Vaginal pessary: a culprit for intraperitoneal bladder perforation

Abstract

Vaginal pessaries are widely considered to be a safe and effective non-surgical management option for women with pelvic organ prolapse. Complications may occur, and are more frequent with improper care and certain device designs and materials. It is imperative to provide information to patients about potential complications. We present the case of a woman in her 70s who presented to the Emergency Department with increasing groin and abdominal pain following a vaginal pessary insertion 2 days prior for grade 3 vaginal vault prolapse. On presentation, her abdomen was markedly distended with guarding. Laboratory investigations showed a significant acute kidney injury with a metabolic acidosis. An initial non-contrast CT showed fluid and inflammatory changes surrounding the bladder, and bladder perforation was suspected. A subsequent CT cystogram showed extravasation of contrast from the bladder into the peritoneal cavity, in keeping with an intraperitoneal bladder rupture. The patient underwent an emergency bladder repair in theatre.

Background

Bladder perforation is a rarely observed phenomenon, typically occurring as a result of trauma or iatrogenic surgical injury. It may be classified as extraperitoneal, intraperitoneal or combined extraperitoneal and intraperitoneal, accounting for 60%, 30% and 10% of cases, respectively.¹ Intraperitoneal bladder perforations require prompt abdominal exploration and repair to prevent peritonitis, intra-abdominal sepsis and death.²

Case presentation

A woman in her 70s presented to the gynaecology clinic with a history of vaginal prolapse symptoms for 2 years. The patient was otherwise well, denying any other symptoms. She had a history of hypertension, type 2 diabetes mellitus and hypercholesterolaemia, for which she was receiving ramipril, amlodipine, metformin and simvastatin. She had a past surgical history of total abdominal hysterectomy for uterine fibroids 30 years previously. Injury to the left ureter during hysterectomy necessitated a relaparotomy and reimplantation of the ureter.

On examination, she had a body mass index of 30 kg/m² and a Pfannenstiel scar from a previous hysterectomy was noted. On vaginal examination, a stage 3 pelvic organ prolapse quantification (POP-Q) vaginal vault prolapse and cystocele was identified. On discussing the management options the patient opted for conservative management and a size 3 Gel horn pessary was inserted by a senior registrar under consultant supervision. The patient previously had a ring pessary inserted at her GP practice but this was not successful. Following the insertion of the pessary she was able to void urine in clinic, and a follow-up appointment was scheduled in 4 months at the pessary clinic for pessary replacement. She was advised to use vaginal oestrogen cream 0.01% twice weekly. Post-pessary insertion instructions and contact information were given to the patient.

Two days later the patient presented to Accident and Emergency with increasing groin and abdominal pain, and an inability to pass urine for almost 48 hours following pessary insertion 60 hours ago.

Initial assessment showed an acutely unwell patient with an early warning score of 7 due to requiring 8 L of oxygen to maintain adequate oxygen saturations, a respiratory rate of 30 breaths/min and a mild tachycardia at 108 beats/min. Her abdomen was tender and distended with evidence of guarding. A urinary catheter was inserted and drained 300 mL of turbid fluid.

An urgent CT scan of the abdomen and pelvis was performed, and the patient was reviewed by the gynaecology team who immediately removed the pessary. On speculum examination, there were no abnormalities detected.

Blood investigations showed a significant acute kidney injury (AKI) with an estimated glomerular filtration rate (eGFR) of 12. An initial arterial blood gas revealed metabolic acidosis (pH 7.25, base excess 8.1 mmol/L, HCO₃ ⁻ 17.8 mmol/L, lactate 5.3 mmol/L). A non-contrast CT scan was performed due to a low eGFR, which showed fluid and inflammatory changes around the bladder with no clear evidence of perforation; however, this was suspected given the clinical scenario and CT findings (figures 1 and 2).

Figure 1.

Non-contrast axial CT scan of the abdomen and pelvis. (A) Large volumes of pericystic free fluid are seen in the paracolic gutters (top arrows) and deep in the pelvis (bottom arrow). A Foley catheter is seen in situ. (B) Pericystic fluid visualised around the hyperdense collapsed bladder.

