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Hypocalcemia 515

every 7 days after diagnosis until stable. After PEARLS & CONSIDERATIONS Client Education
electrolytes are stabilized, recheck monthly Comments It is important to educate clients that this disease
VetBooks.ir • With DOCP, see above. • This disease can mimic others that are more administer therapy (or delayed administration) Diseases and Disorders
for 3-6 months, then q 3-6 months.
requires lifelong treatment and that failure to
may result in a life-threatening crisis. They must
• Subsequent ACTH stimulation testing is of
common (acute kidney injury/anuria, hepatic
no use in patients with spontaneous hypoad-
hypoadrenocorticism is commonly missed
renocorticism; adjustment of prednisone dose disease, GI disease), and the diagnosis of also understand the need for glucocorticoid
dose adjustment in times of stress.
is based on clinical signs while adjustment initially. The CBC can provide a valuable
of mineralocorticoid is based on measured clue; absence of a stress leukogram in an ill SUGGESTED READING
electrolytes. animal suggests hypoadrenocorticism. Lathan P: Hypoadrenocorticism in dogs. In Rand
• DOCP is expensive. Reductions in the dose J, editor: Clinical endocrinology of companion
PROGNOSIS & OUTCOME used or increases in the dosing interval can animals, Ames, IA, 2013, Wiley-Blackwell, pp 1-21.
help control cost. However, initial monitor-
• With treatment and monitoring, prognosis is ing to establish an effective dose/interval is AUTHOR: Patty Lathan, VMD, MS, DACVIM
EDITOR: Ellen N. Behrend, VMD, PhD, DACVIM
excellent, and a normal life span is expected. essential to avoid potentially life-threatening
• At the time of diagnosis of hypoadrenocorti- complications.
cism, azotemia with concurrent isosthenuria
should not be taken to indicate renal failure Technician Tips
and does not necessarily influence the prog- • Make sure that the ACTH is given IV for
nosis (see Pearls & Considerations below). the diagnosis of hypoadrenocorticism.
With treatment of hypoadrenocorticism, • Owners can be taught to give SQ injections
renal function usually returns to normal. of DOCP at home.

Hypocalcemia

BASIC INFORMATION HISTORY, CHIEF COMPLAINT ○ Increasing osteoclastic bone resorption of
Often, complaints relate to underlying cause calcium and phosphorus
Definition of hypocalcemia rather than to hypocalcemia ○ Increasing calcium and decreasing phos-
Serum total calcium < 9.0 mg/dL (<2.2 mmol/L) itself. However, there may be neurologic and/ phorus resorption from renal tubules
dogs; < 8.0 mg/dL (<2.0 mmol/L) cats; or serum or neuromuscular signs (often of abrupt onset). ○ Stimulating conversion of vitamin D
ionized calcium < 5.0 mg/dL (<1.2 mmol/L) • Signs may be intermittent despite persistent to its active form by the renal enzyme
dogs; < 4.5 mg/dL (<1.1 mmol/L) cats hypocalcemia. 1-alpha-hydroxylase
○ Facial rubbing, pawing at face • Inactive vitamin D is absorbed in the
Epidemiology ○ Ear twitching intestine; transported to the liver, where it
SPECIES, AGE, SEX ○ Nervousness, excessive panting is hydroxylated to 25-dihydroxyvitamin D;
• Dogs and cats of either sex and any age; ○ Stiff, stilted, rigid gait it is then transported to the kidney, where
predispositions depends on underlying ○ Muscle tremors it is hydroxylated by 1-alpha-hydroxylase to
cause ○ Seizures the active metabolite 1,25-dihydroxyvitamin
○ Eclampsia (p. 281) D (calcitriol).
○ Hypoparathyroidism (p. 519) PHYSICAL EXAM FINDINGS • Vitamin D increases serum calcium and
○ Protein-losing enteropathy (p. 600) Often, exam findings are related to underlying phosphorus by
cause of hypocalcemia. However, signs may ○ Increasing intestinal absorption of calcium,
RISK FACTORS include phosphorus, and magnesium
• Homemade diets • Muscle rigidity, fasciculations ○ Facilitating PTH-induced bone resorption
• Lactation • Hyperthermia ○ Increasing renal tubular resorption of
• Massive transfusion • Tachyarrhythmias, soft heart sounds, weak calcium and phosphorus
• Parathyroidectomy or bilateral thyroidectomy pulses • Calcitonin decreases serum calcium and
• Phosphate enema • Raised nictitating membranes (cats) phosphorus by
• Protein-losing enteropathy ○ Blocking bone resorption
Etiology and Pathophysiology ○ Decreasing renal tubular resorption of
Clinical Presentation • Calcium homeostasis: 50% of total circulat- calcium and phosphorus
DISEASE FORMS/SUBTYPES ing calcium is ionized (biologically active
Asymptomatic hypocalcemia (common): form), 40% is bound to albumin (storage DIAGNOSIS
• Incidental finding on blood tests form), and 10% is complexed to anions
• Hypocalcemia is mild or has been chronic. (storage form). Diagnostic Overview
Clinical hypocalcemia (less common): • Clinical signs of hypocalcemia occur only The diagnosis is suspected based on the presence
• Patient presented for signs related to when the ionized form is decreased. of facial pruritus, muscle fasciculations, stiff gait,
hypocalcemia. • Serum calcium concentration is tightly and/or seizures, or more often, hypocalcemia
• Hypocalcemia is moderate to severe or has regulated by parathyroid hormone (PTH), is discovered on serum chemistry profile.
developed acutely. vitamin D, and calcitonin. Confirmation requires measurement of ionized
• PTH increases serum calcium by calcium concentration (p. 1320).

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