Secondary Bacterial Peritonitis Research Articles

Evaluation and Management of Tertiary Peritonitis

Tertiary or recurrent peritonitis can occur after any operation for secondary bacterial peritonitis. The major risk factors for the development of tertiary peritonitis include malnutrition, a high Acute Physiology and Chronic Health Evaluation II score, the presence of organisms resistant to antimicrobial therapy, and organ system failure. Most patients with tertiary peritonitis will have fever and leukocytosis, even though other signs of infection may be absent. The management of tertiary peritonitis should include the provision of appropriate physiologic support, the administration of antimicrobial therapy, and operation or intervention to control the source of contamination and to decrease the bacterial load. Antibiotic-resistant organisms and bacteremia are present more commonly and mortality is greater in patients with tertiary peritonitis. Early recognition and effective intervention are critical to achieving a successful outcome.

Epidemiology and pathophysiology of intraabdominal infections (IAI).

Intraabdominal infection continues to be one of the major challenges in general surgery. Whilst the term "peritonitis" means an inflammation of the peritoneum regardless of its etiology, intraabdominal infections encompass all forms of bacterial peritonitis, of intraabdominal abscesses and of infections of intraabdominal organs. Several classification systems have been suggested for peritonitis and intraabdominal infections, respectively. However, neither phenomenological classifications nor classification systems with respect to the origin of bacterial contamination have a proven relevance for the clinical course of this disease. Moreover, most of the studies dealing with secondary peritonitis or intraabdominal infections are ill-comparable because of wide variations of inclusion criteria. Thus the true incidence of secondary bacterial peritonitis is difficult to assess. With respect to its etiology perforation of hollow viscus is the leading cause followed by postoperative peritonitis, ischemic damage of bowel wall, infection of intraabdominal organs and translocation in nonbacterial peritonitis. The anatomic origin of bacterial contamination and microbiological findings are no major predictors of outcome. However, the preoperative physiological derangement, the surgical clearance of the infectious focus and the response to treatment are established prognostic factors. The pathogenesis of intraabdominal infections is determined by bacterial factors which influence the transition from contamination to infection. Intraabdominal adjuvants and the local host response are additionally important. Bacterial stimuli lead to an almost uniform activation response which is triggered by reaction of mesothelial cells and interspersed peritoneal macrophages and which also involves plasmatic systems, endothelial cells and extra- and intravascular leukocytes. The local consequences of this activation are the transmigration of granulocytes from peritoneal capillaries to the mesothelial surface and a dilatation of peritoneal blood vessels resulting in enhanced permeability, peritoneal edema and lastly the formation of protein-rich peritoneal exudate.

Antimicrobial culture and susceptibility testing has little value for routine management of secondary bacterial peritonitis.

The traditional surgical practice of routinely culturing specimens from patients with community-acquired intraabdominal infections, such as appendicitis, contributes little to the management of the individual patient, either initially or later when infectious complications have developed. Instead of performing routine cultures for peritonitis, a modified approach that still facilitates hospital surveillance for microbial resistance patterns should be used.

Hypothesis: Compartmentalization of cytokines in intraabdominal infection

Although the proximal role of systemic cytokines in the infectious-inflammatory cascades is well recognized, the magnitude and meaning of its intraperitoneal levels in peritonitis have received little attention. We hypothesized that in peritonitis a significant and clinically relevant cytokine-mediated inflammatory response is compartmentalized in the peritoneal cavity. MEDLINE was used to search the literature for all articles dealing with experimental, primary, and secondary bacterial peritonitis and cytokines. Bacterial peritonitis is associated with an immense intraperitoneally compartmentalized cytokine response, with plasma levels of cytokines representing only the tip of the iceberg. Although certain amount of cytokines may be beneficial to the peritoneal defense mechanisms, higher levels correlate with adverse outcome. Thus it is plausible to look at acute peritonitis as initially a combined infective (microorganism) and inflammatory (cytokines) process. The clinical significance of the distinction between peritoneal inflammation and infection and the relevance of our findings to the stratification and treatment of peritonitis are discussed. Current surgical and antibiotic therapy for peritonitis is able to clear the peritoneal cavity of infective concentration of bacteria, but many patients continue to die of an uncontrolled activation of the inflammatory cascade. We suggest that one potential venue for therapeutic progress is the modulation of the compartmentalized peritoneal inflammatory response.

Prognosis and treatment of peritonitis. Do we need new scoring systems?

