Pain control for interstitial cystitis/bladder pain syndrome patients undergoing pelvic reconstructive surgery

Introduction: Scant research exists on pain control for interstitial cystitis patients undergoing pelvic reconstructive surgery. Our aim was to compare the perioperative courses in patients with and without interstitial cystitis undergoing pelvic reconstructive surgery performed using primarily monitored anesthesia care with local anesthesia. Methods: A retrospective chart review of surgical cases performed at a single site from November 2015 to July 2018 was performed. Joint non-gynecologic cases were excluded. Data including demographics, intraoperative variables, medication requirements, and postoperative courses were abstracted. Chi-square, independent t, and Mann–Whitney U tests were used to compare interstitial cystitis with non-interstitial cystitis patients. Results: In total, 65 separate cases met inclusion criteria and were analyzed, with 57 individual subjects. Out of the 65 cases, 33 cases were performed on interstitial cystitis patients. Only 2 of the 33 interstitial cystitis patient cases required general anesthesia. Interstitial cystitis patients did not require higher concentrations of 1% lidocaine with epinephrine (average of 3.8 mg/kg) compared to patients without (2.8 mg/kg). There was no difference between groups in perioperative complications, length of recovery, or postoperative narcotic consumption. Conclusion: Perioperative outcomes and pain control do not differ in those with and without interstitial cystitis undergoing pelvic reconstructive surgery. Prolapse surgery can be safely performed on a patient population with a high proportion of chronic pelvic pain using monitored anesthesia care with local anesthesia, without increased morbidity or difficultly with perioperative pain control.

Loss of prostaglandin E2 release from immortalized urothelial cells obtained from interstitial cystitis patient bladders

Interstitial cystitis (IC) is associated with increased activated mast cell numbers in the bladder and impairment of the barrier function of the urothelium. We stimulated immortalized urothelial cells derived from the inflamed region of IC bladders (SR22A or SM28 abn) or from healthy bladders (PD07i or PD08i) with tryptase and measured phospholipase A2 (PLA2) activity and the resultant release of arachidonic acid and prostaglandin E2 (PGE2). Tryptase stimulation of either PD07i or SR22A resulted in similar increases in PLA2 activity and arachidonic acid release. However, tryptase stimulation of SR22A and SM28 abn did not result in a significant increase in PGE2 release compared with the increase in PGE2 release from tryptase-stimulated PD07i and PD08i cells. Expression of mRNA for cyclooxygenase-2 and PGE synthase was lower and mRNA for 15-hydroxyprostaglandin dehydrogenase was higher in SR22A compared with PD07i, suggesting that both decreased synthesis and increased metabolism are responsible for the lack of a PGE2 response in tryptase-stimulated SR22A cells. Since PGE2 is a cytoprotective eicosanoid, the failure to produce this metabolite in cells isolated from the IC bladder may represent an increased susceptibility to damage by proinfammatory stimuli.