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.
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.
Amy Holford, VMD, DACVIM
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.