Placement of an artificial urethral sphincter for treatment of passive urinary incontinence after inadvertent prostatectomy and balloon dilation treatment for stricture formation in a 5-month-old dog.

OBJECTIVE: Describe the management of incontinence with several therapies, culminating with the apparently successful treatment utilizing artificial sphincter placement following an inadvertent prostatectomy. ANIMAL: 5-month-old 7.5-kg male neutered Miniature Schnauzer. CLINICAL PRESENTATION, PROGRESSION, AND PROCEDURES: The patient was referred for dysuria and persistent stranguria following an iatrogenic total prostatectomy and urethrectomy. An extra pelvic urethral anastomosis was performed, followed by hospitalization for 2 weeks with a urinary catheter. The patient was further investigated for persistent stranguria, and a contrast urethrogram revealed a urethral stricture at the anastomosis site, which was treated with fluoroscopic balloon dilation. The stranguria resolved, but an acute nocturnal grade 3 passive urinary incontinence occurred, which was nonresponsive to medical management of phenylpropanolamine hydrochloride and estriol. An artificial urethral sphincter was placed, leading to continence after 5 top-ups to a total volume of 0.9 mL. The patient remained continent for 5.5 weeks before abrupt incontinence recurred, which was resolved by another 0.1-mL top-up. No further signs of incontinence occurred in the 11 months following. TREATMENT AND OUTCOME: The placement of an artificial urethral sphincter successfully managed urinary incontinence in this patient. Continence was achieved with no significant complications other than a transient loss of continence. Long-term follow-up 14 months after sphincter placement revealed that the patient had remained continent since the final sphincter top-up. The owner reported a significant improvement in the patient's quality of life following successful incontinence management. CLINICAL RELEVANCE: This case highlighted the benefits of placing an artificial urethral sphincter in managing urinary incontinence after select cases of prostatectomy in dogs that are unresponsive to medical management.

Cutaneous xanthoma causing hypercalcaemia in a cat.

CASE SUMMARY: A 5-year-old male neutered cat weighing 3.56 kg presented owing to the development of two masses over the dorsal cervical and cranial thoracic areas, as well as weight loss, inappetence and vomiting. Diagnostic tests revealed a grossly lipaemic sample with hypercholesterolaemia (440 mg/dl; reference interval [RI] 90.0-205.0), hypercalcaemia (>16.0 mg/dl [RI 8.0-11.8]) and urine specific gravity 1.022 (RI ⩾1.035). When re-presented 9 months later, fasted blood analyses revealed elevated ionised calcium (1.87 mmol/l [RI 1.11-1.38]), persistently elevated total calcium, normal phosphate and persistent minimally concentrated urine with calcium oxalate dihydrate crystals. Ultrasound-guided fine-needle aspiration of the masses produced blood-tinged purulent fluid with negative culture results. Excisional biopsies of both masses were undertaken, and histopathology was consistent with cutaneous xanthoma. No organisms were identified with special staining, and deep-tissue culture did not grow bacteria or fungi. Postoperatively, repeat fasted biochemical analysis revealed persistent hypercholesterolaemia with normal triglycerides, and normalisation of ionised and total calcium levels. Based on these findings, a diagnosis of cutaneous xanthoma causing hypercalcaemia due to primary dyslipidaemia was made. The cat was reported to be significantly improved in comfort and energy levels postoperatively and a transition to a fat-restricted diet was instituted. Eight months after xanthoma removal no recurrence was reported. RELEVANCE AND NOVEL INFORMATION: To our knowledge, this is the first report of cutaneous xanthoma and associated granulomatous inflammation causing hypercalcaemia due to dyslipidaemia in a cat. Familial hypercholesterolaemia is an example of a primary condition that could cause dyslipidaemia in cats, and further studies are warranted to better describe the genetic characteristics. Xanthoma formation and the resultant granulomatous inflammation should be considered in cases of hypercalcaemia.

Acute and severe haemorrhage following pentosan polysulfate injection in a Cornish Rex.

CASE SUMMARY: A 14-year-old male castrated Cornish Rex cat was referred for lethargy progressing rapidly to collapse in the hours following a subcutaneous injection of a product containing 100 mg/ml pentosan polysulfate sodium and 168 mg/ml glucosamine. Physical examination revealed the cat to be in hypotensive shock with swelling and interstitial oedema around the cranial thorax and caudal cervical regions without cutaneous haemorrhage. Initial diagnostics revealed a severe anaemia (packed cell volume 11%) which later deteriorated further, necessitating a blood transfusion and aggressive fluid therapy. Post-transfusion, the patient remained dyspnoeic and subsequent diagnostics found evidence of pre-existing cardiomyopathy and congestive heart failure. The cat was euthanased 24 h following presentation due to increasing dyspnoea. Post-mortem findings were of severe subcutaneous and intermuscular haemorrhage over the neck and thorax, among other changes. There were no detectable levels of coumarin anticoagulants in the liver. RELEVANCE AND NOVEL INFORMATION: This is the first reported case of acute subcutaneous and intermuscular haemorrhage of this severity suspected to be related to the off-label use of an injectable product containing pentosan polysulfate in a cat. Given the popularity of its use for feline arthritis, there is a need for large-scale clinical trials to evaluate the safety and efficacy of products containing pentosan polysulfate for cats, and any side effects to be reported.

Primary adrenal lymphoma causing hypoaldosteronism in a cat.

CASE SUMMARY: A 10-year-old, 5.1 kg (11.2 lb), male castrated cat was presented with signs of lethargy and decreased appetite at home after being previously healthy. Serum biochemical analysis identified normokalemia (5.1 mmol/l; reference interval [RI] 3.4-5.6 mmol/l) and severe hyponatremia (123 mmol/l; RI 145-158 mmol/l), with an Na/K ratio of 24 (RI 32-41). Baseline serum cortisol was low to normal, but serum aldosterone was markedly decreased with a pre-adrenocorticotropic hormone stimulation concentration of 13 pmol/l (RI 194-388 pmol/l) and post-adrenocorticotropic hormone stimulation concentration of 21 pmol/l (RI 277-721 pmol/l). Hematologic and biochemical analyses were otherwise unremarkable. Abdominal ultrasound revealed bilaterally enlarged adrenal glands with no other abnormalities noted; thoracic radiographs also did not identify any signs of metastasis. Fine-needle aspiration was strongly suggestive of lymphoma of the adrenal glands, and PCR for antigen receptor rearrangement was positive for B-cell clonal expansion; based on these findings, a diagnosis of primary adrenal B-cell lymphoma was made. Stable disease was achieved for a short period of time following vincristine, cyclophosphamide, prednisolone and fludrocortisone therapy, followed by progressive adrenal enlargement and electrolyte derangements that responded to neither doxorubicin nor adjustments in fludrocortisone dosage. Ultrasonographic metastasis was not identified at any time, and other organ derangements were not noted on hematologic or biochemical analyses. The cat was euthanized 55 days after initial presentation. RELEVANCE AND NOVEL INFORMATION: This is the first report of primary adrenal lymphoma in a cat, with presenting signs compatible with hypoaldosteronism. Lymphoma should be a differential for cats presenting with adrenal enlargement or clinical signs and biochemical changes consistent with hypoaldosteronism or hypoadrenocorticism.