Successful conservative management in a dog with substantial urinary bladder ischemia

Abstract

A 7-year-old spayed female pug dog was brought to the veterinary college with a severely and diffusely ischemic urinary bladder secondary to obstructive uroliths in the lower urinary tract. Cystotomy was performed to remove the uroliths and the ischemic bladder was managed with conservative treatment. A recheck abdominal ultrasound 4.5 mo after surgery revealed an abdominal mass that was associated with the urinary bladder. An exploratory laparotomy and partial cystectomy were performed. Histopathology of the mass showed granulomatous inflammation centered on necrotic tissue. The dog recovered well, and long-term prognosis is good. To the best of our knowledge, this is the first veterinary case report describing conservative management of an ischemic urinary bladder. An uncommon complication following cystotomy and the relevant imaging findings is also described. The positive outcome for the dog demonstrated that conservative management may serve as an option for treatment of substantial ischemia of the urinary bladder.

Urolithiasis is a common cause of urethral obstruction in dogs and cats (1). It has been reported that severe urinary bladder distention secondary to lower urinary tract obstruction caused decreased perfusion and ischemia of the bladder wall (2,3).

Surgical management is recommended for extensive urinary bladder ischemia in veterinary medicine. Surgical options include ileocystoplasty, jejunocystoplasty, colonic seromuscular augmentation cystoplasty, a rectus abdominis muscle flap, diversion of ureters, and ureterocolonic anastomosis (4–9) However, these procedures have been reported to have relatively high complication rates in human and veterinary medicine (5–10).

The urinary bladder has high tissue healing capacity and it can regain normal tissue strength in 14 to 21 d after trauma (11). A case report described successful conservative management of extensive urinary bladder ischemia in human medicine (12), but to the authors’ knowledge there is no veterinary literature describing conservative management of ischemic urinary bladder. It is believed that this is the first report of the successful conservative management of substantial urinary bladder ischemia in a dog secondary to lower urinary tract obstruction.

Case description

A 7-year-old spayed female pug dog was referred to the Veterinary Medical Centre at the Western College of Veterinary Medicine, University of Saskatchewan for stranguria and hematuria.

