Iatrogenic rupture of the urinary bladder


Spontaneous rupture occurs from wrong or overzealous attempts to restore patency.

Surgical repair is considered the definitive treatment for rupture of the urinary bladder. In fact, one could state that surgical repair of rents in the excretory pathway of the urinary system is therapeutic dogma. Although this recommendation is logical, there apparently have been no studies to compare surgical versus medical therapy of bladder wall rents by controlled clinical trials.

Carl A. Osborne DVM, Ph.D., Dipl. ACVIM

Clinical experience with nonuremic patients

We found it necessary to evaluate the totality of this therapeutic philosophy in the late 1970s following our experience with iatrogenic rupture of the urinary bladder of an adult male cat with nonazotemic urethral outflow obstruction. At that time, the technique of retrograde positive contrast urethrocystography had just been developed. Following removal of matrix-crystalline urethral plug, a retrograde urethrocystogram was performed to evaluate the lower urinary tract. Overdistention of this cat's urinary bladder at the time of this radiographic procedure was performed resulting in escape of a considerable amount of radio-paque contrast solution into the peritoneal cavity.

The exact site of escape of contrast medium through the bladder wall could not be identified on the radiographs or by evaluation of the serosal surface of the urinary bladder at the time of celiotomy.

A cystotomy was not performed; we had no option but to manage this iatrogenic problem medically. Because the urethra was patent and the cat's urinary bladder remained small because of pollakiuria, therapy was limited to an orally administered antibiotic to prevent ascending bacterial urinary tract infection, as well as modification of diet to minimize struvite crystalluria. During the next five days, the cat had no evidence of uroperitoneum or azotemia. Follow-up low-pressure positive contrast cystography revealed no loss of contrast medium from the bladder into its wall or the peritoneal cavity.

Figure 1: Positive contrast cystogram (lateral view) of the abdomen of a 10-year-old spayed female Golden Retriever illustrats extravasation of contrast solution through the caudoventral aspect of the bladder wall into the peritoneal cavity. The irregularity of the bladder wall at the site of bladder rupture likely is associated with the formation of a blood clot.

During the past 30 years of evaluating feline lower urinary tract disease by retrograde positive contrast urethrocystography, antegrade positive contrast cystourethrography and double-contrast cystography, we have observed leakage of contrast medium from the maximally distended bladder lumen into the peritoneal cavity on several occasions.

Affected cats had hematuria and dysuria but did not have bacterial urinary tract infection. Some had urethral outflow obstruction, but none had post-renal uremia at the time of radiography. In two obstructed male cats, the bladder wall was ruptured during attempts to re-establish urethral patency. In most cases, we could not ascertain the site(s) of discontinuity of the bladder wall by evaluation of positive contrast radiography. We successfully managed all cases by nonsurgical therapy.

Medical management

In our opinion, medical management of iatrogenic rupture of the urinary bladder may be considered, provided:

  • There is no evidence of an underlying atraumatic lesion (neoplasm, etc.) that predisposed the bladder to rupture.

  • The bladder wall is not hypotonic and unable to contract.

  • There is no evidence that the wound's edges are devitalized.

  • There is no evidence of significant urosepsis.

  • There are no other complications requiring celiotomy.

  • The patient can be appropriately monitored for a sufficient time.

Figure 2: Fluroscopic image of a positive contrast cysto-gram (lateral view) of the abdomen of the dog described in Figure 1 obtained four days later. There is no evidence of loss of contrast media through the filling defect in the vertex of the bladder wall into the peritoneal cavity.

When the bladder lumen contains only a small volume of urine, contraction of the bladder musculature often quickly seals the site of disruption. Urine and contrast agents that have accumulated in the peritoneal cavity will be absorbed rapidly and excreted by the kidneys. If the cat is pollakiuric and has a completely patent urethral lumen, then it might be unnecessary to use an indwelling transurethral catheter to prevent filling of the bladder with urine. However, if gentle palpation, ultrasonography or radiography reveal distension of the bladder lumen with urine, then a closed indwelling transurethral catherter system can be used to minimize distension of the bladder wall. A decision to use antibiotics to prevent bacterial UTI should be made on a case-by-case basis. Provided clinical and laboratory findings typical of uroperitoneum and post-renal azotemia do not develop, indwelling catheters may be removed after three to six days. Prior to removal of the catheter, a low-pressure, positive-contrast cystogram can be performed to evaluate the integrity of the bladder wall.

Clinical experience with uremic patients

Spontaneous rupture of the urinary bladder and clinically significant uroperitoneum secondary to urethral outflow obstruction of male cats is an uncommon event. It usually occurs in association with overzealous or incorrect attempts to restore urethral patency. In this setting, patients typically have post-renal uremia associated with varying degrees of fluid, electrolyte and acid-based imbalances.

Compared to rupture of the urinary bladder in nonuremic cats, patients with post-renal uremia often decline rapidly prior to bladder rupture. If the obstruction of urine outflow has been present for several days, the integrity of the entire overdistended bladder wall can be compromised severely.

