Page 166 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

156 ELECTROLYTE DISORDERS

concentration can dramatically increase or decrease daily factors. Acidosis can magnify the effects of hypercalcemia
during treatment suggests that its origin is related to at all serum calcium concentrations by shifting more cal-
extracellular or intravascular fluid volume dynamics. cium to the ionized fraction. The serum phosphorus con-
A favorable outcome is possible in about 50% of centration at the time of hypercalcemia is also an
cases, but several weeks of hospitalization with intensive important modulating factor in clinical decision making
fluid treatment is often needed in those with AIRF, because soft tissue mineralization is potentiated by
especially if oliguric. About 50% of affected dogs can be hyperphosphatemia. Animals with rapid and progressive
expected to develop oliguria or anuria. 169,230,363 Acase development of hypercalcemia usually display serious
of AIRF with a fatal outcome occurred after ingestion of clinical signs that require aggressive therapy.
450 grams of raisins in a vizsla dog despite intensive
treatment, including peritoneal dialysis. 437 Aggressive Definitive Therapy
treatment has been recommended for any dogs suspected Removaloftheunderlyingcauseisthedefinitivetreatment
of having ingested large, or even small, quantities of grapes forhypercalcemia.Mostanimalswithpathologichypercal-
or raisins, including induction of emesis, gastric lavage, and cemia have an associated malignancy that is quickly
administration of activated charcoal, followed by intrave- diagnosed but often not readily treated. Complete exci-
nousfluidtherapyforaminimumof48hours. 230 However, sion of isolated neoplasms (e.g., apocrine gland adenocar-
somedogsmayconsumerelativelylargequantitiesofgrapes cinoma of the anal sac and parathyroid gland adenoma)
or raisins without development of ill effects. abolishes hypercalcemia. In animals with disseminated
Hypercalcemia was reported in a dog with a metastases, multicentric neoplasia, or nonresectable pri-
retained fetus and endometritis. 248 Serum PTH was mary malignancy, the tumor burden and hypercalcemia
suppressed, and 25-hydroxyvitamin D concentration may be decreased by appropriate chemotherapy, radiation
waswithinthenormalrange.Biopsyoftheremoveduterus therapy, and immunotherapy. Chemotherapy may disrupt
documented neutrophilic inflammation but no granulo- neoplastic cellular metabolism to such an extent that
matous inflammation as a possible cause of the hypercalce- the tumor may no longer be able to synthesize enough
mia. Serum iCa was normal 4 days after surgical removal of humoral factors to sustain hypercalcemia. Decreased
the uterus, and serum tCa was normal 6 weeks later. serum calcium concentrations can occur despite a lack of
Humoral hypercalcemia of benignancy is a phrase used obvious reduction in tumor size in these instances.
to describe the association of humoral factors such as Antifungal treatment with amphotericin B, ketocona-
PTHrP and hypercalcemia in the absence of malig- zole, or itraconazole effectively lowers increased serum
nancy. 197,302 One dog with massive mammary gland calcium concentrations in dogs with systemic mycoses
hyperplasia, severe ionized hypercalcemia, and increased as the infectious agent is eradicated and inflammation
PTHrP in the absence of malignancy at necropsy has been resolves. For animals with hypercalcemia associated with
observed (Chew, unpublished observations). This phe- hypoadrenocorticism, replacement therapy with
nomenon has rarely been described in humans. 278,292 mineralocorticoids and glucocorticoids after fluid vol-
ume replacement definitively manages the condition.
TREATMENT OF HYPERCALCEMIA Discontinuing all vitamin D supplementation in animals
with hypervitaminosis D and hypercalcemia removes
Philosophy of Treatment the external cause of intoxication, but excessive body
There is no absolute serum calcium concentration that stores of vitamin D may continue to contribute to hyper-
can be used as a guideline for the decision to treat hyper- calcemia for several weeks.
calcemia aggressively. 113,184 The magnitude of hypercal-
cemia, its rate of development, whether the serum Supportive Therapy
calcium concentration is stable or progressively increas- Supportive therapy is often necessary to decrease serum
ing, and the modifying effects of other electrolyte and calcium concentration to a less toxic level while waiting
acid-base disturbances must all be considered when for a definitive diagnosis to be established, for definitive
deciding on a treatment plan. The clinical condition of treatment to reduce serum calcium concentration perma-
the animal ultimately dictates how aggressive treatment nently, or for chronic management of hypercalcemia when
should be, but a serum calcium concentration of the underlying cause cannot be removed. Box 6-3 and
16 mg/dL or greater has been recommended as a basis Table 6-3 list the general and specific treatments for
for aggressive therapy. 184 Animals with serum calcium the management of hypercalcemia. Unfortunately, no sin-
concentrations approaching 20 mg/dL should be con- gle treatment protocol is consistently effective for all
sidered candidates for crisis management. Animals with causes of hypercalcemia. Consequently, regimens must
serum calcium concentrations less than 16 mg/dL may be tailored for the individual patient. Supportive
also require aggressive treatment, depending on the treatments reduce the magnitude of hypercalcemia by
degrees of neurologic, cardiac, and renal dysfunction increasingrenalcalcium excretion,inhibitingboneresorp-
induced by the hypercalcemia and concurrent deleterious tion, promoting soft tissue deposition of calcium, causing