A 9-year-old castrated male miniature schnauzer was referred to The University of Tennessee Veterinary Medical Center (UTVMC)
for a postoperative oncology consultation. One month earlier, the dog had undergone resection of a 3-cm perianal mass that
was associated with the left anal sac and was firmly adherent to surrounding tissue. Apocrine gland adenocarcinoma had been
diagnosed on histologic evaluation, with surgical margins noted to be "clean but close."
On presentation to UTVMC, the dog was bright and alert. A small area of thickening was noted in the region of the excised
anal sac on digital rectal examination. No abnormalities were seen on a complete blood count and serum chemistry profile.
No evidence of metastatic disease was noted on thoracic or abdominal radiographs; cystic calculi were noted as an incidental
finding. Cytologic examination of an aspirate obtained from the perianal surgical site was difficult to interpret because
of low cellularity; however, findings were suggestive of apocrine gland adenocarcinoma. Surgical excision with biopsy was
recommended. No treatment was provided for the cystic calculi since they were not causing clinical signs.
In surgery, the thickened tissue was excised, along with 40% of the anal sphincter and a portion of the rectal wall. The mass
was marked with ink and sutures before submission. Histologically, the excised tissue included normal-appearing apocrine glands
and a well-demarcated nodule of apocrine gland adenocarcinoma cells that extended close to the deep (cranial) margin.
Postoperative complications included swelling, bruising, constipation, and fecal incontinence. Although anal tone was good,
the dog was unable to effectively terminate defecations because of scar tissue in the region. Because feces in the rectum
were large in diameter and hard on digital palpation, a warm-water enema was administered six days after surgery. The red
rubber catheter was advanced rostral to the rectal sutures to avoid traumatizing the site. Once the impacted feces were removed,
the dog defecated normally. The owners declined follow-up radiotherapy; rechecks were recommended with their veterinarian
every three months, and these were also declined.
Seventeen months after the second surgery, the dog was presented to the teaching hospital for ribbon-shaped feces and straining
to defecate. A left perianal mass (8 x 4.5 x 2.5 cm) and enlarged sublumbar lymph nodes were noted on physical examination.
A complete blood count and serum chemistry profile revealed increased total calcium (16.5 mg/dl; reference range = 10 to 11.9
mg/dl) and ionized calcium (2.03 mmol/L; reference range = 1.26 to 1.39 mmol/L) concentrations. Abdominal radiographic and
ultrasonographic examinations revealed enlarged sublumbar lymph nodes (Figure 1) and a mass in the liver. Two nodules were noted in the pulmonary parenchyma on thoracic radiographs and fluoroscopy; these
were suspected to be metastases.
1. A lateral radiograph of the patient taken 18 months after an initial diagnosis of anal sac adenocarcinoma. Marked sublumbar
lymphadenopathy (arrows) and splenic enlargement are noted.
The dog was treated in the hospital with saline diuresis and, once the dog was well-hydrated, with furosemide to decrease
serum calcium concentrations. Prednisone was prescribed for continued calcium control, and stool softeners were prescribed
to ease defecation. Four days after the dog was released from the hospital, the total serum calcium concentration measured
by the referring veterinarian was normal.
At the two-week recheck, the perianal mass had enlarged slightly. Toceranib phosphate (Palladia—Pfizer Animal Health) therapy
was initiated, and the mass decreased in size within two weeks. After 28 days of treatment with toceranib, the mass size
was stable, and blood calcium concentrations remained normal. The toceranib was continued, and the prednisone was gradually
tapered over two weeks and then discontinued. Thirty-one days after toceranib treatment was initiated, the dog developed anorexia,
vomiting, and diarrhea. The toceranib was temporarily discontinued, and oral metronidazole was administered, after which the
diarrhea resolved. Anorexia and lethargy persisted, however, for seven days, at which time oral famotidine treatment was initiated.
Eleven days after toceranib was discontinued, the dog was reevaluated for persistent lethargy and decreased appetite. The
perianal mass and sublumbar lymph nodes had increased in size, and hypercalcemia (total calcium concentration = 17.3 mg/dl,
ionized calcium concentration = 2.23 mmol/L) was noted on a serum chemistry profile. Toceranib and prednisone therapy were
reinstituted, and the dog was treated with saline diuresis for 16 hours and a single dose of pamidronate (Aredia—Novartis
Pharmaceuticals). The dog's appetite and attitude improved after fluid administration. Its calcium concentrations subsequently
returned to normal, and the prednisone dose was decreased to once a day.
Over the next two months, the dog had intermittent bouts of lethargy, weakness, vomiting, and poor appetite that gradually
increased in frequency and duration and were correlated with the presence of hypercalcemia. Initially, clinical signs resolved
with administration of intravenous fluids, furosemide, famotidine, analgesics, and antiemetics; however, the dog eventually
failed to respond to supportive treatment, and blood urea nitrogen, creatinine, and phosphorus concentrations became mildly
increased. Twenty-three months after the initial surgery and three and a half months after toceranib treatment was initiated,
the dog was euthanized at the owners' request.