To assess the clinical significance of present scoring systems for prognosis and treatment in patients with secondary bacterial peritonitis and to define risk factors for patient survival and outcome not included in the scores. A secondary objective was to review our therapeutic regimens and the need for reoperation with regard to outcome. Prospective observational study. University hospital, secondary referral center. From 1992 to 1995, 92 patients with secondary peritonitis were examined at the University Surgical Clinic, Vienna, Austria. the populations as a whole consisted of 56 men and 36 women with an average age of 56 +/- 19 years. Forty-four percent of patients had postoperative peritonitis. Mortality, multiple organ system failure (MOSF), relaparotomy. The mortality rate in patients with an APACHE II (Adult Physiology and Chronic Health Evaluation) score of less than 15 was 4.8%, while mortality rose to 46.7% in those with a score of 15 or higher (P = .001). The average total mortality rate was 18.5%. The prognosis for patients without organ failure or with failure of one organ system was excellent (mortality rate, 0%); quadruple organ failure, however, had a mortality rate of 90%. Initial thrombocytopenia ( < 60 x 10(9)/L), four-quadrant peritonitis, and diabetes mellitus were associated with significantly higher mortality. Leukopenia (white blood cells, < 6 x 10(9)/L) and inappropriate antibiotic therapy as determined by the antibiogram were mildly significant for higher mortality. The need for relaparotomy resulted in substantially higher mortality (P < .001). The impossibility of definitive operative resolution of the intra-abdominal pathologic findings at initial operation had no significant effect on mortality, possibly because planned reoperations were always carried out in those cases. For patients with definitive resolution at initial operation, it was possible to reduce the traditionally high mortality rate associated with relaparotomy on demand by making the decision for reexploration promptly, within the first 48 hours. Nevertheless, the 52.4% mortality rate observed in those cases was still much higher than the 33% found in patients who were not free of disease after the initial operation. The prognosis in peritonitis is decisively influenced by the health status of the patient at the beginning of treatment and by any concomitant risk factors. As a result, a fairly accurate prediction of the outcome of the disease can initially be made on the basis of the APACHE II score and the MOSF score according to Goris. However, the certainty that severely ill patients with high scores often die has little clinical relevance, since it does not provide any therapeutic alternatives to the attending physician. The decision to perform a relaparotomy must be made as soon as possible, at least before MOSF emerges. Already existing MOSF will lead to the "point of no return."

Peritoneal Dialysis in Liver Disorders

The purposes of this paper is to review the specific role of peritoneal dialysis (PD) in patients with liver disorders. We will pay attention to the confluence of liver diseases and situations for which chronic dialysis treatment is required. Hemodialysis (HD) and peritoneal membranes are safe barriers against the passage of the hepatitis C virus; consequently, while peritoneal effluent or HD ultrafiltrate drained from hepatitis B patients/carriers is infective, that from hepatitis C patients does not appear to present this risk. An important issue is horizontal transmission, which appears to occur with both viruses in HD units, and which is absent in peritoneal dialysis units. The incidence of hepatitis C among continuous ambulatory peritoneal dialysis (CAPD) patients is quite low, while it may reach almost 50%-60% of HD patients in some units. While hepatitis C transmission mechanisms are not completely understood and a vaccine is not available, PD provides some degree of protection when compared with HD, for and-stage renal disease patients. In summary, our experience and that of others, with a total of 19 PD-treated chronic liver disease patients, supports CAPD as the treatment of choice for cirrhotic patients with ascites who require chronic dialysis. Data on peritoneal diffusion of low molecular weight substances revealed a marked increase in most patients. The ultrafiltration capacity was clearly augmented with respect to noncirrhotic patients, making the use of hypertonic bags unnecessary. Hemodynamic tolerance was excellent. Complications and death were mainly related to liver disease complications. Spontaneous bacterial peritonitis (SBP), caused by gram-negative germs, is the most important complication directly related to ascites and may have some points in common with PD-related peritonitis. However, and in contrast to most PD peritonitis, two pathogenetic mechanisms have been suggested for SBP: (1) translocation of bacteria from the gut to the mesenteric lymph nodes, and (2) bacteremia in these patients is secondary to the general abnormal host defense mechanisms. Local factors such as intrahepatic shunting and the impairment of bactericidal activity in ascitic fluid favor the bacteria ascites. The hypothesis of a direct transmural contamination from bowel to ascitic fluid has been relegated to secondary bacterial peritonitis. Would cirrhotic patients with temporal or permanent renal function compromise benefit from peritoneal catheter placement and other PD practices to perform repetitive small ascitic drainages at home? Perhaps the time has arrived when hepatologists and PD nephrologists begin to work shoulder to shoulder in this particular field, as we have a common problem, the peritoneal cavity filled with fluid.

Clinical correlates of anaerobic bacteriology in peritonitis.

