Abstract
CASE DESCRIPTION A 15-year-old spayed female mixed-breed dog was evaluated for a 7-week history of stranguria, pollakiuria, and intermittent urethral obstruction.
CLINICAL FINDINGS On initial evaluation, the patient had persistent stranguria with lack of urine production; after multiple unsuccessful attempts to urinate, a large volume of urine was produced. Prior to voiding the large volume, the urinary bladder was not palpable during examination. Abdominal ultrasonography confirmed caudal displacement of the urinary bladder, and the urethra and trigone could not be located ultrasonographically. Positive-contrast cystourethrography and CT confirmed caudal displacement of the urinary bladder and also revealed trigonal invagination and urethral kinking; dysuria was attributed to these findings.
TREATMENT AND OUTCOME Surgical repositioning of the lower urinary tract was performed. The urinary bladder was moved cranially and was fixed in place along the left lateral aspect of the body wall by cystopexy. After surgery, positive-contrast cystourethrography revealed a more cranial positioning of the urinary bladder and straightening of the urethra with no urethral kinking or trigonal invagination. Immediately after surgery, stranguria had resolved and the patient was able to void normally. Two years after surgery, the dog was reported to be urinating normally.
CLINICAL RELEVANCE Surgical correction of caudal urinary bladder displacement with cystopexy led to resolution of trigonal invagination, urethral kinking, and urethral obstruction in the dog of the present report. Trigonal invagination and urethral kinking, although uncommon findings, should be considered as possible causes of dysuria in dogs.
A15-year-old 1.9-kg (4.2-lb) spayed female mixed-breed dog was referred to the University of California-Davis, Veterinary Medical Teaching Hospital after a 7-week history of stranguria and pollakiuria. Additionally, the dog had clinical signs consistent with intermittent urethral obstruction, including inability to pass urine during posturing.
Hematologic and biochemical analyses were performed 6 weeks prior to referral. No abnormalities were detected on CBC; serum biochemical analysis revealed a mild increase in BUN concentration (39 mg/dL; reference range, 7 to 27 mg/dL), but findings were otherwise unremarkable. Enrofloxacin (7.8 mg/kg [3.5 mg/lb], PO, q 24 h) was administered for 10 days, but no clinical improvement was noted.
Following antimicrobial treatment, abdominal radiography was performed and revealed collapse of the L2-3 intervertebral disk space, but no abnormalities were found related to the urogenital system. During abdominal ultrasonography, the urinary bladder was small in size, difficult to visualize, and reported to have a thickened and irregular wall. The owner was instructed to give the dog pain medication (buprenorphine, 0.07 mg/kg [0.03 mg/lb], PO, q 8 h) as needed at home.
Six days later, the dog returned for vaginoscopy, bacteriologic culture of urine, and urinary bladder wall biopsy. No abnormalities were detected on vaginoscopy. A traumatic catheterization technique with a 3.5F urinary cathetera was used to obtain a urinary bladder wall specimen. Histologic evaluation of the specimen revealed epithelial hyperplasia; however, low-grade transitional cell carcinoma could not be definitively ruled out. Results of urine bacteriologic culture were negative. The dog was prescribed piroxicam (0.3 mg/kg [0.1 mg/lb], PO, q 24 h).
Two weeks later, the dog was brought to an emergency clinic for evaluation after progression of stranguria, worsening signs of discomfort, and passage of only small amounts of urine. On serum biochemical analysis, the BUN concentration (53 mg/dL; reference range, 11 to 33 mg/dL) was mildly increased. During abdominal ultrasonography, the urinary bladder was not visible despite infusing saline (0.9% NaCl) solution (unknown volume) into the urinary bladder.
The dog was referred to the veterinary medical teaching hospital; on initial physical examination, the dog was bright and alert with appropriate mentation. The abdomen was soft, and no signs of pain were found on palpation and no overt masses or organomegaly were detected. The vulva was normal in appearance. Digital rectal examination was not performed because of the small size of the dog. Persistent stranguria was noted during physical examination. Small drops of urine were produced during episodes of prolonged stranguria that lasted several minutes, followed by voidance of a large volume of urine. Prior to the patient voiding a large volume of urine, the urinary bladder was not palpable during physical examination. Other abnormalities detected included a grade 2/6 left apical systolic murmur and severe dental disease.
