Factors predicting recovery of liver function after percutaneous drainage in malignant biliary obstruction: the role of hospital-acquired biliary sepsis

AIM OF THE STUDY: Prolonged cholestasis adversely affects liver function. Hepatic functional recovery is mandatory prior to any surgical or medical intervention. Serum bilirubin levels correlate well with, and are a surrogate marker for, hepatocyte function. We aimed to ascertain factors responsible for slow decline of bilirubin and delayed recovery of liver function following percutaneous drainage in malignant biliary obstruction. MATERIAL AND METHODS: Sixty-seven patients with malignant jaundice who underwent percutaneous biliary drainage (PTBD) were followed until they achieved target bilirubin ≤ 3 mg/dl. According to duration, patients were divided into early (≤ 6 weeks, n = 43) and late (> 6 weeks, n = 24) groups. Various clinical, tumour-related and procedure-related factors were analysed for their contribution to delayed recovery with the χ(2) or t-test. Multi-variate logistic regression analysis was used to predict independent associations. RESULTS: Gallbladder cancer presenting with type I block was the commonest pathology. Overall demographic, clinical, tumour characteristics and procedural details were comparable between groups. Duration of jaundice (p = 0.026), liver involvement (p = 0.041), baseline total (p = 0.001) and direct bilirubin levels (p < 0.001), positive bile cultures with hospital-acquired bacteria (p = 0.031) were significant factors on univariate analysis. Bacterial growth was significantly greater following repeated biliary manipulations. The commonest organisms were Pseudomonas and Citrobacter spp. Number of re-instrumentations, post-procedural biliary sepsis and native biliary organisms were non-contributory. No factor was significant on multivariate analysis. CONCLUSIONS: Factors directly linked to extent and duration of disease are validated as significant contributors to functional recovery after biliary drainage. Biliary sepsis with hospital-acquired organisms, especially following re-interventions is a significant modifiable risk-factor affecting bilirubin decline.