Clinical Rounds: Anal sac adenocarcinoma - Veterinary Medicine
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Clinical Rounds: Anal sac adenocarcinoma
Make rounds with these veterinary specialists and residents for a complete picture of this neoplasia in dogs.



Anal sac adenocarcinoma accounts for about 17% of perianal tumors in dogs. Most affected dogs are older (average age, 10 to 11 years), and some, though not all, studies report a predisposition in females.1-4 Clinical signs may include tenesmus or perineal swelling, although the mass may be an incidental finding in one-third of animals.1-4 A diagnosis of anal sac adenocarcinoma is suspected based on a palpable thickening of the anal sac or a mass in that region, particularly in dogs with hypercalcemia or sublumbar lymph node enlargement. Definitive diagnosis is based on cytologic examination of an aspirate or histologic examination of a biopsy sample.

Medical perspective
Amy Holford, VMD, DACVIM

Amy Holford, VMD, DACVIM
Paraneoplastic syndrome with resultant hypercalcemia and hyperphosphatemia is noted in 25% to 50% of dogs with anal sac adenocarcinoma.1-4 Dogs with hypercalcemia may not exhibit any clinical signs or may exhibit polyuria, polydipsia, muscular weakness, vomiting, and constipation. Animals with hypercalcemia of malignancy associated with anal sac adenocarcinoma have a decreased parathyroid hormone (PTH) concentration and an increased PTH-related protein concentration.5 In contrast, dogs with primary hyperparathyroidism have no measureable PTH-related protein concentration and normal or increased PTH concentration in the face of an increased ionized calcium concentration.

Besides the clinical signs listed above, hypercalcemia may also result in renal failure from metastatic mineralization, particularly if the calcium-phosphorus product is > 60 to 80.5 Mild hypercalcemia with no evidence of renal failure does not require aggressive therapy if the patient is able to maintain adequate hydration. Acute treatment of marked hypercalcemia includes rehydration if the patient is dehydrated and subsequent saline diuresis at two to three times maintenance fluid rates.5

Once dogs are well-hydrated and volume-expanded, furosemide is administered (5 mg/kg initial intravenous bolus, followed by 2 to 4 mg/kg every eight to 12 hours orally, intravenously, or subcutaneously) during diuresis to promote calcium excretion in the urine. Diuresis and furosemide treatments may be continued until the calcium-phosphorus product decreases to < 60. Electrolytes and magnesium concentrations should be monitored, and supplementation should be provided when necessary. Additional treatments include corticosteroids and bisphosphonates such as pamidronate. Corticosteroids decrease bone resorption and intestinal absorption of calcium and promote renal calcium excretion. Dogs are commonly treated with prednisone or prednisolone (1 to 2 mg/kg orally b.i.d.), and gastroprotectants may be administered concurrently.5 Bisphosphonates inhibit osteoclastic activity and, therefore, bone resorption. In dogs with decreased renal function, the toxicity of bisphosphonates can be minimized by administering them as a two-hour infusion rather than a one-time injection. The infusion can be repeated in one to four weeks if the patient is still hypercalcemic.

During treatment of severe hypercalcemia, hydration should be frequently assessed by physical examination (body weight, skin turgor, mucous membrane wetness) and, in critical patients, by measurement of central venous pressures. Use of diuretics or bisphosphonates in a patient that is dehydrated or has renal compromise can be extremely dangerous, potentially resulting in renal failure or exacerbation of already present renal disease.


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