Your activity: 4 p.v.

Microbiology and therapy of peritonitis in peritoneal dialysis

Microbiology and therapy of peritonitis in peritoneal dialysis
Author:
John M Burkart, MD
Section Editors:
Thomas A Golper, MD
Steve J Schwab, MD, FACP, FASN
Deputy Editors:
Eric N Taylor, MD, MSc, FASN
Keri K Hall, MD, MS
Literature review current through: Dec 2022. | This topic last updated: Nov 16, 2021.

INTRODUCTION — Peritonitis is one of the major complications of peritoneal dialysis and remains the primary reason that patients switch from peritoneal dialysis to hemodialysis [1,2]. This topic reviews the microbiology and therapy of peritonitis in continuous peritoneal dialysis. The approach to the diagnosis of peritonitis, including exclusion of other intra-abdominal diseases, is discussed separately:

(See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis".)

Risk factors, prevention, and diagnosis are discussed elsewhere:

(See "Risk factors and prevention of peritonitis in peritoneal dialysis", section on 'Epidemiology'.)

(See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis".)

MICROBIOLOGY

Overview — The vast majority of peritonitis cases are caused by bacteria. Approximately 3 to 5 percent are caused by fungi, mostly Candida species [3-5]. A viral etiology of peritonitis has been postulated in some cases, although viral infection as a cause of peritonitis has not been proven conclusively [6].

Approximately 45 to 65 percent of cases are caused by gram-positive organisms and 15 to 35 percent by gram-negative organisms [4,5,7-10]. More than one organism has been reported in 1 to 4 percent of cases [3,4]. (See 'Polymicrobial peritonitis' below.)

Failure to identify an organism is common. Two series reported 20 to 40 percent of cases that were culture negative [3,4,11]; in the later series, the high percentage may have reflected failure to obtain a peritoneal dialysate sample prior to initiation of antibiotic treatment [4]. Culture-negative peritonitis is treated with empiric antibiotics and has a clinical course that is similar to that of coagulase-negative Staphylococcus infection [5,12,13]. (See 'Culture-negative peritonitis' below.)

The most common source of peritonitis is intraluminal contamination; typically, this occurs if the patient uses suboptimal sterile technique for connecting or disconnecting the catheter to perform exchanges ("touch contamination"). Other sources of peritonitis include periluminal (contamination due to extension of bacteria from exit-site or tunnel infection), visceral (contamination via bacteria from bowel) and vaginal (rarely). In addition, peritonitis can develop via hematogenous dissemination from a remote source.

Gram positive — Gram-positive pathogens include coagulase-negative Staphylococcus spp, Streptococcus spp, Staphylococcus aureus, Enterococcus spp, and Corynebacterium spp. The sources of infections are discussed elsewhere. (See "Risk factors and prevention of peritonitis in peritoneal dialysis", section on 'Source of infection'.)

Coagulase-negative Staphylococcus is the most common cause of peritonitis. In one of the more recent studies, coagulase-negative staphylococci caused 60 percent of infections caused by gram-positive organisms and 39 percent of infections overall [10]. Streptococcus spp caused 20 percent of gram-positive infections and 13 percent of infections overall. S. aureus, Enterococcus spp, and Corynebacterium spp caused 6, 6, and 4 percent of gram-positive infections, respectively, and 4, 4, and 2.5 percent of infections overall.

The relative percentages of peritonitis caused by staphylococci have changed over time [4,9]. The use of Y systems (or flush before fill) has reduced the incidence of coagulase-negative staphylococcal peritonitis due to touch contamination but has a lesser protective effect against other causes of infection [14,15]. As a result, there has been a reduction in the overall rate of peritonitis due to staphylococci, with a relative increase in the incidence of peritonitis due to S. aureus.

Enterococcus infections may be due to touch contamination or from the gastrointestinal tract. The frequency of vancomycin-resistant enterococci (VRE) has increased [16]. Major risk factors include prior exposure to vancomycin and cephalosporins. (See "Vancomycin-resistant enterococci: Epidemiology, prevention, and control".)

Gram negative — Gram-negative organisms can be from the bowel, skin, urinary tract, contaminated water, or animal contact [17,18]. In some centers, preventive measures aimed at reducing peritonitis due to touch contamination have resulted in a percentage increase in gram-negative organisms as the cause of peritonitis and exit-site infections [19]. (See "Risk factors and prevention of peritonitis in peritoneal dialysis", section on 'Prevention' and "Peritoneal catheter exit-site and tunnel infections in peritoneal dialysis in adults", section on 'Prevention'.)

Common causes of gram-negative peritonitis include Escherichia coli, Klebsiella spp, and Pseudomonas aeruginosa (33, 25, and 12 percent of the gram-negative infections in one study, respectively) [10].

Fungal — Fungal peritonitis is uncommon in peritoneal dialysis patients. The presenting signs and symptoms associated with fungal peritonitis are similar to those seen with bacterial peritonitis. The approach to such patients is discussed separately. (See "Fungal peritonitis in peritoneal dialysis".)

Fungal infection is an indication for immediate catheter removal. (See 'Indications for catheter removal' below.)

TREATMENT — The major treatment for peritoneal dialysis-associated peritonitis is antimicrobial therapy. We may also adjust the dialysis prescription to prevent clotting of the catheter or volume overload that occurs as a result of changes in peritoneal membrane characteristics during infection. In some cases, catheter removal is required to eradicate infection.

