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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic inflammatory response syndrome (SIRS) is the clinical expression of the action of complex intrinsic mediators of the acute phase reaction. SIRS can be precipitated by events such as infection, trauma, pancreatitis, and surgery. At times, SIRS can compromise the function of various organ systems resulting in Multiple Organ Dysfunction Syndrome (MODS). SIRS and MODS are graded expressions of the inflammation associated with acute illness. Mild forms are frequent in general wards for both medical and surgical patients but those with severe forms require intensive care. Clinicians should learn to identify SIRS in their patients at an early stage to determine the underlying cause and treatment before the SIRS progresses to a more severe form.
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PMID:The systemic inflammatory response syndrome: definitions and aetiology. 951 Oct 80

Antithrombin III (AT III) is the physiological inhibitor of thrombin and other serine proteases of the clotting cascade. In the development of sepsis, septic shock and organ failure, the plasma levels of AT III decrease considerably, suggesting the concept of a substitution therapy with the inhibitor. A decrease of AT III plasma levels might also be associated with other pathological disorders like trauma, burns, pancreatitis or preclampsia. Activation of coagulation and consumption of AT III is the consequence of a generalized inflammation called SIRS (systemic inflammatory response syndrome). The clotting cascade is also frequently activated after organ transplantation, especially if organs are grafted between different species (xenotransplantation). During the past years AT III has been investigated in numerous corresponding disease models in different animal species which will be reviewed here. The bulk of evidence suggests, that AT III substitution reduces morbidity and mortality in the diseased animals. While gaining more experience with AT III, the concept of substitution therapy to maximal baseline plasma levels (100%) appears to become insufficient. Evidence from clinical and preclinical studies now suggests to adjust the AT III plasma levels to about 200%, i.e., doubling the normal value. During the last few years several authors proposed that AT III might not only be an anti-thrombotic agent, but to have in addition an anti-inflammatory effect.
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PMID:Antithrombin III in animal models of sepsis and organ failure. 951 81

Severe acute pancreatitis is a two-phase systemic disease. The first phase is a clinical response resulting from systemic effects of proinflammatory mediators called SIRS (systemic inflammatory response syndrome), that may lead to multiple organ failure and death. The second phase, if the process is not reversed by natural defences or treatment, may be accompanied by local complications such as infected pancreatic necrosis. The severity of the disease must be established early to identify patients requiring intensive monitoring and support. The clinico-biochemical score (Ranson score) is about 80% accurate at 48 hours but is not accurate before this time; the APACHE II system has the sensitivity to predict severe pancreatitis in 61% of patients on admission. Although not perfect, the prognostic systems of severity remain better than clinical judgement. SIRS followed by local complications is accompanied by increased energy requirements and, with the absence of oral intake, a persistently negative nitrogen balance and mineral and micronutrient deficiencies. Thus, early nutritional support is indicated. Formerly, total parenteral nutrition was the standard practice for providing exogenous nutrients avoiding pancreatic stimulation. The use of early enteral feeding has recently been evaluated. Gastric atony and obstruction of the duodenum by pancreatic oedema or necrosis have been overcome by delivering enteral nutrition to the jejunum, distal to the ligament of Treitz; in this position, regular diets do not stimulate pancreatic secretions. The efficacy, tolerance, clinical outcome and cost of enteral nutrition suggest that this feeding route should be preferred in patients with severe acute pancreatitis.
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PMID:[Nutrition in acute pancreatitis]. 1058 62

SIRS, MODS, and MOF are not diseases or even syndromes. They are simply clinical descriptors of people that are sick. They are symptoms and signs of various stages of illness progressing to death in the modern organ supporting ICU. They are catchy, popular acronyms but they cannot be treated specifically, and then only by support of organ functions. To help our patients and improve morbidity and mortality we must focus on specific diseases. Although ventilator associated pneumonia and pancreatitis may both produce an inflammatory response, cytokine-mediator activation and SIRS, they must each be treated in a different way. I believe that SIRS has led us astray.
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PMID:A debate on the subject "Are SIRS and MODS important entities in the clinical evaluation of patients?" The con position. 1113 6

