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

Since the introduction of the LeVeen modification of the peritoneovenous shunt (PVS) in 1974, these devices have been placed in a relatively large number of patients. The most common indication has been for medically intractable ascites in the setting of chronic liver disease. A review of a series of studies shows that we can expect approximately an 18% perioperative overall mortality rate, a 46% survival rate at 21 months, and loss of ascites in 59% of the survivors at 18 months. The PVS has not been shown by prospective trials to prolong survival significantly in patients with either intractable ascites or the hepatorenal syndrome (HRS), although it may shorten hospitalizations, compared with medical controls. A few well-documented cases of reversal of the HRS have been documented. The best results of PVS therapy have been evident in those patients with milder liver disease. The loss of ascites need not correlate with a functioning shunt. Alcohol abstinance is associated with hepatic functional recovery and may relate to the disappearance of renal sodium retention, resulting in shunt occlusion due to low flow. A number of serious complications with the PVS have been described. Nutritional repletion follows successful shunting, but might, in part, relate to simultaneous alcohol abstention. The more common complications of coagulopathy and fluid overload are preventable by total ascitic drainage at the time of surgery. Shunt patency remains a clinical problem. Only 18.6% of the total shunts placed functioned in the survivors at 2 yr. Perioperative infections with staphylococcal and Gram-negative organisms occur. Postoperative bacterial peritonitis or septicemia requires shunt removal for cure.
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PMID:The peritoneovenous shunt: expectations and reality. 219 58

A case of successive coagulopathies post peritoneovenous shunt in the same patient is presented. These coagulopathies occurred after a LeVeen valve insertion with ascitic fluid evacuation, and after reopening the shunt with ascitic fluid evacuation, with the peritoneal cavity washed and replaced with normal saline solution. This case illustrates the fact that peritoneal lavage and the replacement of the ascites with normal saline decrease the severity of the coagulopathy but do not prevent it completely. Peritoneal lavage and ascitic fluid replacement when a LeVeen valve is inserted, should be performed in selected cases, especially those who had a recently treated bacterial peritonitis.
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PMID:Failure of ascitic fluid replacement for prevention of coagulopathy post peritoneovenous shunt. Case report. 234 54

Many advances have been made in the understanding, diagnosis, and management of severe complications of liver disease. The pathogenesis of hepatic encephalopathy remains a challenge. Several toxins including ammonia, mercaptans, short-chain fatty acids, benzodiazepine-like substances, GABA-like substances, and impaired glutamatergic neurotransmission are at the top of the list of candidates. Use of the benzodiazepine antagonists is an experimental but promising new therapy in patients with hepatic encephalopathy. In patients with cirrhosis, spontaneous bacterial peritonitis (SBP) remains a common and highly lethal complication. The diagnosis of SBP is based on the polymorphonuclear cell count in the ascites and confirmed by culture of ascitic fluid. Early diagnosis and aggressive treatment has reduced mortality of SBP from greater than 90 per cent to 30 to 50 per cent. The appearance of cerebral edema in severe acute hepatocellular failure is associated with high mortality and conventional neurologic signs may be unreliable indicators of brain swelling. Current management of cerebral edema in fulminant hepatocellular failure may include early placement of an extradural sensor for continuous monitoring of intracranial pressure, so that short-term measures can be instituted making later liver transplantation safer. Coagulopathy remains a serious problem in patients with liver disease. Exchange plasmapheresis is a promising short-term adjuvant therapy. However, liver transplantation should be considered the definitive treatment for fulminant hepatocellular failure. The gastroenterologist often encounters multiorgan failure in patients with severe liver disease. Liver transplantation is now an important therapeutic consideration in almost every patient with severe, irreversible liver disease. Efforts should be targeted to early diagnosis of irreversible disease and coordination of patient care with a liver transplant center.
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PMID:Major complications of acute and chronic liver disease. 304 45

