Challenging cases in internal medicine: A dog with an enlarged prostate and bloody preputial discharge - Veterinary Medicine
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Challenging cases in internal medicine: A dog with an enlarged prostate and bloody preputial discharge
These clinicians puzzled over this neutered dog's clinical signs and diagnostic test results, which seemed to indicate a disease only found in intact males.


Definitive diagnosis and treatment

Figure 3: A normal testicle obtained from a young male dog after routine orchiectomy (left) and the testicle obtained surgically from the patient in this report (right). The white arrows indicate the vas deferens of the normal testicle. The black arrows indicate the absence of a vas deferens in the testicle on the right.
Before we performed an abdominal exploratory, another abdominal ultrasonographic examination was conducted to search for evidence of retained testicular tissue. Again, detailed abdominal ultrasonographic evaluation revealed no findings consistent with retained testicular tissue. However, ultrasonographic evaluation of the subcutaneous tissues cranial to the scrotum on the left side identified tissue consistent with testicular tissue. Firm pressure applied medially to this region caused the testicle to become palpable just cranial to the scrotum, but release of this pressure caused the testicle to return to its deep subcutaneous site, again making it nonpalpable on routine scrotal palpation. With this new information, a castration was performed after the testicle was identified during surgical exploration of the prescrotal subcutaneous tissues on the dog's left side. Gross examination of the testicle revealed the absence of a vas deferens (Figure 3). The dog recovered from the exploratory successfully and was discharged pending histopathologic examination of the testicular tissue.

Histopathologic examination of this testicle revealed an interstitial (Leydig) cell tumor along with testicular atrophy and degeneration with aspermia. There was no microscopic evidence of a vas deferens in any section of the testicle evaluated. The epididymis was devoid of sperm, and no evidence of a vas deferens arising from the epididymal tissue was noted.

Figure 4: A lateral radiograph of the caudal abdomen taken seven weeks after castration. The black arrow indicates a much smaller prostate compared with presurgical radiographs (Figure 1). The white arrow indicates the urinary bladder.
Recheck examination of this dog seven weeks after the castration revealed a markedly smaller prostate on rectal palpation compared with previous examinations. Additionally, the preputial discharge had resolved. Repeat abdominal radiographs confirmed the absence of prostatomegaly noted on previous examinations (Figure 4).


Benign prostatic hyperplasia

Benign prostatic hyperplasia is a common, spontaneous, age-related condition in sexually intact male dogs. The condition increases in frequency with age, and nearly 95% of intact male dogs are affected by 9 years of age.1 Mild inflammatory changes in the prostate are commonly associated, without bacteria.2 Benign prostatic hyperplasia commonly causes no clinical signs in affected animals; however, if the prostate gland is markedly enlarged, a dog may experience constipation, tenesmus, or thin stools secondary to dorsal prostatic compression of the rectum.1-4 Also, intermittent, clear to light-yellow to hemorrhagic urethral discharge may occur in some dogs. Although signs consistent with urethral compression such as dysuria or stranguria are common in affected men, they are rarely present in dogs.1 At the time of initial presentation, this dog may have had a staphylococcal prostatitis, but this was not confirmed. Confirmation would have required quantitative culture of prostatic fluid obtained by aspiration, ejaculation, or prostatic massage. It is evident that antimicrobial therapy did not eliminate the urethral discharge, while castration did.

Table 5: Testosterone Concentrations in Normal Intact Dogs and Dogs with Common Testicular Disorders*
The pathophysiology of benign prostatic hyperplasia is not completely understood, but dihydrotestosterone, which is irreversibly converted from testosterone by the action of 5α-reductase in prostatic epithelial cells, is accepted as a key hormone in stimulating enhancement of prostate growth.1,4,5 Other hormones (estrogen, prolactin, growth hormone) have been implicated in its pathophysiology as well.1,4 The dog in this report had circulating testosterone concentrations well within the ranges expected for intact dogs despite its castrated status. However, there are conflicting reports regarding serum testosterone concentrations in cryptorchid dogs. One group of researchers reported no significant difference in serum testosterone concentrations between unilaterally cryptorchid dogs and normal control dogs.6 In contrast, another group of researchers7 reported a tendency for lower serum testosterone concentrations in unilaterally and bilaterally cryptorchid dogs during sexual development as compared with normal age-matched dogs both before and after administration of a luteinizing hormone-releasing hormone analogue.8 Blood testosterone concentrations may help differentiate among intact, castrated, and bilaterally cryptorchid dogs (Table 5).9

Diagnosing benign prostatic hyperplasia involves noting typical clinical signs and detecting prostatic enlargement by palpation and abdominal imaging. Palpating the dog in this report revealed an enlarged, symmetric, and nonpainful prostate, which is consistent with benign prostatic hyperplasia. Complete blood count and serum chemistry profile findings are typically unaffected by uncomplicated hyperplasia, while urinalysis results may be normal, or may reveal hematuria without pyuria or bacteriuria.1,3,4 The mild azotemia noted in this dog was not present on subsequent examinations. We suspected a prerenal cause such as subclinical dehydration or a high-protein meal rather than a renal azotemia since the urine specific gravity was 1.032.10 The mild thrombocytopenia and hepatosplenomegaly were considered clinically insignificant in this dog; however, potential exposure to tick-borne pathogens was not determined serologically. The hypercholesterolemia was likely associated with postprandial hypercholesterolemia, as these samples were obtained when the dog was not fasted. The mild hypercalcemia noted on initial examination was considered consistent with the mild hemoconcentration and was not present in subsequent serum chemistry profile results. The results of all other diagnostic tests (abdominal radiography and ultrasonography, prostatic biopsy and fine-needle aspiration, and prostatic fluid cytology) were deemed consistent with a diagnosis of benign prostatic hyperplasia.

Treatment of benign prostatic hyperplasia is required only when clinical signs warrant, as was the case with the dog in this report. The most effective treatment is castration, which decreases prostate size by 50% within three weeks postoperatively and by 70% within nine weeks.1,4 In this dog, the prostate size was reduced and the clinical signs were completely alleviated by seven weeks after surgery. Several medical options (e.g. diethylstilbestrol, progestins, flutamide, finasteride, tamoxifen citrate) are available for breeding animals or those with inherent anesthetic risks, but none are as effective (physiologically or cost-wise) as castration, and the use of some of these drugs is associated with side effects.1-5


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