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Abstract

We present two cases of peritonitis shortly after endoscopic examination of the large bowel with polypectomy in patients on continuous ambulant peritoneal dialysis (CAPD) despite the standard preventive measure to drain the dialysate from the abdomen prior to the procedure. We have reviewed the current literature on this topic. These cases demonstrate that the administration of prophylactic broad-spectrum antibiotics next to the drainage of the abdomen prior to colonoscopy in CAPD patients should be considered as recommended in the International Society for Peritoneal Dialysis (ISPD) guidelines 2005.

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Introduction Peritonitis is an inflammation of the peritoneum, the thin membrane that lines the abdominal wall and covers the organs within. The inflammation is caused by a bacterial or fungal infection of this membrane. There are three major types of peritonitis. Primary peritonitis is caused by the spread of an infection from the blood and lymph nodes to the peritoneum. This type of peritonitis is rare -- less than 1% of all cases of peritonitis are primary. The more common type of peritonitis, called secondary peritonitis, is caused when the infection comes into the peritoneum from the gastrointestinal or biliary tract. And the last is tertiary a persistent or recurrent infection after adequate initial therapy. These cases of peritonitis are very serious and can be life threatening if not treated quickly. Peritonitis is most often caused by introduction of an infection into the otherwise sterile peritoneal environment through organ perforation, but it may also result from other irritants, such as foreign bodies, bile from a perforated gall bladder or a lacerated liver, or gastric acid from a perforated ulcer. Women also experience localized peritonitis from an infected fallopian tube or a ruptured ovarian cyst. Patients may present with an acute or insidious onset of symptoms, limited and mild disease, or systemic and severe disease with septic shock. The peritoneum, which is an otherwise sterile environment, reacts to a variety of pathologic stimuli with a fairly uniform inflammatory response. Depending on the underlying pathology, the resultant peritonitis may be infectious or sterile (ie, chemical or mechanical). Infections in the peritoneum are further divided into generalized (peritonitis) and localized (intra-abdominal abscess). This article focuses on the diagnosis and management of infectious peritonitis and abdominal abscesses because of the tertiary part, where the treatment is in-adequate.

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Case Report Peritonitis in CAPD patients after colonoscopy is a known complication. A retrospective study from Hong Kong revealed an average risk of peritonitis after colonoscopy of 6.3% in 77 CAPD patients after 97 endoscopic procedures. Colonic biopsy or other interventions such as polypectomies apparently did not increase the risk of peritonitis. After colonoscopy in CAPD patients it is thought that bacteria may translocate to mesenteric lymph nodes, then to portal circulation resulting eventually in systemic bacteraemia with peritoneal seeding. In CAPD patients the glucose-containing fluid in the peritoneal cavity impairs the local immune response by diluting cytokines and reducing the macrophage level. The function of mesothelial surface and cells, another local host defence system, may be altered due to presence of dialysis solution. Further, activated cytokines and macrophages are constantly removed by daily changes of the dialysate. All these factors may facilitate bacterial growth in the peritoneal cavity even with a small inoculum of bacteria.

Signs and Symptoms: The signs and symptoms of peritonitis include:

Swelling and tenderness in the abdomen with pain ranging from dull aches to severe, sharp pain

Fever and chills Loss of appetite Thirst

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Nausea and vomiting Limited urine output Inability to pass gas or stool

Causes: Primary peritonitis is usually caused by liver disease. Fluid builds up in the abdomen, creating a prime environment for the growth of bacteria. Secondary peritonitis is caused by other conditions that allow bacteria, enzymes, or bile into the peritoneum from a hole or tear in the gastrointestinal or biliary tracts. Such tears can be caused by pancreatitis, a ruptured appendix, stomach ulcer, Crohn's disease, or diverticulitis. Peritoneal dialysis, which uses the blood vessels in the peritoneum to filter waste from your blood when your kidneys are not able to do so, also may cause peritonitis.

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Risk Factors: The following factors may increase the risk for primary peritonitis:
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Liver disease (cirrhosis) Fluid in the abdomen Weakened immune system Pelvic inflammatory disease

Risk factors for secondary peritonitis include:
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Appendicitis (inflammation of the appendix) Stomach ulcers

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Torn or twisted intestine Pancreatitis Inflammatory bowel disease, such as Crohn's disease or ulcerative colitis Injury caused by an operation Peritoneal dialysis Trauma

Diagnosis: Peritonitis can be life threatening, so the doctor will first conduct a physical examination to determine whether you need surgery to correct the underlying problem. The doctor will feel and press the abdomen to detect any swelling and tenderness as well as signs that fluid has collected in the area. The doctor may also listen to bowel sounds and check for difficulty breathing, low blood pressure, and signs of dehydration. The following procedures also may be performed:
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Blood tests -- to see if there is bacteria present in your blood Samples of fluid from the abdomen -- identify the bacteria causing the infection CT scan -- identifies fluid in the abdomen, or an infected organ X-rays -- detect air in the abdomen, which indicates that an organ may be torn or perforated.