Antimicrobial therapy — Treatment recommendations are based on expert opinion. Systematic reviews have shown no single, optimal antibiotic agent or combination of agents [20,21].

Empiric antibiotics — Empiric antibiotics should be initiated as soon as possible after specimens obtained for cell count, Gram stain, and culture [22]. Coverage should be provided for both gram-positive and gram-negative organisms [22-25]. The initial regimen should be selected based on local sensitivity data for organisms that commonly cause peritonitis [22,26,27] and whether a patient has recently received antimicrobial therapy for another indication.

We agree with the 2016 International Society for Peritoneal Dialysis (ISPD) guidelines that recommended the following approach to initial empiric antibiotic coverage [22]:

Gram-positive organisms may be covered by vancomycin or a first-generation cephalosporin (such as cefazolin). In centers with a high rate of methicillin-resistant organisms, vancomycin should be used.

Gram-negative organisms may be covered by a third- or fourth-generation cephalosporin (such as cefepime or ceftazidime), an aminoglycoside, or aztreonam [24].

Antibiotics may be adjusted based on the Gram stain if an organism is demonstrated. Gram-negative coverage may be omitted or stopped if the Gram stain shows only gram-positive organisms, and gram-positive coverage may be omitted or stopped if only gram-negative organisms are observed. If the Gram stain reveals yeast or other fungus, antifungal agents should be started and the patient prepared for possible catheter removal depending on the final culture results [23]. Fungal infection is an indication for prompt catheter removal. (See "Fungal peritonitis in peritoneal dialysis".)

Details regarding dosing and administration of antibiotics are discussed below. (See 'Antibiotic dosing and administration' below.)

After culture and sensitivity results are available

Single bacterial organism — The regimen should be adjusted after a specific organism is identified [22] and may be further adjusted based on clinical response [22-24,28-31]. Patients with cultures demonstrating methicillin-resistant S. aureus warrant treatment with vancomycin; patients with methicillin-sensitive S. aureus warrant treatment with a first-generation cephalosporin such as cefazolin, if feasible.

We generally do not use intraperitoneal quinolones, even if culture results suggest that the organism may be sensitive [32]. Although in vitro sensitivity testing may suggest efficacy of a quinolone, in vivo results may be different due to biofilm formation [33]. In addition, the use of quinolones increases the risk for the development of Clostridioides difficile infection and has been associated with an overall increase in quinolone resistance. (See "Clostridioides difficile infection in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use' and "Fluoroquinolones", section on 'Important resistance patterns'.)

There are no high-quality, randomized studies that have examined the optimal duration of antibiotics. We select the duration of antibiotics based on the organism. We treat coagulase-negative Staphylococcus and Streptococcus infections for two weeks; all other gram-positive infections and all gram-negative infections are treated for three weeks because infections with these organisms are usually more severe and difficult to eradicate, although this has not been shown to improve outcomes [34]. (See 'Prognosis' below.)

An exception is patients with coagulase-negative Staphylococcus infection who had a previous infection with the same organism; we treat such patients for three weeks, which may result in a higher cure rate [35].

Polymicrobial peritonitis — Polymicrobial infection (either multiple gram-negative organisms or both gram-positive and gram-negative organisms) has been reported in 1 to 4 percent of cases of peritoneal dialysis-associated peritonitis [3,4].

Peritonitis due to multiple enteric organisms or mixed gram-negative/gram-positive organisms should raise concern for a concurrent intra-abdominal condition such as ischemic bowel or diverticular disease. In such cases, imaging studies and surgical consultation should be obtained [23,24,36]. (See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis", section on 'When to suspect secondary peritonitis'.)

Empiric broad-spectrum antimicrobial therapy should include coverage for anaerobes and gram-negative enteric bacilli. We generally treat with metronidazole plus vancomycin plus an aminoglycoside or ceftazidime. Catheter removal is typically necessary. We continue antibiotics for a minimum of two weeks after the catheter is removed. Antibiotics need to be given orally or intravenously once the catheter is removed. (See 'Indications for catheter removal' below.)

Culture-negative peritonitis — Failure to identify an organism is common. Two series reported 20 to 40 percent of cases that were culture negative [3,4].

Patients with culture-negative peritonitis are treated with empiric antibiotics covering both gram-positive and negative organisms. (See 'Empiric antibiotics' above.)

We repeat the cell count and culture after three days of empiric therapy. If there is improvement in cell count and clinical status after three days and cultures continue to show no growth, we continue either vancomycin or a first-generation cephalosporin for a total of two weeks.

If the repeat cell count shows no improvement after three days of antibiotics, we perform additional evaluation for other causes of culture-negative peritonitis.

The differential diagnosis for infectious causes of culture-negative peritonitis includes mycobacterial and fungal pathogens, Nocardia, and Legionella. Evaluation for mycobacterial and fungal pathogens consists of mycobacterial and fungal cultures, respectively. Nocardia may be detected with bacterial or mycobacterial culture. Legionella is usually diagnosed via serology. (See "Clinical manifestations and diagnosis of nocardiosis" and "Clinical manifestations and diagnosis of Legionella infection".)

Nonmicrobial causes of sterile peritonitis include endotoxin contamination of the dialysate, an adverse reaction to icodextrin (a component of peritoneal dialysis solution), allergic reactions, or reaction to intraperitoneal or retroperitoneal disease [37-45]. Icodextrin dialysate-associated peritonitis occurs either immediately or after several months of exposure [42,44,46,47]. (See "Peritoneal dialysis solutions", section on 'Glucose polymer-containing solutions (icodextrin)'.)