We report a case of synchronous gas gangrene and spontaneous bacterial peritonitis associated with liver cirrhosis. The patient was a 52-year-old man who was being followed for decompensated liver cirrhosis. He experienced sudden onset lower abdominal pain with distension and pain in the left leg. A bullous lesion, with crepitation, later appeared in the thigh and showed air-bubbles on X-ray. Eschericia coli was cultured from ascites and the bullous lesions; there was associated gas gangrene. The patient died of bacteremia with disseminated intravascular coagulopathy 26 h after admission, despite receiving intensive care. We discuss the route of bacteria causing the spontaneous bacterial peritonitis and simultaneous gas gangrene.
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PMID:Liver cirrhosis with synchronous gas gangrene and spontaneous bacterial peritonitis due to E. coli. 908 80

Chronic liver diseases are potentially evolving clinical situations which, independently by the etiology, could proceed towards progressive liver structural and functional impairments. The only efficient treatment is orthotopic liver transplantation. Chronic liver diseases, and up to 40% of liver cirrhosis, are initially asymptomatic, but cirrhosis is the most frequent cause of death among non-neoplastic digestive diseases. Important elements complicating a decompensated liver cirrhosis are ascites, hepatic encephalopathy, digestive bleeding and jaundice. Acute liver failure (ALF) is the expression of a clinical state, that is common to many conditions sharing severe liver structural and functional impairments. In patients affected by decompensated liver cirrhosis, ALF could be triggered by several factors, while the death is caused by bleeding episodes, hepato-renal syndrome, spontaneous bacterial peritonitis or hepatocarcinoma. In patients affected by chronic liver diseases, the diagnosis of ALF is based on progressively increasing jaundice, encephalopathy and coagulopathy. Recent clinical trials have evaluated the efficacy of extrahepatic liver support systems, either artificial or bio-artificial, in treating episodes of ALF in chronic liver patients. The preliminary results indicate a potential use of such systems in blood detoxification, but they also showed limits in increasing patient survival.
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PMID:[Acute liver failure in chronic hepatic disease. Clinico-therapeutic evaluation]. 1101 9

Sepsis is a systemic inflammatory response to the presence of infection, mediated via the production of many cytokines, including tumour necrosis factor (TNF-), interleukin (IL)-6, and IL-1, which cause changes in the circulation and in the coagulation cascade. There is stagnation of blood flow and poor oxygenation, subclinical coagulopathy with elevated D-dimers, and increased production of superoxide from nitric oxide synthase. All of these changes favour endothelial apoptosis and necrosis as well as increased oxidant stress. Reduced levels of activated protein C, which is normally anti-inflammatory and antiapoptotic, can lead to further tissue injury. Cirrhotic patients are particularly susceptible to bacterial infections because of increased bacterial translocation, possibly related to liver dysfunction and reduced reticuloendothelial function. Sepsis ensues when there is overactivation of pathways involved in the development of the sepsis syndrome, associated with complications such as renal failure, encephalopathy, gastrointestinal bleed, and shock with decreased survival. Thus the treating physician needs to be vigilant in diagnosing and treating bacterial infections in cirrhosis early, in order to prevent the development and downward spiral of the sepsis syndrome. Recent advances in management strategies of infections in cirrhosis have helped to improve the prognosis of these patients. These include the use of prophylactic antibiotics in patients with gastrointestinal bleed to prevent infection and the use of albumin in patients with spontaneous bacterial peritonitis to reduce the incidence of renal impairment. The use of antibiotics has to be judicious, as their indiscriminate use can lead to antibiotic resistance with potentially disastrous consequences.
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PMID:Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club. 1583 23

