The role of extra-hepatic bile duct resection in the surgical management of gallbladder carcinoma. A first meta-analysis

ObjectiveTo systematically evaluate the clinicopathological and prognostic value of extra-hepatic bile duct resection (EHBDR) in the surgical management of patients with gallbladder carcinoma (GBC), especially in non-jaundiced patients.MethodsPubMed, EMBASE and the Cochrane Library were searched up to March 1^st 2021 for comparative studies between bile duct resected and non-resected groups. RevMan5.3 and Stata 13.0 software were used for the statistical analyses.ResultsEHBDR did not correlate with a better overall survival (OS) (P = 0.17) or disease-free survival (P = 0.27). No survival benefit was also observed in patients with T2N1 (P = 0.4), T3N0 (P = 0.14) disease and node-positive patients (P = 0.75), rather, EHBDR was even harmful for patients with T2N0 (P = 0.01) and node-negative disease (P = 0.02). Significantly higher incidences of recurrent disease (P = 0.0007), postoperative complications (P < 0.00001) and positive margins (P = 0.02) were detected in the bile duct-resected group. The duration of postoperative hospital stay between the two groups was comparable (P = 0.58). Selection bias was also detected in our analysis that a significantly higher proportion of advanced lesions with T3-4 or III-IV disease was observed in the bile duct-resected group (P < 0.00001). EHBDR only contributed to a greater lymph yield (P = 0.01).ConclusionEHBDR has no survival advantage for patients with GBC, especially for those with non-jaundiced disease. Considering the unfairness of comparing OS between jaundiced patients receiving EHBDR with non-jaundiced patients without EHBDR, we could only conclude that routine EHBDR in non-jaundiced patients is not recommended and future well-designed studies with more specific subgroup analyses are required for further validation.     

Cirrhosis is independently associated with complications and mortality following operative treatment of acetabular fractures

IntroductionPatients with cirrhosis are at higher risk for morbidity after injury. Acetabular fractures represent a highly morbid injury pattern. Few studies have specifically examined an effect of cirrhosis on risk of complications after acetabular fracture. We hypothesized that cirrhosis is independently associated with increased risk of inpatient complications following operative treatment of acetabular fractures.MethodsAdults patients with acetabular fracture who underwent operative treatment were identified from Trauma Quality Improvement Program data from 2015 to 2019. Patients with and without cirrhosis were matched on a propensity score predicting cirrhotic status and inpatient complications based on patient, injury, and treatment characteristics. The primary outcome was overall complication rate. Secondary outcomes included serious adverse event rate, overall infection rate, and mortality.ResultsAfter propensity score matching, 137 cirrhosis+ and 274 cirrhosis- remained. No significant differences existed in observed characteristics after matching. Compared to cirrhosis- patients, cirrhosis+ patients experienced 43.4% (83.9 vs 40.5%, p < 0.001) greater absolute risk difference of any inpatient complication, 29.9% (51.8 vs 21.9%, p < 0.001) greater absolute risk difference of serious adverse events, 28.5% (41.6 vs 13.1%, p < 0.001) greater absolute risk difference of any infection, and 2.9% (2.9% vs 0.0%, p = 0.02) greater absolute risk difference of inpatient mortality.ConclusionCirrhosis is associated with higher rates of inpatient complications, serious adverse events, infection, and mortality among patients undergoing operative repair of acetabular fracture.Level of EvidencePrognostic Level III.     

Future directions in managing aniridia-associated keratopathy

Congenital aniridia is a panocular disorder that is typically characterized by iris hypoplasia and aniridia-associated keratopathy (AAK). AAK results in the progressive loss of corneal transparency and thereby loss of vision. Currently, there is no approved therapy to delay or prevent its progression, and clinical management is challenging because of phenotypic variability and high risk of complications after interventions; however, new insights into the molecular pathogenesis of AAK may help improve its management. Here, we review the current understanding about the pathogenesis and management of AAK. We highlight the biological mechanisms involved in AAK development with the aim to develop future treatment options, including surgical, pharmacological, cell therapies, and gene therapies.