Initial management should be designed to correct the polysystemic consequences of post-renal uremia, especially hyperkalemia, acidemia and dehydration. Once the patient's fluid, electrolyte and acid-base disorders have been corrected, patency of the urethra should be re-established. An indwelling urethral catheter (closed system) can be used to minimize continued loss of urine into the peritoneal cavity.

If necessary, a peritoneal dialysis type of catheter can be placed in the abdomen to facilitate removal of fluid from the peritoneal cavity. As soon as the patient's overall condition has been stabilized, the specific nature and timing of additional diagnostic procedures and surgical or medical therapy should be considered.

When formulating diagnostic and therapeutic plans, care must be used to determine the initial cause(s) of urethral outflow obstruction, the site and size of the rent in the bladder wall and the time-related trends of change in the status associated with clinical abnormalities.

Figure 3: Positive contrast cystogram (lateral view) of the abdomen of the dog described in Figure 1 obtained 18 days later. The reduction in the size of the filling defect in the bladder wall and the marked reduction in irregularity of the mucosal surface at this site are consistent with healing of the rupture site.

Surgical repair of the large rent in the bladder wall certainly is consistent with conventional knowledge and clinical wisdom. However, it is of interest that in three out of 14 previously normal dogs with surgically induced untreated bladder ruptures, spontaneous sealing of 3-centimeter incision sites in the bladder vertex occurred within 45 hours (Burrows et al. Amer J Vet Res 35: 1083-1088, 1974). Three dogs recovered without the benefit of transurethral indwelling catheterization, fluid therapy or antibiotic therapy. We also observed remission of uroperitoneum and post-renal uremia in an adult female Beagle with an induced struvite urocystolith that obstructed the bladder neck. Therapy consisted of restoration of urine outflow by dislodging the urocystolith from the bladder neck into the bladder lumen, intermittent abdominocentesis, and parenteral administration of lactated Ringer's solution. Following this experience we also have managed successfully azotemic patients with ruptured urinary bladders by nonsurgical protocols.

Case report

A 10-year-old spayed female Golden Retriever was admitted to the Veterinary Medical Center because of rear limb weakness that lasted several weeks. The owner's indicated that the dog had difficulty rising to a standing position and was reluctant to climb stairs. All other body systems were normal. Physical examination revealed that the dog was overweight (body condition score of 4 points on a 5-point scale), and had musculoskeletal signs consistent with hip dysplasia and osteoarthritis.

Abdominal palpation revealed marked distension of the urinary bladder. Unfortunately, application of excessive digital pressure to the abdomen by a trainee resulted in rupture of the urinary bladder. This was unexpected, especially since the dog had no history of urinary tract disease.

Further evaluation of the patient revealed no evidence of an underlying disorder of the lower urinary tract that would predispose her to bladder rupture. Urinalysis performed on a sample of urine obtained by transurethral catheterization following bladder rupture revealed changes consistent with trauma, for example, numerous red blood cells in the urine sediment and moderate proteinuria. There was no evidence of inflammation; in-vitro bacterial culture was negative. The urine specific gravity was 1.042. Results of a CBC and serum chemistry profile were normal (serum urea nitrogen = 22 mg/dl and serum creatinine = 1.6 mg/dl). Retrograde positive contrast cystography revealed escape of radiopaque contrast solution from the bladder lumen through the bladder wall into the peritoneal cavity (Figure 1). Initial treatment of the iatrogenic rupture of the bladder wall consisted of an indwelling transurethral catheter attached to a closed drainage system.

The dog was given an oral antibiotic (Clavamox) to minimize the risk of ascending bacterial infection associated with the indwelling catheter.

The indwelling catheter was removed after four days. Just before removal of the catheter, a urine sample was obtained from the bladder lumen for urinalysis and aerobic bacterial culture. Results of the urinalysis revealed no abnormalities with the exception of mild hematuria (red blood cells = 15 to 20 per 450X magnification; specific gravity = 1.047). The urine was bacteriologically sterile. Also, prior to removal of the urinary catheter, radiopaque contrast solution was injected through it under fluoroscopy. Extravasation of contrast solution through the bladder wall into the peritoneal cavity was not observed (Figure 2). Peritoneal fluid was not detected around the serosal surface of the urinary bladder. The serum concentrations of creatinine (1.0 mg/dl) and urea nitrogen (17 mg/dl) were normal.

Evaluation of the patient two weeks later revealed no abnormalities of the urinary tract. A positive contrast cystogram revealed that the contrast solution was retained in the bladder lumen (Figure 3). Urinalysis results and the serum concentrations of creatinine (1.2 mg/dl) and urea nitrogen (18 mg/dl) were normal. Follow-up of the patient during the next five years revealed no evidence of lower urinary tract disease.

What is the point?

The point to be emphasized is that surgical closure might not be necessary to successfully manage all patients with ruptured urinary bladders. If the margins of the walls of tears in the bladder wall are not devitalized, and if they remain in close apposition by maintaining the bladder lumen in a nondistended state for an appropriate period, then it is plausible that these conditions would simulate those created by use of surgical sutures.

We are not advocating an all-or-none choice. Since the clinical status of patients with ruptured urinary bladders can vary from that characterized by only hematuria and dysuria to life-threatening post-renal uremia, a range of surgical and medical options should be considered.

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