Thoracic radiography revealed mild left atrial enlargement and a dilated right cranial lobar bronchus. Abdominal radiography revealed chronic degenerative changes at the L2-3 intervertebral disc space; no radioopaque urinary calculi were visible. During abdominal ultrasonography, the urinary bladder was located caudally, and identification of the trigone and proximal portion of the urethra was not possible because of the position of the bladder within the pelvis. No ultrasonographic abnormalities were identified within the visible urinary bladder lumen or wall. There was an ill-defined, hypoechoic 1.1-cm nodule within the liver. The remainder of the abdominal viscera appeared ultrasonographically normal.
Urine was collected via ultrasound-guided cystocentesis. Urinalysis revealed a urine specific gravity of 1.026, pH of 6, urine protein concentration of 25 mg/dL (reference limit, no measurable protein), few transitional cells, hyaline casts, and rare WBCs but no RBCs on sediment examination. Urine bacteriologic culture results were negative. Cytologic examination of free catch urine was performed to look for evidence of neoplastic transitional cells, and none were found.
On the basis of the history and initial diagnostic findings, the differential diagnoses for stranguria and pollakiuria (with the presence of a large urinary bladder) included mechanical or functional outflow tract obstruction. Given the dog's intermittent ability to pass large amounts of urine, functional causes or intermittent mechanical causes were considered most likely. Possible causes for intermittent mechanical obstruction included neoplasia, radiolucent uroliths, or an infectious or inflammatory cause resulting in cystitis and urethritis; the intermittent nature of the dysuria was not consistent with a fixed obstruction. Functional causes such as neurologic dysfunction, urethral spasm, or reflex dyssynergia (functional outflow tract obstruction) were also considered to be possible etiologies.
A plan was made to perform digital rectal examination, positive-contrast cystourethrography via fluoroscopic evaluation, cystoscopy, and urethroscopy under general anesthesia. The dog was premedicated with oxymorphone (0.05 mg/kg [0.02 mg/lb], IM) and atropine (0.02 mg/kg [0.01 mg/lb], IM). Anesthesia was induced with propofol (2.6 mg/kg [1.2 mg/lb], IV) and maintained with isoflurane in oxygen. No abnormalities were detected on digital rectal examination. The cystoscopeb could not be passed beyond the distal third of the urethra. In addition, manual expression of the urinary bladder was not possible. During fluoroscopic evaluation, the urinary bladder was moderately full, and all but the most cranial apex of the urinary bladder was located in an intrapelvic location.
Positive-contrast cystourethrography was performed to view the anatomic positioning of the urinary bladder and urethra with fluoroscopy. The dog was placed in right lateral recumbency, and an 0.018-inch hydrophilic, angled guidewirec was introduced into the urinary bladder via the urethral orifice by use of cystoscopic guidance. A 5F red rubber catheterd was passed over the guidewire and introduced into the urinary bladder. The guidewire was removed, and the urinary bladder was distended with a 50:50 mixture of saline solution and iodinated contrast medium.e When the urinary bladder was sufficiently distended, the catheter was withdrawn in a retrograde fashion while positive contrast medium was injected; this allowed for evaluation of the urethra along its course. Fluoroscopic evaluation revealed that the urinary bladder was caudally displaced within the pelvic canal and the urethra was tortuous in its course. The displacement of the urinary bladder was most markedly apparent on the ventrodorsal projection (Figure 1). There was a transient but repeatable, small rounded filling defect in the region of the trigone, suspected to represent an invagination of the urinary bladder wall; however, a mass lesion could not be definitively ruled out. Abdominal pressure was increased by gently pressing the abdominal wall during injection of the contrast medium. As the pressure increased, the urinary bladder shifted caudally, resulting in kinking of the proximal portion of the urethra.