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Etiology Primary Peritonitis SBP occurs in the absence of an apparent intra-abdominal source of infection and is observed almost exclusively in patients with ascites from chronic liver disease. Contamination of the peritoneal cavity is thought to result from translocation of bacteria across the gut wall or mesenteric lymphatics and, less frequently, via hematogenous seeding in the presence of bacteremia. Approximately 10-30% of patients with cirrhosis and ascites develop SBP.1 The incidence rises with ascitic fluid protein contents of less than 1 g/dL (which occurs 15% of patients) to more than 40%, presumably because of decreased ascitic fluid opsonic activity.

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More than 90% of cases of SBP are caused by a monomicrobial infection. The most common pathogens include gram-negative organisms (eg, Escherichia coli [40%], Klebsiella pneumoniae [7%], Pseudomonas species, Proteus species, other gram-negative species [20%]) and gram-positive organisms (eg, Streptococcus pneumoniae [15%], other Streptococcus species [15%], Staphylococcus species [3%]) (see Table 2). Anaerobic microorganisms are found in less than 5% of cases, and multiple isolates are found in less than 10%. Secondary peritonitis SP is by far the most common form of peritonitis encountered in clinical practice. It is caused by perforation or necrosis (transmural infection) of a hollow visceral organ with bacterial inoculation of the peritoneal cavity. (See Table 1 for differential diagnoses.) The pathogens involved in SP differ in the proximal and distal GI tract. Gram-positive organisms predominate in the upper GI tract, with a shift toward gram-negative organisms in the upper GI tract in patients on long-term gastric acid suppressive therapy. Contamination from a distal small bowel or colon source initially may result in the release of several hundred bacterial species (and fungi); host defenses quickly eliminate most of these organisms. The resulting peritonitis is almost always polymicrobial, containing a mixture of aerobic and anaerobic bacteria with a predominance of gram-negative organisms (see Table 2). As many as 15% of patients who have cirrhosis with ascites who were initially presumed to have SBP have SP. In many of these patients, clinical signs and symptoms alone are not sensitive or specific enough to reliably differentiate between the 2 entities. A thorough history,

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evaluation of the peritoneal fluid, and additional diagnostic tests are needed to do so; a high index of suspicion is required. Peritoneal abscess Peritoneal abscess describes the formation of an infected fluid collection encapsulated by fibrinous exudate, omentum, and/or adjacent visceral organs. The overwhelming majority of abscesses occurs subsequent to SP. Approximately half of patients develop a simple abscess without loculation, whereas the other half of patients develop complex abscesses secondary to fibrinous septation and organization of the abscess material. Abscess formation occurs most frequently in the subhepatic area, the pelvis, and the paracolic gutters, but it may also occur in the perisplenic area, the lesser sac, and between small bowel loops and their mesentery. The incidence of abscess formation after abdominal surgery is less than 1-2%, even when the operation is performed for an acute inflammatory process. The risk of abscess increases to 10-30% in cases of preoperative perforation of the hollow viscus, significant fecal contamination of the peritoneal cavity, bowel ischemia, delayed diagnosis and therapy of the initial peritonitis, and the need for reoperation, as well as in the setting of immunosuppression. Abscess formation is the leading cause of persistent infection and development of tertiary peritonitis.

Tertiary peritonitis Tertiary peritonitis represents the persistence or recurrence of peritoneal infection following apparently adequate therapy for SBP or SP, often without the original visceral organ

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pathology. Patients with tertiary peritonitis usually present with an abscess, or phlegmon, with or without fistulization. Tertiary peritonitis develops more frequently in immunocompromised patients and in persons with significant preexisting comorbid conditions. Although rarely observed in uncomplicated peritoneal infections, the incidence of tertiary peritonitis in patients requiring ICU admission for severe abdominal infections may be as high as 50-74%. Patients who develop tertiary peritonitis demonstrate significantly longer lengths of stay in the ICU and hospital, higher organ dysfunction scores, and higher mortality rates (50-70%). Resistant and unusual organisms (eg, Enterococcus, Candida, Staphylococcus, Enterobacter, Pseudomonas species) are found in a significant proportion of cases of tertiary peritonitis. Most patients with tertiary peritonitis develop complex abscesses or poorly localized peritoneal infections that are not amenable to percutaneous drainage. Antibiotic therapy appears to be less effective in tertiary peritonitis than in all other forms of peritonitis, and up to 90% of patients will require reoperation for additional source control.

