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

Eleven episodes of spontaneous bacterial empyema were identified in eight cirrhotic patients with ascites. Criteria for spontaneous bacterial empyema included positive pleural fluid culture or polymorphonuclear cell concentration greater than 500 cells/mm3, evidence of pleural effusion before an infectious episode and transudate characteristics during infection. In five cases, spontaneous bacterial empyema was culture-negative and was associated with spontaneous bacterial peritonitis. Ascitic fluid was culture-negative in two of these cases and culture-positive in three. Blood cultures were negative in all five of these cases. In six cases spontaneous bacterial empyema was culture-positive (Escherichia coli in four, Klebsiella pneumoniae in one and Clostridium perfringens in one). Four of these patients had the same organism in ascites; one had culture-negative spontaneous bacterial peritonitis and one had no infection of ascites. Blood cultures were positive in four of these patients; three died. Death was more frequent in patients with positive cultures than in those with negative ones (p less than 0.05). Patients with hydrothorax are prone to spontaneous bacterial empyema. This infection probably occurs through hematogenous seeding, but transfer of infected ascites from the abdominal cavity through the diaphragm cannot be excluded. Patients with spontaneous bacterial empyema may be asymptomatic or may be seen with fever, chills and dyspnea. Spontaneous bacterial empyema must be differentiated from parapneumonic empyemas. The presence of pleural effusion before the infectious episode, fluid characteristics and the organisms isolated are the clues for differential diagnosis. Treatment includes antibiotics; chest tube insertion probably is not necessary.
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PMID:Spontaneous bacterial empyema in cirrhotic patients: analysis of eleven cases. 217 97

Spontaneous bacterial empyema (SBEM) is an infection of a preexisting hydrothorax in cirrhotic patients and has seldom been reported. To determine its incidence and primary characteristics, all cirrhotic patients with pleural effusion underwent thoracentesis at our hospital either on admission or when an infection was suspected. Pleural fluid (PF) study included biochemical analysis, polymorphonuclear (PMN) leukocyte count, and culture by two methods: conventional and modified (inoculation of 10 mL of PF into a blood culture bottle at the bedside). SBEM was defined according to previously reported criteria: PF culture positive or PMN count greater than 500 cells/micro L, and exclusion of parapneumonic effusions. Sixteen of the 120 (13 percent) cirrhotic patients admitted with hydrothorax had 24 episodes of SBEM. In 10 of the 24 episodes (43 percent), SBEM was not associated with spontaneous bacterial peritonitis (SBP). PF culture was positive by the conventional method in 8 episodes (33 percent) and by the modified method (blood culture inoculation) in 18 (75 percent) (P = .004, McNemar). The microorganisms identified in PF were Escherichia coli in 8 episodes, Streptococcus species in 4, Enterococcus species in 3, Klebsiella pneumoniae in 2, and Pseudomonas stutzeri in 1. All episodes were treated with antibiotics without inserting a chest tube in any case. Mortality during treatment was 20 percent. We conclude that SBEM is a common complication of cirrhotic patients with hydrothorax. Almost half of the episodes were not associated with SBP; thus, thoracentesis should be performed in patients with cirrhosis, pleural effusion, and suspected infection. Culture of PF should be performed by inoculating 10 mL into a blood culture bottle at the bedside.
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PMID:Spontaneous bacterial empyema in cirrhotic patients: a prospective study. 866 23

Although fluid analysis usually is the first step toward identifying the cause of pleural effusion in patients with cirrhosis and ascites, there are no available data on the reliability of this approach, therefore, we retrospectively evaluated hematologic and biochemical parameters from pleural fluid analysis in 21 patients with hepatic hydrothorax (with proven peritoneal-pleural communication) and 6 patients with primary pleural disease (2 with tuberculosis, 3 with parapneumonic effusion, and 1 with empyema). The criteria developed by Light were diagnostic of pleural "exudate" in only one of six patients with primary pleural disease, concentrations of leukocytes, total protein (TP), albumin, and lactic dehydrogenase (LDH) in both fluids were measured and pleural fluid-to-ascites ratios of these measurements were calculated. Only ratio values for leukocytes and TP were higher in the group of patients with primary pleural disease compared with those with hepatic hydrothorax. Ratio values for leukocytes and TP overlapped between both groups during baseline conditions and during episodes of spontaneous bacterial peritonitis and pleuritis. We conclude that pleural fluid analysis has limited diagnostic efficacy in the patient with cirrhosis. Data collected by other methods--clinical and radiologic--should assist in arriving at the correct diagnosis.
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PMID:Evaluation of pleural fluid in patients with cirrhosis. 945 75

