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Infection After Pancreatic Surgery: Superficial and Deep Thoughts.

Whether one believes that all surgical site infections (SSIs) are preventable, procedure-specific SSI is increasingly used as a measure of surgical quality. Although its appropriateness as a quality measure can be debated, a better understanding of factors associated with SSI may inform strategies for risk reduction. However, the common practice of combining the 3 levels of SSI—superficial, deep, and organ-space—into a single SSI index may obfuscate through aggregation, particularly for complex intra-abdominal procedures such as pancreatic resection. In this issue of JAMA Surgery, Elliott and colleagues1 analyze single-institution and national hepatopancreaticobiliary-specific National Surgical Quality Improvement Program data for pancreatic resection to determine whether factors associated with wound infection are distinct from those associated with organ-space infection. Multivariate analysis indicated that the presence of a biliary stent was associated with wound infection but not organ-space SSI, whereas gland texture was more strongly associated with organ-space SSI (and was difficult to distinguish from the complication of pancreatic fistula). We learn much by mining clinical databases such as the National Surgical Quality Improvement Program, but we must also be careful not to confuse correlation with causation or to focus on putative risk factors that may prove to be surrogate markers. Consider preoperative biliary stent, identified as a risk factor for wound infection but not organ-space SSI. Although avoidance of unindicated biliary stents is undoubtedly good practice, what makes us believe that stent avoidance per se will reduce the rate of SSI? Indeed, we lack a plausible mechanism whereby the presence of a biliary stent would differentially affect wound infection but not intraperitoneal infection. Clearly, we are missing something. We might fill our gaps if the database captured more relevant data fields, for example, the duration of bile duct stenting, the use of periprocedural antibiotics at the time of stent placement and during the preoperative weeks, the use of neoadjuvant chemotherapy, and the presence of malnutrition associated with preoperative jaundice. Without mechanism, we encounter the limits of database mining. We must encourage parallel investigations that better elucidate the bacteriology of leaks. The mechanisms of intra-abdominal infection probably differ after pancreaticoduodenectomy and distal pancreatectomy. Pancreatic anastomotic leak after pancreaticoduodenostomy almost inevitably involves early contamination by enteric organisms and interaction of pancreatic juice with intestinal enterokinase, features that are lacking, at least initially, with a leak after distal pancreatectomy. Further insights will likely also depend on advances in understanding of host-microbiome interactions in surgical patients.2 Finally, we must be careful to consider unintended consequences of our strategies for risk reduction. The recommendation to extend the duration of antibiotic prophylaxis must be balanced against concerns over the emergence of antibiotic-resistant hospital pathogens and Clostridium difficile infection.