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BILIARY STRICTURE AFTER NECROTIZING PANCREATITIS: AN UNDERAPPRECIATED CHALLENGE
Thomas K. Maatman, Department of Surgery, Indiana University School of Medicine, Indianapolis, IN
Introduction:
Benign biliary stricture occurs secondary to bile duct injury, anastomotic narrowing, or chronic inflammation. The profound locoregional inflammatory response in necrotizing pancreatitis (NP) creates challenging biliary strictures; this problem has not been systematically categorized. We sought to define the incidence and natural history of biliary stricture caused by NP.
Methods:
A prospectively maintained institutional NP database was retrospectively reviewed between 2005-2019 to identify patients developing biliary stricture. Patients were excluded if death occurred prior to NP resolution, biliary stricture was present prior to NP onset, or they were lost to follow up. Biliary stricture was identified on cholangiopancreatography as any narrowing of the extrahepatic biliary tree that measured less than 75% of the diameter of the unaffected duct. Risk factors for biliary stricture development were identified by comparing demographic information, comorbidities, and NP-associated clinical variables between patients with and without biliary stricture. Univariate analysis was performed using independent groups t-test, chi-squared test, and ANOVA. Multivariable analysis was performed on risk factors identified in univariate analysis.
Results:
A total of 743 NP patients were treated; 64 died and 13 were lost to follow up leaving 666 for analysis. Mean follow up was 3.5 ± 3.3 years. Biliary stricture developed in 108 (16%) patients. Median time from NP onset to biliary stricture diagnosis was 4.2 months (range, 14 days-9.6 years). Presentation was most commonly clinical or biochemical jaundice, n = 30 (28%) each. Significant risk factors identified on multivariable analysis were splanchnic vein thrombosis and head parenchymal necrosis (Table 1). Portal and superior mesenteric vein thrombosis were most strongly associated with biliary stricture; isolated splenic vein thrombosis was also associated with biliary stricture. 106 (98%) patients had intervention. Endoscopy provided definitive treatment in 83%. Median time to stricture resolution was 6.0 months after onset (range, 1 month-8.3 years). A mean of 3.3 ± 2.3 procedures were performed (Figure 1). Surgery was required in 22 (20%) patients; five patients underwent surgery as the first intervention (N = 3) or after percutaneous stenting of biliary stricture (N = 2) and 17 patients after a median of 8 months (range, 2-26 months) of endoscopic treatment. Operative treatment of biliary stricture was more likely in patients with infected necrosis (OR, 3.2; 95% CI, 1.1-9.0; P = 0.02) or NP disease duration ≥6 months (OR, 5.7; 95% CI, 1.8-18.2; P = 0.002), but was not associated with stricture length.
Conclusion:
Biliary stricture occurs frequently after necrotizing pancreatitis and is associated with splanchnic vein thrombosis and pancreatic head necrosis. Surgical correction is required in 20%.
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