Hepatic hydrothorax is the accumulation of ascitic fluid in the pleural space and requires the same treatment as ascites: salt restriction, diuretics, and paracentesis. Refractory hydrothorax appears when there is no response to those measures and its management is not well established. Videothoracoscopy is a promising therapy that permits the detection and closure of diaphragmatic defects, and when used with pleurodesis resulted in long-lasting control of hydrothorax in six of eight patients without appreciable morbidity. The transjugular intrahepatic portosystemic shunt is an effective therapy in more than 75% of refractory hydrothorax cases. Hepatic encephalopathy and worsening of liver function in some patients are the main adverse effects. Spontaneous bacterial empyema, the infection of a hydrothorax, was reported in 13% of 120 cirrhotic patients with hydrothorax. Forty percent of the episodes of spontaneous bacterial empyema were not associated with spontaneous bacterial peritonitis. The sensibility of pleural fluid culture improves inoculating pleural fluid into a blood culture bottle at the bedside. Patients with refractory hydrothorax or those having an episode of spontaneous bacterial empyema should be considered candidates for liver transplantation.
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PMID:Hepatic hydrothorax. 1081 41

In 1996, the International Ascites Club defined "refractory ascites" as ascites that cannot be mobilized by medical therapy or that recurs early after initial mobilization despite continued treatment. Of all patients with ascites, 5% to 10% will become refractory to medical therapy. Management of refractory ascites should attempt to control fluid accumulation, reduce the likelihood of developing complications such as spontaneous bacterial peritonitis (SBP) and the hepatorenal syndrome, and improve the patient's nutritional status and overall well-being. Measures to control ascites accumulation include documenting medication and dietary compliance and eliminating potentially nephrotoxic agents that promote sodium retention. Large volume paracentesis is an effective first step in managing these patients and can be performed routinely in an outpatient setting. When more than 5 L of fluid are removed during a paracentesis, intravenous albumin should be infused to reduce the likelihood of the patient developing postparacentesis circulatory dysfunction. Transjugular intrahepatic portosystemic shunt (TIPS) placement effectively eliminates ascites; however, there is no convincing evidence that the shunt improves mortality. Furthermore, it is associated with frequent complications of encephalopathy and shunt malfunction. We feel TIPS should be reserved for patients requiring extremely frequent paracentesis, those who develop significant postparacentesis circulatory dysfunction, or those with hepatic hydrothorax. Patients who have evidence of SBP should be treated with antibiotics and intravenous albumin infusion. Patients who have had a previous episode of SBP or an ascitic fluid protein level of less than 1.0 should receive prophylactic antibiotics. Overall, the prognosis for patients with refractory ascites remains grim, and liver transplantation is the only definitive therapy. Appropriate candidates should be identified promptly and referred for transplant evaluation.
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PMID:Treatment of refractory ascites. 1708 86

Spontaneous bacterial empyema, defined as spontaneous infection of the pleural fluid, represents a distinct complication of hepatic hydrothorax with a different pathogenesis, clinical course and treatment strategy from those of empyema secondary to pneumonia. Nearly 40% of episodes of spontaneous empyema are not associated with spontaneous bacterial peritonitis (SBP) or even ascites. The condition portends a poor prognosis, and is frequently under-diagnosed. This article reviews the pathogenesis, diagnosis and management of spontaneous bacterial empyema.
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PMID:Spontaneous bacterial empyema in liver cirrhosis: an underdiagnosed pleural complication. 1956 97

