Abstract
A 6-year-old, spayed female Labrador retriever was presented with clinical signs of stranguria, pollakiuria, and hematuria of 12 weeks’ duration. A bacterial urinary tract infection, diffuse polypoid cystitis, and emphysematous cystitis were diagnosed. Antibiotic therapy combined with extensive resection of the mucosa and submucosa associated with polypoid lesions resulted in complete resolution of clinical signs and resolution of the remaining polypoid lesions. Polypoid cystitis is an uncommon but clinically relevant and reversible condition of the urinary bladder. Resection of mucosa and submucosa of the urinary bladder in dogs with polypoid cystitis may be a useful surgical treatment and can be considered as an alternative to partial cystectomy or mucosal resection.
Introduction
Polypoid cystitis is an uncommonly recognized but clinically relevant condition of the lower urinary tract in dogs.1–2 Associated with bacterial urinary tract infection, cystic calculi, and chronic bladder catheterization, polypoid cystitis has been speculated by some to be a precursor to malignancy.1–4 Prior reports on the surgical management of this condition in dogs describe partial cystectomy and local mucosal or submucosal excision for discrete lesions.1–2 The purpose of this report is to describe the successful surgical management of diffuse polypoid cystitis using a submucosal resection technique.
Case Report
A 6-year-old, 36-kg, spayed female Labrador retriever was presented to The Ohio State University Veterinary Teaching Hospital (OSUVTH) for evaluation of chronic hematuria. The hematuria began approximately 12 weeks prior to presentation and was grossly apparent throughout the course of urination. Straining and an increased sense of urgency to urinate were also noted initially. A urinary tract infection was diagnosed by analysis of a voided sample at the referring veterinary facility, but no culture was performed at that time. Stranguria and pollakiuria resolved following empirical treatment with amoxicillin (400 mg per os [PO] q 12 hours) for 10 days, but the hematuria persisted. Sulfadimethoxine and ormetoprim (960 mg PO q 24 hours) were then administered for 20 days without resolution of the hematuria.
On presentation to OSUVTH, the dog was bright, alert, responsive, and had a body condition score of 4/5. Physical examination revealed a recessed vulva, but findings were otherwise unremarkable. Gross hematuria was noted during hospitalization. Concurrent medical conditions included idiopathic epilepsy and chronic colitis. These conditions were being effectively managed by the referring veterinarian with phenobarbital, potassium bromide, and tylosin powder.
Laboratory Findings
A complete blood count (CBC), serum biochemical profile, urinalysis, and urine culture from a sample obtained by cystocentesis were performed. The CBC was within normal limits. Abnormalities noted on serum biochemical profile included elevations in alanine aminotransferase (77 IU/L, normal 10 to 55 IU/L), alkaline phosphatase (4006 IU/L, normal 15 to 120 IU/L), and corticosteroid-induced alkaline phosphatase (3841 IU/L, normal 0 to 6 IU/L). Urinalysis revealed a specific gravity of 1.009, a pH of 7.0, 3+ protein, 3+ blood, three to five white blood cells per high-power field (HPF), zero to one squamous epithelial cells per HPF, too-numerous-to-count red blood cells, and unspecified bacteria. Quantitative urine culture identified >30,000 colony-forming units per mL of Klebsiella spp. The organism was resistant to ampicillin but was susceptible to first-generation cephalosporins and sulfa antibiotics. Culture of the bladder wall obtained at the time of surgery yielded many Klebsiella spp. that were resistant to ampicillin and intermediately susceptible to sulfas.
Diagnostic Imaging
Abdominal and thoracic radiography and abdominal ultrasonography were performed. The thoracic radiographs were unremarkable. Plain abdominal radiographs revealed the presence of gas in the bladder wall, consistent with emphysematous cystitis. Ultrasound revealed bladder wall emphysema and the presence of numerous, polypoid lesions radiating from multiple locations on the bladder wall. A generalized increase in bladder wall thickness (9 mm) was also noted, with the bladder moderately distended with urine.
Cystoscopy
Cystoscopic evaluation of the lower urinary tract was performed preoperatively using an adult human rigid cystoscopea (4 × 300 mm, with 30° viewing angles).
On entering the vestibule, the only abnormality noted was the presence of follicles diffusely distributed on the mucosa. The urethral mucosa was slightly hyperemic in appearance, and blood-tinged urine was noted; however, no sites of active hemorrhage were observed within the urethra itself. Multiple fingerlike to nodular masses were observed arising from all areas of the bladder mucosa [Figure 1⇓]. No normal bladder mucosa was observed, and the masses began to hemorrhage with minimal bladder distension.
