Posterior reconstruction during robotic-assisted radical cystectomy with intracorporeal orthotopic ileal neobladder: description and outcomes of a simple step

A posterior reconstruction (PR) might improve the fluidity and delicacy of the maneuvers related to the neovesico-urethral anastomosis during robotic-assisted radical cystectomy (RARC). Our objective is to describe in detail the surgical steps of PR and to assess its feasibility and functional outcomes. The data regarding patients undergoing a totally intracorporeal RARC with neobladder and PR for high-grade and/or muscle-invasive urothelial cancer of the bladder at Karolinska University Hospital between October 2015 and November 2016 by a single surgeon (PW) were reviewed. Prior to the anastomosis, a modified posterior Rocco’s repair involving the Denonvillier’s fascia, the rhabdosphincter, and the posterior side of the ileal neobladder neck was performed. The steps are shown in a video at https://doi.org/10.1089/vid.2019.0029. The primary outcome was urinary continence; the secondary outcomes were urinary leakage, intermittent catheterization, and complications related to the reconstructive steps. Eleven male patients with a median age and BMI of 67 years and 24, respectively, underwent RARC with PR associated to the neovesico-urethral anastomosis. Overall and posterior reconstruction time were 300′ (195–320) and 6′ (4–7), respectively. The daytime and nighttime continence rates were 100% and 44% at 12 months, respectively; the median pad weight was 3.5 g and 108 g at daytime and nighttime, respectively. One urinary leakage from the urethrovesical anastomosis was treated conservatively. Two patients perform intermittent catheterization. The posterior reconstruction during RARC is safe and feasible, providing good continence rates. It supported a careful suturing of the anastomosis as well as an uncomplicated catheter placement

Metabolic acidosis may be as protective as hypercapnic acidosis in an ex-vivo model of severe ventilator-induced lung injury: a pilot study

<p>Abstract</p> <p>Background</p> <p>There is mounting experimental evidence that hypercapnic acidosis protects against lung injury. However, it is unclear if acidosis <it>per se </it>rather than hypercapnia is responsible for this beneficial effect. Therefore, we sought to evaluate the effects of hypercapnic (respiratory) versus normocapnic (metabolic) acidosis in an ex vivo model of ventilator-induced lung injury (VILI).</p> <p>Methods</p> <p>Sixty New Zealand white rabbit ventilated and perfused heart-lung preparations were used. Six study groups were evaluated. Respiratory acidosis (RA), metabolic acidosis (MA) and normocapnic-normoxic (Control - C) groups were randomized into high and low peak inspiratory pressures, respectively. Each preparation was ventilated for 1 hour according to a standardized ventilation protocol. Lung injury was evaluated by means of pulmonary edema formation (weight gain), changes in ultrafiltration coefficient, mean pulmonary artery pressure changes as well as histological alterations.</p> <p>Results</p> <p>HPC group gained significantly greater weight than HPMA, HPRA and all three LP groups (P = 0.024), while no difference was observed between HPMA and HPRA groups regarding weight gain. Neither group differ on ultrafiltration coefficient. HPMA group experienced greater increase in the mean pulmonary artery pressure at 20 min (P = 0.0276) and 40 min (P = 0.0012) compared with all other groups. Histology scores were significantly greater in HP vs. LP groups (p < 0.001).</p> <p>Conclusions</p> <p>In our experimental VILI model both metabolic acidosis and hypercapnic acidosis attenuated VILI-induced pulmonary edema implying a mechanism other than possible synergistic effects of acidosis with CO2 for VILI attenuation.</p

Studies on production and function of pulmonary nitric oxide [Elektronisk resurs]

Nitric oxide is involved in pulmonary vascular and bronchial regulation and appears to be of paramount importance in the adaptation of the pulmonary circulation at birth. Nitric oxide is present in exhaled gas. The main objective of the present study was to investigate the physiological regulation of pulmonary nitric oxide production, considering factors that are known to be important during pulmonary adaptation at birth, with special reference to the role of nitric oxide in the regulation of pulmonary vascular function. An animal model for continuous analysis of single-breath quantification of lower airway nitric oxide, by chemiluminescence, in vivo was established. The findings show that respiratory system nitric oxide formation is stimulated by stretch-sensitive and [beta]1-adrenoceptor sensitive calcium dependent processes, where the stretch-sensitive process can be blocked by gadolinium. The marked increase in pulmonary vascular resistance upon gadolinium, by far exceeding that attained by direct blockade of NO synthase, suggests that one or several other powerful vasodilators are activated by stretch during pulmonary breathing-induced excursions. The [beta]1-adrenoceptive mechanism is activated by adrenaline released from the adrenals. Carbon dioxide exerts a rapid inhibitory effect on pulmonary nitric oxide formation and especially when nitric oxide formation is stimulated by stretch. It is likely that the findings presented here represent important regulatory mechanisms on pulmonary nitric oxide production, and therefore are of importance for extrauterine pulmonary adaptation at birth and continuous ventilation/perfusion matching throughout extrauterine life