Excerpt
Although this is a timely study, given the current interest in and increasing number of prophylactic pancreatic stents being placed during ERCP, there remain several issues that require clarification. It is well known that ERCP in general can lead to transient bacteremia in 15% to 27% of cases. This is not often clinically significant and does not warrant routine antibiotic prophylaxis.2–6 Ascending cholangitis is an uncommon complication occurring on an average in about 1% to 2% of ERCPs.7–9 There also exist data regarding the risk of infection from placement of preoperative biliary stents in malignancies, demonstrating a clinically relevant microbial impact on patients, with Coliforms and enterococcus being the most common organisms cultured from surgical specimens.10 There are, however, no published data regarding the risk of infection specifically related to indwelling pancreatic stents. The authors use the term “clinically significant bacteria,” but this statement is somewhat of a reach as there were no data reported that clearly demonstrated a link between the bacteria found and clinical outcome. One patient with Enterobacter septicemia already had cholangitis, and it is quite likely that the bacteria may have originated from the biliary tract.
Furthermore, it was interesting that the majority of prophylactic pancreatic stent placements were during ERCPs performed for cholangitis. This is somewhat surprising as this group of patients is considered to be at low risk for post-ERCP pancreatitis and rarely warrants prophylactic pancreatic stent placement. Given this high incidence of cholangitis, one cannot help but wonder whether this issue may be the principal reason for bacterial colonization of the pancreatic stents and not the duration of placement.
There have been numerous studies reporting pancreatic stent-induced changes to the pancreatic duct over time.11,12 Smith et al13examined 61 patients with pancreatic stents and found that 80% developed stent-induced changes on their subsequent pancreatograms. A canine model was used to show the pathologic changes associated with pancreatic stents including inflammation, parenchyma atrophy, and fibrosis.14 The authors of the current study hypothesized that bacterial colonization of pancreatic stents may be responsible for pancreatic duct damage. Infection or bacterial colonization has never been invoked in the past as a mechanism, making this theory an intriguing one. Hill and colleagues, however, do not provide any background scientific data to support this hypothesis, and we believe that this assumption cannot be supported solely on the basis of their study data.
In addition, there are also flaws in the study design that include its retrospective design and the fact that there was no uniformity with either: (a) type of pancreatic duct stent used, (b) method of collecting pancreatic stents, or (c) assessing which portion had been inside the pancreatic duct. It is unclear what, if any, contribution stent flanges or length may have made to findings of bacterial colonization. It is also unclear how the pancreatic stents were collected, in what media they were preserved for analysis, and the condition of the endoscope that they were retrieved through.