Exit site infection (ESI) is an important clinical problem in peritoneal dialysis (PD) patients and is a significant cause of peritonitis and catheter loss. While most ESIs are caused by skin commensals, rising incidence of atypical and resilient organisms such as mycobacteria, Pseudomonas and Burkholderia species has been observed. The diagnosis and management of these emerging pathogen remain difficult and poorly defined. This chapter highlights the evaluation and management of ESI in PD patients. The clinical features, microbiology, and ultrasonographic findings are discussed. The general and specific management of ESI due to different organisms will also be elaborated. ESI is usually a clinical diagnosis, but the use of bedside ultrasound can help assess for any collection around the cuff and tunnel tract involvement. Topical prophylaxis remains an effective way to prevent ESI. While the majority ESIs are related to skin flora and can be managed successfully by topical or systemic antimicrobials, clinicians should be alert to the emergence of resistant and atypical microorganisms. Surgical treatment should be reserved for ESI refractory to medical treatment or those with associated peritonitis.
- exit site infection
- peritoneal dialysis
Peritoneal dialysis (PD) is an important modality of renal replacement therapy and is gaining popularity in both developed and developing countries . While PD is associated with lower treatment costs and better patient autonomy when compared to hemodialysis, the practice of PD is also burdened with various infectious and noninfectious complications. PD catheter (also known as Tenckhoff catheter) is an essential device for the performance of PD exchanges. However, the implantation of a PD catheter is associated with infective complications such as exit site infection (ESI), tunnel tract infections, and peritonitis. Repeated or fulminant PD peritonitis heralds adverse clinical outcomes such as catheter loss, peritoneal failure and patient mortality [2–4]. Therefore, prevention of peritonitis plays a crucial role in the care of PD patients. In this context, ESI constitutes a significant risk factor for peritonitis, and thus prevention and appropriate management of ESI can substantially diminish the risk of PD-related peritonitis [2–5], and thus improve overall patient outcomes.
2. Pathogenesis and microbiology of exit site infection in peritoneal dialysis patients
In most PD patients, colonization with microorganisms occurs shortly after the implantation of PD catheter. Colonization does not equate clinical infection, but predisposes PD patients to ESI, especially after exit site traumatization. Bacterial colonization of exit site is frequently followed by formation of biofilm, which promote further bacterial growth and void the colonizing microorganisms from antimicrobial treatments. The organisms that colonize the exit site are often the same pathogens responsible for ESI . Common pathogens to cause ESI in PD patients include
2.1. Staphylococcus aureus
2.2. Coagulase-negative staphylococcus
2.3. Other Gram-positive organisms
2.4. Pseudomonas aeruginosa
2.5. Other Gram-negative organisms and anaerobes
Gram-negative bacilli are also important causes of ESI, and
Rapidly growing atypical mycobacteria are more frequent causative agents for ESI than
3. Clinical features and evaluation of exit site infection in peritoneal dialysis patients
ESI is characterized by purulent discharge from the exit site, and with or without erythema or induration at the exit site [2, 22]. Although erythema around the PD catheter in the absence of purulent discharge may represent early signs of ESI, this can also be normal skin reaction to recently implanted PD catheter or exit site traumatization. The presence of crust around the exit site or positive cultures from exit site without signs of inflammation, however, does not indicate an ESI. The spectrum of severity of ESI can range from increased crust formation, to erythema around the exit site, to serous or purulent discharge, to abscess formation, and to tunnel tract involvement. In this context, different grading systems have been proposed to document the clinical severity of ESI [22, 23]. Assessment of the exit site involves gross inspection of the exit site, palpation of the tunnel tract and expression of discharge from the exit site. The discharge should be sent for microbiological examination (Gram smear, culture and sensitivity pattern), which can guide further treatment decisions. Ultrasonography has also been used to assess ESI, especially with regard to local collections and tunnel tract involvements . In this context, sonolucent zone (>1 mm thick) surrounding the external cuff after a course of appropriate antimicrobial therapy and the involvement of the internal cuff portends adverse clinical outcomes .
