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Multiple Organ Dysfunction (multiple + organ_dysfunction)

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Medical Sciences100%

Terms modified by Multiple Organ Dysfunction

  • multiple organ dysfunction syndrome
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    Selected Abstracts

    BIOCHEMICAL MARKERS OF CARDIAC INJURY IN NORMAL AND SURVIVING VERSUS NON-SURVIVING SEPTICEMIC NEONATAL FOALS

    JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue S1 2004
    SF Peek
    Although myocardial injury can be a significant component of multiple organ dysfunction (MODS) in association with septicemia in critically ill human patients, it is as yet an undefined clinical entity in equine septicemia. With septicemia as the leading cause of death in neonatal foals, a better understanding of the pathophysiology, diagnosis and treatment of MODS will be important in further improving survival rates. We designed a prospective study to establish normal ranges for cardiac troponin I (cTnI), T (cTnT) and CKMB mass in healthy 24,48 hour old foals, as well as septicemic neonatal foals seen over a 2-year period in a teaching hospital. We also performed a comparison of these biomarkers in surviving and non-surviving septicemic foals. Sepsis was judged on the basis of the presence of any of the 3 following criteria: blood culture positive at admission, admission sepsis score ,11, or 3 or more sites of infection during hospitalization in foals ,14 days of age. cTnI was measured by the ACCESS® (Beckman Coulter), cTnT was measured using the Elecsys 2010® Immunoassay (Roche), and CKMB mass measurements were performed using the Elecsys 2010®. Each parameter was described using range and 95th and 50th percentile. Comparisons were made for each parameter between normal and septic foals as well as surviving and non-surviving septic foals using the non-parametric Wilcoxon's rank sum test. Significance was set at p<0.05. There were 52 control foals and 38 septic foals of which 22 survived. Significant differences were documented for CKMB between septicemic and normal foals, but not for cTnT or cTnI. However, CKMB and cTnT were significantly lower in surviving versus non-surviving septicemic foals. The 50th and 95th percentiles alongside the ranges for the normal foal population were 0.14, 0.49, (0.01,0.51) ,g/L for cTnI, 0.009, 0.03, (0.009,0.04) ,g/L for cTnT and 2.3, 7.4, (0.4,9.3) ,g/L for CKMB. Our findings suggest that myocardial injury is a component of MODS during septicemia in foals, and that quantitatively significant increases in CKMB and cTnT are seen in non-surviving septicemic foals versus survivors. [source]

    Critical role of the vascular endothelial cell in health and disease: a review article

    JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2004
    Todd C. Duffy DVM
    Abstract Objective: To review the human and veterinary literature on the role of the vascular endothelial cell in health, as well as during hypoxic and inflammatory disease states. Data sources: Data from human and veterinary literature were reviewed through a Pubmed search and a manual search of the references listed in articles covering some aspect of vascular endothelial cell function. Human data synthesis: The development of techniques that allow the maintenance and growth of endothelial cells in culture has produced an explosion of new research in the area of endothelial cell physiology. This plethora of data has revealed the critical role that vascular endothelial cells play in both health and disease states. Interspecies variations can occur with respect to the vascular endothelial cell physiology and its response to pathologic conditions. Veterinary data synthesis: There is a paucity of information regarding the role of the vascular endothelial cell in health or disease of small animals. Many human studies use species cared for by veterinarians, providing information that may be applied to small animals and that may be used to construct future studies. Conclusion: An organ system itself, the vascular endothelium is an essential component of all organs in the body. The endothelial cell lining functions to maintain selective permeability between the blood and the tissue it supplies, regulate vascular tone, sustain blood fluidity through regulation of coagulation, and modulate interaction of leukocytes with the interstitium and inflammatory reactions. During disease states, the endothelial cell functions locally to limit the boundaries of the disease process. If these functions are not controlled, they can become a part of the pathogenic process, contributing to blood stasis and thrombosis, potentiation of local inflammation and interstitial edema formation, subsequent tissue hypoxia, and multiple organ dysfunction. Pharmacological investigations targeting the modulation of endothelial function during disease states have not yet advanced treatment protocols. Since all critically ill animals are at risk for some degree of endothelial cell dysfunction, treatment regimens should focus on promoting capillary blood flow and tissue oxygen delivery. [source]

    Role of mast cells in the development of pancreatitis-induced multiple organ dysfunction

    BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 2 2002
    M. Dib
    Background: Activated mast cells can produce and release a number of inflammatory mediators involved in the pathophysiology of acute conditions. The aim of the present study was to evaluate the role of activated tissue mast cells in the pathogenesis of multiple organ dysfunction syndrome following acute pancreatitis (AP). Methods: AP was induced by the intraductal infusion of 5 per cent sodium taurodeoxycholate in the rat. Some 30 min before induction of AP, a mast cell stabilizer (sodium cromoglycate (SCG)) or antihistamines (pyrilamine, cyproheptadine, meclizine and amitriptyline) were administered intra peritoneally. Plasma exudation of radiolabelled albumin, histamine, myeloperoxidase (MPO), monocyte chemoattractant protein (MCP) 1 and adhesion molecules (platelet endothelial cell adhesion molecule (PECAM) 1 and L-selectin) were measured. Results: The mast cell stabilizer significantly reduced plasma exudation in the pancreas, colon and lungs (P < 0·05), decreased the release of histamine at 1 h (P < 0·05), and reduced MPO activity and MCP-1 levels in the colon and lungs (P < 0·05) but not in the pancreas. Expression of PECAM-1 and L-selectin on total circulating leucocytes in rats with AP and SCG pretreatment did not differ from that in sham controls, while levels in animals that had AP and saline pretreatment were half of those seen following sham operation. Conclusion: Activation of mast cells after induction of AP is involved in the development of endothelial barrier dysfunction in both the pancreas and extrapancreatic organs/tissues, particularly in the lungs and colon. This may, at least partly, contribute to the sequential development of multiple organ dysfunction and organ/tissue-specific endothelial barrier dysfunction. © 2002 British Journal of Surgery Society Ltd [source]

    Extracorporeal membrane oxygenation bridge to adult heart transplantation

    CLINICAL TRANSPLANTATION, Issue 3 2010
    Jennifer Chia-Ying Chung
    Chung JC, Tsai PR, Chou NK, Chi NH, Wang SS, Ko WJ. Extracorporeal membrane oxygenation bridge to adult heart transplantation. Clin Transplant 2010: 24: 375,380. © 2009 John Wiley & Sons A/S. Abstract:, Extracorporeal membrane oxygenation (ECMO) can rescue some critical patients with circulatory collapse when intra-aortic balloon pump (IABP) and ventricular assist devices (VAD) are not suitable. A subset of these patients can use ECMO for direct bridging, or indirect double bridging via VAD to heart transplantation (HTx). For these patients, we identified risk factors for unsuccessful ECMO bridging, with survival to receiving either HTx or VAD as the measure of success. The characteristics evaluated were age, sex, body mass index, pre-ECMO cardiopulmonary resuscitation (CPR), IABP use, dialysis use, sequential organ failure assessment (SOFA) score, and the etiology of cardiomyopathy. From January 1995 to August 2007, there were 70 adult ECMO patients with the intent to bridge to HTx (male: 55, age: 46 ± 14 yr). Thirty-one patients (44%) were successful in bridging. A stepwise multivariate logistic regression analysis found that age > 50 yr (p = 0.003), pre-ECMO CPR (p = 0.001) and SOFA score > 10 at ECMO initiation (p = 0.018) were significant independent predictors of unsuccessful bridging. Direct VAD implantation, if possible, is preferable to double bridging in patients over 50 yr. Also, elective ECMO support before hemodynamic deterioration to cardiac arrest or multiple organ dysfunction would improve rates of successful ECMO bridging. [source]

    Trauma: physiology, pathophysiology, and clinical implications

    JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2006
    DACVA, DACVECC, William Muir DVM
    Abstract Objective: To review the physiology, pathophysiology, and consequences of trauma. The therapeutic implications of hypovolemia, hypotension, hypothermia, tissue blood flow, oxygen delivery, and pain will be discussed. Data Sources: Human and veterinary clinical and research studies. Human and veterinary data synthesis: Trauma is defined as tissue injury that occurs more or less suddenly as a result of violence or accident and is responsible for initiating hyothalamic,pituitary,adrenal axis, immunologic and metabolic responses that are designed to restore homeostasis. Tissue injury, hemorrhage, pain, and fear are key components of any traumatic event. Trauma and blood loss result in centrally integrated autonomic-mediated cardiovascular responses that are designed to increase heart rate, systemic vascular resistance, and maintain arterial blood pressure (ABP) to vital organs at the expense of blood flow to the gut and skeletal muscle. Severe trauma elicits exuberant physiologic, immunologic, and metabolic changes predisposing the animal to organ malfunction, a systemic inflammatory response, infection, and multiple organ dysfunctions. The combination of both central and local influences produces regional redistribution of blood flow among and within tissue beds which, when combined with impaired vascular reactivity, leads to maldistribution of blood flow to tissues predisposing to tissue hypoperfusion and impaired oxygen delivery and extraction. Gut blood flow and viability may serve as a sentinel of patient survival. These consequences are magnified in animals suffering from pain or that become hypothermic. Successful treatment of traumatized animals goes beyond the restoration of blood pressure and urine output, is dependent on a fundamental understanding of the pathophysiologic processes responsible for the animals current physical status, and incorporates the reduction of pain, stress, and the systemic inflammatory response and methods that restore microcirculatory blood flow and tissue oxygenation. Conclusions: Severe trauma is a multifaceted event and is exacerbated by hypothermia, pain, and stress. Therapeutic approaches must go beyond the simple restoration of vascular volume and ABP by maintaining tissue blood flow, restoring tissue oxygenation, and preventing systemic inflammation. [source]