Page 1049 - Cote clinical veterinary advisor dogs and cats 4th

520 Hypoparathyroidism, Primary

○ Weakness, decreased activity (especially ○ Formulas to correct serum calcium to discontinued because dietary calcium is
usually adequate.
in cats) account for serum albumin or protein • Parenteral calcium administration is usually
VetBooks.ir ○ Facial rubbing Advanced or Confirmatory Testing needed while awaiting oral vitamin D and
concentrations are NOT recommended.
• Less common
oral calcium supplementation to take effect:
○ Biting/licking paws
○ Behavior changes (e.g., being restless,
evaluating concurrent serum ionized calcium
rate infusion (60-90 mg/kg q 24h; do not
nervous, anxious, aggressive, reluctant • Hypoparathyroidism is confirmed by ○ 10% calcium gluconate IV by constant-
to be touched) and PTH concentrations; both usually are add to bicarbonate-containing fluids). SQ
○ Excessive panting decreased. administration (p. 515) should not be used
○ Vomiting, diarrhea, weight loss • A low-normal serum PTH concentration due to the potential for calcinosis cutis
is inappropriate if ionized calcium is low; and skin necrosis. Calcium chloride is not
PHYSICAL EXAM FINDINGS in a patient with a low ionized calcium, a recommended; perivascular administration
• Neuromuscular signs; raised nictitans possible serum PTH concentration that is decreased can cause tissue necrosis and sloughing.
(cats) or low-normal supports a diagnosis of ○ Monitor serum calcium concentrations
• Additional findings may include hyper- hypoparathyroidism. q 12-24h and adjust dose to maintain
thermia (from muscle fasciculation), tense serum calcium concentration between
abdomen, thin body condition, or cataracts. TREATMENT 8-9.5 mg/dL (2.0-2.4 mmol/L). When
• Physical exam may be normal. serum calcium concentrations have been
Treatment Overview consistently above 8 mg/dL (2 mmol/L)
Etiology and Pathophysiology • The goal of therapy is to increase serum total for 48 hours, parenteral calcium can be
• Naturally occurring disease is most com- calcium above the threshold for clinical signs tapered and discontinued over 3-5 days
monly due to immune-mediated destruction and maintain it just below or at the low by increasing the dosing interval.
or idiopathic atrophy of the parathyroid end of the reference range (e.g., 8-9.5 mg/ Maintenance/long-term chronic treatment:
glands. Hypoparathyroidism can also result dL [2-2.4 mmol/L]). Lifelong therapy for • Vitamin D should be slowly tapered to the
from parathyroid or thyroid surgery. primary hypoparathyroidism is required. lowest dose possible to maintain low-normal
• In normal animals, hypocalcemia results in Hypocalcemia caused by parathyroidectomy or slightly below normal calcium concentra-
increased PTH secretion. However, with can be transient as long as ≥ 1 parathyroid tions. Lifelong therapy is required for primary
hypoparathyroidism, the parathyroid glands gland remains. hypoparathyroidism.
are unable to respond. • Therapy must be individualized, and frequent
• Loss of PTH results in sustained, potentially monitoring and adjustment of drug dosages Possible Complications
severe hypocalcemia and hyperphosphatemia. are required. Overtreatment resulting in • Overzealous treatment with vitamin D may
○ Hypocalcemia results from decreased hypercalcemia must be avoided. result in hypercalcemia and soft-tissue (renal)
calcium resorption from bone, decreased • The need for acute emergency therapy varies, mineralization.
intestinal calcium absorption, and depending on the severity of presenting signs. • Severe, extensive calcinosis cutis and epi-
increased renal calcium excretion. • Referral is indicated if 24-hour care and dermal necrosis after SQ administration of
○ Hyperphosphatemia occurs due to in-house serum calcium monitoring cannot calcium gluconate for hypoparathyroidism
decreased renal phosphate excretion. be provided during the stabilization period. have been described in dogs and a cat.
• Loss of the membrane-stabilizing effect • Because lack of PTH results in hyperphos-
of ionized calcium on nerve cells causes Acute General Treatment phatemia and calcitriol increases intestinal
increased central and peripheral nervous For hypocalcemic tetany (p. 515) phosphorus absorption, hyperphosphatemia
tissue excitability. may occur. A low-phosphorus diet (e.g.,
Chronic Treatment formulated for chronic kidney disease) and a
DIAGNOSIS Subacute/early chronic treatment: phosphate binder (e.g., aluminum hydroxide)
• Oral vitamin D may be indicated.
Diagnostic Overview ○ Calcitriol is the preparation of choice.
Concurrent hypocalcemia and hyperphospha- It is faster- and shorter-acting than Recommended Monitoring
temia in a patient with normal renal function ergocalciferol and much less likely to • During the stabilization phase, patients
strongly suggests primary hypoparathyroidism. cause hypercalcemia but more expensive. should be observed 24 hours/day for seizures
The diagnosis is confirmed by evaluating Initial dosage: 0.01-0.015 mcg/kg PO q and other signs of hypocalcemia.
concurrent serum ionized calcium and PTH 12h × 3-4 days. Maintenance dosage: • Initially, serum calcium and phosphorus
concentrations. 0.005-0.015 mcg/kg PO q 24h. Time to concentrations should be measured at least
maximal effect is 1-4 days. Time required q 12h, then with decreasing frequency as
Differential Diagnosis for relief of toxicosis is 1-14 days. serum calcium concentration stabilizes.
Hypocalcemia (pp. 515 and 1239) ○ Ergocalciferol is rarely used due to its When patients are stable on maintenance
long half-life and potential for persistent oral vitamin D therapy, evaluation of serum
Initial Database hypercalcemia (up to 18 weeks). calcium and phosphorus concentrations is
• CBC and urinalysis: unremarkable ○ Dihydrotachysterol is no longer available. recommended q 3-6 months.
• Serum biochemical profile: hypocalcemia • Oral calcium
and hyperphosphatemia, normal renal ○ Dose: 25 mg/kg elemental calcium q PROGNOSIS & OUTCOME
parameters. Measure serum magnesium (Mg) 8-12h
as well. ○ The amount of elemental calcium per With careful treatment and monitoring,
• Confirm hypocalcemia. tablet varies with the preparation (p. prognosis is excellent.
○ Repeat calcium measurement on a separate 1205). Calcium carbonate is preferred;
blood sample. Use of EDTA plasma or 750 mg of calcium carbonate contains PEARLS & CONSIDERATIONS
EDTA contamination of sample causes a 300 mg of elemental calcium.
falsely low result. ○ After serum calcium concentration is stable Comments
○ Measure serum ionized calcium concentra- and the patient is eating well, oral calcium • Always measure serum Mg in a patient with
tion. can be tapered over 2-3 weeks and then apparent primary hypoparathyroidism. If

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