4. Prevention of exit site infection in peritoneal dialysis patients
Proper care of the exit site constitutes an integral component in the prevention of ESI. In the early postoperative period (~first 2 weeks), the exit site should be kept dry until it is well healed . The exit site should be covered with sterile dressing and the change of dressing should be performed by experienced nursing staff before the patient is properly trained. After completion of PD training, the patient should be able to clean the exit site with antiseptic agents (e.g., povidone iodine or chlorhexidine) on daily or alternate day basis, and the exit site be constantly covered with sterile dressings .
Hand hygiene is a key measure to decrease ESI in PD patients. Good hand hygiene practices should be undertaken by patients, helpers and healthcare providers during routine handling of the PD catheter and its exit site . In this regard, 70% alcohol-based hand rub is the most effective hand-sanitizing agent to be used before and after the handing of PD catheter and its exit site . Alternative hand-sanitizing agents include antimicrobial-containing (e.g., 4% chlorhexidine) soap .
Although the exit site prophylaxis with mupirocin has curbed
5. Management of exit site infection in peritoneal dialysis patients
5.1. General principles (Figure 1)
Exit site care and local dressing constitutes the cornerstone in the management of ESI. Topical antiseptics (e.g., mupirocin, gentamicin ointment) are all viable options for dressing of exit sites. Other alternatives such as hypertonic saline solution can be considered in selected cases (e.g.,
5.2. Management of exit site infection due to specific organisms
5.2.1. Methicillin-sensitive or resistant
First-generation cephalosporins (e.g., cephazolin) or penicillinase-resistant penicillins (e.g., cloxacillin) can be used in MSSA ESI . Parenteral vancomycin has established clinical efficacy in the treatment of MRSA ESI, tunnel tract tunnel infection and peritonitis in PD patients . In this context, intravenous (IV) vancomycin (1 g every 5–7 days for a minimum of 14 days) is a standard treatment of MRSA exit site or tunnel tract infection in PD patients . However, rising MIC to vancomycin remains a valid concern for the use of vancomycin in MRSA infection. Other viable choices for MRSA infections in PD patients include teicoplanin, daptomycin, linezolid, tigecycline, and quinupristin-dalfopristin. Teicoplanin is a glycopeptide that exhibits activity and efficacy profile resembling vancomycin, and has the merit of longer half-life and superior tolerability than vancomycin. Daptomycin is an approved treatment of complicated MRSA soft-tissue infections and bacteremia (with or without infection endocarditis) in a dosage of 6 mg/kg/day [38, 39]. In CKD stage 4 or 5 patients, the dosage of daptomycin should remain unchanged but the frequency be reduced to every 48 hours . Linezolid (600 mg B.I.D., IV or PO) can be used for the treatment of MRSA skin infection as well as community- or hospital-acquired MRSA pneumonia [41, 42]. No dosage modification is required for linezolid in dialysis patients but one should be aware of the side effects such as myelosuppression and lactic acidosis . Tigecycline demonstrates promising
5.2.2. Pseudomonas aeruginosa
Topical treatments (e.g., gentamicin ointment) can be used as adjunctive treatment for mild
5.2.3. Other Gram-negative organisms
In general, ESI due to Gram-negative organisms are susceptible to second- or third-generation cepholosporins [2, 22]. However, there is increasing prevalence of ESBL-producing Gram-negative organisms. Carbapenems should be considered in patients with previous history of ESBL-producing organisms or when the ESI do not respond to second- or third-generation cephalosporins .
The treatment regimen for atypical mycobacterium ESI is dependent on the organisms identified as well as the susceptibility/resistance profiles. In general, the regimen should consist of at least two or more antimycobacterial agents (e.g., parenteral aminoglycosides, fluoroquinolones, tetracyclines and macrolides), and prolonged therapy is generally required [2, 21]. In this context, a combination of oral fluoroquinolones, tetracyclines (doxycycline or minocycline), macrolides (clarithromycin or azithromycin) or cotrimoxazole can be administered for
5.2.5. Fungal exit site infection
Fungal ESI is rare clinical entity and there are limited data regarding the optimal management of fungal ESI. It is important to exclude contamination when fungus is isolated from the exit site, and removal of PD catheter should be considered if there is established fungal ESI to avoid fungal peritonitis.
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