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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bacterial infections are an important complication of cirrhosis, particularly in hospitalized patients. In this article we review the prevalence, risk factors, and pathogenesis of bacterial infections in cirrhosis, focusing on the mechanisms of bacterial translocation such as impaired immunity and bacterial overgrowth, as well as maneuvers that may inhibit bacterial translocation and could be used not only to prevent infections but also to ameliorate the hyperdynamic circulatory state of cirrhosis. We also review the clinical features and management of the most common infection in cirrhosis, spontaneous bacterial peritonitis (SBP), specifically the evidence behind the therapy of acute SBP, the role of albumin, and the role of antibiotics in the prophylaxis of high-risk patients. It has been recognized that SBP and other bacterial infections lead to the systemic inflammatory response syndrome, sepsis, and multiorgan failure. We review the pathogenesis and management of these complications, the role of adrenal insufficiency, and the utility of intensive care prognostic models.
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PMID:Bacterial infections, sepsis, and multiorgan failure in cirrhosis. 1829 75

Sepsis is physiologically viewed as a proinflammatory and procoagulant response to invading pathogens. There are three recognized stages in the inflammatory response with progressively increased risk of end-organ failure and death: sepsis, severe sepsis, and septic shock. Patients with cirrhosis are prone to develop sepsis, sepsis-induced organ failure, and death. There is evidence that in cirrhosis, sepsis is accompanied by a markedly imbalanced cytokine response ("cytokine storm"), which converts responses that are normally beneficial for fighting infections into excessive, damaging inflammation. Molecular mechanisms for this excessive proinflammatory response are poorly understood. In patients with cirrhosis and severe sepsis, high production of proinflammatory cytokines seems to play a role in the worsening of liver function and the development of organ/system failures such as shock, renal failure, acute lung injury or acute respiratory distress syndrome, coagulopathy, or hepatic encephalopathy. In addition, these patients may have sepsis-induced hyperglycemia, defective arginine-vasopressin secretion, adrenal insufficiency, or compartmental syndrome. In patients with cirrhosis and spontaneous bacterial peritonitis (SBP), early use of antibiotics and intravenous albumin administration decreases the risk for developing renal failure and improves survival. There are no randomized studies that have been specifically performed in patients with cirrhosis and severe sepsis to evaluate treatments that have been shown to improve outcome in patients without cirrhosis who have severe sepsis or septic shock. These treatments include recombinant human activated C protein and protective-ventilation strategy for respiratory failure. Other treatments should be evaluated in the cirrhotic population with severe sepsis including the early use of antibiotics in "non-SBP" infections, vasopressor therapy, hydrocortisone, renal-replacement therapy and liver support systems, and selective decontamination of the digestive tract or oropharynx.
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PMID:Severe sepsis in cirrhosis. 2037 75

Cirrhosis has many complications regardless of the aetiology. Complications include splenomegaly, ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome and hepatocellular carcinoma and also linked to abnormalities in the endocrine system, including abnormal sex hormone metabolism, thyroid disease, osteoporosis, and, most recently identified, adrenal insufficiency. This prospective cohort study was done to evaluate the impact of adrenocortical insufficiency on clinical parameters in haemodynamically stable cirrhotic patients with ascites and had been performed at the inpatient of GHPD Department, BIRDEM, Dhaka, Bangladesh from April 2011 to March 2012. A total of fifty three (53) patients fulfilling inclusion criteria were included in the study. Patients were divided into two groups: Group A (patients of normal adrenal function) and Group B (patients of insufficient adrenal function) and those were followed up for the next 6 months. In Group A, the total number of patients was 25(47%) and in Group B it was 28(53%). Between two groups, mean age difference and gender difference were not statistically significant (p value was 0.278 and 0.933, respectively). Group B patients had significant higher CLD duration (p=0.004). Haematemesis and/or maelena was significantly lower in Group B at follow up (p=0.0001) due to significant higher number of band ligation in this group (p=0.009). Hepatic encephalopathy was significantly higher in Group B at enrollment (p=0.028) and at follow up (p<0.001). During the period of follow up, significant higher number of patients had developed hepatic encephalopathy in Group B compared to Group A (p<0.05). There was statistically significant higher number of patients had SBP (p=0.031) in Group B at follow up. During the period of follow up, only 1(4%) patient in Group A and 5(18%) patients in Group B died. There was no significant difference of number of death between two groups (p=0.196). Adrenal insufficient decompensated cirrhotic patients have higher morbidities.
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PMID:Impact of Adrenocortical Insufficiency on Clinical Parameters in Haemodynamically Stable Cirrhotic Patients with Ascites. 2891 7