Tuberculous peritonitis (TP) is rare in the United States (<2% of all causes of peritonitis), but it continues to be a significant problem in developing countries and among patients with human immunodeficiency virus (HIV). The presenting symptoms are often nonspecific and insidious in onset (eg, low-grade fever, anorexia, weight loss). Many patients with TP have underlying cirrhosis and more than 95% of patients with TP have evidence of ascites on imaging studies, and more than half of these patients have clinically apparent ascites. In most cases, chest radiographic findings in patients with TP peritonitis are abnormal; active pulmonary disease is uncommon (<30%). Results on Gram stain of ascitic fluid are rarely

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positive, and culture results may be falsely negative in up to 80% of patients. A peritoneal fluid protein level greater than 2.5 g/dL, a lactate dehydrogenase (LDH) level greater than 90 U/mL, or a predominantly mononuclear cell count of greater than 500 cells/µL should raise suspicion but have limited specificity for the diagnosis. Laparoscopy and visualization of granulomas on peritoneal biopsy specimens, as well as cultures (requires 4-6 wk), may be needed for the definitive diagnosis; however, empiric therapy should begin immediately. Chemical peritonitis Chemical (sterile) peritonitis may be caused by irritants such as bile, blood, barium, or other substances or by transmural inflammation of visceral organs (eg, Crohn disease) without bacterial inoculation of the peritoneal cavity. Clinical signs and symptoms are indistinguishable from those of SP or peritoneal abscess, and the diagnostic and therapeutic approach should be the same.

Discussion In the 2005 guidelines for CAPD peritonitis of the International Society for Peritoneal Dialysis (ISPD) drainage of the peritoneal cavity and antibiotic prophylaxis with ampicilline, an aminoglycoside with or without metronidazole intravenously prior to colonoscopy is recommended. However, due to the lack of prospective trials there is scarce evidence to support this recommendation. Therefore, this guideline is not widely accepted and implemented. In the

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current guidelines of the Dutch Federation of Nephrology (NfN) the use of prophylactic antibiotics additionally to drainage of the dialysate before colonoscopy is recommended. However it is mentioned that this is currently not daily practice in the Netherlands. Furthermore, these nephrology guidelines are widely unknown among gastroenterologists who are responsible for the planning and performance of endoscopic procedures. In the current guidelines of the American Society for Gastrointestinal Endoscopy (ASGE), the British Society of Gastroenterology (BSG)6 and the European Society of Gastrointestinal Endoscopy (ESGE),7 the risk of peritonitis in PD patients is not mentioned. No advice is given about antibiotic prophylaxis in these patients prior to colonoscopy. In 2009, two colonoscopies in 32 CAPD patients were performed in our hospital with one episode of peritonitis. Although peritonitis after colonoscopy in CAPD patients might be a rare event, it may lead to serious complications in the short and long term and even to death. Recurrent peritonitis remains the primary reason to switch from PD to haemodialysis. In distinction, the prophylactic use of a single-dose antibiotic prior to colonoscopy has almost no risks.

The implementation of the ISPD guidelines should be considered in every endoscopy unit performing colonoscopies in CAPD patients. We strongly recommend the use of antibiotic prophylaxis next to drainage of the peritoneal cavity prior to colonoscopy in CAPD patients as advised in the ISPD guidelines. A clear, interdisciplinary communication over these patients between gastroenterologist and nephrologist is important to prevent this serious complication.

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Conclus ion CAPD peritonitis after colonoscopy is not a rare event. It may lead to serious morbidity. With our cases we have demonstrated that drainage of the peritoneal cavity prior to endoscopy is not sufficient to prevent infectious complications. We therefore recommend implementing the current ISPD guidelines to use additional antibiotics. The gastroenterologist should be familiar with this guideline.

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References 1. Piraino B, et al. Peritoneal dialysis-related infections recommendation: 2005 update. Perit Dial Int. 2005;25(2):107-31. 2. Yip T, Tse KC, Lam MF, Cheng SW, Lui SL, Tang S, et al. Risks and outcomes of peritonitis after flexible colonoscopy in CAPD patients. Perit Dial Int. 2007;27(5):560-4. 3. Brulez HF, Verbrugh HA. First-line defense mechanisms in the peritoneal cavity during peritoneal dialysis. Perit Dial Int. 1995;15(7 Suppl):S24-33.

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4. Richtlijnen Peritoneale Dialyse gerelateerde infectie. Nederlandse Federatie voor Nefrologie 2007. http://www.nefro.nl/uploads/6y/mb/ 6ymb3ASlqwnBj7rGmYMtNw/Richtlijn-PDgerelateerde-infecties.2007.pdf 5. Antibiotic prophylaxis for GI endoscopy. ASGE guidelines. Gastrointest Endosc. 2008;67:791-8. 6. Allison MC, Sandoe JAT, Tighe R, Simpson IA, Hall RJ, Elliot TSJ. Antibiotic prophylaxis in gastrointestinal endoscopy. Gut. 2009;58: 869-80. 7. European Society for Gastrointestinal Endoscopy. Guideline: Antibiotic prophylaxis for gastrointestinal endoscopy 1998. http://www.esge.com/ assets/downloads/pdfs/guidelines/antibiotic_prolax.pdf. 8. Perez Fontan M, et al. Peritonitis-related mortality in patients undergoing chronic peritoneal dialysis. Perit Dial Int. 2005;25(3):274-84. 9. Voinescu CG, Khanna R. Peritonitis in peritoneal dialysis. Int J Artif Organs. 2002;25(4):249-60.

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