of early systemic inflammatory response syndrome (SIRS) in the development of multiorgan dysfunction syndrome (MODS) and death from acute pancreatitis. Methods: Data for all patients with a diagnosis of acute pancreatitis between January 2000 and December 2004 were reviewed. Serum C-reactive protein (CRP), Acute Physiology And Chronic Health Evaluation (APACHE) II scores and presence of SIRS were recorded on admission and at 48 h. Marshall organ dysfunction scores were calculated during the first week of presentation. Presence of SIRS and raised serum CRP levels on admission and at 48 h were correlated with the cumulative organ dysfunction scores in the first week. Results: A total of 759 patients with acute pancreatitis were identified, of whom 45 (5·9 per cent) died during the index admission. SIRS was identified in 162 patients on admission and was persistent in 138 at 48 h. The median (range) cumulative Marshall score in patients with persistent SIRS was significantly higher than that in patients in whom SIRS resolved and in those with no SIRS (4 (0,12), 3 (0,7) and 0 (0,9) respectively; P < 0·001). Thirty-five patients (25·4 per cent) with persistent SIRS died from acute pancreatitis, compared with six patients (8 per cent) with transient SIRS and four (0·7 per cent) without SIRS (P < 0·001). No correlation was observed between CRP level on admission and Marshall score (P = 0·810); however, there was a close correlation between CRP level at 48 h and Marshall score (P < 0·001). Conclusion: Persistent SIRS is associated with MODS and death in patients with acute pancreatitis and is an early indicator of the likely severity of acute pancreatitis. Copyright © 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] | ||||||||||