Page 149 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Calcium: Hypercalcemia and Hypocalcemia 139

Effects of Hypercalcemia on Other Organs hypercalcemia as transient or persistent, pathologic or
Anorexia, vomiting, and constipation can result from nonpathologic, mild or severe, progressive or static,
hypercalcemia by reduction of the excitability of gastroin- and acute or chronic is helpful in determining its cause.
Persistent, pathologic hypercalcemia occurs most often
testinal smooth muscle and from direct effects on the cen-
in association with malignancy. Most studies in dogs attri-
tral nervous system. Gastric hyperacidity and subsequent
bute hypercalcemia to malignancy in more than 50% of
gastric ulceration caused by increased secretion of gastrin 46,166,586
the cases, although in one series malignancy
and direct stimulation of hydrogen ion secretion from 314
accounted for only one third of the cases.
parietal cells by hypercalcemia may account for some of
Hypoadrenocorticism, renal failure, primary hyper-
the vomiting. Gastrin concentration was increased in four
parathyroidism, hypervitaminosis D, and inflammatory
of six dogs with hypercalcemia in one preliminary
report. 66 Increased gastrin concentration occurs second- disorders sporadically account for hypercalcemia in dogs.
In a study of 109 dogs with ionized hypercalcemia, 58%
ary to reduced renal clearance as a consequence of the
had underlying neoplasia, 17% had renal failure, 13% were
hypercalcemia. Decreased excitability of skeletal muscle
diagnosed with hyperparathyroidism, 5% had hypoadre-
contributestogeneralizedweakness.Lethargyiscommonly 375
nocorticism, and 3% had vitamin D toxicity. It is often
observed in severe hypercalcemia because of direct effects
difficult to determine the cause of hypercalcemia in
onthecentralnervoussystemandrarelycanprogresstostu-
por and coma. Seizures and muscle twitching are unusual animals with mild or transient hypercalcemia. No defini-
neuromuscular manifestations of hypercalcemia. 271 tive diagnosis could be made for 2% to 9% of hypercalce-
166,586
Clinically important cardiac effects of hypercalcemia mic dogs in two reports. No definitive diagnosis
are not commonly detected in dogs and cats, but PR– was reported in 13% of cats with hypercalcemia in one
interval prolongation and QT–interval shortening can report, but the actual percentage is much higher based
be observed on the electrocardiogram. Serious on sample submissions to veterinary endocrinology
511
arrhythmias (including ventricular fibrillation) can be laboratories.
caused by the direct effects of severe hypercalcemia or In serum samples from 332 hypercalcemic cats, 80%
had parathyroid-independent hypercalcemia, 10% had
may be a consequence of mineralization of cardiac tissue.
parathyroid-dependent hypercalcemia, and 10% were
Hypertension has been demonstrated in humans and rats 61
equivocal. Approximately 10% of these hypercalcemic
during both acute and chronic hypercalcemia. The
cats had PTHrP levels above the reference range,
increase in blood pressure is proportional to the increase
in serum calcium concentration in acute studies. 97 In a suggesting malignancy as the cause. Hypercalcemic cats
have parathyroid-independent hypercalcemia more com-
study of acute hypercalcemia, hypertension was
monly than dogs. Samples from 5722 hypercalcemic dogs
attributed to a direct effect of calcium on vascular smooth
from the same laboratory categorized the hypercalcemia
muscle and to an indirect effect of calcium to increase
as parathyroid dependent in about 40%, parathyroid
secretion of catecholamine with activation of adrenergic 466
receptors. 165 Whether hypertension is a clinically relevant independent in 50%, and equivocal in 10%.
complication in dogs and cats with hypercalcemia is GENERAL APPROACH TO
unknown.
DIAGNOSTIC WORKUP OF PATIENTS
MECHANISMS AND DIFFERENTIAL WITH HYPERCALCEMIA
DIAGNOSIS OF HYPERCALCEMIA It is important to ensure that the hypercalcemia initially
Increased entry of calcium into ECF, decreased egress of detected is repeatable, especially if the magnitude of
calcium from ECF, reduced plasma volume, or a combi- hypercalcemia is modest. The likely cause of the hypercal-
nation of these factors must occur for hypercalcemia to cemia will be obvious in some patients from findings in
develop (Fig. 6-11). Increased calcium input can arise the history (hypervitaminosis D) or from physical exami-
from increased intestinal absorption, increased bone nation (masses and effusions). When the cause is not
resorption, or increased renal tubular reabsorption of cal- immediately apparent, body cavity imaging with chest
cium. Decreased glomerular filtration and decreased radiographs, abdominal radiographs, and abdominal
bone accretion result in decreased egress of calcium from ultrasound is recommended to determine whether
ECF. Volume contraction is common in the presence of organomegaly or infiltrative processes are present that
hypercalcemia because of the effects of anorexia, could account for the hypercalcemia. Fine needle aspira-
vomiting, and obligatory polyuria. The mechanisms of tion, needle biopsy, or wedge biopsy of abnormal
hypercalcemia vary with the specific causes, but much tissues will often yield the cause of the hypercalcemia.
attention has been focused on the importance of Patients with cytopenia (neutropenia, anemia, and
increased bone resorption. thrombocytopenia) should undergo bone marrow evalu-
Box 6-2 provides a list of possibilities in the differential ation if the diagnosis has not already been established by
diagnosis of hypercalcemia. Characterization of the other means. Bone marrow evaluation in the absence of