We discontinue exchanges that contain icodextrin. We review all medications to look for potential allergens. (See "Fungal peritonitis in peritoneal dialysis", section on 'Laboratory findings and diagnosis' and "Abdominal tuberculosis", section on 'Peritoneal tuberculosis'.)

Other measures depend on how the patient looks. If the patient is doing well clinically, our approach is to stop antibiotics and continue to observe with one follow-up culture two weeks after completion of antibiotic therapy.

If the patient continues to be symptomatic with persistently elevated cell counts, we remove the catheter. (See 'Indications for catheter removal' below.)

Antibiotic dosing and administration — Intraperitoneal administration of antibiotics is preferred to intravenous administration, unless the patient appears septic [22-24]. Intraperitoneal administration provides optimal local antibiotic concentration. In the majority of patients, infection is localized to the peritoneum and a few cell layers lining the peritoneal cavity and intra-abdominal viscera. Bacteremia is uncommon in peritoneal dialysis-associated peritonitis. The commonly used antibiotics, including vancomycin, cephalosporins, and aminoglycosides, can be mixed in the same dialysis bag without loss of bioactivity.

Intraperitoneal antibiotics can be administered either continuously (with antibiotics given in each exchange) or intermittently (given once daily for almost all antibiotics, with a few exceptions where every other bag dosing is recommended). We initiate therapy with intermittent dosing for ease-of-use reasons, though occasionally switch to continuous dosing if the patient does not respond to intermittent dosing (see 'Monitoring clinical response' below). However, many clinicians initiate therapy with continuous dosing. Continuous and intermittent intraperitoneal dosing regimens have similar rates of treatment failure and relapse [20].

Intraperitoneal antibiotics that are administered intermittently must dwell for at least six hours (table 1 and table 2). For patients on chronic ambulatory peritoneal dialysis (CAPD), this would be during the overnight dwell; whereas, for patients on automated peritoneal dialysis (APD), this would be the daytime dwell.

Specific considerations apply to patients using cycler therapy (APD). When patients set up their cycler, they will connect two or three bags of fluid for the overnight dwells, some of which may be used for the daytime dwell(s), and then often attach a different bag of fluid to be used for the daytime dwell(s). The typical daytime dwell often uses a different dialysate bag (different percent dextrose or icodextrin) than the overnight dwells. As a result, if the clinician is prescribing intermittent dosing, then the prescribed antibiotic should be added to the daytime dwell that is intended to dwell at least six hours. If the clinician wishes to use continuous dosing, the clinician and home training team need to remember that after the first overnight fill, the cycler draws fluid from all the overnight bags. Thus, when continuous dosing in APD is used, it is important to add antibiotics in the dose concentration (usually dosed in mg/L (table 1 and table 2)) to all bags.

Serum drug levels for vancomycin and aminoglycosides are commonly monitored to facilitate dosing and prevent toxicity since systemic absorption occurs with intraperitoneal administration of antibiotics. However, this practice is not universal, and many clinicians do not monitor drug levels.

Monitoring clinical response — We monitor the patient's clinical response daily to make sure symptoms are stable or starting to improve. Clinical improvement should be observed within 48 hours of initiating therapy [24]. (See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis", section on 'Evaluation'.)

By 48 hours, the fluid should be less cloudy. We repeat cell counts to assess response to therapy [24]. The cell count should be decreasing from baseline obtained on presentation. Methods for obtaining peritoneal fluid and evaluation of cell counts are described elsewhere. (See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis", section on 'Peritoneal fluid analysis'.)

The absence of improvement in the cell count suggests lack of response to treatment. In a study of 565 consecutive episodes of peritonitis, a persistent dialysate cell count >1000 by the third day of peritonitis was associated with a 64 percent likelihood of treatment failure [48].

If the patient does not appear to be improving clinically by 48 hours and cultures demonstrate a susceptible organism, we switch from intermittent to continuous dosing [49]. (See 'Antibiotic dosing and administration' above.)

Some organisms may require the addition of a second antibiotic:

For S. aureus infections, we add rifampin if there is no or little clinical response by 48 hours. In one retrospective study of 245 patients with S. aureus peritonitis, adjuvant rifampin therapy was associated with a lower risk for relapse or repeat peritonitis [31].

For gram-negative infections, we add a second antibiotic based on sensitivities if there is no response at 48 hours [50,51]. However, there are no good studies that support this practice, and some clinicians prefer to continue with single antibiotic rather than risk the potential toxicity associated with an additional agent.

If a cloudy effluent persists after five days of appropriate antibiotic therapy, we remove the catheter [24]. (See 'Indications for catheter removal' below.)

Antifungal prophylaxis — Treatment with systemic antibiotics is a major risk factor for the development of fungal peritonitis among peritoneal dialysis patients. Antifungal prophylaxis during the course of antibiotic therapy may reduce the risk of subsequent fungal peritonitis. (See "Fungal peritonitis in peritoneal dialysis", section on 'Causes and risk factors'.)

There is no consensus on the optimal approach to prevention of fungal peritonitis [52]. We administer antifungal prophylaxis among patients on peritoneal dialysis who are treated with antibiotics for longer than three days, regardless of the site of infection. However, others favor administration of antifungal prophylaxis with any antibiotic course lasting longer than one day [53-60]. (See "Fungal peritonitis in peritoneal dialysis".)

