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

There is dispute about the cause of Beethoven's death; alcoholic cirrhosis, syphilis, infectious hepatitis, lead poisoning, sarcoidosis and Whipple's disease have all been proposed. In this article all primary source documents related to Beethoven's terminal illness and death are reviewed. The documents include his letters, the report of his physician Andreas Wawruch, his Conversation Books, the autopsy report, and a new toxicological report of his hair. His terminal illness was characterised by jaundice, ascites, ankle oedema and abdominal pain. The autopsy data indicate that Beethoven had cirrhosis of the liver, and probably also renal papillary necrosis, pancreatitis and possibly diabetes mellitus. His lifestyle for at least the final decade of his life indicated that he overindulged in alcohol in the form of wine. Alcohol was by far the most common cause of cirrhosis at that period. Toxicological analysis of his hair showed that the level of lead was elevated. During the eighteenth and early nineteenth centuries, lead was added illegally to inexpensive wines to sweeten and refresh them. These findings strongly suggest that liver failure secondary to alcoholic cirrhosis, associated with terminal spontaneous bacterial peritonitis, was the cause of death. This was complicated in the end stages by renal failure. If the presence of endogenous lead was verified by analysis of Beethoven's skeletal remains, it would suggest that the lead was derived from wine that he drank. Lead poisoning may account for some of his end-of-life symptoms. There is little clinical or autopsy evidence that Beethoven suffered from syphilis.
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PMID:Beethoven's terminal illness and death. 1721 30

The key pathogenic mechanism initiating spontaneous bacterial peritonitis (SBP) is bacterial translocation (BT), a process through which enteric bacteria cross the intestinal barrier and infect the mesenteric lymph nodes, thus entering the blood circulation and ascitic fluid. The high rate of bacterial translocation in cirrhosis is due to injury to the three pilars composing the intestinal mucosal barrier (the balance of intraluminal bacterial flora, the integrity of the intestinal epithelial barrier, and the local immune system). Blood dissemination and microbial growth in ascitic fluid resulting from SBP are a consequence of damage to the immune system in cirrhosis. Hyperproduction of proinflammatory cytokines and other vasoactive substances contributes to the arterial vasodilation and renal failure that frequently complicate the course of SBP. Even in the absence of SBP, translocation of bacteria and bacterial products from the intestinal lumen contribute to systemic inactivation of immune cells in cirrhosis.
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PMID:[Physiopathology of bacterial translocation and spontaneous bacterial peritonitis in cirrhosis]. 1733 15

Hepatorenal syndrome is complication of the advanced cirrhosis characterized by functional renal failure and changes of systemic blood pressure due to increased activity of endogenous vasoactive systems. Functional renal failure is due to severe renal cortical ischemia and reduction of glomerular filtration rate (GFR) developing in the late stages of cirrhosis. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to arterial vasodilatation located in the splanchnic circulation. Reduced effective arterial blood volume triggers a compensatory response with activation of systemic and renal vasoconstrictor systems. At the same time, the ascites becomes refractory in some patients, as it is no longer responsive to diuretic treatment. These changes result from combination of deteriorating liver function and increasing portal pressure, further splanchnic vasodilatation, increase of circulating vasoconstrictors, and decrease of renal blood flow and GFR. Hepatorenal syndrome can be precipitated by shock, infection, nephrotoxic drugs, bleeding, surgery or large volume paracentesis. Renal failure may be rapidly progressive (type I HRS) or may develop more slowly (type II HRS), which is usually associated with refractory ascites. The diagnosis of HRS is based on established diagnostic criteria aimed at excluding the nonfunctional causes of renal failure. The prognosis of patients with HRS is very poor. Liver transplantation remains the only curative treatment for the time being. Pharmacological therapies based on the use of vasoconstrictor drugs may serve as a bridge to liver transplantation. Prevention of HRS by albumin infusion is recommended in patients with spontaneous bacterial peritonitis and by pentoxifylline in patients with the acute alcoholic hepatitis.
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PMID:[Hepatorenal syndrome]. 1750 77

We herein report a case of spontaneous bacterial peritonitis (SBP) caused by Staphylococcus epidermidis in an adult patient on regular hemodialysis (due to terminal renal failure caused by hypertension) and not on immunosuppressive therapy.
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PMID:Spontaneous bacterial peritonitis in terminal renal failure. 1796 96

Accumulation of fluid as ascites is the most common complication of cirrhosis. This is occurring in about 50% of patients within 10 years of the diagnosis of cirrhosis. It is a prognostic sign with 1-year and 5-year survival of 85% and 56%, respectively. The most acceptable theory for ascites formation is peripheral arterial vasodilation leading to underfilling of circulatory volume. This triggers the baroreceptor-mediated activation of renin-angiotensin-aldosterone system, sympathetic nervous system and nonosmotic release of vasopressin to restore circulatory integrity. The result is an avid sodium and water retention, identified as a preascitic state. This condition will evolve in overt fluid retention and ascites, as the liver disease progresses. Once ascites is present, most therapeutic modalities are directed on maintaining negative sodium balance, including salt restriction, bed rest and diuretics. Paracentesis and albumin infusion is applied to tense ascites. Transjugular intrahepatic portosystemic shunt is considered for refractory ascites. With worsening of liver disease, fluid retention is associated with other complications; such as spontaneous bacterial peritonitis. This is a primary infection of ascitic fluid caused by organisms originating from large intestinal normal flora. Diagnostic paracentesis and antibiotic therapy plus prophylactic regimen are mandatory. Hepatorenal syndrome is a state of functional renal failure in the setting of low cardiac output and impaired renal perfusion. Its management is based on drugs that restore normal renal blood flow through peripheral arterial and splanchnic vasoconstriction, renal vasodilation and/or plasma volume expansion. However, the definitive treatment is liver transplantation.
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PMID:Fluid retention in cirrhosis: pathophysiology and management. 1818 68