On examination, abdominal palpation revealed a large urinary bladder and severe abdominal pain at mid-abdomen. The remainder of the physical examination was unremarkable. Abdominal radiographs showed a markedly dilated urinary bladder with a large amount of variously shaped mineral opaque cystoliths occupying most of the lumen. A few irregular mixed mineral and soft tissue opaque structures were present in mid-abdomen. These were ureteroliths or intestinal foreign bodies (Figure 1 a, b). A complete blood (cell) count (CBC) identified a mild neutrophilia with severe left shift and toxic change [white blood cells (WBC): 20.5 × 10⁹/L, reference range (RR): 4.9 to 15.4 × 10⁹/L; band neutrophil: 18%, absolute number: 3.69 × 10⁹/L, RR: 0 to 0.1 × 10⁹/L]. Marked azotemia (urea: 39.4 mmol/L, RR: 3.5 to 11.4 mmol/L; creatinine: 501 μmol/L, RR: 41 to 121 μmol/L), and moderate hyperkalemia (potassium: 6.7 mmol/L, RR: 3.8 to 5.6 mmol/L) were noted on the serum biochemistry panel. Venous blood gas analysis suggested compensated metabolic acidosis and concurrent respiratory alkalosis (pH: 7.368, RR: 7.35 to 7.45; pCO₂: 26.2 mmHg, RR: 45 to 50 mmHg; HCO₃–: 14.7 mEq/L, RR: 24 to 28 mEq/L; base excess: −8.4 mEq/L, RR: −4 to +4 mEq/L). Retrograde urohydropropulsion under sedation was unsuccessful in resolving the urethral obstruction. Cystocentesis was performed removing approximately 300 mL of dark red urine. Urinalysis revealed pyuria and hematuria with abundant bacteria [WBC: 40 to 50/hpf with some clumps; red blood cells (RBC): 80 to 90/hpf; abundant cocci bacteria/hpf ]. Supportive care including intravenous Ringer’s lactate solution (Baxter Corporation, Mississauga, Ontario), maropitant (Cerenia; Zoetis Canada, Kirkland, Quebec), 1 mg/kg body weight (BW), IV, pantoprazole (Fresenius Kabi, Toronto, Ontario), 1 mg/kg BW, IV, and butorphanol (Torbugesic; Zoetis Canada), 0.4 mg/kg BW, IV, was administered and a plan for surgical intervention was developed. Retrograde urohydropropulsion was attempted and was successful under general anesthesia prior to surgery. A midline celiotomy was performed, and abdominal exploration revealed a small amount of serosanguinous peritoneal fluid. The urinary bladder appeared diffusely dark purple in color indicating lack of perfusion (Figure 2). There were concerns regarding tissue viability as the urinary bladder wall bled minimally from the cystotomy site. A ventral midline incision of the bladder was made to allow complete mucosal visualization and cystoliths were removed. The mucosal surface of the bladder wall was sloughing and had a dark purple coloration similar to that of the serosal surface. The intraoperative findings were reported to the owner and treatment options were considered. The options discussed included ileocystoplasty, a muscle flap, diversion of ureters, and conservative management with an indwelling urinary catheter. The owner elected to proceed with conservative management, and a 12-Fr Foley urinary catheter was placed. A sample of tissue from the bladder was obtained before the cystotomy site was closed with 3–0 PDSII in simple continuous pattern. A Jackson-Pratt (JP) drain (Cardinal Health Canada, Mississauga, Ontario) was placed in the abdomen for a management of possible subsequent bladder rupture and uroabdomen. The dog recovered from surgery uneventfully. Azotemia and hyperkalemia resolved in the following days. Bacterial culture of the urinary bladder tissue revealed Staphylococcus pseudintermedius infection which was susceptible to most of the tested antibiotics. The dog was monitored in the ICU with the indwelling urinary catheter. No fluid flowed out through the JP drain and the drain was removed 3 d after surgery, at which time the dog was clinically stable, the urinary catheter was removed, and voluntary urination was observed. The dog was discharged with cephalexin (Novopharm, Toronto, Ontario), 26 mg/kg BW, PO, q12h, 1 d after urinary catheter removal. Uroliths were submitted to the Canadian Veterinary Urolith Centre for quantitative analysis and the results showed 95% struvite and 5% calcium phosphate. Feeding urinary prescription diet and encouraging more water intake were recommended.

Figure 1.

Right lateral (a) and VD (b) views of abdominal radiographs showing a large amount of sharply marginated, variously shaped and sized, homogenously mineral opaque cystoliths occupying most of the urinary bladder. The few irregularly mixed mineral and soft tissue opaque structures presenting in mid-abdomen could be ureteroliths or intestinal foreign bodies.

Figure 2.

In the first surgery, the entire serosal surface of the urinary bladder is dark purple in color.

Two weeks after surgery, the dog showed hematuria and mild urinary incontinence; results of urine bacterial culture showed Enterococcus faecium infection. Marbofloxacin and chloramphenicol (unknown doses and manufacturers) were administered by the referring veterinarian according to antibiotic susceptibility testing. After completion of the antibiotic treatment, the owner reported no clinical signs. A routine check by the referring veterinarian 3.5 mo after surgery revealed a positive urinary culture with Enterococcus faecalis. An abdominal ultrasound showed a vermiform structure in the urinary bladder. The dog was reexamined at our hospital 4.5 mo after surgery and was clinically normal. A CBC and serum biochemistry were unremarkable. Abdominal ultrasound revealed a hyperechoic structure within the bladder which shifted with a positional change of the dog (Figure 3 a). A diverticulum at the apex of the urinary bladder (Figure 3 b) extended cranially into a large sac-like structure. This large structure was filled with heterogeneously hyperechoic debris. (Figure 3 c). No ureteroliths were present. The dog underwent exploratory laparotomy and the urinary bladder appeared healthy with no necrosis observed. However, there was adhesion of omentum, small intestine, and colon to the urinary bladder. There was an approximate 9 cm round and firm mass adherent to the right cranial body wall and peritoneum within the abdomen, which appeared to be connected to the urinary bladder through the diverticulum-like structure extending from the apex of the urinary bladder (Figure 4 a). The adhesion around the mass was broken down, and the mass, diverticulum, and the apex of the bladder were removed en bloc. The bladder was assessed through the cystectomy site, a free-floating yellow soft structure, approximately 3 to 4 cm in length was seen (4 b). The abdominal mass and yellow structure in the urinary bladder were submitted for bacterial culture separately. Both culture results indicated Enterococcus faecalis infection. The dog recovered from surgery without major complication and was discharged the next day with amoxicillin/clavulanic acid (AventiCLAV; Aventix, Burlington, Ontario), 13 mg/kg BW, PO, q12h, for 7 d. Histopathology results of the mass cranial to the urinary bladder showed granulomatous inflammation centered on necrotic mesenteric adipose tissue and surrounded by variably mature granulation tissue. In addition, histopathology indicated that the structure in the urinary bladder was composed of necrotic debris with bacterial colonies, crystalline material, and refractile foreign material. The refractile foreign material was histopathologically similar to suture material. At 4 wk after surgery and at a recheck appointment with the referring veterinarian, the dog had no clinical signs and was doing well. Urine bacterial culture showed Enterococcus faecalis infection. Considering that the dog had subclinical bacteriuria, no further treatment was recommended at this time.

