The role of bladder hydrodistension as an important diagnostic and therapeutic tool in bladder pain syndrome/interstitial cystitis (BPS/IC), as popularized by Messing and Stamey in 1978, has been significantly questioned within the last years. For many decades the “disease-specific” glomerulations, petechial mucosal bleedings, have been regarded to be pathognomonic for BPS/IC and, thus, included in the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) criteria to better define patients suffering from this disease [1]. As a proposed scale for disease severity, glomerulations have even been graded with regard to their extension and intensity [2].

A recent review of publications on glomerulations in BPS/IC showed no consistent relationship between glomerulations and the diagnosis of BPS/IC. Several studies were not able to demonstrate a link between symptom severity and the number of glomerulations. Some investigators also observed that the grade of glomerulations may change with time. Glomerulations were observed in healthy asymptomatic populations as well as in symptomatic populations with another primary diagnosis. In summary, the authors found no convincing evidence that glomerulations should be included in the diagnosis or phenotyping of BPS/IC [3].

The fact that hydrodistension gives temporary symptom relief to a considerable number of BPS/IC patients was first reported by Bumpus in 1930 [4] and made it one of the few available therapeutic regimens for many years. Even in 2017, the mechanism for this symptom remission is not understood. Partial sensory denervation of suburothelial nerve plexus by hydrodistension pressure is one of the presumed mechanisms for symptom remission, and axonal degeneration has been observed in animal studies after bladder overdistension [5]. Chai found a significant increase of urinary heparin-binding epidermal growth factor (HB-EGF) and a significant decrease of urinary anti-proliferative factor (APF) after in vivo bladder stretch [6]. Bägli described an increased expression of RHAMM (receptor for hyaluronic acid mediated motility) after bladder stretch, which may be an early step for tissue repair in response to injured bladder tissue [7]. Within the last 15 years, no more studies on the physiologic effects of bladder hydrodistension have been published, and only two publications from this period refer to the clinical outcome of this procedure:

Glemain reported on the results of 32 BPS/IC patients that were treated prospectively by continuous balloon dilatation of the bladder for 3 h under epidural anesthesia. The intravesical pressure used was equal to the patients mean arterial pressure. Pain resolution was maintained for 6 months in 60% of patients, and for 1 year in 43.3%. Results were better for patients with a cystometric bladder capacity ≥150 cc before treatment [8].

Hoke treated 106 BPS/IC patients with bladder hydrodistension, of whom 48 simultaneously received a transvaginal trigonal block with 0.25% bupivacaine/1% lidocaine under cystoscopic guidance. Patients with and without trigonal block perceived a significant improvement in pain scores, with no difference between both groups. Distension times of 2 and >5 min did not give statistically different results [9].

A recent publication followed patients after a combination of hydrodistension and fulguration of Hunner’s ulcers. The mean time to therapeutic failure (defined as restart with any disease-specific therapy) was 28.5 months in Hunner type and 25.2 months in non-Hunner type disease, with no significant difference for both types of disease [10]. However, it is not clear which procedure was responsible for this long-term symptom improvement and if the combination was necessary to achieve these good results.

Sequential therapy with hydrodistension and intravesical instillation of hyaluronic acid under general anesthesia was performed by several authors: Ahmad found a 74% response rate in 17 patients [11], and Shao reported on a 77.8% response rate at 6 and a 50% response rate at 9 months (compared to 33.3% and 20% with heparin instillations) [12]. Good immediate response with this regimen was also reported by Yang [13].

No publications exist on the long-term course of patients with repeated bladder hydrodistensions after symptom recurrence. Hydrodistension never cures BPS/IC. Whether repeat fulgurations/resections or bladder distensions add to the disease caused bladder wall fibrosis is not known. It is therefore uncertain if aggressive therapy like fulguration/resection or hydrodistension carries a potential negative effect. Theoretically, repeat fulgurations/resections over many years might result in chronic injury to the bladder wall and lead to bladder fibrosis and shrinkage. Whether such changes reflect merely the natural course of the disease or are augmented by these attempts at therapy is unknown. The fibrotic small capacity bladder is the classical indication for bladder augmentation or urinary diversion. Thus, the price to be paid for temporary symptom improvement could be major surgery at a later phase of life. This is important information for patients who are offered hydrodistension for symptomatic relief, since alternative therapeutic regimens do not bear this theoretical consequence.

With this information, the value of bladder hydrodistension in BPS/IC management will most probably be minimized in the future. In principle, the procedure has been performed with roughly the same standards throughout the last decades. The ESSIC definition from 2008 established a maximum intravesical pressure of 80 cm H₂O for 5 min, and glomerulations observed after hydrodistension were rated grade I to III with regard to their extension [2].

Instead of general or spinal anesthesia, local anesthesia with electromotive administration (EMDA) of intravesical lidocaine may be used for painless hydrodistension of the bladder [14]. Rosamilia reported on 21 women who underwent hydrodistension after EMDA with lidocaine and dexamethasone [15]. A good response was observed in 85% of patients 2 weeks after treatment, with 63% still responding at 2 months. 25% of patients were still free of symptoms at 6 months. The same regimen was used by Riedl in 13 patients, and 62% showed complete symptom resolution after an average 4.5 months [16].

Bladder hydrodistension is not a riskless procedure. In the original textbook chapter by Nehra and Vardi, the incidence of bladder ruptures was 8%. Vesical necrosis following hydrodistension has also been reported [17–19]. These events are severe complications that require major surgery for repair and need to be communicated to patients before the intervention.