Issues related to selection and dosing of antifungal prophylaxis are discussed separately. (See "Fungal peritonitis in peritoneal dialysis", section on 'Prevention'.)

Dialysis prescription

Rapid exchanges — We perform one to two rapid in-and-out exchanges prior to the administration of antibiotics if the patient is having significant pain. Rapid exchanges reduce pain and may reduce the inflammatory burden and endotoxin load but have little effect on the duration of peritonitis or likelihood of cure [61,62]. If rapid exchanges are performed, dialysate containing 1.5 percent dextrose should be used so that ultrafiltration is not excessive.

Addition of heparin to dialysate — Heparin (500 units/L of dialysate) may be added when fibrin strands are observed in dialysate or when there is a history of clogging of the catheter. Heparin helps to lyse and/or prevent fibrin clots [62]. Heparin is otherwise not added even if dialysate is cloudy (as it almost always is in setting of peritonitis).

Adjustment for volume overload — Patients commonly become volume overloaded during episodes of peritonitis because there is decreased ultrafiltration by dialysis. Decreased ultrafiltration is due to an increase in the solute transport rate that results in rapid equilibration of fluid and solute across the peritoneal membrane and the reabsorption of fluid from the peritoneal cavity into the blood. (See "Management of hypervolemia in peritoneal dialysis patients", section on 'Related to dialysis'.)

We adjust the prescription in such patients to treat volume overload. We use hypertonic (4.25 percent) dextrose solutions or icodextrin for one or two exchanges per day. We may also reduce the dwell time. Reducing the dwell time removes the fluid from the peritoneum before it can be reabsorbed. (See "Management of hypervolemia in peritoneal dialysis patients", section on 'Icodextrin dialysate' and "Management of hypervolemia in peritoneal dialysis patients", section on 'Additional exchange'.)

In the absence of hypervolemia, we generally do not change the dwell time or number of exchanges. Theoretically, long dwell times (four to six hours) may be preferred to short dwell times in patients with peritonitis because they are associated with higher numbers of functional intraperitoneal macrophages and immunoglobulin G (IgG) concentrations [2,63]. However, there are no conclusive data that this improves outcomes, and, as noted, long dwells may result in decreased ultrafiltration.

Cessation of dialysis — In general, we do not stop peritoneal dialysis in the setting of peritonitis. Early studies suggested that stopping peritoneal dialysis for 48 hours after giving one dose of antibiotics resulted in a high cure rate [64,65]. However, this approach is not favored for multiple reasons. Such patients would require hemodialysis, which is associated with additional risks associated with vascular catheter placement and the hemodialysis procedure. In addition, withholding peritoneal dialysis in patients with severe peritonitis may increase the risk of encapsulating peritoneal sclerosis [66]. (See "Encapsulating peritoneal sclerosis in peritoneal dialysis patients", section on 'Risk factors'.)

However, stopping peritoneal dialysis may be necessary in severe cases of peritonitis in which the catheter is removed. (See 'Indications for catheter removal' below.)

Indications for catheter removal — Occasionally, catheter removal is required to eradicate infection. We remove the catheter in the following circumstances [23,24]:

Refractory peritonitis, defined as peritonitis that does not respond to appropriate antibiotics within five days.

Relapsing peritonitis, defined as a repeat episode of peritonitis within four weeks of completion of an antibiotic course. The repeat episode is caused by the same organism that caused the initial episode or follows an episode of culture-negative peritonitis. We may also remove the catheter if the patient develops a repeat episode of peritonitis with the same species within two months of completion of an antibiotic course. (See 'Culture-negative peritonitis' above.)

Fungal or mycobacterial peritonitis.

Peritonitis occurring in association with intra-abdominal pathology, such as an abscess, perforation, or infarcted bowel.

Culture-negative peritonitis with persistent symptoms and high peritoneal white blood cell count.

Early catheter removal in patients with refractory peritonitis reduces mortality and avoids prolonged episodes of peritonitis that could damage the peritoneal membrane [67,68]. In a report describing 636 episodes of peritonitis and 16 deaths, the catheter was removed between the 5th and the 10th day in six patients who died and after 10 days in seven patients who died [68].

Simultaneous catheter removal and a new catheter replacement are acceptable for relapsing peritonitis if the dialysate can be cleared first [23,69,70].

Simultaneous catheter replacement is not possible for refractory peritonitis, fungal peritonitis, or peritonitis associated with intra-abdominal pathology. In these settings, there should be a minimum period of three to four weeks between the time of catheter removal and new catheter placement. We treat with oral or intravenous antibiotics for a minimum of two weeks after the catheter is removed.

Limited data exist concerning success with peritoneal dialysis catheter reinsertion because of catheter removal for severe peritonitis [71]. Reported success rates range from 30 to 55 percent at follow-up of 20 to 24 months, with overall mortality of 19 to 36 percent [72,73]. Technique failure was most common in those with increased dialysis vintage.

PROGNOSIS

Mortality — The reported peritonitis-associated mortality is 2 to 6 percent [2,5,12,13,74]. The mortality risk is highest with fungal pathogens, gram-negative organisms, and S. aureus [12,74]. In one retrospective Spanish study of 565 patients (693 episodes of peritonitis), mortality rates of 28, 19, and 15 percent were associated with fungus, enteric organisms, and S. aureus, respectively [74].

