Page 182 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

172 ELECTROLYTE DISORDERS

decrease renal synthesis of calcitriol. Decreased developed in about 6% of cats postthyroidectomy. 399
concentrations of calcitriol contribute to hypocalcemia Hypocalcemia resolved in all cats within 6 days
via decreased intestinal calcium absorption. Hypocalce- with therapy. Bilateral thyroidectomy results in loss of
mia unrelated to low PTH concentrations may arise the two internal parathyroid glands, and hypoparathy-
from increased uptake of calcium by bone after rapid roidism is permanent in patients in which the external
correction of long-standing hyperparathyroidism or parathyroid glands are completely removed during bilat-
hyperthyroidism, both of which are associated with loss eral thyroidectomy. Hypocalcemia and hypoparathyroid-
of bone calcium before treatment (“hungry bone” ism do not develop if the two external parathyroid glands
syndrome). 548,567,617 are not excised or damaged during thyroidectomy.
Definitive diagnosis of primary hypoparathyroidism is Normocalcemia can be maintained with one completely
based on the combination of clinical signs (see Box 6-5), functional parathyroid gland.
low iCa concentration, and PTH concentration Hypoparathyroidism is usually transient when the
inappropriatelylow to the magnitude ofionized hypocalce- external parathyroid glands are retained but have their
mia. Hypoparathyroidism is the only possible diagnosis blood supply disrupted (parathyroid gland ischemia after
when low serum calcium concentration, high serum physical trauma, vessel stretching, suture, cautery, or
phosphorus concentration, normal renal function, and transection) during surgery. Permanent hypoparathy-
low PTH concentration are present in combination. Low roidism is rare, but it may take as long as 3 months to
serum calcium and high serum phosphorus concentrations be certain whether remaining parathyroid tissue can
can be encountered during nutritional and renal secondary recover by hyperplasia. 51,446,504 Similar injury to parathy-
hyperparathyroidism, after phosphate-containing enemas, roid glands can occur during any extensive surgery of the
241,301
and during tumor lysis syndrome, but PTH is increased neck in dogs or cats or after exploration of the neck
in all of these conditions. for unilateral parathyroid gland removal. Restored vascu-
PTH should be measured in patients with lar supply to damaged parathyroid tissue seems unlikely as
chronic hypocalcemia of undetermined cause. Primary the mechanism for recovery from hypocalcemia. It is
hypoparathyroidism requires lifelong treatment, and con- more likely that hyperplasia and hypertrophy of parathy-
firmation of the diagnosis with PTH measurement is roid gland remnants left behind during surgery or ectopic
recommended. It is not necessary to measure PTH rou- parathyroid tissue achieve sufficient mass to synthesize
tinely in patients with postsurgical hypocalcemia because adequate amounts of PTH. Experimental cats subjected
this effect is usually transient and the cause obvious. PTH to parathyroidectomy predictably developed hypocalce-
concentrations should be determined for patients in mia and low serum PTH concentration, but, interest-
which hypocalcemia does not resolve. Absolute hypo- ingly, the hypocalcemia resolved, although the PTH
parathyroidism is present if a PTH concentration below concentrations remained low. 188 Autotransplantation of
the reference range is detected simultaneously with hypo- parathyroid tissue after bilateral thyroparathyroidectomy
calcemia. Relative hypoparathyroidism is present if PTH was associated with reduced morbidity and rapid return
concentration is inappropriately low but remains within of serum calcium concentrations to normal in experimen-
the normal reference range. Increased serum phosphorus tal cats. 425
and decreased calcitriol concentrations provide further Long-standing ionized hypercalcemia causes normal
support for a diagnosis of hypoparathyroidism. 232 parathyroid tissue to atrophy. If hypercalcemia is
nonparathyroid in origin, PTH concentrations will
Causes of Hypoparathyroidism already be low. Rapid correction of hypercalcemia results
The causes of hypoparathyroidism can be divided into in hypocalcemia because the atrophic parathyroid glands
three categories: (1) suppressed secretion of PTH with- cannot respond immediately to the need for increased
115,145
out parathyroid gland destruction, (2) sudden cor- PTH secretion. Surgical removal of a single parathyroid
rection of chronic hypercalcemia, and (3) absence or gland tumor (usually an adenoma) commonly causes
destruction of the parathyroid glands. The most common postoperative hypocalcemia in this manner. Hypocalce-
category of hypoparathyroidism in dogs and cats is mia severe enough to require treatment is likely to
absence or destruction of the parathyroid glands. develop within 24 to 48 hours. Nearly 50% of dogs with
Postoperative hypocalcemia developed 1 to 3 days primary hyperparathyroidism can be expected to develop
after thyroidectomy in approximately 20% to 30% of clinical signs of hypocalcemia 3 to 6 days after surgical
cats. 51,187,190,223,609 Some cats developed hypocalcemia removal of a parathyroid gland tumor. Hypocalcemia is
as late as 1 to 2 weeks after surgery. The surgical tech- more likely to develop in dogs with higher presurgical
nique used for thyroidectomy influences the chances that iCa concentrations. More than one half of hyperpar-
hypocalcemia will develop, and hypocalcemia occurred in athyroid dogs exhibit a rapid decrease in serum iCa con-
more than 80% of cats when original extracapsular tech- centration that normalizes within 24 hours of surgery.
nique was used. 187 When a modified intracapsular dissec- Serum iCa concentrations in the remaining dogs usually
tion technique was used, transient hypocalcemia normalize by 2 or 3 days after surgery, but some require as