The occurrence of BT has been well documented in experimental animal models of hemorrhagic shock, trauma, severe burns, cirrhosis, pancreatitis, and bacterial overgrowth. Translocation of viable bacteria and endotoxins into mesenteric lymph nodes and other gut-associated lymphatic tissue is thought to activate a complex interplay of mediators that initiates the SIRS. Multiple humoral and cellular systems cause synthesis, expression, and release of inflammatory mediators, such as toxic oxygen radicals, proteolytic enzymes, adherence molecules, and various cytokines. A massive sustained proinflammatory response can ultimately result in irreversible multiple organ dysfunction. Because BT is associated with splanchnic hypoperfusion, the cornerstone of therapy involves rapid resuscitation and restoration of tissue perfusion. If a septic focus can be identified, it should be removed. Gut protectants, promotility agents, antioxidants, and immune-enhancing diets have shown promise in improving length of survival in these critically ill patients.
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PMID:Bacterial translocation: clinical implications and prevention. 1238 Jan 71

The authors define pathogenetics correlations as a acute necrotizing pancreatitis complicated by infection and bacterial translocation. Acute necrotizing pancreatitis infection occurs for gastrointestinal bacterial translocation due to structural and functional modifications of intestinal mucosa. These modifications are results of mucosa ischemic-reperfusion system caused by systemic emodynamic instability in micro- and macro-circulation of splanchnic district. Emodynamic systemic instability has a central role in different multiple physiopathologic phenomena (ipovolemic shock; pancreatic shock, SIRS), which is caused by acute pancreatic necrosis and carries to common way established by severe systemics emodinamics modifications; these changes promote growth of adverse events which conduce by means of process previously described to bacterial translocation and infection of acute pancreatic necrosis. Indeed, emodynamic systemic instability of any etiology, can determine for one way bacterial translocation and on the other acute ischemic pancreatitis; both phenomena concur lead to cause beginning of acute necrotizing pancreatitis complicated by infection. The authors confirm that improved knowledge of acute pancreatic necrosis complicated by infection and own pathogenetic correlations with bacterial translocation, allows the realization of therapeutic measures aimed to prophylaxis of infection of acute pancreatic necrosis. Central emodynamic stability regularization of splanchnic perfusion and antibiotic prophylaxis, have a central role in prophylaxis of infection of acute pancreatic necrosis. Antibiotic is given by systemic (imipenem e.v.) and selective decontamination of gastrointestinal tract (SDD). SDD provides for oral antibiotic prophylaxis (PTA protocol) and systemic antibiotic prophylaxis (cefotaxime and gentamicin), in addition to microbiologic and gastrointestinal monitoring. If on the one hand the role of SDD about mortality reduction is not clear, however, on the other it is well recognized capacity of reduction the intercurrents and pulmonary infections. Other Authors think that SDD is insignificant on early mortality, whereas, is a good option to reduce late and overall mortality of acute pancreatic necrosis complicated by infection.
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PMID:[Acute pancreatic necrosis complicated by infection and gastro-intestinal translocation: pathogenesis correlation and therapeutic implication]. 1282 May 85

Acute pancreatitis is a disease with a wide variety of pathophysiologies, ranging from mild to severe condition. In about 80% to 90% of cases, acute pancreatitis presents as a mild inflammation with low morbidity and mortality, self-reversing to normal condition within 3-4 days. However, the natural course of severe pancreatitis progresses into SIRS and necrosis of the pancreas and its surrounding tissue. And infection of the necrotic tissue develops in sepsis and organ failures. Therefore, the initial management for acute pancreatitis would significantly contribute on the early prognosis. The first step includes not only diagnosis but also initial treatment according to etiological assessment and severity stratification. The summarization of initial management revealed as follows: monitorings of temperature, pulse rate, blood pressure, urine output volume, abdominal pain etc, and treatments of cardio-pulmonary care with sufficient fluid resuscitation, pain control, resting of pancreas etc. As the treatment of the initial management after initial onset, the significances of nasogastric tube drainage, prophylactic use of broadspectrum antibiotics, continuous infusion of protease inhibitors, use of H2 receptor antagonists, control by enteral nutrition and so on have been discussed. And also the indications of total parenteral nutrition, selective digestive decontamination and the efficacies of peritoneal lavage, continuous hemodiafiltration and continuous arterial infusion of protease inhibitor and antibiotics have been reviewed. For those events, the evidences were collected by a systemic search of MEDLINE and Japan Centra Revues Medicina. And then practical recommendations were also graded and introduced to provide a framework for clinitians to manage acute pancreatitis as a guideline. This paper described a part of those recommendations.
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PMID:[Essential therapeutic strategies for acute pancreatitis--guidelines for initial treatment and their significance]. 1555 88