Peritonitis is also associated with increased mortality from noninfectious causes. In a study of 1316 peritoneal dialysis patients who died while being treated with peritoneal dialysis or within 30 days of transfer to hemodialysis, there was a much greater risk of having had peritonitis within the four months prior to death compared with the rest of the year, even though the immediate cause of death was not attributed to peritonitis in the majority of cases [75]. In particular, there was a marked increase in the risk of having had peritonitis in the 30 days prior to death among patients who died of cardiovascular, cerebrovascular, or peripheral vascular disease (odds ratio 3.4, 95% CI 2.4-4.6). Similar findings were reported in a study of 1321 peritoneal dialysis patients, which found that peritonitis was independently associated with increased risks of all-cause, cardiovascular, and infection-related mortality in patients dialyzed for longer than two years [76].

Secondary peritonitis is associated with a worse prognosis [36,77,78]. In one report, 11 of 26 patients with secondary peritonitis died [77] compared with an overall peritonitis-associated mortality of approximately 2 to 3 percent among all peritoneal dialysis patients with peritonitis [13]. In the study of secondary peritonitis, mortality correlated with the specific causes of peritonitis (particularly infarcted bowel), the time to diagnosis, and definitive surgical intervention. (See "Unique aspects of gastrointestinal disease in dialysis patients".)

Peritonitis due to extended-spectrum beta-lactamase- or carbapenemase-producing gram-negative organisms is associated with higher mortality [79]. Peritonitis due to multidrug-resistant gram-negative pathogens may occur in patients who have previously received broad-spectrum antimicrobial therapy, who have resided in a long-term care facility, or who are from a region where such organisms are endemic.

Catheter removal — Most cases of peritoneal dialysis-associated peritonitis resolve with outpatient antibiotic treatment [80]. The risk of having to remove the catheter to eradicate infection is approximately 20 percent with variability between centers and with individual organisms [80]. Coagulase-negative staphylococci, streptococci, and culture-negative peritonitis have the lowest risk of failure without catheter removal (<20 percent); corynebacteria, enterococci, S. aureus, and non-Pseudomonas gram-negative peritonitis have a moderate risk of requiring catheter removal (20 to 40 percent); Pseudomonas has the highest risk of requiring catheter removal (>40 percent) [80-83].

The risk of requiring catheter removal increases if there is a concurrent exit-site or tunnel infection [84].

Transfer to hemodialysis — Peritonitis results in a 5 to 20 percent risk of patients needing to switch to hemodialysis [12,80-83,85,86]. Organisms that are considered moderate or high risk for requiring catheter removal (corynebacteria, enterococci, S. aureus and non-Pseudomonas gram negatives, fungus, and Pseudomonas) are associated with higher risk of switching to hemodialysis compared with coagulase-negative Staphylococcus, Streptococcus, and culture-negative peritonitis [80-83].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Beyond the Basics topic (see "Patient education: Peritoneal dialysis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

General principles – Peritonitis is a major complication of peritoneal dialysis and is the primary reason patients switch from peritoneal dialysis to hemodialysis. The majority of peritonitis cases are caused by bacteria; a small percentage of cases are caused by fungi, mostly Candida species. (See 'Introduction' above and 'Microbiology' above.)

Treatment – Treatment for peritoneal dialysis-associated peritonitis consists of antimicrobial therapy; in some cases, catheter removal is also warranted. Additional therapies may include the addition of heparin to dialysate and rapid exchanges to reduce symptoms. (See 'Treatment' above.)

Antimicrobial therapy – Initial empiric antibiotic coverage for peritoneal dialysis-associated peritonitis consists of coverage for gram-positive organisms (by vancomycin or a first-generation cephalosporin) and gram-negative organisms (by a third-generation cephalosporin, an aminoglycoside, or aztreonam). Intraperitoneal administration of antibiotics is preferred to intravenous administration, unless the patient appears septic. The regimen should be adjusted based on culture and sensitivity data. (See 'Antimicrobial therapy' above.)

Polymicrobial peritonitis – Peritonitis due to multiple enteric organisms or mixed gram-negative/gram-positive organisms should raise concern for a concurrent intra-abdominal condition such as ischemic bowel or diverticular disease. (See 'Polymicrobial peritonitis' above.)

Culture-negative peritonitis – Culture-negative peritonitis should be treated with empiric antibiotic therapy that covers both gram-positive and negative organisms. A repeat cell count and culture should be obtained after three to five days of empiric therapy and determines further therapy. Our approach is detailed above. (See 'Culture-negative peritonitis' above.)

Indications for catheter removal – Indications for catheter removal include relapsing or refractory peritonitis, fungal or mycobacterial peritonitis, peritonitis associated with intra-abdominal pathology, and culture-negative peritonitis with persistent symptoms. (See 'Indications for catheter removal' above.)

Prognosis – Most episodes of peritoneal dialysis-associated peritonitis resolve with outpatient antibiotic treatment. Approximately 20 percent require catheter removal to eradicate infection. There is a reported associated mortality of 2 to 6 percent. (See 'Prognosis' above.)

