Objective To report on the safety and efficacy of rectus sheath blocks, ‘topped‐up’ using bilateral rectus sheath catheters (RSCs), in patients undergoing major open urological surgery. Methods The RSCs were inserted under ultrasound guidance into 200 patients between April 2008 and August 2011, of whom 106 patients underwent radical retropubic prostatectomy (RRP) and 94 underwent open radical cystectomy (ORC). A retrospective case‐note review was undertaken. Outcomes included technical success and complication rates of the insertion and use of RSC, visual analogue pain scores, additional analgesia requirements and length of hospital stay (LOS). Results All RSCs were successfully placed without complication and used for a mean of 3.6 days for ORC and 2.1 days for RRP. Early removal occurred in 6.49% of patients. Low overall pain scores were reported in both groups. Patients were more likely to require a patient‐controlled analgesia system in the ORC group but the overall need for additional analgesia was low in both groups, reducing significantly after the initial 24 h. In combination with an enhanced recovery programme, LOS reduced from 17.0 to 10.8 days in the ORC group and from 6.2 to 2.8 days in the RRP group. Conclusion The use of RSCs appears to offer an effective and safe method of peri‐operative analgesia in patients undergoing major open urological pelvic surgery.

Objectives• To describe our experience with the implementation and refinement of an enhanced recovery programme (ERP) for radical cystectomy (RC) and urinary diversion.• To assess the impact on length of stay (LOS), complication and readmission rates. Patients and Methods• In all, 165 consecutive patients undergoing open RC (ORC) and urinary diversion between January 2008 and April 2013 were entered into an ERP.• A retrospective case note review was undertaken.• Outcomes recorded included LOS, time to mobilisation, complication rates within the first 30 days (Clavien-Dindo classification) and readmissions.

We localized the sites of vasodilation of inhaled nitric oxide (NO), a selective pulmonary vasodilator, and sodium nitroprusside (SNP) in isolated rat lungs. The sites were determined by analyzing the arterial, venous, and double-occlusion data with a two-resistor (small arteries and veins) three-capacitor (large arteries, large veins, and capillaries) model of the pulmonary vascular bed. Inhaled NO (170 and 670 ppm) and SNP (22.5 and 45.0 micrograms) decreased the small-artery resistance by 7.4 +/- 1.6, 17.2 +/- 2.2, 14.2 +/- 2.8, and 21.4 +/- 3.4% and the small-vein resistance by 13.5 +/- 3.2, 20.3 +/- 3.4 (SNP of 22.5 micrograms not significant), and 9.3 +/- 3.3%, respectively, in blood-perfused lungs (n = 12). Similar results were observed in Krebs-perfused lungs (n = 12). Capillary compliance was unaffected by inhaled NO and SNP. SNP increased the large-artery capacitance by 40.0 +/- 8.6 and 69.3 +/- 9.7%, whereas inhaled NO had no effect. SNP increased the large-vein capacitance by 31.0 +/- 8.7 and 48.0 +/- 10.7%, whereas inhaled NO had no effect in blood-perfused lungs. However, in Krebs-perfused lungs inhaled NO and SNP (45.0 micrograms only) increased the large-vein capacitance by 43.3 +/- 11.9, 41.4 +/- 14.2, and 44.2 +/- 11.0%. In conclusion, in blood-perfused isolated rat lungs inhaled NO and SNP dilate small-resistance arteries and veins, whereas SNP but not inhaled NO dilates larger capacitance arteries and veins. Furthermore, blood appears to prevent the downstream vasodilation by inhaled NO on larger capacitance pulmonary veins.

We determined the direct effects of thiopental, ketamine, midazolam, etomidate, and propofol on pulmonary vascular resistance (PVR), the relationship of the direct effects to the baseline PVR, and the possible interaction with functional endothelium. The intravenous anesthetics were injected randomly into 1) endothelium-intact isolated rat lungs which were either unconstricted or constricted with angiotensin II (n = 10), and 2) lungs with endothelial injury produced by electrolysis (n = 10). In endothelium-intact lungs thiopental (0.5 and 5.0 mg/kg) and etomidate (3.0 mg/kg) significantly (P < 0.05) increased PVR by 3% +/- 1%, 30% +/- 7%, and 29% +/- 5%, respectively. Ketamine (3.0 and 100 mg/kg) and propofol (20 mg/kg) significantly (P < 0.05) decreased the PVR by 6% +/- 1%, 15% +/- 1%, and 8% +/- 1%, respectively. Midazolam (0.3 and 3.0 mg/kg) and smaller doses of etomidate (0.3 mg/kg) and propofol (2.0 mg/kg) did not affect PVR. These responses did not vary with the baseline PVR over a twofold range. The effects of thiopental, ketamine, etomidate, and midazolam were not altered by endothelial injury. In contrast to the vasodilation produced by propofol in normal lungs, propofol (20 mg/kg) significantly (P < 0.05) increased the PVR by 8% +/- 2% after endothelial injury. In conclusion, this study demonstrates that thiopental and etomidate are direct pulmonary vasoconstrictors, ketamine and propofol are direct pulmonary vasodilators, and midazolam has no direct effects in the isolated rat lung. Further, these effects on pulmonary vasculature do not vary with baseline PVR, and only propofol appears to have endothelium-dependent effects.

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