Lateral (A and C) and ventrodorsal (B) positive-contrast cystourethrographic projections of the pelvic region in a 15-year-old spayed female mixed-breed dog that was evaluated for a 7-week history of stranguria, pollakiuria, and intermittent urethral obstruction. For positive-contrast cystourethrography, a mixture of contrast medium and saline (0.9% NaCl) solution was infused via urethral catherization to distend the urinary bladder and urethra. Notice the caudal position of the urinary bladder within the pelvic canal. Urethral kinking (black arrows) is evident as a result of caudal displacement of the urinary bladder. Notice the region of trigonal invagination (white arrows). In the lateral views, notice that as the urinary bladder is displaced further caudally (C), the degree of urethral kinking increases, compared with the less caudally displaced position (A).
Citation: Journal of the American Veterinary Medical Association 251, 7; 10.2460/javma.251.7.818
Given the malpositioning of the urinary bladder, a perineal hernia was considered as a possible differential diagnosis; however, several variables did not support this finding, including that the dog was a small-breed spayed female with no history of trauma and the lack of any obvious abnormalities on digital rectal or perineal examination. Furthermore, stranguria and dysuria associated with perineal herniation are reported to be secondary to retroflexion of a herniated urinary bladder, which was not the situation for the dog of the present report.1,2
To further investigate the possibility of perineal hernia and to evaluate the filling defect observed on positive-contrast cystourethrography, contrast CT imaging was performed. Contiguous images (slice thickness, 2.5 mm) of the abdomen and 0.6-mm-thick reformatted CT images were obtained and reviewed. The urinary bladder was located within the pelvic canal, and the tortuous urethra was appreciated (Figure 2). The mucosa on the caudal aspect of the urinary bladder appeared mildly irregular, and the cranial aspect of the urinary bladder wall was thickened, consistent with cystitis. A mass lesion was not present within the trigone of the urinary bladder, and there was no evidence of perineal herniation. A large amount of granular mineral opacity was present within the gallbladder and cystic duct, and the L2-3 intervertebral disk space and the endplates were sclerotic and irregular.
Lateral (A) and ventrodorsal (B) postcontrast CT reconstructed images of the abdominal and pelvic regions of the dog in Figure 1. Contrast is present within the urinary bladder and urethra, and denotes the pelvic location of the urinary bladder as well as the kinking of the urethra (arrowheads).
Citation: Journal of the American Veterinary Medical Association 251, 7; 10.2460/javma.251.7.818
On the basis of the results of diagnostic imaging, the cause of the dog's dysuria was determined to be intermittent mechanical outflow obstruction, secondary to urinary bladder hypermobility with caudal displacement into the pelvic cavity, resulting in intermittent trigonal invagination and urethral kinking. Once consulted, the dog's owners elected surgical repositioning of the urinary bladder and urethra. The patient was positioned in dorsal recumbency, and the hair on the ventral aspect of the abdomen was clipped. The surgical site was prepared with aseptic technique and draped. During the standard midline approach to the abdomen, only the apex of the urinary bladder was visible, as most of the bladder was displaced caudally into the pelvic canal (Figure 3). No other abnormalities were found in the abdominal cavity during exploration.
Intraoperative images of the dog in Figure 1. Notice the caudally displaced urinary bladder (star) within the pelvic canal (A) and the urinary bladder (star) after cranial traction (B).
Citation: Journal of the American Veterinary Medical Association 251, 7; 10.2460/javma.251.7.818
To allow for postoperative positive-contrast cystourethrography, an introducer sheath was placed into the urethra prior to cystopexy. To place the sheath, a 22-g over-the-needle catheterf was introduced into the urinary bladder at the apex and the needle was removed. A 0.018-inch hydrophilic, angled guidewire was then passed through the over-the-needle catheter and advanced caudally, extending out the urethral orifice and vulva. A 5F introducer sheathg was then passed over the guidewire (retrograde) into the urinary bladder and sutured to the vulva with 3-0 nylon.h The urinary bladder was pulled cranially with stay sutures and positioned along the left lateral aspect of the body wall. A 2-cm incision was made into the transversus abdominus muscle with a No. 15 scalpel blade, and a corresponding portion of the serosa of the urinary bladder was abraded with gauze. The body wall and urinary bladder were sutured together with 2 parallel lines of simple continuous 3-0 polypropylene suturesi to complete a cystopexy. The abdomen was closed routinely.
