Page 162 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

152 ELECTROLYTE DISORDERS

concentration after excision of autonomously secreting calcium, but increased osteoclastic bone resorption and
parathyroid tissue. 233 calcium reabsorption from renal distal tubules may also
Ultrasound-guided chemical ablation was used safely contribute.
and effectively as an alternative treatment to surgery in Vitamin D intoxication and hypercalcemia may result
eight dogs with a solitary parathyroid gland mass and from excessive dietary supplementation or may be caused
hypercalcemia. 336 Serum tCa and iCa concentrations iatrogenically during the treatment of hypoparathyroid-
were within reference ranges 24 hours after treatment ism. Accurate dosing with cholecalciferol and
in seven dogs and within 5 days in one dog. Transient ergocalciferol is difficult because they have a slow onset
hypocalcemia developed in four dogs during the first 5 and prolonged duration of action. 40,530 Hypercalcemia
days after treatment; one dog required treatment for developed in 7 of 16 hypoparathyroid dogs during treat-
hypocalcemic tetany. Dysphonia was noted in two of ment with vitamin D and calcium salt supplementation. 40
eight dogs in this study, but Horner syndrome, laryngeal Ingestion of toxic plants that contain glycosides of
paralysis, and death were not encountered as has been calcitriol (e.g., Cestrum diurnum, Solanum malacoxylon,
described with ethanol injection of thyroid glands of and Trisetum flavescens) is a potential cause of hypercalce-
hyperthyroid cats. 213,592,612 It is likely that the low vol- mia in small animals. 428 Vitamin D toxicity associated
ume of ethanol injected into a single parathyroid mass with ingestion of C. diurnum has been reported in a
provides less potential for leakage beyond the parathyroid cat. 151 C. diurnum, day-blooming jessamine, has
mass. In a review of treatment of 110 dogs with primary achieved increasing popularity as a house plant and
hyperparathyroidism, 72% of ethanol ablation procedures should not be confused with jasmine, which is an indoor
resulted in a control of hypercalcemia. 464 Hypercalcemia climbing plant without active vitamin D metabolites. 85
resolved in 1 to 4 days, and remained within normal limits A diagnosis of hypervitaminosis D in dogs and cats
for a median of 540 days. increased with the introduction of cholecalciferol-
Ultrasonographically guided radiofrequency heat containing rodenticides in 1985, but this source of intox-
ablation of parathyroid masses in dogs has become the ication is less common today. Cholecalciferol bait is deliv-
preferred treatment at some referral hospitals. In one ered as pellets that are palatable to some animals and are
study, 11 dogs with either one or two masses on ultraso- very toxic when ingested. One manufacturer claimed a
nography were treated by radiofrequency heat following low hazard to dogs (oral median lethal dose, 88 mg/
anesthesia and insertion of a 20-gauge over-the-needle kg), but toxicity at a lower dosage (10 mg/kg) was
catheter into the mass. 455 Hypocalcemia developed in five demonstrated. 162,228 High-risk groups include dogs
of the eight successfully treated dogs, all of which weighing 12 kg or less and those younger than 9 months.
required treatment. The only other adverse effect was a Recovery from previous cholecalciferol toxicity can be a
transient voice change in one dog. In 49 dogs with pri- risk factor for subsequent occurrence because removal
mary hyperparathyroidism treated with heat ablation, of the source from the premises may not be possible. 112
90% of procedures resulted in a control of hypercalce- Toxicity in four cats has also been reported. 390,441 One
mia. 464 Hypercalcemia resolved in 1 to 6 days, and reason for the few reports of vitamin D toxicity in cats
remained within normal limits for a median of 581 days. is that they appear to be resistant to cholecalciferol toxic-
ity when the diet is otherwise complete and balanced. 534
Hypervitaminosis D Clinical signs are usually vague and include anorexia,
Hypervitaminosis D refers to toxicity resulting from lethargy, vomiting, tremors, constipation, and polyuria.
excess cholecalciferol (vitamin D 3 ) or ergocalciferol (vita- These signs are usually attributed to the effects of
min D 2 ). Metabolites of vitamin D can also exert toxicity, hypercalcemia. Hypercalcemia is reversible with early
and the term hypervitaminosis D has been extended clin- and aggressive therapy by providing enough time for
ically to include toxicity from 25-hydroxyvitamin D, 25-hydroxyvitamin D to be eliminated from the
107,149,162
dihydrotachysterol, and 1,25-dihydroxyvitamin D body. Death occurred in approximately 45%
(calcitriol), as well as newer analogues of calcitriol. Vita- of dogs after developing hypercalcemia from hypervita-
min D toxicity is better referred to as 25-hydroxyvitamin minosis D in early reports, 162,228,344,500 but the survival
D toxicity, because vitamin D is rapidly transformed into rate was higher in dogs of a later series. 107
this metabolite in vivo. 199 Vitamin D and its immediate Hypercalcemia usually develops within 24 hours after
metabolite, 25-hydroxyvitamin D, have little biologic ingestion, 228 and hypercalcemia is often severe unless
activity at physiologic concentrations because they have serum samples were obtained within 24 hours of inges-
low binding affinity for the VDR. Pharmacologic tion. Mild hyperphosphatemia is often noted. Azotemia
concentrations of 25-hydroxyvitamin D that occur dur- is initially absent but can develop subsequently. Serum
ing hypervitaminosis D exert hypercalcemic effects, creatinine concentration usually is less than 3 mg/dL
because 25-hydroxyvitamin D competes with calcitriol unless treatment has been delayed, in which case azotemia
for binding to the VDR in target tissues. 162,404 Hypercal- may be marked. It may take as long as 72 hours for
cemia results from increased intestinal absorption of azotemia to develop as a result of renal lesions caused