Introduction

Acute abdominal pain with diverse etiologies is commonly evaluated in the small animal emergency room. Seminoperitoneum is an uncommon cause in dogs with few cases reported.^1–3 Seminoperitoneum is defined as spermatozoa within the peritoneal cavity.⁴

Spermatozoa are normally immune-privileged due to the presence of a blood–testis barrier (BTB). Sertoli cell tight junctions and gap junctions create this barrier of the seminiferous epithelium.^5–7 Immune cells of the canine testes reside in the interstitial compartment and blood vessels. T lymphocytes and macrophages are the only immune cells present normally.⁷ The immune system creates a response when the BTB is disrupted.

Autoimmune orchitis is a cause of infertility in dogs, characterized by an increase in T and B lymphocytes, plasma cells, and macrophages, with possible antisperm antibodies within the testes. These cells are also found within the seminiferous tubules, demonstrating disruption of the BTB.^6,7

Spermatozoa extravasation may occur from a chronic spermatocele at the site of a previous vasectomy, testicular and epididymal injury, epididymal congenital occlusion, stenosis or occlusion of the genital tract secondary to infectious orchitis and epididymitis, or degeneration of the seminiferous epithelium with aging. The extravasated fluid elicits an inflammatory response comprised primarily of macrophages and some lymphocytes. This chronic granulomatous inflammation and fibrosis results in a spermatozoa granuloma.^1,8–10

Scrotal contents are considered an extension of the abdominal cavity because the surrounding vaginal tunic is continuous with the peritoneum.¹¹ Semen within the peritoneal cavity incites an inflammatory response comprised of nondegenerate neutrophils that phagocytize the spermatozoa along with macrophages.^3,4 In many mammals, rare complications of seminoperitoneum include formation of antisperm antibodies, anaphylaxis, septic peritonitis, and formation of adhesions.^2,3

Previous case reports theorized mechanisms of seminoperitoneum in female dogs such as the pressure of the copulatory lock forcing semen retrograde through uterine tubes and disruption of a recently ligated uterine stump. The latter had evidence of peritonitis secondary to Escherichia coli infection, suspected to be from the male or female genitalia.^2,3 Copulatory lock pressure may have an increased risk of causing seminoperitoneum with mismatch breeding (i.e., large dog and small bitch) or a diseased genital tract at risk of perforation. Vaginal mucosa injury is less likely because, to prepare for the copulatory lock, there is estrogen-induced thickening during proestrus.³ A report described rupture of the uterine body; however, spermatozoa were not detected in the peritoneal effusion. β-Hemolytic streptococcus from the male or female genitalia was suspected to be at least a component of peritonitis, with or without apparent seminoperitoneum.² Traumatic perforation of the genital tract during artificial insemination may also be considered.³

There are fewer reported cases of seminoperitoneum in male dogs. A report of an adult male Chihuahua described a uroperitoneum as well as peritoneal extracellular and phagocytosed spermatozoa and lubricant gel. The mechanism of this seminoperitoneum was postulated to be either traumatic urethral catheterization and retrograde hydropropulsion of a cystine urolith or transient urinary bladder leakage after cystocentesis.¹²

A report of an adult male Weimaraner with a history of an intra-abdominal vasectomy described a seminoperitoneum and inflammatory peritoneal effusion. This dog had a suspected spermatocele on ultrasound, indicating an accumulation of sperm in the ductus deferens and potential leakage of sperm at the previous vasectomy site. It was not definitive if these findings were incidental or the cause of the dog’s lethargy, inappetence, and discomfort; however, it is the only known report of seminoperitoneum as a complication of a vasectomy.¹ This case report describes another example of a seminoperitoneum associated with peritoneal effusion and inflammation in a vasectomized dog.

Case Report

An 8 yr old male German shorthaired pointer was presented to the University of Wisconsin Veterinary Care (UWVC) emergency service with a 2 hr history of acute onset kyphosis, a stilted gait, and excessive panting. He had no other clinical signs of systemic illness. There was no witnessed trauma, breeding event, mounting behavior, or known toxin exposure. He was a hunting dog in Northern Wisconsin but had not been hunting for several months. Significant medical history includes a vasectomy performed under the care of previous owners at an unknown age.

The dog presented to UWVC with abdominal pain, an enlarged painful left testis, scrotal edema, and an enlarged nonpainful prostate. No other clinically significant findings were observed from the musculoskeletal examination, neurologic examination, and the remainder of the physical examination.

Imaging Diagnostics

A point of care ultrasound revealed scant peritoneal effusion, and abdominal radiographs revealed prostatomegaly. An abdominal ultrasound revealed an enlarged prostate that was heterogeneously hyperechoic with smooth margins and multiple small round anechoic structures throughout. The abdominal ultrasound also confirmed a small amount of anechoic free fluid within the peritoneum and retroperitoneum along the left kidney. The peritoneal effusion was aspirated and submitted for cytology and culture.

The testes were subjectively enlarged with heterogeneous echotexture on ultrasound. The epididymides were enlarged and heterogeneously hypoechoic with moderate flow on color Doppler. The ductus deferentes were markedly enlarged and tortuous at the level of the testicles with ill-defined proximal portions (Figure 1).

