Spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis (SBP) is a bacterial infection of ascitic fluid in patients with decompensated cirrhosis. The modifier 'spontaneous' distinguishes this from surgical peritonitis. The infecting organisms are usually enteric gram-negatives which have translocated from the bowel. Symptoms of infection occur in most patients with SBP, including fever, abdominal pain, mental status changes, and ileus. A high index of suspicion should exist for SBP in patients with cirrhosis and ascites. Diagnostic abdominal paracentesis can be undertaken with minimal risk and should be performed in all patients admitted to the hospital, during times of worsening clinical appearance, or when gastrointestinal bleeding occurs. The ascitic fluid polymorphonuclear cell count is the most sensitive test in evaluating for infection. Cultures of the ascitic fluid are helpful in identifying the organism and are best performed by bedside injection of blood culture bottles. Ascites total protein, lactate dehydrogenase, and glucose levels can assist in distinguishing SBP from secondary peritonitis. Empirical therapy is recommended after paracentesis if suspicion for infection exists. Cefotaxime is the best-studied antibiotic for this purpose and has excellent penetration into ascites with no nephrotoxicity. Prophylaxis should be limited to high-risk settings. Mortality rates in SBP have declined dramatically, largely due to earlier detection and improved therapy.     

自发性细菌性腹膜炎

自发性细菌性腹膜炎(spontaneous bacterial peritonitis,SBP)在肝硬化患者的发生率为10.0%～25.0%,重型肝炎患者SBP的发生率为17.7％～47.0％。 一、细菌学及其耐药性的变迁 SBP感染多来自肠道细菌,绝大多数为单一细菌感染,厌     

Spontaneous bacterial peritonitis

Opinion statement Spontaneous bacterial peritonitis (SBP) is the prototypical ascitic fluid infection occurring in patients with advanced liver disease and ascites. The key to successful treatment of SBP is a knowledge of appropriate antibiotic regimens and an understanding of the setting in which infection develops, particularly those individuals at high risk for infection. A high index of suspicion should lead to early diagnostic paracentesis and ascitic fluid analysis. Treatment of SBP involves the use of nonnephrotoxic broad-spectrum antibiotics expected to cover the typical bacterial flora associated with SBP. SBP typically involves infection with a single organism, with Escherichia coli, Klebsiella spp, and Streptococcus spp responsible for nearly three fourths of cases. The treatment of choice is cefotaxime 2 g given intravenously every 8 hours for a total of 5 days. The antibiotic regimen is adjusted based on the results of ascitic fluid cultures. Other antibiotic regimens for SBP are less well studied. Given the significant morbidity and mortality rates associated with SBP, efforts to prevent its development and recurrence with antibiotic prophylaxis are warranted. The most extensively studied form of prophylaxis involves selective intestinal decontamination (SID) with the oral fluoroquinolone norfloxacin. Individuals with low-protein ascites (ascitic fluid total protein < 1g/dL) benefit from SID with norfloxacin 400 mg daily during times of hospitalization. Long-term primary prophylaxis during outpatient management of individuals awaiting liver transplantation with severe ascites and advanced liver failure should also be considered. Patients with cirrhosis and upper gastrointestinal bleeding should receive norfloxacin 400 mg twice daily for 1 week following their bleed. Those individuals surviving an episode of SBP should be treated with norfloxacin 400 mg daily until the risk of SBP is removed by definitive resolution of the ascites or liver transplantation surgery. Although the infection-related mortality associated with SBP has decreased to less than 10%, hospitalization-related mortality remains as high as 30% as a result of the severe underlying liver disease in which the infection arises and the marked generation of cytokines and nitric oxide resulting from the infection. Recently, the simultaneous administration of intravenous albumin and antibiotics for SBP has been shown to result in the decreased development of azotemia and hospitalization-related mortality. Further improvement in the outcomes of SBP will require treatments targeting this cytokine cascade rather than the development of more potent antibiotics.     

Spontaneous bacterial peritonitis.

SBP is an infection of ascites that occurs in the absence of a local infectious source. It is mainly a complication of cirrhotic ascites, with a prevalence of 15% to 19% (when culture-negative cases are included). Gram-negative enteric bacteria are the causative agents in more than 70% of cases. SBP is probably the consequence of bacteremia due to defects in the hepatic reticuloendothelial system and in the peripheral destruction of bacteria by neutrophils, with secondary seeding of an ascitic fluid deficient in antibacterial activity. Patients with advanced liver disease and low ascitic fluid protein concentrations seem to have an increased susceptibility to SBP. A diagnostic paracentesis should be performed in any cirrhotic patient who suddenly deteriorates or presents with any compatible symptom of SBP, most frequently fever or abdominal pain, or both. A PMN count greater than 500/mm3 is indicative of SBP, and treatment with intravenous broad-spectrum antibiotics should be initiated immediately. Although the mortality of an acute episode of SBP decreases with early therapy, it is still high (approximately 50%), and patients who survive an episode of SBP have a high frequency of recurrence. Mortality seems to be related to the severity of the underlying liver disease, because only a third of patients die from sepsis and prophylactic antibiotics decrease the frequency of SBP but do not seem to improve long-term survival.     

Spontaneous bacterial peritonitis]

Patients with liver cirrhosis and ascites suffer from spontaneous bacterial peritonitis (SBP) in up to 25%. The typical clinical signs are abdominal pain with tenderness and fever. 30% have no signs of peritonitis. Then clinical worsening, encephalopathy, rising serum creatinine levels, and therapy resistant ascites may be the only clinical features. SBP must be differentiated from bacterascites and culture negative neutrocytic ascites by the polymorphonuclear neutrophil (PMN) count in the ascites and the presence of positive culture results, which has prognostic implications. Gram negative rods from the colon play an important etiological role in SBP. Gastrointestinal bleeding, lack of serum complement, a low ascites protein and the extent of intrahepatic shunts predispose to SBP. Then, prophylaxis with the comparable drugs neomycin and norfloxacin is indicated. Coexisting encephalopathy has to be treated by the therefore effective neomycin. Otherwise, norfloxacin is the drug of choice because of better acceptance and lower costs. Chemical parameters of the ascites (pH value less than 7.4; LDH and lactate greater than serum levels; glucose less than 50 mg%) help to assess the severity of peritonitis. The course of ascitic PMN under therapy and the time of persisting positive cultures can discriminate SBP from secondary peritonitis. Antibiotics of choice are amoxicillin-clavulanic acid and cefotaxime. Short course therapy (5 days) is a effective as long course therapy (10 days). Today SBP is no more life-threatening because diagnosis, prophylaxis and therapy have improved. However, complication rate of patients with liver cirrhosis and ascites has not changed.     

Spontaneous bacterial peritonitis in Wilson's disease

Spontaneous bacterial peritonitis associated with Wilson's disease has been previously reported in only one case. We report two cases where this infection developed and seriously complicated the course of illness. As with spontaneous bacterial peritonitis occurring with other underlying diseases, early diagnosis and treatment are critical to improved outcome. Recognition that it can occur with Wilson's disease is important, and paracentesis should be performed without delay when suspicious features are present.