Recent surgical reports indicate that for patients with secondary bacterial peritonitis, surgeons do not routinely use the identification of the bacterial pathogens and determination of their antimicrobial susceptibilities in choosing antimicrobial therapy. Further, some surgeons advocate abandoning the routine practice of obtaining culture specimens from patients with complicated appendicitis, because the data from the clinical laboratory have not been found to have an impact on postoperative care. We review the rationale for continued surveillance of and implementation of bacteriological data in treatment of secondary peritonitis. We also describe in detail the anaerobic flora of secondary peritonitis, the unique susceptibility patterns of these organisms, and the specific virulence factors of anaerobes, particularly Bacteroides fragilis. The fact that clinical investigations sometimes result in treatment failure when gram-negative anaerobes are resistant to the antimicrobials used or when complete antimicrobial susceptibility data are not available emphasizes the need for accurate and early knowledge of the bacteriologic characteristic of the flora of the operative site. We emphasize the relationship of in vitro susceptibility of intraoperative isolates with clinical outcome. We propose a cooperative trial that would demonstrate that successful antimicrobial therapy should be based on the susceptibility of the flora of the operative site, which correlates with clinical outcome.

Antibiotic Treatment for Surgical Peritonitis

The charts of 480 patients with secondary bacterial peritonitis were reviewed. The antibiotics used were compared with the culture and sensitivity data obtained at surgery, and the outcomes of patients were evaluated. Patients treated with a single broad-spectrum antibiotic had a better outcome than patients treated with multiple drug treatment. Inadequate empiric antibiotic treatment was associated with poorer outcome than any other type of treatment. The outcome of this inadequate treatment group could not be improved by any antibiotic response to culture and sensitivity information after operation. Those patients treated with antibiotic coverage for anticipated organisms and having no cultures taken did as well as patients having cultures taken. Surgeons typically ignore culture data after operation, and only 8.8% of patients in this study had an appropriate change in antibiotic treatment after operation. A benefit from obtaining operative cultures could not be identified.

Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis

To prospectively assess the value of an algorithm in differentiating spontaneous from secondary bacterial peritonitis, we performed serial paracenteses in 43 episodes of ascitic fluid infection (28 spontaneous and 15 secondary) in 40 patients. The algorithm involved identification of (a) secondary peritonitis associated with gut perforation, based on previously proposed criteria in patients with neutrocytic ascites (ascitic fluid total protein > 1 g/dl, glucose < 50 mg/dl, and lactate dehydrogenase greater than the upper limit of normal for serum) and (b) separation of spontaneous from secondary peritonitis (unassociated with perforation) based on the response of the ascitic fluid cell count to antibiotic therapy. The perforation criteria had 100% sensitivity in detecting episodes of actual gut perforation; their specificity, however, was low (45%). After 48 h of treatment the concentration of ascitic fluid neutrophils was below the baseline pretreatment value in all episodes of spontaneous peritonitis but in only two thirds of the patients with secondary peritonitis. This algorithm is useful in (a) identifying patients who have infected ascites associated with perforation of an intraabdominal viscus, and (b) differentiating spontaneous from nonperforation secondary peritonitis on the basis of the response of the ascitic fluid cell count to appropriate antibiotic therapy. The optimal time for repeat paracentesis in patients with infected ascites appears to be 48 h after initiation of treatment.

Mononuclear Phagocyte Thromboplastin and Endotoxin in Patients with Secondary Bacterial Peritonitis

Endotoxin levels and mononuclear phagocyte thromboplastin activities in samples from peripheral blood and peritoneal fluid were determined in nine patients with secondary bacterial peritonitis (appendicitis with perforation, or diverticulitis) and in five control patients (uncomplicated duodenal ulcer or gallbladder stones). None or only negligible amounts of endotoxin, always less than 0.01 ng/dl (contamination), and no growth of bacteria were detected in controls. In the patients with peritonitis, peritoneal fluid samples always contained gram-negative bacteria, and large amounts (mean, 31.6 ng/dl) of endotoxin were seen. Plasma from these patients also contained endotoxin (mean, 0.56 ng/dl) despite negative blood cultures. Mononuclear phagocytes from controls had low thromboplastin values, whereas both circulating monocytes and peritoneal macrophages from peritonitis patients showed a substantial increase (multifold) of thromboplastin.

Bacterial Peritonitis Secondary to a Perinephric Abscess. Case Report and Differentiation From Spontaneous Bacterial Peritonitis

Abstract A cirrhotic patient is described who presented with Escherichia coli septic arthritis as the first manifestation of a perinephric abscess. Results of baseline abdominal paracentesis were unremarkable. After 10 days of antibiotics, abdominal paracentesis was repeated because of recurrence of fever; E. coli peritonitis was confirmed. Subsequent autopsy revealed a perinephric abscess. Development of bacterial peritonitis during antibiotic treatment is distinctly unusual in the spontaneous form of peritonitis and should raise suspicion of secondary bacterial peritonitis.

