Cystoscopic-guided scissor transection of intramural ectopic ureters as a novel alternate minimally invasive treatment option to laser ablation in female dogs: 8 cases (2011-2020).

OBJECTIVE: To evaluate the safety and efficacy of cystoscopic-guided scissor transection of ectopic ureters (CST-EU) in female dogs. ANIMALS: 8 incontinent female dogs with intramural ectopic ureters. PROCEDURES: For this retrospective case series, data were collected from medical records of dogs that underwent CST-EU to relocate the ectopic ureteral orifice to an anatomically normal trigonal location between June 2011 and December 2020. Outcome after hospital discharge was determined using owner telephone questionnaires. RESULTS: Ectopic ureters were bilateral in 4 of the 8 dogs, and all dogs had other urogenital tract anomalies. Owner questionnaire follow-up was available for 7 dogs, and results indicated 6 dogs had improved urinary continence immediately following the procedure. At the last follow-up (44 to 3,384 days after CST-EU), 3 of the 7 dogs were completely continent with CST-EU alone, 3 others became continent or were markedly improved with the addition of medications for urethral sphincter mechanism incompetence, and 1 required ureteroneocystostomy, colposuspension, and an artificial urethral sphincter to become fully continent. Owners of 5 of the 7 dogs reported that they considered the outcome of CST-EU as good to excellent, and all owners reported that they would consider having CST-EU performed again should they have another incontinent dog. Complications were minor, and only 3 dogs showed transient lower urinary tract signs after CST-EU. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated CST-EU could provide a safe, effective, minimally invasive alternative in the absence of laser technology for the treatment of intramural ectopic ureters in female dogs.

Management of hypoadrenocorticism (Addison's disease) in dogs.

Hypoadrenocorticism (HOAC; Addison's disease) is an endocrine condition seen in small animal practice. Dogs with this disease can present in a variety of ways from acute hypovolemic collapse to vague, chronic, waxing, and waning clinical signs. In the most common form of this disease, animals have both mineralocorticoid and glucocorticoid deficiency, resulting in hyponatremia and hyperkalemia, and signs of cortisol deficiency. The etiology may be immune-mediated destruction of the adrenal cortex, drug-induced adrenocortical necrosis (mitotane), enzyme inhibition (trilostane), or infiltrative processes such as neoplastic or fungal disease. Much less commonly, dogs have signs of cortisol deficiency, but no electrolyte changes. This is referred to as atypical HOAC. The veterinarian needs to have a clinical suspicion for HOAC to make a diagnosis in a timely manner. Treatment of dogs with an acute presentation prioritizes correcting the hypovolemia, hyperkalemia, acidosis, and hypoglycemia. Fluid therapy addresses most of these issues, but other directed therapies may be required in the most severe cases. For chronic management, all patients with Addison's disease will require replacement of glucocorticoids (usually prednisone), and most patients require replacement of mineralocorticoids with either desoxycorticosterone pivalate or fludrocortisone. Atypical Addisonians do not require mineralocorticoid supplementation, but electrolytes should be monitored in case the need arises in the future. The prognosis for dogs treated for HOAC promptly and appropriately is excellent; most patients die from other diseases. However, if the diagnosis is missed, patients may die as a consequence of HOAC. Thus, knowledge of the hallmarks of Addison's disease is imperative.

Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005).

OBJECTIVE: To compare dogs with glucocorticoid-deficient hypoadrenocorticism (GDH) with those with mineralocorticoid- and glucocorticoid-deficient hypoadrenocorticism (MGDH) and determine prevalence, historical and clinicopathologic markers, and outcome of dogs with GDH. DESIGN: Retrospective case series. ANIMALS: 46 dogs with hypoadrenocorticism. PROCEDURES: Records in the veterinary medical database at Purdue University were searched for dogs in which hypoadrenocorticism had been diagnosed at the Veterinary Teaching Hospital from 1985 to 2005. Data pertaining to signalment, history, a minimum clinicopathologic database, treatment, and outcome were collected. Dogs with hypoadrenocorticism were classified as having MGDH if hyponatremia, hyperkalemia, or both were detected and as having GDH if hyponatremia and hyperkalemia were absent. Dogs were excluded if they had ever been treated with mitotane or had been treated with > 1 dose of corticosteroids within a month prior to the ACTH-stimulation test. RESULTS: 35 dogs with MGDH and 11 dogs with GDH met the inclusion criteria. Dogs with GDH were older at the time of diagnosis and had a longer duration of clinical signs prior to diagnosis than those with MGDH. Dogs with GDH were more likely to be anemic, hypoalbuminemic, and hypocholesterolemic than dogs with MGDH. CONCLUSIONS AND CLINICAL RELEVANCE: GDH was more common than reported in a referral hospital population of dogs with primary hypoadrenocorticism. Definitive diagnosis of GDH remains a clinical challenge. Absence of a stress leukogram in dogs with signs of illness (especially relating to the gastrointestinal tract) warrants further investigation. Most dogs with primary cortisol deficiency do not develop mineralocorticoid deficiency.