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Imaging diagnoses of the urogenital system included bilateral orchitis and epididymitis secondary to either infectious (i.e., bacterial such as Brucellosis spp, fungal, viral) or noninfectious inflammatory etiologies. An infiltrative neoplastic process could not be ruled out at this time. The enlarged ductus deferentes may have been secondary to the reported vasectomy or to inflammation related to the orchitis and epididymitis. The prostatic changes were interpreted as benign prostatic hyperplasia and prostatic cysts, consistent with the intact status; however, prostatitis could not be ruled out.

The remainder of the abdominal ultrasound revealed a mildly diffusely heterogeneous spleen with normal flow on color Doppler, likely representing splenic extramedullary hematopoiesis or lymphoid hyperplasia. These splenic changes may also represent infectious splenitis or an infiltrative neoplasm. The caudal pole of the left adrenal gland was mildly enlarged at 0.83 cm (expected maximal dimension of 0.74 cm),¹³ likely a normal variant but may represent functional or nonfunctional nodular hyperplasia, adenoma, or a neoplasm (i.e., adenocarcinoma, pheochromocytoma). The right adrenal gland size was within reference limits with a small hyperechoic focus of the caudal pole, likely representing dystrophic mineralization or fibrosis. The liver, gallbladder, kidneys, urinary bladder, pancreas, gastrointestinal tract, and lymph nodes appeared normal.

Additional Diagnostics

Blood work included a venous blood gas, biochemical profile, and complete blood count. The alkaline phosphatase activity was moderately elevated at 408 U/L (reference interval 20–157 U/L), and the remainder of the blood work had no significant abnormalities. Differentials for the moderately increased alkaline phosphatase activity include primary and secondary hepatopathy and hyperadrenocorticism considering the mildly enlarged left adrenal gland.

A urinalysis and urine aerobic culture obtained via cystocentesis revealed a pH of 8.0, 2+ protein, 4+ protein sulfosalicylic acid, a specific gravity of 1.054, no casts seen, 1–5 red and white blood cells per high-power field, rare transitional cells, few triple phosphate crystals, no bacteria seen, minimal debris, and no bacterial growth. A urinary protein to creatinine ratio was not performed.

The peritoneal effusion was submitted for cytologic analysis and aerobic culture. Total protein and total nucleated cell count were not performed owing to particulate material within the specimen. Two direct smears, two squash preparations of the particulate material, and a cytocentrifuged slide were prepared. The samples were highly cellular, and nucleated cells were predominantly poorly preserved neutrophils. Neutrophils occasionally contained phagocytosed sperm head, sperm tails, or both. Many sperm heads, with and without tails, were free in the fluid background (Figure 2). There were fewer macrophages, eosinophils, and lymphocytes. The interpretation was seminoperitoneum with marked neutrophilic inflammation. The peritoneal effusion aerobic culture and serum Brucella canis rapid slide agglutination test were both negative.

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Discussion

Vasectomy, involving disruption of the ductus deferens, is an uncommon surgical sterilization technique in the dog.^1,14 The ductus deferens can be accessed by exteriorization with a prescrotal approach or by laparoscopy with an intra-abdominal approach.^14–16 However, because a vasectomy does not hinder steroidogenesis, orchiectomy is the recommended alternative, which diminishes unwanted sexual behaviors and androgen-dependent diseases.^1,14–16 Reported complications of vasectomy in the dog include transitory orchitis, hydrocele, incisional complications (e.g., self-trauma, swelling, seroma, cellulitis, infection, dehiscence), and recurrent autogenic scrotal dermatitis.^1,8,9,15

Spermatoceles and sperm granulomas are additional potential complications. The previously described report of a Weimaraner suggested the plausibility of direct extravasation of spermatozoa into the peritoneal cavity resulting from an intra-abdominal vasectomy and formation of spermatocele. The German shorthaired pointer in this case report was diagnosed with orchitis and epididymitis based on enlarged epididymides and ductus deferentes; however, these findings also may be evidence of spermatoceles. The technique of this dog’s vasectomy is unknown, but an intra-abdominal approach is reasonable to consider given the development of seminoperitoneum.

Both the Weimaraner and German shorthaired pointer had cytologic evidence of extracellular and phagocytosed spermatozoa in the peritoneal effusion, which contribute, at least in part, to peritoneal inflammation and effusion formation and possibly to the German shorthaired pointer’s acute abdominal pain and the Weimaraner’s discomfort. The Weimaraner’s reported discomfort was not further localized or definitively determined to be a result of the seminoperitoneum. The German shorthaired pointer’s acute abdominal pain also could be referred genitalia pain from periorchiepididymitis.

In the absence of testicular histopathology, other etiologies of periorchiepididymitis cannot be ruled out, including autoimmune, infectious (e.g., E coli, Proteus vulgaris, Staphylococcus sp., Streptococcus sp., blastomycosis and other fungi, Mycoplasma canis, Rickettsia rickettsia, and canine distemper virus), neoplastic, and traumatic.^18–21 The testicular ultrasound findings are similar to those seen with spermatic cord torsions, although bilateral torsions are less likely.^19,22

Conclusion

This case is the second known reported seminoperitoneum in a vasectomized dog. The pathophysiology of the seminoperitoneum was not definitively determined. Bilateral orchiectomy with histopathology would have provided more detail. This information was lost to follow-up. This case emphasizes the importance of thoroughly evaluating the urogenital system in vasectomized dogs presenting with acute abdominal pain or peritoneal effusion. Additionally, abdominal ultrasound and ruling out peritoneal effusion or other intra-abdominal abnormalities should be considered in vasectomized dogs presenting with urogenital abnormalities.