Spontaneous vs secondary bacterial peritonitis. Differentiation by response of ascitic fluid neutrophil count to antimicrobial therapy.

A retrospective chart review revealed 24 patients who had at least one subsequent ascitic fluid neutrophil count within 14 days of the ascitic fluid analysis that was diagnostic of spontaneous bacterial peritonitis. The neutrophil count decreased (after antibiotic therapy was started) at an exponential rate, with a half-life of 34 +/- 35 hours. In none of four episodes of secondary bacterial peritonitis was there an exponential decline in neutrophil count after antimicrobial therapy was initiated. In fact, the first follow-up neutrophil count was greater than the baseline value in all four episodes. The response pattern of the ascitic fluid neutrophil count to antimicrobial therapy is helpful in differentiating spontaneous from secondary bacterial peritonitis.

Spontaneous vs Secondary Bacterial Peritonitis

Spontaneous vs Secondary Bacterial Peritonitis

Bacterial peritonitis secondary to a perinephric abscess. Case report and differentiation from spontaneous bacterial peritonitis

A cirrhotic patient is described who presented with Escherichia coli septic arthritis as the first manifestation of a perinephric abscess. Results of baseline abdominal paracentesis were unremarkable. After 10 days of antibiotics, abdominal paracentesis was repeated because of recurrence of fever; E. coli peritonitis was confirmed. Subsequent autopsy revealed a perinephric abscess. Development of bacterial peritonitis during antibiotic treatment is distinctly unusual in the “spontaneous” form of peritonitis and should raise suspicion of secondary bacterial peritonitis.

Secondary bacterial peritonitis in cirrhotic patients with ascites.

Bacterial peritonitis in patients with cirrhosis has a wide variety of clinical presentations. We report a group of 21 cirrhotic patients with secondary peritonitis from intra-abdominal sources. Seven had infected ascites. All of them had unrecognized secondary peritonitis which was diagnosed and treated as spontaneous (primary) bacterial peritonitis (SBP). Ascitic fluid analysis yielded a mean white blood cell count of 23,750 +/- 10,935/cu mm with 91.5% polymorphonuclear leukocytes, significantly higher than patients surveyed with SBP, 1,757 +/- 2,154/cu mm (P less than .001). Ascitic fluid protein levels were also higher than those typically seen in SBP: 4.4 +/- 1.5 gm/dl vs 0.8 +/- 0.4 gm/dl (P less than .001). The ascites: serum protein ratio was consistent with an exudate in those patients with secondary peritonitis (0.7 +/- 0.2) in contrast to typically infected transudate in patients with SBP (0.15 +/- 0.05) (P less than .001). Bacteriologic determination was similar: single organisms with Escherichia coli the most common. Often the clinical features and ascitic fluid analysis will not differentiate spontaneous from secondary peritonitis. It is, therefore, clinically prudent to consider secondary bacterial peritonitis in cirrhotic patients, especially with ascitic fluid WBC counts in excess of 5,000/cu mm and protein levels of greater than or equal to 2.5 gm/dl. Noninvasive diagnostic procedures should be included to search for sources of intra-abdominal infection.

The adjuvant effect of peritoneal fluid in experimental peritonitis. Mechanism and clinical implications.

At laparotomy, many surgeons routinely instill crystalloid solutions into the peritoneal cavity, presumably to dilute out necrotic debris, bacteria, and adjuvant substances which foster bacterial growth. We examined the effect on mortality, bacterial growth, clearance, and phagocytosis of various volumes of saline instilled into the peritoneal cavity of rats during Escherichia coli peritonitis. Minimal intraperitoneal bacterial growth was seen after the introduction of a nonlethal inoculum of viable E. coli in 1 ml of saline, while administration of an identical inoculum in 30 ml of saline intraperitoneally (i.p.) led to increased 48-hour mortality (p less than 0.01), and associated rapid bacterial proliferation (p less than 0.01). Clearance of nonviable radiolabelled E. coli from the peritoneal cavity was delayed, bacterial association with host peritoneal leukocytes was decreased, and blood uptake of radiolabelled bacteria was diminished in animals receiving 30 ml of saline i.p., compared to controls which received the identical inoculum in 1 ml of saline i.p. The clinical relevance of these studies is manifold: (1) they provide a possible explanation why patients with ascites due to cirrhosis or the nephrotic syndrome, or those patients undergoing peritoneal dialysis are more susceptible to primary and secondary bacterial peritonitis, possibly on the basis of impaired peritoneal clearance or diminished phagocytosis and, (2) although irrigation of the peritoneal cavity with crystalloid solution would seem prudent during laparotomy, these solutions must be removed prior to closure to prevent interference with normal peritoneal host defense mechanisms.