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WSV18-0310
UROLOGY
URINARY INCONTINENCE IN MALE DOGS
B. Gerber1
1Vetsuisse Faculty University of Zurich,
Clinic for Small Animal Internal Medicine, Z├╝rich, Switzerland
Urinary incontinence in male dogs
Urinary incontinence is involuntary loss of urine during the filling phase of the bladder. Male dogs are less often affected by this problem than female dogs. Causes of urinary incontinence in dogs can be divided in congenital and acquired causes. Congenital causes can be ectopic ureters, congenital urethral sphincter mechanism incompetence, persistent urachus, bladder diverticula, hypoplasia of the bladder, prostate, or urethra, and hypospadia. Acquired causes can be hyperreflexia of the detrusor muscle, acquired urethral sphincter mechanism incompetence, detrusor atony because of bladder over distention, prostatic disease, neoplastic disease of the bladder, prostate or urethra, or neurologic disease (lower motor neuron disease).
While congenital urinary incontinence often starts in early life, acquired urinary incontinence can occur at any time. However, congenital diseases can become clinical later in life. For instance ectopic ureters can appear later in life because of the urethral closure pressure decreasing with age. Also neutering can decrease the urethral sphincter pressure and uncover an ectopic ureter.
Incontinence can be continuous and the dog loses urine all the time. In this case, the urethral closure is constantly overwhelmed. This might occur with ectopic ureters. Oftentimes the dogs only lose urine while sleeping.
In this case the urethral pressure is overcome by the bladder pressure only after a certain filling volume in the bladder. This might be the case in urethral sphincter mechanism incompetence. Incontinence only when the dog is excited might indicate detrusor hyperreflexia. Urinary tract infection can occur together with other causes of urinary incontinence or can be the cause of the incontinence. With diseases like ectopic ureters or urethral sphincter mechanism incompetence the dogs urinate normally, while with diseases like urinary tract infection or neoplasia pollakiuria or stranguria can be seen.
The size of the bladder before and after urination can help to differentiate causes of urinary incontinence. A bladder that is always small indicates continuous loss of urine, a bladder that is not empty after urination indicates an obstructive lesion or detrusor atony. A bladder that is atonic and easy to express indicates lower motor neuron disease or overflow incontinence.
43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS
25-28 September, 2018 | Singapore
concentration compared with clinical control as assessed by owner perception9. Results indicated that baseline cortisol and pre-trilostane cortisol were better than the post-ACTH stimulation cortisol at differentiating between dogs with excellent clinical control and those that were inadequately controlled. The pre-trilostane cortisol
was slightly better that the baseline cortisol and had
the added benefit of being more useful at signalling potential oversuppression. It is this measurement that
is now recommended for monitoring trilostane therapy. Broadly speaking a pre-trilostane cortisol > 40 and < 138 nmol/L, > 138 nmol/l or < 40 nmol/L indicates adequate, inadequate or excessive control, respectively. However, interpretation should only be carried out in light of clinical findings. Dogs with persistent clinical signs despite adequate cortisol concentration may still require an increased dose or frequency of administration. Dogs
with good clinical control and cortisol concentrations suggestive of inadequate control may benefit from split dosing and dogs with excessive cortisol control may benefit from a lower dose. Dogs presenting ill when on trilostane therapy warrant an ACTH stimulation test to fully evaluate adrenal reserve.References
1. Griebsch, Lehnert C, Williams GJ et al. Effect of trilostane on hormone and serum electrolyte concentrations in dogs with pituitary-dependent hyperadrenocorticism. J Vet Intern Med; 2014; 28; 160-165.
2. Bonadio CM, Feldman EC, Cohen TA et al. Comparison of adrenocorticotropic hormone stimulation test results started 2 versus 4 hours after trilostane administration in dogs with naturally occurring hyperadrenocorticism. J Vet Intern Med; 2014; 28; 1239-43.
3. Midence JN, Drobatz KJ, Hess RS Cortisol concentrations in well-regulated dogs with hyperadrenocorticism treated with trilostane. J Vet Intern Med; 2015; 29; 1529-33.
4. Arteaga A, Dhand NK, McCann T et al. Monitoring the response of canine hyperadrenocorticism to trilostane treatment by assessment of acute phase protein concentrations. J Small Anim Pract; 2010; 51; 204-209.
5. Cook AK, Bond KG Evaluation of the use of baseline cortisol concentration as a monitoring tool for dogs receiving trilostane as a treatment for hyperadrenocorticism. J Am Vet Med Assoc; 2010; 237; 801-805.
6. Galac S, Biujtels JJCWM, Kooistra HS Urinary corticoid:creatinine ratios in dogs with pituitary-dependent hypercortisolism during trilostane treatment. J Vet Intern Med; 2009; 23; 1214-19.
7. Burkhardt WA, Boretti FS, reusch CE et al. Evaluation of baseline cortisol, endogenous ACTH, and cortisol/ACTH ratio to monitor trilostane treatment in dogs with pituitary-dependent hypercortisolism. J Vet Intern Med; 2013; 27; 919-923.
8. Boretti FS, Holzthum J, Reusch CE Lack of association between clinical signs and laboratory parameters in dogs with hyperadrenocorticism before and during trilostane treatment. SAT Schweizer Archiv fur Tierheilkunde; 2016; 158; 631-638.
9. Macfarlane L, Parkin T, Ramsey I Pre-trilostane and three-hour post-trilostane cortisol to monitor trilostane therapy in dogs. Vet Record; 2016; doi:10.1136/ vr.103744.






































































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