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Peritonitis in Peritoneal Dialysis
Peritoneal dialysis (PD) is the modality of kidney replacement therapy in about 15% of the dialysis population worldwide. Despite the advances in technology and antibiotic therapy, peritonitis remains a major cause of technique failure and morbidity in PD patients. Although only 4% of peritonitis episodes are a direct cause of mortality, peritonitis is a contributing factor to death in 16% of PD patients. Furthermore, peritonitis accounts for 30% of PD technique failure and 15% to 35% of patient hospitalization.
Reporting of Peritonitis Rate
Peritonitis rates should be reported as number of episodes per patient-year rather than as the interval in months between episodes. Every PD program should monitor the peritonitis rate at least yearly. In addition to the overall peritonitis rate, other parameters that could be considered for regular monitoring include peritonitis rates of specific organisms, the percentage of patients per year who are peritonitis free, and the antimicrobial susceptibilities of the infecting organisms. Some centers also monitor the incidence of death associated with peritonitis, which is often defined as death with active peritonitis or within 4 weeks of a peritonitis episode, or any death during the hospitalization for a peritonitis episode.
There are substantial variations in the peritonitis rate between countries as well as between different centers of the same country, but a reasonable target for any PD center should be within 0.5 episodes per year of treatment. Many centers now report a peritonitis rate of 0.2 to 0.3 episodes per year of treatment.
Risk Factors
The risk factors for peritonitis include patient, technique, and environment related ( Table 27.1 ). However, although many risk factors listed in Table 27.1 are labeled as “modifiable,” there is often a lack of published evidence that modifying these risk factors would reduce peritonitis rates. There is a strong association between PD catheter-related infections (either exit site or tunnel infection) and subsequent peritonitis. Early detection of and prompt antibiotics therapy for catheter-related infections are important steps to reduce the risk of peritonitis.
Table 27.1
Risk Factors for Peritonitis
| Nonmodifiable | Modifiable | |
|---|---|---|
| Patient related |
|
|
| Technique related |
|
|
| Environment related |
|
|
Older patients are at risk, but patients below 20 years of age also have higher risk than middle-aged ones. The socioeconomic status of patients is associated with peritonitis risk. Patients with fewer than 9 years of education have twice as high a peritonitis rate compared to those with over 12 years of education. Depression (e.g., as indicated by a Beck Depression Inventory score) is also associated with the risk of peritonitis.
PD patients with diabetes are at particularly high risk for peritonitis because of multiple mechanisms. Diabetes adversely affects peritoneal defense mechanisms by interfering with the migration of phagocytic cells into the peritoneum. Formation of advanced glycation end products further suppresses the phagocytic activity of resident peritoneal macrophages. Impaired vision and dexterity increase the risk of touch contamination. Concomitant autonomic neuropathy results in a decrease in intestinal motility or slow colonic transit time, which favors bacterial overgrowth and increases the risk of peritonitis due to enteric organisms.
Patients with Staphylococcus aureus nasal carriage have a higher risk for S. aureus peritonitis. Intranasal mupirocin ointment reduces S. aureus exit site infections but is less effective in preventing peritonitis. Intermittent nasal mupirocin application may further prevent redevelopment of S. aureus carriage, and the incidence of antibiotic resistance does not seem to be increased.
Several reports suggest a seasonal variation in the incidence of PD-related peritonitis, with peak incidence in the months that are hot and humid. Keeping a cool and dry living environment may reduce the risk of peritonitis, particularly in tropical countries.
Pathogenesis and Causative Organisms
Bacteria could invade the peritoneal cavity through several routes: intraluminal (via touch contamination during PD exchange), periluminal (as a result of catheter-related infections), intestinal (via transmural spread through the bowel wall), systemic (secondary to septicemia or hematogenous spread), and rarely ascending (through the vagina).
The causative organism can be isolated from the PD effluent in over 90% of peritonitis episodes using appropriate culture techniques. With the extensive use of the “flush before fill” technology and double-bag disconnect systems, Gram-positive and Gram-negative organisms accounted for about 40% and 30% of all peritonitis episodes, respectively ( Fig. 27.1 ). Among the Gram-negative organisms, the Enterobacteriaceae family, which is often labeled as “enteric bacteria,” is the most common. However, there are substantial variations in the prevalence of individual organisms as well as the spectrum of antibiotic resistance between different centers. Each PD unit should take note of its own local data in order to design the optimal management and quality-improvement strategies.