One of the most common manifestations of the development of portal hypertension in the patient with cirrhosis is the appearance of ascites. Once ascites develops, the prognosis worsens and the patient becomes susceptible to complications such as bacterial peritonitis, hepatic hydrothorax, hyponatremia, and complications of diuretic therapy. As the liver disease progresses, the ascites becomes more difficult to treat and many patients develop renal failure. Most patients can be managed by diuretics which, when used correctly, will control the ascites. Spontaneous bacterial peritonitis can be treated effectively, but portends a worse prognosis. Once the ascites becomes refractory to diuretics, liver transplantation is the best option, although use of transjugular intrahepatic portosystemic shunts will control the ascites in many patients. Lastly, the development of hepatorenal syndrome indicates the patient's liver disease is advanced, and transplantation again is the best option. However, use of vasoconstrictors may improve renal function in some patients, helping in their management while they await a liver transplant.
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PMID:Management of refractory ascites and hepatorenal syndrome. 2108 Feb 46

Identification and treatment of advanced hepatitis C virus (HCV) infection is often challenging. Accurate fibrosis staging can be performed only by liver biopsy. For patients with advanced fibrosis (Metavir score, F3 or F4), progression to decompensated liver disease occurs at a rate of approximately 5% per year and progression to hepatocellular carcinoma occurs at a rate of 1% to 2% per year. Liver decompensation primarily results from altered hepatic blood flow caused by liver scarring and is characterized by ascites and its complications (hepatorenal syndrome, hepatic hydrothorax, and spontaneous bacterial peritonitis), hepatic encephalopathy, bleeding varices, and coagulopathy. Patients with advanced fibrosis need to be regularly monitored for evidence of decompensated disease, and complications need to be aggressively managed. This article summarizes a presentation by Kenneth E. Sherman, MD, at the IAS-USA live continuing medical education course, Management of Hepatitis C Virus in the New Era, held in New York City in April 2011.
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PMID:Advanced liver disease: what every hepatitis C virus treater should know. 2194 90

Advanced liver disease is associated with hypoxemia and respiratory failure by various mechanisms. Patients with cirrhosis are especially prone to episodes of decompensation requiring intensive care unit admission and management. Such patients may already be in acute liver failure or have decompensated due to a concurrent illness such as spontaneous bacterial peritonitis, sepsis, encephalopathy, varices, or hepatorenal syndrome. Acute respiratory distress syndrome is one of the main reasons for intensive care unit admission and mortality. Overall, critically ill cirrhotic patients frequently progress to multiorgan failure requiring mechanical ventilation. Caring for such patients is therefore understandably complex and extremely challenging. Patients with end-stage liver disease are especially at risk for developing acute respiratory failure and hypoxemia secondary to hepatopulmonary syndrome, portopulmonary hypertension, and hepatic hydrothorax. They should therefore be screened for these conditions because failure to recognize and adequately treat these serious complications of cirrhosis may have devastating consequences. This article is based on a review of the current literature on how to approach and manage acute respiratory failure in advanced liver disease, which is important to intensivists, anesthesiologists, and physicians as a whole.
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PMID:Acute respiratory failure complicating advanced liver disease. 2244 64

Ascites formation in patients with cirrhosis, portal hypertension, or both usually results from hyperdynamic circulatory dysfunction, where the retention of sodium and water is associated with the activation of the sympathetic and renin-angiotensin-aldosterone systems. The presence of ascites indicates the development of liver decompensation. Furthermore, complications seen in conjunction with ascites such as spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic hydrothorax may result in increased morbidity and mortality. Although nonpharmacological, pharmacological, and surgical approaches have been introduced and clinically practiced, their therapeutic effects are still suboptimal or limited by their potential side effects, such as large-volume paracentesis-induced postparacentesis circulatory dysfunction. Herein, we discuss strategies to prevent and properly manage ascites-related complications, including a review of the literature and controlled studies that assess these strategies.
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PMID:Management of ascites in patients with liver cirrhosis: recent evidence and controversies. 2349 63


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