Figure 2.

Non-contrast sagittal CT scan of the abdomen and pelvis. The pessary is clearly visualised. High density bladder with a large volume of pericystic fluid.

After the patient had received 2 L of fluid, the blood gas was repeated which showed worsening metabolic acidosis (pH 7.09, lactate 9.0 mmol/L). The eGFR on the gas was 6.

A contrast-enhanced CT scan of the abdomen and pelvis was performed following initial fluid resuscitation. Free fluid in the abdomen was seen, with a distribution unusually centred around the bladder involving the intraperitoneal and extraperitoneal spaces. The urinary bladder was collapsed with a Foley’s catheter in situ (figure 3). The reporting radiologist suggested that such appearances may be secondary to urosepsis, although a bladder perforation could not be entirely excluded.

Figure 3.

CT scan of the pelvis. The contrast has been administered via a catheter. (A) A Foley catheter is seen in the bladder being filled with contrast. (B) Bladder filled with contrast (arrow). (C) The arrow indicates the defect in the right lateral wall of the urinary bladder. (D) The arrow indicates the urinary bladder (with air (black)/fluid (white) level secondary to catheterisation). Extraluminal contrast is also demonstrated.

A CT cystogram was subsequently performed. 200 mL of diluted water-soluble contrast was instilled via the Foley’s catheter to distend the bladder to look for any contrast leak from a potential bladder perforation. Extravasation of contrast from the bladder into the peritoneal cavity around the small bowel loops was identified, which was in keeping with an intraperitoneal bladder perforation.

Treatment

The patient was reviewed by the urology team and underwent an exploration via laparotomy 18 hours following admission, where the bladder was visualised. Around 700 mL of free fluid was drained from the abdominal cavity, but no obvious defect was seen in the visualised bladder wall. The bladder was distended with methylene blue saline via a catheter. In the right lateral aspect of the bladder a small area of blue discolouration was seen underneath the peritoneum; however, no contrast extravasated into the abdomen. It is possible that the rupture was rather subtle or difficult to visualise, especially if it was located in a complex anatomical position.

Outcome and follow-up

The patient required critical care admission postoperatively. During the procedure she was profoundly septic and required intravenous fluid resuscitation and large doses of norepinephrine. Initially, in critical care, her vasopressor requirements were high, and she required continuous veno-venous haemodiafiltration (CVVHDF) for stage 3 AKI. She also received intravenous piperacillin-tazobactam for 5 days.

Her clinical condition gradually improved over the admission, allowing her vasopressor requirements to decrease and the CVVHDF to be stopped. She was extubated on day 6 postoperatively and was clinically stable. She was discharged from critical care and transferred to the ward on day 7. A post-surgical ureteroscopy did not identify any abnormalities (figure 4). The patient recovered gradually and was discharged home on day 28 with a suprapubic catheter (SPC) in situ.

Figure 4.

Post-surgical ureteroscopy showing a normal pelvicalyceal system bilaterally (A) and normal appearance of both ureters (B).

On day 4 after discharge the patient unfortunately presented with a blocked SPC, for which it was spigotted. A urinary catheter was inserted which drained clear urine. One week later she attended the ambulatory urology unit for a trial without a catheter with her SPC in situ. The SPC was removed but she only managed to pass small amounts of urine (150 mL) with post-void residual volumes of 150 mL on bladder scan. In the context of a recent bladder injury, the decision to continue catheterisation despite a residual urine volume of 150 mL is guided by the need to minimise bladder pressure, promote healing and prevent complications like urinary leakage or infection. While 150 mL residual urine may not typically pose a problem, its presence warrants cautious management in this scenario to support optimal bladder recovery and mitigate potential risks associated with the injury. Therefore, the decision for urethral re-catheterisation was made and she was referred to the community district nurses for ongoing catheter management.

