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Hypercalcemia 491

Client Education SUGGESTED READING AUTHOR & EDITOR: Ellen N. Behrend, VMD, PhD,
• Efficacy of treatment for occult HAC is Behrend EN, et al: Occult hyperadrenocorticism: DACVIM
VetBooks.ir • If occult HAC warrants treatment and the veterinary therapy XV, St. Louis, 2014, Elsevier, Diseases and Disorders
unknown.
is it real? In Bonagura J, et al, editors: Current
patient responds, treatment is for life.
pp 221-224.
○ Hypoadrenocorticism is a potential com-
plication if trilostane or mitotane are used.

Hypercalcemia

BASIC INFORMATION • Various observations possible, depending on resorption of calcium from bone, pro-
underlying cause motes renal conservation of calcium, and
Definition ○ Lymphadenopathy possible with malig- enhances intestinal absorption of calcium.
Increase in serum total and/or ionized calcium nancy or granulomatous/fungal disease ○ 50% of PHPTH dogs have serum PTH
concentrations ○ Small kidneys in pets with CKD (p. 169). concentrations within reference limits,
○ Bone pain with some metastatic diseases indicative of autonomous and excessive
Epidemiology ○ Slow heart rate and/or poor pulse quality hormone secretion (e.g., adenoma)
SPECIES, AGE, SEX may be noted with hypoadrenocorticism • Hypercalcemia of malignancy: neoplastic
• Dogs or cats of either sex and any age, (p. 512). cells elaborate parathyroid hormone–related
depending on the underlying cause ○ Rectal palpation may reveal mass with anal protein (PTHrP; actions similar to parathy-
• Juvenile healthy dogs and cats: mild hyper- sac apocrine gland adenocarcinoma (ASAGA roid hormone).
calcemia is common. [p. 29]). Because anal sac masses may be • Granulomatous disease: elaboration of
• Hypercalcemia in adult dogs and cats is found incidentally, rectal palpation should PTHrP-like substances
always worrisome. be routine part of physical exam of dogs. • Idiopathic hypercalcemia of cats (poorly
understood) (p. 492)
GENETICS, BREED PREDISPOSITION Etiology and Pathophysiology ○ Rule out underlying neoplasia.
Depends on cause; inherited predisposition • Approximate reference ranges for serum total ○ Predisposed to urolith formation
for primary hyperparathyroidism (PHPTH) and ionized calcium concentrations: • CKD: renal secondary hyperparathyroidism
in the keeshond ○ Dogs: total: 9.5-11.5 mg/dL (2.32- • Vitamin D toxicosis (rodenticide or human
3.06 mmol/L); ionized: 1.2-1.4 mmol/L prescription medications such as calcipot-
CONTAGION AND ZOONOSIS ○ Cats: total 9.0-11.5 mg/dL (2.20- riene): heightened vitamin D–mediated
Common-source infections possible with 3.04 mmol/L); ionized: 1.2-1.4 mmol/L intestinal calcium absorption, renal calcium
systemic mycoses • Dystrophic, soft-tissue mineralization, conservation
specifically of nephrons, is more likely to • Juvenile: bone growth
GEOGRAPHY AND SEASONALITY occur if the product of calcium × phosphorus
Granulomatous diseases (systemic mycoses, concentrations > 60-80 mg/dL. DIAGNOSIS
schistosomiasis): specific geographic distributions • Approximately 50% of circulating calcium
is ionized, 40% is protein bound (mostly Diagnostic Overview
ASSOCIATED DISORDERS to albumin), and 10% is bound to other History, absence or presence of worrisome clinical
Mineralization of nephrons due to hyperphos- molecules (e.g., lactate, citrate). signs (e.g., anorexia, severe weight loss), physical
phatemia, despite serum calcium concentrations Dogs: exam, and serum phosphate concentrations
within reference ranges, may contribute to • The most common causes of hypercalcemia in should allow the differential diagnosis to be
progression of chronic kidney disease (CKD). dogs (% of affected dogs with hypercalcemia) refined, directing additional testing (p. 1233).
Hypercalcemia with low-normal to decreased include lymphoma (15%-30%), vitamin D
serum phosphate concentrations (e.g., PHPTH) toxicosis (expected), CKD (<5%), hypoad- Differential Diagnosis
is not commonly associated with tissue miner- renocorticism (≈25% in association with See above and Hypercalcemia (p. 1232).
alization or nephron damage. hyperkalemia), ASAGA (≈25%), PHPTH
(expected), multiple myeloma (≈20%), Initial Database
Clinical Presentation histoplasmosis (uncommon), blastomycosis • CBC: depends on cause (e.g., nonregenerative
HISTORY, CHIEF COMPLAINT (uncommon), and various other malignancies anemia if CKD; monocytosis if systemic
• Polyuria/polydipsia (p. 812) (uncommon). mycosis)
• Malaise: lethargy, weakness, inappetence, • In general, all these conditions in dogs are • Serum chemistry panel
weight loss; mild with hypercalcemia alone. associated with worrisome clinical signs, ○ Azotemia (i.e., increased blood urea
• Lower urinary tract signs in 30%-50% of dogs except dogs with PHPTH. nitrogen [BUN], creatinine, and phospho-
with PHPTH due to cystic calculi and/or Cats: rus): severe dehydration, kidney disease,
urinary tract infection (e.g., pollakiuria, stran- • Most commonly reported disease associa- hypoadrenocorticism
guria, hematuria, and apparent incontinence) tions are malignancy (lymphoma, squamous ○ Hyperkalemia: hypoadrenocorticism, acute
• If the underlying cause is a condition other cell carcinoma), kidney disease, idiopathic kidney injury; NOTE: in vitro hemolysis
than PHPTH (e.g., neoplasia, toxin, Addison’s hypercalcemia, and urolithiasis. can increase serum potassium in the Akita
disease), more worrisome signs may be present. • Less common disorders include PHPTH. and Japanese Tosa breeds.
Mechanisms of causative disorders: ○ Hypophosphatemia: PHPTH, hypercal-
PHYSICAL EXAM FINDINGS • PHPTH (p. 499) cemia of malignancy
• No physical finding is pathognomonic for ○ Autonomous secretion of parathyroid ○ Hyperphosphatemia: CKD, vitamin D
a specific cause of hypercalcemia. hormone (PTH) activates osteoclastic toxicosis, hypoadrenocorticism
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