Extended hospital stay after radical cystectomy with enhanced recovery protocol.

INTRODUCTION: To evaluate the reasons leading to an extended hospital stay (EHS) in patients undergoing radical cystectomy (RC) with postoperative enhanced recovery after surgery (ERAS) protocol. MATERIALS AND METHODS: A total of 509 patients underwent RC and urinary diversion with ERAS between May 2012 and March 2017. The protocol includes no bowel preparation, early feeding, predominantly non-narcotic pain control and µ opioid antagonists. Non-consenting/lost to follow up patients, and those with non-urothelial carcinoma were excluded. We defined EHS as ≥ 5 postoperative days and compared the cohort to those with a LOS of ≤ 4 days. Demographics including modifiable and non-modifiable factors as well as in-house complications as possible contributing factors to EHS was reviewed. RESULTS: There were 279/509 (54.8%) patients had an EHS. Median age was 73 years, 82.4% were male, and 36.6% had a Charlson comorbidity index (CCI) of > 2. Univariate analysis demonstrated that age > 65 years, CCI > 2, increased operative time, anemia requiring transfusion and non-orthotopic diversion were associated with EHS. On multivariate analysis, advanced age, operative time, postop transfusion, CCI > 2 as well as surgeon specific preferences was associated with EHS. Within EHS patients, 86% stayed due to an in-house complication; ileus (34.3%), anemia requiring transfusion (9.8%), UTIs (9.4%) and atrial fibrillation (8.5%). CONCLUSIONS: Advanced age, operative time, postop transfusion, CCI > 2 and surgeon-specific preferences are associated with an EHS following RC with ERAS. The common causes of EHS are in-house complications, mainly ileus.

Iron sucrose impairs phagocytic function and promotes apoptosis in polymorphonuclear leukocytes.

BACKGROUND: With the recent implementation of bundling reimbursement policy, the use of intravenous (IV) iron preparations for the management of anemia in the end-stage renal disease (ESRD) population has dramatically increased. Iron overload increases the risk of infections in individuals with or without kidney disease. IV iron administration in ESRD patients impairs bacteriocidal capacity of polymorphonuclear leukocytes (PMNs) against Escherichia coli. These preparations consist of an elemental iron core and a carbohydrate shell. In addition to the iron core, the carbohydrate shell may affect PMNs. We therefore examined the effect of iron sucrose, a commonly used preparation, on phagocytic capacity of PMNs from a group of normal individuals against Gram-positive (Staphylococcus aureus) and Gram-negative (E. coli) bacteria. METHODS: Iron sucrose was added to heparinized blood samples at pharmacologically-relevant concentrations and incubated for 4 and 24 h at 37°C to simulate in vivo condition. Blood samples mixed with equal volume of saline solution served as controls. To isolate the effects of the carbohydrate shell, blood samples were co-treated with the iron chelator, desferrioxamine. RESULTS: Iron sucrose caused significant PMN apoptosis and dose-dependent suppression of phagocytic function against both Gram-positive and Gram-negative bacteria. These abnormalities were prevented by desferrioxamine which precluded contribution of the carbohydrate shell to the PMN dysfunction. CONCLUSIONS: At pharmacologically-relevant concentrations, iron sucrose promotes apoptosis and inhibits phagocytic activities of PMNs. The deleterious effect of iron sucrose is mediated by its elemental iron core, not its carbohydrate shell, and as such may be shared by other IV iron preparations.