Discussion

Pelvic organ prolapse is the downward descent of the female pelvic organs into or through the vagina due to muscular or ligamental weakness. Vaginal pessaries are a well-recognised treatment for providing pelvic anatomical support and have been widely used in clinical practice.^{3 4}

While pessaries are generally considered a safe and effective treatment option, complications may occur. The most common side effects include vaginal discharge, vaginal bleeding and new bladder or bowel symptoms. Serious complications such as vesicovaginal fistula, rectovaginal fistula and erosion have all been reported.⁵ Rarely, they may cause life-threatening complications such as bowel incarceration, obstructive uropathy and urosepsis.⁶ There is no reported literature of bladder perforation as a possible complication, yet it is imperative to be aware of bladder perforation as a possible sequel of urinary retention from any cause. We wish to highlight that, although extremely rare, bladder perforation should be a recognised life-threatening complication following pessary insertion in a patient with urinary retention.

Bladder perforation is a rare clinical phenomenon, characterised by an intraperitoneal and/or an extraperitoneal bladder wall laceration.⁷ While plain and CT cystography have remarkable sensitivity (90–95%) and specificity (100%), the clinical identification of bladder perforation may be challenging.^{8 9}

Intraperitoneal injury is caused by a sudden increase in intravesical pressure of a distended bladder secondary to a traumatic event. In our case, it is likely due to bladder distension secondary to urinary retention post-pessary insertion with a late presentation. Perforations usually occur at the dome of the bladder, as this is the primary area of weakness.¹⁰ The management of intraperitoneal bladder ruptures hinges closely on prompt identification and surgical intervention. Intraperitoneal urine extravasation can lead to peritonitis, AKI and sepsis and has a mortality rate of over 20% if not recognised early.¹¹ Men are more likely to sustain a bladder injury than women, yet women are at a higher risk of having an undiagnosed injury.¹²

Conservative management of intraperitoneal bladder perforations has been described, yet this remains an area of contention. Non-operative management has been shown to be successful in multiple studies looking at intraperitoneal bladder perforations during transurethral resection of bladder tumour, spontaneous bladder perforations and bladder perforations due to blunt trauma.^13–16 Such management is achieved by an indwelling urethral catheter and/or percutaneous peritoneal drainage. As yet there is no standard for conservative management of intraperitoneal bladder perforations, but some authors have suggested that the duration of drainage should be 7–14 days, with cystography performed prior to catheter removal.¹³

Nonetheless, surgery remains the mainstay of treatment. An open bladder repair commonly uses a two-layer suture closure technique to ensure a watertight seal. Of note, there is no evidence that two-layer closure is superior to single-layer closure.^{17 18} More recently, laparoscopic repairs are being increasingly performed for patients with intraperitoneal bladder perforations, conferring the advantages of shorter hospital stay, reduced use of postoperative analgesia and reduced postoperative complications. Excellent outcomes have been observed with laparoscopic procedures.¹⁹ It should be noted that laparoscopy should only be performed in stable patients where there is no concern for multi-organ trauma; thus, this would not have been suitable for our patient.

In conclusion, vaginal pessaries are generally considered a safe intervention for women with vaginal prolapse. Serious complications have been rarely reported in the literature and it is imperative for clinicians to be aware of such complications. Patients should receive counselling regarding complications and have awareness regarding when to report their symptoms to a medical professional. Bladder perforation is a rare pelvic condition that may be difficult to identify clinically. A high index of suspicion is pivotal in making the diagnosis. The atypical nature of our case conveys an important message to clinicians. Bladder perforation must be considered as a differential diagnosis if a patient presents with urinary retention following insertion of a vaginal pessary.

Learning points.

• Urinary bladder ruptures have a high level of morbidity and risk of mortality if left untreated.

• Women should be asked to void before and after pessary placement prior to leaving the clinic to ensure that the pessary is not causing urinary obstruction, as advised in the UK Continence Society guideline pathway.

• While relatively rare, patients should be counselled on the red flag symptoms to look out for, including an inability to void urine and the necessity to seek urgent medical attention in such circumstances.

• CT cystography is a highly sensitive and specific investigation for detecting bladder perforation, and imaging protocols should be adhered to.

Ethics statements

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