  1. Holley JL, Praino BM. Complications of peritoneal dialysis: Diagnosis and management. Semin Dial 1990; 3:245.
  2. Stablein DM, Nolph KD, Lindblad AS. Timing and characteristics of multiple peritonitis episodes: a report of the National CAPD Registry. Am J Kidney Dis 1989; 14:44.
  3. Port FK, Held PJ, Nolph KD, et al. Risk of peritonitis and technique failure by CAPD connection technique: a national study. Kidney Int 1992; 42:967.
  4. Kim DK, Yoo TH, Ryu DR, et al. Changes in causative organisms and their antimicrobial susceptibilities in CAPD peritonitis: a single center's experience over one decade. Perit Dial Int 2004; 24:424.
  5. Mujais S. Microbiology and outcomes of peritonitis in North America. Kidney Int Suppl 2006; :S55.
  6. Lewis SL. Recurrent peritonitis: evidence for possible viral etiology. Am J Kidney Dis 1991; 17:343.
  7. Oo TN, Roberts TL, Collins AJ. A comparison of peritonitis rates from the United States Renal Data System database: CAPD versus continuous cycling peritoneal dialysis patients. Am J Kidney Dis 2005; 45:372.
  8. Kan GW, Thomas MA, Heath CH. A 12-month review of peritoneal dialysis-related peritonitis in Western Australia: is empiric vancomycin still indicated for some patients? Perit Dial Int 2003; 23:465.
  9. Kavanagh D, Prescott GJ, Mactier RA. Peritoneal dialysis-associated peritonitis in Scotland (1999-2002). Nephrol Dial Transplant 2004; 19:2584.
  10. Whitty R, Bargman JM, Kiss A, et al. Residual Kidney Function and Peritoneal Dialysis-Associated Peritonitis Treatment Outcomes. Clin J Am Soc Nephrol 2017; 12:2016.
  11. Bunke M, Brier ME, Golper TA. Culture-negative CAPD peritonitis: the Network 9 Study. Adv Perit Dial 1994; 10:174.
  12. Bunke CM, Brier ME, Golper TA. Outcomes of single organism peritonitis in peritoneal dialysis: gram negatives versus gram positives in the Network 9 Peritonitis Study. Kidney Int 1997; 52:524.
  13. Ghali JR, Bannister KM, Brown FG, et al. Microbiology and outcomes of peritonitis in Australian peritoneal dialysis patients. Perit Dial Int 2011; 31:651.
  14. Burkart JM, Hylander B, Durnell-Figel T, Roberts D. Comparison of peritonitis rates during long-term use of standard spike versus Ultraset in continuous ambulatory peritoneal dialysis (CAPD). Perit Dial Int 1990; 10:41.
  15. Grützmacher P, Tsobanelis T, Bruns M, et al. Decrease in peritonitis rate by integrated disconnect system in patients on continuous ambulatory peritoneal dialysis. Perit Dial Int 1993; 13 Suppl 2:S326.
  16. Troidle L, Kliger AS, Gorban-Brennan N, et al. Nine episodes of CPD-associated peritonitis with vancomycin resistant enterococci. Kidney Int 1996; 50:1368.
  17. Wood CJ, Fleming V, Turnidge J, et al. Campylobacter peritonitis in continuous ambulatory peritoneal dialysis: report of eight cases and a review of the literature. Am J Kidney Dis 1992; 19:257.
  18. Holley JL, Bernardini J, Piraino B. Polymicrobial peritonitis in patients on continuous peritoneal dialysis. Am J Kidney Dis 1992; 19:162.
  19. Piraino B, Bernardini J, Florio T, Fried L. Staphylococcus aureus prophylaxis and trends in gram-negative infections in peritoneal dialysis patients. Perit Dial Int 2003; 23:456.
  20. Ballinger AE, Palmer SC, Wiggins KJ, et al. Treatment for peritoneal dialysis-associated peritonitis. Cochrane Database Syst Rev 2014; :CD005284.
  21. Wiggins KJ, Johnson DW, Craig JC, Strippoli GF. Treatment of peritoneal dialysis-associated peritonitis: a systematic review of randomized controlled trials. Am J Kidney Dis 2007; 50:967.
  22. Li PK, Szeto CC, Piraino B, et al. ISPD Peritonitis Recommendations: 2016 Update on Prevention and Treatment. Perit Dial Int 2016; 36:481.
  23. Piraino B, Bailie GR, Bernardini J, et al. Peritoneal dialysis-related infections recommendations: 2005 update. Perit Dial Int 2005; 25:107.
  24. Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections recommendations: 2010 update. Perit Dial Int 2010; 30:393.
  25. Teitelbaum I. Vancomycin for the initial therapy of peritonitis: don't throw out the baby with the bathwater. Perit Dial Int 2001; 21:235.
  26. Lye WC. Empirical treatment of CAPD peritonitis: to each his own? Perit Dial Int 2004; 24:416.
  27. Van Biesen W, Vanholder R, Vogelaers D, et al. The need for a center-tailored treatment protocol for peritonitis. Perit Dial Int 1998; 18:274.
  28. Flanigan MJ, Lim VS. Initial treatment of dialysis associated peritonitis: a controlled trial of vancomycin versus cefazolin. Perit Dial Int 1991; 11:31.
  29. Gucek A, Bren AF, Hergouth V, Lindic J. Cefazolin and netilmycin versus vancomycin and ceftazidime in the treatment of CAPD peritonitis. Adv Perit Dial 1997; 13:218.