Diagnosis
From a case-reporting point of view, the diagnosis of PD-related peritonitis is confirmed when at least two of the following conditions are present: (1) symptoms and signs of peritoneal inflammation; (2) cloudy PD effluent with an elevated leukocyte count (> 100/μL) or neutrophil predominance (> 50%) in the PD effluent; and (3) presence of bacteria in the PD effluent by Gram stain or culture. In clinical practice, however, PD patients presenting with cloudy effluent should be presumed to have peritonitis. It is important to initiate empiric antibiotic therapy in these patients as soon as possible. There are other causes of cloudy peritoneal effluent (e.g., chemical peritonitis, eosinophilia of the effluent, hemoperitoneum, and rarely, malignancy and chylous effluent), but the risk of serious consequences of peritonitis (i.e., relapse, catheter removal, permanent transfer to hemodialysis, and death) are much higher if treatment is not promptly initiated. Although a number of novel diagnostic techniques have been explored, there is insufficient evidence to recommend their routine clinical use.
Clinical Assessment
Assessment of the patient should include history taking for possible touch contamination, adherence with sterile dialysis technique, recent invasive procedures that may have led to peritonitis, and change in bowel habits (either diarrhea or constipation). Physical examination should focus on abdominal and vital signs. The presence of features that suggest systemic sepsis (i.e., high fever or hypothermia, hypotension, tachycardia, tachypnea, or altered mental state) would favor the use of intravenous instead of intraperitoneal antibiotic therapy. Catheter exit site and tunnel should be examined for features of concomitant catheter-related infections, which may be the cause of the peritonitis.
Microbiological Investigations
The diagnosis of peritonitis and the subsequent management of PD-related peritonitis depends on a timely specimen collection with the appropriate technique. After the initial clinical assessment, PD effluent should be obtained before the addition of antibiotics, and the specimen should be sent immediately to the laboratory for absolute cell count and differential counts as well as bacterial culture. If the specimen is collected after rapid PD cycles (with a dwell time less than 2 hours), the percentage of neutrophils rather than the total leukocyte cell count should be used for the diagnosis of peritonitis.
PD effluent cell count is important because it can differentiate cellular elements of the peritonitis from other causes of cloudy PD effluent (e.g., fibrin, chyle). Most of the leukocytes in the PD effluent of untreated peritonitis should be neutrophils or lymphocytes. A high proportion of eosinophils should raise the suspicion of allergic peritonitis, which usually happens soon after starting PD due to allergy to plasticizers. Tuberculous peritonitis should be suspected if there is a predominance of lymphocytes or macrophages in the PD effluent. It should be noted that cell lysis may occur after 24 to 48 hours of specimen collection, and the cell morphology would not be identified if specimen handling is delayed.
Traditionally, PD effluent is collected in universal sterile bottles for bacterial culture. The fluid specimen is centrifuged, and the sediment is used for Gram stain and plate culture. However, the yield of this method is low. The latest International Society for Peritoneal Dialysis (ISPD) guidelines recommend the use of blood-culture bottles for the bacterial culture of PD effluent because nutrients inside this system facilitate the growth and identification of any causative organism. If immediate delivery to the laboratory is not possible, the inoculated culture bottles should be incubated at 37°C. Centrifugation of a large volume of PD effluent (e.g., 50 mL) followed by resuspension of the sediment and inoculation in the standard blood culture media further increases the yield by 5 to 10 times, but the technique is cumbersome. Blood cultures are not necessary unless there is clinical suspicion of systemic sepsis.
Management
Patients presenting with cloudy PD effluent should be presumed to have peritonitis, and empiric antibiotic therapy should be started once appropriate microbiological specimens have been obtained, and there is no need to wait for the result of any laboratory test. The latest ISPD guidelines recommend center-specific selection of empiric antibiotic regimens that cover both gram-positive and gram-negative organisms. In general, Gram-positive organisms may be covered by vancomycin or a first-generation cephalosporin, while Gram-negative organisms may be covered by aminoglycoside or a third-generation cephalosporin. The choice should depend on the local antibiotic sensitivity of individual PD centers.
Fig. 27.2 summarizes the overall management algorithm of PD-related peritonitis. The authors favor cefazolin over vancomycin for Gram-positive coverage so as to minimize the risk of the emergence of vancomycin-resistant organisms. Although short-term aminoglycoside therapy is safe and provides good Gram-negative coverage, repeated or extended courses of aminoglycoside should be avoided because of the risk for both vestibular toxicity and ototoxicity.
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