A characteristic feature of all inflammatory disorders is the excessive recruitment of leukocytes to the site of inflammation. The loss of control in trafficking these cells contributes to inflammatory diseases. Leukocyte recruitment is a well-orchestrated process that includes several protein families including the large cytokine subfamily of chemotactic cytokines, the chemokines. Chemokines and their receptors are involved in the pathogenesis of several diseases. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is caused by an uncontrolled systemic inflammatory response resulting from clinical events including major surgery, trauma, multiple transfusions, severe burns, pancreatitis, and sepsis. Systemic inflammatory response syndrome involves activation of alveolar macrophages and sequestered neutrophils in the lung. The clinical hallmarks of ARDS are severe hypoxemia, diffuse bilateral pulmonary infiltrates, and normal intracardiac filling pressures. The magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ARDS. Recent evidence shows that activated leukocytes and chemokines play a key role in the pathogenesis of ARDS. The expanding number of antagonists of chemokine receptors for inflammatory disorders may hold promise for new medicines to combat ARDS.
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PMID:Chemokines in acute respiratory distress syndrome. 1559 Oct 40

Clinical observations of Babesia canis infection in 63 dogs during a 1-year period are summarised, demonstrating the pathogenicity of the Babesia strain endemic in Hungary. Most patients had babesiosis in the spring and autumn, correlating with the seasonal activity of ticks. Male animals appeared in higher numbers, probably due to an overrepresentation of outdoor dogs. Uncomplicated babesiosis was diagnosed in 32 cases. The disease affected dogs of any age in this study. Symptoms were similar to those published from other parts of the world: lethargy, fever, splenomegaly, pallor, icterus, haemoglobinuria and presence of ticks were the most common observations. Thrombocytopenia, lymphopenia and neutropenia were frequent haemogram changes. Imidocarb appeared to be highly effective in eliminating the Babesia infection. Thirty-one animals demonstrated babesiosis with complications. Most Rottweilers (7/9) developed complicated disease. Old age was a risk factor for multiple complications. Multiple organ manifestations had poor prognosis. Hepatopathy (44%), pancreatitis (33%), acute renal failure (ARF; 31%) and disseminated intravascular coagulation (DIC; 24%) were frequent complications, while immune-mediated haemolytic anaemia (IMHA; 10%), acute respiratory distress syndrome (ARDS; 6%) and cerebral babesiosis (3%) were rarely observed. There was a significant difference between the mean age of dogs having uncomplicated disease, babesiosis with a single complication and babesiosis with multiple complications (3.4, 4.8 and 8.6 years, respectively, p < 0.001). The recovery rate (78, 68 and 25%, respectively, p = 0.005) and mortality rate (3, 21 and 67%, respectively, p < 0.001) also tended to differ significantly in these groups. Systemic inflammatory response syndrome (SIRS) and DIC are two possible pathways leading to multiple organ dysfunction syndrome (MODS) in babesiosis. DIC was found to predict MODS more sensitively in this study than SIRS: there were 6 animals developing MODS out of 11 identified with DIC, while only 5 dogs developed MODS out of 22 having SIRS.
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PMID:Clinical manifestations of canine babesiosis in Hungary (63 cases). 1702 Jan 40

Selenium is an essential micronutrient for humans. Critically ill patients with Systemic Inflammatory Response Syndrome (SIRS) and Multiple Organ Dysfunction (MOD) -such as severe sepsis, trauma, severe pancreatitis and critical burns- are exposed to severe oxidative stress. These patients exhibit decreased serum Selenium and selenoenzymes like Glutathione Peroxidase and Selenoprotein P. Selenoenzymes play a major role in protecting cells against lipid peroxidation and they are involved in the inflammatory response regulation. The degree of selenium deficiency correlates with disease severity and the incidence of mortality. In the past years, some clinical trials have studied Selenium supplementation effects in critical illness with SIRS-MOD. This therapeutic strategy could improve the outcome and prognosis in critically ill patients. Few small trials have demonstrated Selenium supplementation beneficial effects, reducing the rate of infectious complications and length of hospital stay. However, no clinical trials using Selenium supplementation in high doses have yet demonstrated significant improvement in mortality. The aims of this review are to evaluate: a) Selenium metabolism, b) the role of selenoenzymes during critical illness, c) clinical studies using Selenium alone or in combination with other antioxidants in critically ill patients and d) to analyze current parenteral Selenium replacement strategies and their results. Further multicentre, well designed randomized, double blind clinical trials about Selenium supplementation in critically ill patients with SIRS and MODS are required and appear to be attractive, necessary and challenging.
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PMID:[Selenium in critically ill patients with systemic inflammatory response]. 1761 71


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