Cystoscopic appearance of the bladder prior to surgery. Notice the diffuse polypoid appearance and absence of normal mucosa.
Surgery
Exploratory celiotomy and cystotomy were performed to obtain samples for culture and histological evaluation and to debulk the mucosal masses. The liver was mildly enlarged, and the urinary bladder was hyperemic with a diffusely thickened wall. A liver biopsy was obtained. Numerous tortuous vessels were apparent on the serosal surface of the urinary bladder. A ventral cystotomy was performed, and a full-thickness portion of the bladder wall was resected for histological evaluation as well as aerobic and anaerobic tissue cultures.
Following sample collection, cefazolin sodium (22 mg/kg intravenously [IV]) was administered. The mucosal surface of the bladder appeared hyperemic with diffusely distributed, small, broad-based polypoid structures and longitudinal folds [Figure 2⇓]. The lesions were superficially fri-able and bled easily, but they were tightly adhered to underlying structures. No regions of normal bladder mucosa were identified. Elevation of the mucosal polypoid tissue was first attempted with the aid of saline injection.b This technique proved to be unsuccessful, because the affected tissue was too tightly adhered to the underlying submucosa. Subsequently, Metzenbaum scissors were used to elevate and resect the diseased tissue between the submucosa and muscularis. Excision was continued from the apex of the bladder to the trigone. Numerous polypoid lesions located caudal to the trigone were not excised. Dilute epinephrine (<10 drops, final concentration ≤0.1 mg/mL) was applied topically to the exposed seromuscular layer to stimulate vasoconstriction. Prior to closing the cystotomy, a urinary catheter was placed aseptically. Because the holding layer of the bladder was excised, the bladder was closed in two layers with 3-0 poliglecaprone 25c in a simple continuous pattern, followed by a continuous Lembert pattern.
Appearance of bladder lumen at the time of surgery. Note the lack of normal mucosa.
Postoperative Care
Following surgery, urine output was monitored. In addition to receiving tylosin powder, phenobarbital, and potassium bromide for concurrent conditions, the dog was given hydromorphone (0.05 mg/kg IV up to q 4 hours as needed) for pain and cefazolin sodium (22 mg/kg IV q 8 hours) until the morning after surgery. Cephalexin (1 g PO q 12 hours) was then instituted and continued for 30 days. Urine production (2 mL/kg per hour) was noted to be appropriate, and the hematuria began to resolve within 24 hours of surgery, at which time the urinary catheter was removed. The dog was discharged to the owner 2 days postoperatively.
Histopathology
Histopathology of the urinary bladder was consistent with severe, widespread, polypoid cystitis that was characterized by marked submucosal edema with dilated lymphatics, neutrophilic and histiocytic infiltrates, epithelial hyperplasia with minimal dysplasia, multifocal hemorrhage, and mild, multifocal hemosiderosis. In addition, occasional lymphatics containing rafts of normal-appearing, hyperplastic epithelial cells were identified. Marked margination of neutrophils and mild, multifocal degeneration of individual epithelial cells with occasional formation of intraepithelial cysts were also noted. Histopathology of the liver was consistent with fluid or glycogen accumulation, suggestive of steroid hepatopathy.
Case Follow-up
During the first week after the dog was discharged, the client reported that the hematuria resolved, despite the presence of some degree of stranguria and pollakiuria. These clinical signs gradually improved and resolved without additional treatment.
One month after the bladder mucosal and submucosal resection, follow-up abdominal ultrasonography and cystoscopy were performed in conjunction with an episioplasty for the recessed vulva. The urinary bladder had a completely normal ultrasonographic and cystoscopic appearance [Figure 3⇓]. Urine samples, obtained by cystocentesis for culture after 2 weeks of antibiotic therapy and 3 days after discontinuing the antibiotics, were negative for bacterial growth. Another urine culture performed 2 weeks after the episioplasty also was negative. Recommendations were for the urine to be cultured every 3 months for the next year or if clinical signs recurred. Three months postoperatively, no gross hematuria, stranguria, or pollakiuria were seen.
Cystoscopic appearance of the bladder 4 weeks after surgery. Normal mucosal surface and vascularity are seen throughout the bladder. The central hemorrhagic lesion in the image is secondary to cystocentesis.
