There are few clinical conditions encountered by the Urogynaecologist that causes more patient and clinician frustration as Bladder Pain Syndrome (BPS). This frustration is due to the delay and difficulty in diagnosis, chronicity of disabling symptoms and unsatisfactory treatment responses. BPS diagnosis is heavily dependent on the patient history of bladder pain and relies primarily on the exclusion of confusable disorders affecting the urinary bladder and pelvis. Many patients must try several treatment options before finding a treatment that gives them relief. However, despite excellent care, some never find relief of their pain. The aim of the study was to characterize the pain and functionality of the bladder in patients with BPS using urodynamic examination.

We performed a cross-sectional study of 24 female patients with Bladder Pain Syndrome. All participants completed a written consent form. The Central Sensitization Inventory and Kings Health Questionnaires were completed. Urodynamic assessment was undertaken on each participant. The bladder was filled at a rate of 80mls/min and important urodynamic variables recorded. During assessment, women were asked to report their pain using the Likert numeric pain scale at cystometric capacity and post void. Subsequently, participants were randomly assigned to receive either 20mls of 2% alkalinized lidocaine, or 20mls of 0.9% normal saline into their bladders. These solutions were allowed to remain in-situ for 20 minutes and pain score repeated. The above urodynamic protocol was again repeated.

There was a significant volume increase for all urodynamic sensations post lidocaine treatment. In addition, pain scores were significantly reduced post lidocaine treatment. In contrast, there was no difference in urodynamic parameters or pain scores in the saline controls. Individual analysis revealed that there was a lack of analgesic effect in 5 participants who received lidocaine, with a corresponding deterioration in their urodynamic parameters, similar to the saline controls. These five participants reported a significantly worse bladder related quality of life on the King’s health Questionnaire than the lidocaine responders and there was a tendency toward central sensitivity syndromes on the central sensitization inventory.

Lidocaine causes a reduction in pain perception, as well as increases bladder volumes in the majority of patients with BPS. These patients appear to have a peripherally mediated disease state, and peripheral treatment targets are deemed appropriate. However, in those patients with more severe disease and associated central sensitivity syndromes, there was no response to lidocaine treatment. This could represent disease progression.

We have successfully used urodynamics to characterize the pain and functionality of the bladder in BPS patients. The failed response to treatment in five lidocaine treated participants implies disease progression. These patients warrant further characterization of their disease as peripheral treatment targets as not predicted to have effect.