  30. Khairullah Q, Provenzano R, Tayeb J, et al. Comparison of vancomycin versus cefazolin as initial therapy for peritonitis in peritoneal dialysis patients. Perit Dial Int 2002; 22:339.
  31. Szeto CC, Chow KM, Kwan BC, et al. Staphylococcus aureus peritonitis complicates peritoneal dialysis: review of 245 consecutive cases. Clin J Am Soc Nephrol 2007; 2:245.
  32. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis 2010; 50:133.
  33. Valdés-Sotomayor J, Cirugeda A, Bajo MA, et al. Increased severity of Escherichia coli peritonitis in peritoneal dialysis patients independent of changes in in vitro antimicrobial susceptibility testing. Perit Dial Int 2003; 23:450.
  34. Altmann P, Butter K, Cunningham J, et al. CAPD peritonitis: 10 or 21 days of treatment. Kidney Int 1984; 26:544.
  35. Szeto CC, Kwan BC, Chow KM, et al. Coagulase negative staphylococcal peritonitis in peritoneal dialysis patients: review of 232 consecutive cases. Clin J Am Soc Nephrol 2008; 3:91.
  36. Kern EO, Newman LN, Cacho CP, et al. Abdominal catastrophe revisited: the risk and outcome of enteric peritoneal contamination. Perit Dial Int 2002; 22:323.
  37. de Freitas DG, Gokal R. Sterile peritonitis in the peritoneal dialysis patient. Perit Dial Int 2005; 25:146.
  38. Sewell DL, Golper TA, Hulman PB, et al. Comparison of large volume culture to other methods for isolation of microorganisms from dialysate. Perit Dial Int 1990; 10:49.
  39. Seow YY, Iles-Smith H, Hirst H, Gokal R. Icodextrin-associated peritonitis among CAPD patients. Nephrol Dial Transplant 2003; 18:1951.
  40. Borràs M, Martin M, Fernández E. Sterile peritonitis outbreak related to icodextrin treatment. Perit Dial Int 2004; 24:87.
  41. Mangram AJ, Archibald LK, Hupert M, et al. Outbreak of sterile peritonitis among continuous cycling peritoneal dialysis patients. Kidney Int 1998; 54:1367.
  42. MacGinley R, Cooney K, Alexander G, et al. Relapsing culture-negative peritonitis in peritoneal dialysis patients exposed to icodextrin solution. Am J Kidney Dis 2002; 40:1030.
  43. Foggensteiner L, Baylis J, Moss H, Williams P. Timely initiation of dialysis--single-exchange experience in 39 patients starting peritoneal dialysis. Perit Dial Int 2002; 22:471.
  44. Tintillier M, Pochet JM, Christophe JL, et al. Transient sterile chemical peritonitis with icodextrin: clinical presentation, prevalence, and literature review. Perit Dial Int 2002; 22:534.
  45. Touré F, Lavaud S, Mohajer M, et al. Icodextrin-induced peritonitis: study of five cases and comparison with bacterial peritonitis. Kidney Int 2004; 65:654.
  46. Boer WH, Vos PF, Fieren MW. Culture-negative peritonitis associated with the use of icodextrin-containing dialysate in twelve patients treated with peritoneal dialysis. Perit Dial Int 2003; 23:33.
  47. Glorieux G, Lameire N, Van Biesen W, et al. Specific characteristics of peritoneal leucocyte populations during sterile peritonitis associated with icodextrin CAPD fluids. Nephrol Dial Transplant 2003; 18:1648.
  48. Chow KM, Szeto CC, Cheung KK, et al. Predictive value of dialysate cell counts in peritonitis complicating peritoneal dialysis. Clin J Am Soc Nephrol 2006; 1:768.
  49. Fish R, Nipah R, Jones C, et al. Intraperitoneal vancomycin concentrations during peritoneal dialysis-associated peritonitis: correlation with serum levels. Perit Dial Int 2012; 32:332.
  50. Szeto CC, Chow VC, Chow KM, et al. Enterobacteriaceae peritonitis complicating peritoneal dialysis: a review of 210 consecutive cases. Kidney Int 2006; 69:1245.
  51. Jain AK, Blake PG. Non-Pseudomonas Gram-negative peritonitis. Kidney Int 2006; 69:1107.
  52. Piraino B, Bernardini J, Brown E, et al. ISPD position statement on reducing the risks of peritoneal dialysis-related infections. Perit Dial Int 2011; 31:614.
  53. Wong PN, Lo KY, Tong GM, et al. Prevention of fungal peritonitis with nystatin prophylaxis in patients receiving CAPD. Perit Dial Int 2007; 27:531.
  54. Záruba K, Peters J, Jungbluth H. Successful prophylaxis for fungal peritonitis in patients on continuous ambulatory peritoneal dialysis: six years' experience. Am J Kidney Dis 1991; 17:43.
  55. Robitaille P, Mérouani A, Clermónt MJ, Hébert E. Successful antifungal prophylaxis in chronic peritoneal dialysis: a pediatric experience. Perit Dial Int 1995; 15:77.
  56. Wadhwa NK, Suh H, Cabralda T. Antifungal prophylaxis for secondary fungal peritonitis in peritoneal dialysis patients. Adv Perit Dial 1996; 12:189.
  57. Lo WK, Chan CY, Cheng SW, et al. A prospective randomized control study of oral nystatin prophylaxis for Candida peritonitis complicating continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1996; 28:549.
  58. Thodis E, Vas SI, Bargman JM, et al. Nystatin prophylaxis: its inability to prevent fungal peritonitis in patients on continuous ambulatory peritoneal dialysis. Perit Dial Int 1998; 18:583.
