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Activation of Pancreatic Enzyme Plus Bacterial Infection Plays an Important Role in the Pathogenic Mechanism of Clinically Relevant Popf After Pancreaticoduodenectomy
Kenichiro Uemura*, Yoshiaki Murakami, Takeshi Sudo, Yasushi Hashimoto, Naru Kondo, Naoya Nakagawa, Hayato Sasaki, Kenjiro Okada, Hiroki Ohge, Taijiro Sueda Surgery, Hiroshima University, Hiroshima, Japan
Background: Postoperative pancreatic fistula (POPF) after pancreaticoduodenectomy (PD) is relatively common, and remains a major cause of morbidity and surgical mortality. However, the underlying pathogenic mechanism of POPF, with the exception of technical error, still remains unclear. We previously reported that postoperative pancreatitis after PD plays an important role in the pathogenic mechanism of POPF after PD. We hypothesized that the bacterial infection in addition to the activation of pancreatic enzyme around the pancreatico-enteric anastomosis could be associated with occurrence of clinically relevant POPF (CR-POPF) after PD. Objectives: We retrospectively analyzed the possible association of postoperative pancreatitis, bacterial colonization in the surgical drain, and CR-POPF after PD using prospectively collected data base. Methods: 250 consecutive patients undergoing PD were included. All patients were administered prophylactic antibiotics, which were selected based on perioperative bile cultures. POPFs were diagnosed by International Study Group Pancreatic Fistula (ISGPF) criteria. Hyperamylasemia was defined as serum amylase more than 3 times the upper limit of the reference value. Closed suction drains were inserted along the pancreatico-enteric anastomosis, and surgical drains were examined bacteriologically when they were removed. Results: Of 250 patients, 23% developed POPF; Grade A in 16%, Grade B in 6%, and Grade C in 1%. A total of 32% of the patients had hyperamylasemia on postoperative day (POD) 1, and the presence of hyperamylasemia on POD1 was closely associated with the development of POPF (p<0.01). A total of 43% of the patients had bacterial colonization in the surgical drain. In the patients without bacteria in surgical drain, only 1% of the patients developed CR-POPFs, while 29% of the patients with bacteria in surgical drain developed CR-POPFs (p<0.01). Moreover, in the patients without hyperamylasemia and no bacterial colonization in the surgical drain, no patients developed CR-POPF, while 60% of the patients with CR-POPF had both hyperamylasemia and bacterial colonization in the surgical drain (p<0.01). Conclusion: Bacterial infection in addition to activation of pancreatic enzyme around the pancreatico-enteric anastomosis might play an important role in the pathogenic mechanism of CR-POPF after PD. Prevention of postoperative pancreatitis of remnant pancreas with infection control might be an area of focus for reducing the incidence of CR-POPF after PD.
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