After surgery, while the dog was still under anesthesia, positive-contrast cystourethrography was performed to evaluate the location of the urinary bladder and urethra. Iodinated contrast medium was injected into the urinary bladder via the introducer, and the urinary bladder was found to be in a normal position within the abdominal cavity. Iodinated contrast medium was injected into the urethra as the sheath was pulled caudally, revealing a straight urethral course without urethral kinking that had been present before surgery (Figure 4).
Lateral positive contrast cystourethrographic projection of the pelvic region of the dog in Figure 1 after cystopexy. Notice the normally positioned urinary bladder and lack of trigonal invagination and urethral kinking.
Citation: Journal of the American Veterinary Medical Association 251, 7; 10.2460/javma.251.7.818
The dog recovered from anesthesia without complication. Oxymophone (0.03 mg/kg [0.01 mg/lb], IV, q 12 h) was continued after surgery for pain control for 2 days, and tramadol (2.1 mg/kg [1.0 mg/lb], PO, q 8 h) was initiated after that time.
Following surgery, the dog remained pollakiuric but there was no evidence of stranguria or urethral obstruction, as the dog was able to void urine normally. The dog had minor urinary incontinence, with small drops of urine evident after lying down for an extended period. The dog was discharged from the hospital 3 days after surgery. Seven days after surgery, the dog was reevaluated by the referring veterinarian and was reported to be urinating normally with no observations of pollakiuria, stranguria, or urinary incontinence. Seventeen days after surgery, the dog was re-evaluated by the referring veterinarian. Physical examination findings were within reference limits, and there were no signs of stranguria or incontinence, although the dog was still urinating every 2 to 3 hours. Follow-up 2 years after surgery revealed that the dog was urinating normally, with no related abnormal clinical signs.
Discussion
The dog of the present report had severe caudal displacement of the urinary bladder, with secondary trigonal invagination, and urethral kinking, resulting in intermittent urethral obstruction. This disease complex accounted for the initial clinical signs observed in this patient.
Abnormal caudal displacement of the urinary bladder, also termed pelvic bladder, can be an incidental finding in patients that have no clinical signs of an abnormality.3,4 Diagnosis can be made with contrast radiography, by assessment of trigone location in relation to the cranial edge of the pelvis when the urinary bladder is fully distended. Results of a previous study5 suggested that a urinary bladder is considered as intrapelvic when 5% of the craniocaudal dimension is within the pelvic canal; however, because of variation in urinary bladder location with the degree of distention, a urinary bladder may falsely be thought to have an intrapelvic location if it is not fully distended at the time of evaluation.3 Traditionally, in veterinary medicine, a pelvic bladder has been thought to be present from birth and not an acquired condition, as was expected to be the case for the dog of the present report.
During positive-contrast cystourethrography in the dog of the present report, the urinary bladder was maximally distended with a mixture of saline solution and contrast medium. During infusion, the urinary bladder apex did not shift cranially as the urinary bladder became maximally filled, indicating true existence of a pelvic bladder. The caudal displacement of the urinary bladder was most markedly apparent on ventrodorsal projections. To the authors’ knowledge, neither trigonal invagination nor tortuosity and kinking of the urethra, as observed on positive-contrast cystourethrography and CT in this dog, has been reported previously in dogs with a pelvic bladder. Jackson et al6 evaluated normal continent dogs with voiding cystourethrography and found caudal movement of the urinary bladder and a tortuous proximal portion of the urethra during micturition. This demonstrates the extent of urethra and urinary bladder neck mobility in clinically normal dogs. As voiding cystourethrography was not performed in the dog of the present report, the anatomic positioning of the urinary bladder and urethra during active voiding was not known. However, the dysuria in combination with the extent of urethral tortuosity and kinking and the hypermobility of the urethra and urinary bladder neck in this dog at a time without active voiding was considered to be outside of normal variation.
The clinical sign most commonly thought to be associated with pelvic bladder in dogs is urinary incontinence; however, as noted, pelvic bladders are also found incidentally in dogs with no abnormal clinical signs. Dogs with pelvic bladder that develop signs of urinary incontinence are reported to have a high prevalence of urethral sphincter mechanism incompetence.7 The dog of the present report did not have prior urinary incontinence; however, it is hypothesized that the pathophysiologic cause of caudal urinary bladder displacement in this dog was different from what has previously been reported.