Discussion
Polypoid cystitis is an uncommon condition of the urinary bladder, characterized by the formation of multiple, raised, proliferative lesions protruding from the bladder mucosa. Though lesions are commonly solitary, multifocal, or found in clusters, microscopic and diffuse lesions have also been reported.1–3,5–7
Although its exact cause is unknown, polypoid cystitis has been suggested to be associated with bacterial urinary tract infections and/or chronic urethral catheterization.1–6,8–10 Other causes of chronic mucosal irritation, such as cystic calculi, have also been suggested to be associated with polypoid cystitis.1 Although polypoid cystitis is generally considered to be reversible after treatment of any associated condition, it also has been suggested as a preneoplastic phenomenon.1,4,5,8,9 In this dog, a bacterial urinary tract infection was identified as a concurrent condition, and no evidence of malignancy was identified histopathologically. In addition, no history of prior urinary tract catheterization or cystic calculi was known.
In dogs, traditional surgical treatment of polypoid cystitis involves partial cystectomy for full-thickness excision, although local mucosal and submucosal excisions are also described.1,2 Full-thickness excision is particularly important when the potential for malignancy exists. In this dog, the polypoid changes appeared to involve all of the bladder mucosa, making partial cystectomy a less desirable option. Although at least 75% of the urinary bladder can be excised as long as the trigone is preserved,11 such a radical cystectomy in this dog would not have allowed complete surgical excision and would have resulted in a temporary reduction in the bladder’s reservoir capacity. Mucosal and submucosal resection was chosen over full-thickness partial cystectomy because of the extensive, diffuse nature of the lesions; the lack of response to appropriate antibiotic therapy; and the clinical suspicion that the lesions were benign polypoid cystitis with the presence of concurrent emphysematous cystitis. Using this technique, an estimated 80% of the diseased bladder mucosa was excised, and a full-thickness biopsy was obtained (to rule out malignancy) while maintaining the bladder’s reservoir capacity.
Following surgery, bladder healing is rapid and nearly complete.11 Healing occurs through a combination of epithelial regeneration and formation of scar tissue, as well as smooth-muscle proliferation and hypertrophy.11 The urinary bladder can regain nearly 100% of its original strength within 2 to 3 weeks of cystotomy or partial cystectomy.11 In addition, when the urinary bladder lining has been stripped by curettage or denuded by laser resection, the epithelial cells from the terminal ureters and urethra have been demonstrated to proliferate and migrate, completely resurfacing the bladder within 30 days.12,13 In the dog of our study, the bladder mucosa could not be separated from the underlying submucosa, so excision of both layers was determined to be necessary. Because this required removal of the submucosal holding layer, the bladder was closed in two layers as a precaution. Follow-up cystoscopy confirmed that bladder resurfacing was able to take place within 30 days, and the residual macroscopic polypoid lesions were no longer present.
Bacterial urinary tract infection with concurrent emphysematous cystitis was an unusual clinical finding in this dog. While emphysematous cystitis is typically associated with diabetes mellitus, several veterinary reports document its presence in nondiabetic animals.14–16 Numerous organisms, including Klebsiella spp., have been implicated.14–17 The bacterial utilization of glucose, albumin, and other substrates is believed to result in the production of gas-filled vesicles.14–16 Resolution of this condition is possible with proper antibiotic therapy and/or resolution of glucosuria when present.14–16
An episioplasty was performed in this dog 1 month after cystotomy. This procedure was performed because of a recessed vulva that may have been a factor predisposing to urinary tract infections. Episioplasty is an important and successful procedure to consider in dogs with chronic urinary tract infections and a recessed vulva.18
Conclusion
Despite incomplete surgical excision of the polypoid tissue in this dog, complete resolution of all clinical signs and remaining lesions occurred within 1 month of surgery. This suggests that polypoid cystitis is a reversible condition of the urinary bladder; however, until more is known regarding its pathogenesis and potential for malignant transformation, aggressive management of polypoid cystitis is warranted. If an underlying cause of mucosal irritation, such as a urinary tract infection, is identified, it should be treated aggressively. Surgical excision by partial cystectomy or mucosal and submucosal resection should be considered in cases where the polypoid lesions result in clinical signs of urethral or ureteral obstruction; when lesions do not respond to appropriate medical therapy; or when obtaining a definitive diagnosis is necessary.
Footnotes
References