Conditions that necessitate surgery frequently arise in patients with chronic liver disease and cirrhosis. Because cirrhosis has the ability to cause physiologic derangements in every organ system in the body, clinicians face significant challenges in preoperative preparation of the patient with cirrhosis in order to decrease postoperative morbidity and mortality. Emergent operations add an extra dimension of complexity to the clinical picture, due to limited preoperative time to prepare the patient with cirrhosis for surgery. In cases of severely decompensated cirrhosis, clinicians should have in their armamentarium possible alternatives to surgery that can be used to temporize the emergent nature of the disease and improve patient outcomes. The classification of cirrhotic liver disease by Child and Turcotte was initially utilized to predict mortality in patients undergoing surgically placed shunts for portal hypertensive bleeding. Subsequent studies have pointed to the fact that other general and thoracic surgery procedures can be assigned predicted mortality rates according to a similar classification scheme, the modified Child-Pugh score. Patients with cirrhosis facing surgery should undergo a careful history and physical examination and should be accurately placed into a designated Child-Pugh category. Because the modified Child-Pugh class is the most reliable determinant of postoperative morbidity and mortality, every attempt should be made to upgrade a patient's class in a favorable direction prior to surgery. Patients should be carefully evaluated for the presence of ascites and dietary alterations. In addition, medical management with diuretics should be employed to prevent postoperative ascites leak and possible infectious complications including bacterial peritonitis. Perhaps one of the most feared complications in the patient with cirrhosis facing surgery is hemorrhage. Because the liver is vital in maintenance of coagulation homeostasis, several pharmacologic adjuncts may be administered to correct any coagulopathy in the peri-operative period. Several diseases such as cholelithiasis and peptic ulcer disease are known to be more prevalent in the cirrhotic patient, and clinicians treating these diseases should have a thorough understanding of the pathophysiology of cirrhosis and portal hypertension. Patients with cirrhosis and portal hypertensive bleeding that are considered good surgical candidates (ie, Child-Pugh class A) may benefit from surgical portasystemic shunt in contrast to angiographically placed portacaval shunt (ie, transjugular intrahepatic portosystemic shunt ) due to the lack of durable patency and cost effectiveness in the latter. In patients with cirrhosis awaiting orthotopic liver transplantation, TIPS may be a lifesaving temporizing technique that is utilized as a bridge to transplantation.
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PMID:Management of the cirrhotic patient that needs surgery. 1631 65

Massive ascites and hepatorenal syndrome (HRS) are frequent complications of liver cirrhosis. Thus, effective therapy is of great clinical importance. This concise review provides an update of recent advances and new developments. Therapeutic paracentesis can be safely performed even in patients with severe coagulopathy. Selected patients with a refractory or recurrent ascites are good candidates for non-surgical portosystemic shunts (TIPS) and may have a survival benefit and improvement of quality of life. Novel pharmaceutical agents mobilizing free water (aquaretics) are currently under test for the therapeutic potential in patients with ascites. Prophylaxis of hepatorenal syndrome in patients with spontaneous bacterial peritonitis is recommended and should be considered in patients with alcoholic hepatitis. Liver transplantation is the best therapeutic option with long-term survival benefit for patients with HRS. To bridge the time until transplantation, TIPS or Terlipressin and albumin are good options. Albumin dialysis can not be recommended outside prospective trials.
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PMID:Progress in treatment of massive ascites and hepatorenal syndrome. 1648 62

The coagulopathy of liver disease is complex and often unpredictable. Despite clear evidence of an increased tendency for bleeding in patients who have cirrhosis, many circumstances also promote local and systemic hypercoagulable states. The consequences of hypercoagulability include the obvious morbidity and mortality of portal vein thrombosis, deep vein thrombosis, and pulmonary embolism, but possibly also include other end-organ syndromes, such as portopulmonary hypertension, hepatorenal syndrome, and spontaneous bacterial peritonitis. A more subtle contribution also could be responsible for progression of early fibrosis to decompensated cirrhosis. Future research is needed to elucidate specific mechanistic pathways that might lead to local hypercoagulation and the clinical interventions that might prevent morbidity and mortality related to hypercoagulation in patients who have cirrhosis.
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PMID:Hypercoagulation in liver disease. 1915 Mar 15

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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