  59. Williams PF, Moncrieff N, Marriott J. No benefit in using nystatin prophylaxis against fungal peritonitis in peritoneal dialysis patients. Perit Dial Int 2000; 20:352.
  60. Moreiras-Plaza M, Vello-Román A, Sampróm-Rodríguez M, Feijóo-Piñeiro D. Ten years without fungal peritonitis: a single center's experience. Perit Dial Int 2007; 27:460.
  61. Zelenitsky S, Barns L, Findlay I, et al. Analysis of microbiological trends in peritoneal dialysis-related peritonitis from 1991 to 1998. Am J Kidney Dis 2000; 36:1009.
  62. Voinescu CG, Khanna R. Peritonitis in peritoneal dialysis. Int J Artif Organs 2002; 25:249.
  63. Vlaanderen K, Bos HJ, de Fijter CW, et al. Short dwell times reduce the local defence mechanism of chronic peritoneal dialysis patients. Nephron 1991; 57:29.
  64. Cairns HS, Beckett J, Rudge CJ, et al. Treatment of resistant CAPD peritonitis by temporary discontinuation of peritoneal dialysis. Clin Nephrol 1989; 32:27.
  65. Pagniez DC, MacNamara E, Fortin F, et al. Withdrawal of continuous ambulatory peritoneal dialysis to treat mild peritonitis. BMJ 1988; 297:1174.
  66. Burkart JM. Short, long, or no dwells for PD-associated peritonitis. Semin Dial 1998; 11:257.
  67. Siva B, Hawley CM, McDonald SP, et al. Pseudomonas peritonitis in Australia: predictors, treatment, and outcomes in 191 cases. Clin J Am Soc Nephrol 2009; 4:957.
  68. Digenis GE, Abraham G, Savin E, et al. Peritonitis-related deaths in continuous ambulatory peritoneal dialysis (CAPD) patients. Perit Dial Int 1990; 10:45.
  69. Mitra A, Teitelbaum I. Is it safe to simultaneously remove and replace infected peritoneal dialysis catheters? Review of the literature and suggested guidelines. Adv Perit Dial 2003; 19:255.
  70. Singhal MK, Vas SI, Oreopoulos DG. Treatment of peritoneal dialysis catheter-related infections by simultaneous catheter removal and replacement. Is it safe? Perit Dial Int 1998; 18:565.
  71. Pérez-Fontán M, Rodríguez-Carmona A. Peritoneal catheter removal for severe peritonitis: landscape after a lost battle. Perit Dial Int 2007; 27:155.
  72. Cox SD, Walsh SB, Yaqoob MM, Fan SL. Predictors of survival and technique success after reinsertion of peritoneal dialysis catheter following severe peritonitis. Perit Dial Int 2007; 27:67.
  73. Szeto CC, Chow KM, Wong TY, et al. Feasibility of resuming peritoneal dialysis after severe peritonitis and Tenckhoff catheter removal. J Am Soc Nephrol 2002; 13:1040.
  74. Pérez Fontan M, Rodríguez-Carmona A, García-Naveiro R, et al. Peritonitis-related mortality in patients undergoing chronic peritoneal dialysis. Perit Dial Int 2005; 25:274.
  75. Boudville N, Kemp A, Clayton P, et al. Recent peritonitis associates with mortality among patients treated with peritoneal dialysis. J Am Soc Nephrol 2012; 23:1398.
  76. Ye H, Zhou Q, Fan L, et al. The impact of peritoneal dialysis-related peritonitis on mortality in peritoneal dialysis patients. BMC Nephrol 2017; 18:186.
  77. Tzamaloukas AH, Murata GH, Fox L. Peritoneal catheter loss and death in continuous ambulatory peritoneal dialysis peritonitis: correlation with clinical and biochemical parameters. Perit Dial Int 1993; 13 Suppl 2:S338.
  78. Harwell CM, Newman LN, Cacho CP, et al. Abdominal catastrophe: visceral injury as a cause of peritonitis in patients treated by peritoneal dialysis. Perit Dial Int 1997; 17:586.
  79. Yip T, Tse KC, Lam MF, et al. Risk factors and outcomes of extended-spectrum beta-lactamase-producing E. coli peritonitis in CAPD patients. Perit Dial Int 2006; 26:191.
  80. Htay H, Cho Y, Pascoe EM, et al. Center Effects and Peritoneal Dialysis Peritonitis Outcomes: Analysis of a National Registry. Am J Kidney Dis 2018; 71:814.
  81. O'Shea S, Hawley CM, McDonald SP, et al. Streptococcal peritonitis in Australian peritoneal dialysis patients: predictors, treatment and outcomes in 287 cases. BMC Nephrol 2009; 10:19.
  82. Cho Y, Badve SV, Hawley CM, et al. Peritoneal dialysis outcomes after temporary haemodialysis transfer for peritonitis. Nephrol Dial Transplant 2014; 29:1940.
  83. Gregory MC, Duffy DP. Toxic shock following staphylococcal peritonitis. Clin Nephrol 1983; 20:101.
  84. Millikin SP, Matzke GR, Keane WF. Antimicrobial treatment of peritonitis associated with continuous ambulatory peritoneal dialysis. Perit Dial Int 1991; 11:252.
  85. Guo A, Mujais S. Patient and technique survival for patients on PD in the US in large national cohorts. Kidney Int 2003; 64:S3.
  86. Pulliam J, Li NC, Maddux F, et al. First-year outcomes of incident peritoneal dialysis patients in the United States. Am J Kidney Dis 2014; 64:761.
Topic 1882 Version 38.0

References