Figure 3.

a — Abdominal ultrasound reveals a hyperechoic tissue in the urinary bladder which shifts with positional change of the dog. b — A diverticulum at the apex of the urinary bladder. c — The diverticulum extending cranially into a large sac-like structure which filled with heterogeneously hyperechoic debris.

Figure 4.

a — An approximately 9-cm round and firm mass adhering to the right cranial body wall and peritoneum within the abdomen, which connects to the urinary bladder through the diverticulum-like structure extending from the apex of the urinary bladder. b — There is a non-adherent yellow soft structure in the urinary bladder, approximately 3 to 4 cm in length.

Discussion

Uroliths in dogs and idiopathic cystitis plugs and uroliths in cats are the most common causes of urethral obstruction (1). Prolonged obstruction potentially leads to excessive intraluminal urinary tract pressure, resulting in tissue ischemia or necrosis (2,3). In cases in which over 90% of the urinary bladder is estimated to be ischemic, the currently reported surgical options in veterinary medicine are ileocystoplasty, jejunocystoplasty, colonic seromuscular augmentation cystoplasty, a rectus abdominis muscle flap, diversion of ureters to the prepuce or vagina, and ureterocolonic anastomosis (4–9). Postoperative complications of these advanced surgical interventions include excess mucus production, bacterial infections, pyelonephritis, dehiscence of ureters, ureteral stricture or obstruction, intermittent urinary incontinence, and urine stasis (5–9). In human medicine, augmentation cystoplasty is used to treat patients with small-capacity, high-pressure, poorly compliant or unstable urinary bladders that fail to improve with pharmacological or conservative management. However, contraindications for augmentation cystoplasty such as intrinsic bowel disease, renal impairment, or noncompliance were discussed (10). Before surgical intervention is considered, any comorbidity should be taken into consideration. Moschouris et al (12) opted for conservative management for extensive urinary bladder ischemia due to multiple comorbidities, and the patient had a favorable outcome.

In our report, the urinary bladder was markedly and diffusely ischemic. Conservative management of the ischemic bladder was chosen, with the intention of relying on the robust healing capacity of urinary bladder (13,14). To the best of our knowledge, this is the first case report in veterinary medicine which describes conservative management of an ischemic bladder in a dog. The origin of the mass cranial to the urinary bladder was undetermined. It could be a focal area of bladder dehiscence along the previous suture line with a focal peritonitis. Furthermore, the yellow structure floating in the bladder was likely necrotic tissue sloughed off from the bladder wall mixing with potential suture material from an area of focal bladder wall dehiscence.

We concluded that conservative management for bladder ischemia may serve as an initial treatment option rather than highly invasive procedures which include risk of complications. It is proposed that if bladder ischemia is noted in a timely fashion and the underlying cause is corrected, the bladder may remain viable and advanced procedures are unnecessary. If conservative management fails to return the dog to adequate urinary function or if urinary bladder leakage is detected, reconstruction of the urinary bladder or diversion surgeries could be considered.