Preventing PD Peritonitis: What’s the Evidence?

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Peritoneal dialysis associated peritonitis
is the second commonest cause of death among PD patients (35/1000 years) and
the most common cause of treatment failure. It confers a CV risk of 7 times
normal for 6 months following the bacteremia, so we need to remain ever
vigilant when dealing with PD patient, and its worth refreshing our knowledge
on how to prevent this feared complication. There is a paucity
of high quality evidence for many of the most fundamental questions in PD. Such
is the lack of evidence, the International Society for Peritoneal Dialysis (ISPD)
have issued a consensus document where they state they are unable to issue
formal guidelines.
The best resources I have found on the
topic are a Kidney International supplement from 2006, and the ISPD document already mentioned. In the first instance, which patients are at risk of developing
peritonitis? The best described risk factors are
hypoalbuminemia (similar to the association in haemodialysis patients), Staph
aureus  carriage at inception of dialysis
(HR 1.53), initiation of PD early after catheter insertion (HR 0.98/day), PD
after transplant failure (HR 2.18), lower hemoglobin (HR 0.88/gram/l), faster PD
transport rates (HR 2.92) and previous peritonitis. A special risk group to consider are those PD patients undergoing
invasive procedures such as endoscopy or IUD insertion. There is evidence that
antibiotic prophylaxis using cephalosporins may help reduce peritonitis rates.
The cornerstone of peritonitis prevention
is minimizing contamination risk with effective hand washing and immaculate
exchange technique. Specialized nurse-led training is key. If peritonitis
occurs, retraining and re-education are the most important interventions. Home
visits by PD nurses can cut recurrence rates in half, and should be performed
where possible. A Cochrane review could find no RCT data to support any particular insertion technique,
catheter type, number of cuffs or positioning. It demonstrated that of all
catheter-related interventions designed to prevent peritonitis in PD, only
disconnect (twin-bag and Y-set) systems have been proved to be effective. Topical antibiotic prophylaxis is a
standard of care and there are multiple RCTs demonstrating the efficacy of
mupirocin cream application at the exit site. Ointment is to be avoided as it
can erode the catheter polymer.  In
contrast, nasal mupirocin is more difficult to justify. Cochrane point out that
while there is trial data that nasal mupirocin reduces exit-site/tunnel
infection, it has no effect on peritonitis rates. Preoperative intravenous
prophylaxis reduces early peritonitis but not exit-site/tunnel infection. 
Recent published trials in the area of
antimicrobial prophylaxis have been disappointing. They include the Honeypot
study, discussed previously on RFN, which demonstrated the application of
honey to exit sites approximately doubled the risk of developing peritonitis in
diabetic patients. The MP3 study published in JASN in 2012 found polysporin to increase rates
of fungal exit site infections without any improvement in primary outcomes of
exit site infection or peritonitis. Finally, a special mention goes to cats,
who are responsible for at least 25 case reports of pastuerella peritonitis, as
well as an assortment of other bugs. Not to be outdone, rodents feature  in the case reports also, coining the term “hamster
bite peritonitis” caused by pastuerella aerogenes.
In summary, technique and continuing
re-education are of fundamental importance, as are topical antibiotics to
prevent exit site infection.  Beyond
this, trial data are severely lacking and local opinion and consensus must guide
practice.
Authored by Eoin O’Sullivan

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