In women, alterations in the urethrovesicular axis resulting from decreased urethral support by the pubocervical fascia and the increase in laxity of the anterior vagina wall leading to stretching of the urinary bladder neck and proximal portion of the urethra are some of the pathophysiologic causes of stress urinary incontinence.8 The decrease in urethral and urinary bladder neck support results in hypermobility of both, impairing the pressure transmission during increased abdominal pressure.9 These incidents occur secondary to historical surgical procedures in the pelvic canal, neurologic disease that affects the nervous supply of the urogenital tract, childbirth, and estrogen deficiency at menopause with resultant atrophy of periurethal supportive tissues.10 On the basis of findings in women with stress urinary incontinence, the dog in the present report may have had a similar disease process of pelvic organ hypermobility; however, our patient had intermittent urethral obstruction resulting from intermittent urethral kinking and not urinary incontinence. The urethral and urinary bladder neck hypermobility and malpositioning may have been the result of historical parturition in the dog of the present report many years before when it was a young adult and decreased pelvic canal supportive tissues from lack of estrogen secondary to ovariohysterectomy, although this cannot be confirmed.
In humans, abnormal displacement of the pelvic organs beyond the normal anatomic confines is termed pelvic organ prolapse; this condition occurs frequently in elderly women. Pelvic organ prolapse can involve malpositioning of any of the pelvic floor organs, including the urinary bladder, vagina, uterus, and rectum.11 The degree of pelvic organ prolapse is staged on the basis of the extent of the organ prolapse, with 0 being least and 4 being most severely affected.11 In humans, the relationship between the vaginal and urethral attachments and the variable sheets of fibromuscular tissue, pubocervical fascia, or endopelvic fascia is important in maintaining appropriate positioning of these pelvic organs. In the presence of pelvic organ prolapse, the musculofascial vaginal support mechanism is deficient.12 The dog of the present report had a disease process similar to what is found in humans with cystoceles, in which the decrease in urethral support by the surrounding tissues results in caudal displacement of the urethra and the urinary bladder neck.
In women with mild to moderate prolapse (< stage 1), stress urinary incontinence is the most commonly associated clinical sign and is reported to be the result of denervation injury, decreased collagen content of the surrounding tissue, decreased smooth muscle support, and lack of estrogen.12 However, with advancement of the anterior prolapse, voiding dysfunction (difficulty with urinary bladder emptying) and obstructive voiding (hesitancy, weak or prolonged flow, intermittent flow, and the need to change position to facilitate micturition) have been reported to be common clinical signs seen in 30% to 60% of the patients with severe pelvic organ prolapse (> stage 3).13 Urodynamic testing in patients with severe pelvic organ prolapse is consistent with obstruction (urethral kinking, urethral compression, pressure dissipation, and urinary bladder outlet obstruction) with high voiding pressure.14,15 The clinical signs of dysuria and intermittent (positional) urethral obstruction in the dog of the present report were similar to the clinical signs reported in humans with more advanced pelvic organ prolapse.
To our knowledge, this is the first report of a dog with intermittent mechanical outflow tract obstruction secondary to caudal urinary bladder displacement and subsequent trigonal invagination and urethral kinking. There was a similar clinical report16 in a 6-month-old alpaca with urinary bladder outlet obstruction secondary to pelvic bladder; the alpaca underwent cystopexy and also had a favorable outcome.
Acknowledgments
No third-party funding or support was received in connection with the writing or publication of the manuscript.
Footnotes
Argyle Sterile Tom Cat Catheter, Covidien, Mansfield, Mass.
Panoview Telescope II (8.5F × 18 cm), Richard Wolf Medical, Vernon Hills, Ill.
Weasel wire, Infiniti Medical, Menlo Park, Calif.
Red rubber catheter, Bard Medical, Murray Hill, NJ.
Isovue 370, Bracco Diagnostics, Princeton, NJ.
BD Medical Systems, Franklin Lakes, NJ.
Vascular introducer sheath with dilator, Infiniti Medical, Menlo Park, Calif.
Ethilon suture, Ethicon Inc, Somerville, NJ.
Prolene suture, Ethicon Inc, Somerville, NJ.
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