Hepatorenal syndrome (HRS) is a functional renal failure that frequently develops in patients with advanced cirrhosis and severe impairment in systemic circulatory function. Traditionally it has been considered to be the consequence of a progression of the splanchnic arterial vasodilation occurring in these patients. However, recent data indicate that a reduction in cardiac output also plays a significant role. There are two different types of HRS. Type-2 HRS consists of a moderate and steady or slowly progressive renal failure. It represents the extreme expression of the circulatory dysfunction that spontaneously develops in patients with cirrhosis. The main clinical problem in these patients is refractory ascites. Type-1 HRS is a rapidly progressive acute renal failure that frequently develops in closed temporal relationship with a precipitating event, commonly spontaneous bacterial peritonitis. In addition to renal failure, patients with type-1 HRS present deterioration in the function of other organs, including the heart, brain, liver, and adrenal glands. Type-1 HRS is the complication of cirrhosis associated with the worst prognosis. However, effective treatments of HRS (vasoconstrictors associated with intravenous albumin, transjugular intrahepatic portacaval shunt, albumin dialysis) that can improve survival have recently been introduced.
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PMID:Pathogenesis and treatment of hepatorenal syndrome. 1829 79

The two most widely used experimental models of advanced liver disease are the administration of carbon tetrachloride, and common bile duct ligation (BDL), however, neither has been systematically evaluated as a model of hepatorenal syndrome (HRS). The BDL model in rats, studied at diverse time points, induced a progressive renal dysfunction without structural changes in the kidney. The authors concluded that BDL is a good model for further studies of HRS and its treatment. However, the renal impairment observed at the acute phase of the BDL model is based on a different pathophysiology than that of HRS. Specifically, in acute obstructive jaundice, cholemia predominates over parenchymal liver disease (reversible at this stage without portal hypertension or cirrhosis) and independently induces negative inotropic and chronotropic effects on the heart, impaired sympathetic vasoconstriction response and profound natriuresis and diuresis that might lead to volume depletion. In addition, systemic endotoxemia contributes to the prerenal etiology of renal impairment and promotes direct nephrotoxicity and acute tubular necrosis. On the other hand, the renal failure observed in the chronic BDL model (with development of biliary cirrhosis, portal hypertension and ascites) shares pathophysiological similarities with HRS, but the accordance of the chronic BDL model to the diagnostic criteria of HRS (e.g. absence of spontaneous bacterial peritonitis, no renal function improvement after plasma volume expansion) should have been confirmed. In conclusion, we think that the BDL model is not suitable for the study of the natural history of HRS, but the chronic BDL model might be valid for the study of established HRS and its potential therapies.
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PMID:Bile duct ligation in rats: a reliable model of hepatorenal syndrome? 1868 Feb 30

Continuous ambulatory peritoneal dialysis (CAPD) is used to treat end-stage renal failure in an increasing number of patients. CAPD has an advantage over hemodialysis in that it allows patients greater freedom to perform daily activities; it also provides other clinical benefits. However, the long-term effectiveness of CAPD is limited by complications, which have various causes. Complications with an infectious cause include bacterial peritonitis, tuberculous peritonitis, and infections of the catheter exit site and tunnel. Noninfectious complications include catheter dysfunction, dialysate leakage, hernias, and sclerosing encapsulating peritonitis. Many imaging modalities-radiography, ultrasonography, peritoneal scintigraphy, computed tomography (CT), and magnetic resonance (MR) imaging-are useful for characterizing these complications. CT peritoneography and MR peritoneography are techniques specifically suited to this purpose. Imaging plays a critical role in ensuring that complications are detected early and managed appropriately.
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PMID:Complications of continuous ambulatory peritoneal dialysis. 1932 58

Hepatorenal syndrome (HRS) is a type of renal failure that occurs in patients with advanced cirrhosis. It is a result of splanchnic arterial vasodilation, renal vasoconstriction, reduced effective arterial volume, and potentially reduced cardiac output. Often, HRS is a fatal complication, and the only definitive treatment currently available is liver or liver-kidney transplantation. A number of other treatment modalities have been tested for the management of HRS, but most evidence is derived from small noncontrolled studies. The primary role of these treatment options is to provide a bridge to liver transplantation. Treatment may also provide acute reversal of renal failure and some symptomatic relief, but relapse is a common occurrence. The best therapeutic options appear to be those that reverse portal hypertension, splanchnic vasodilation, and/or renal vasoconstriction. Vasopressin analogs, particularly terlipressin, have emerged as the preferred pharmacologic therapies for management of HRS. Albumin is an appropriate adjunctive therapy to terlipressin and can be used to prevent HRS in patients with spontaneous bacterial peritonitis. Transjugular intrahepatic portosystemic shunt may provide a surgical option for qualified patients with HRS. Octreotide is ineffective as monotherapy but may be used as adjunctive therapy to other vasoactive agents. Dopamine agonists, endothelin antagonists, natriuretic peptides, and nitric oxide synthase inhibitors have not been effective for reversing HRS. Artificial hepatic support therapies have demonstrated the ability to improve laboratory abnormalities in patients with HRS, but their effect on clinical outcomes has not been determined. The role of renal replacement therapies or the newer artificial hepatic support therapies need further evaluation before they can be routinely recommended.
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PMID:Treatment of hepatorenal syndrome. 1979 93

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


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