Page 1276 - Clinical Small Animal Internal Medicine

1214 Section 11 Oncologic Disease

gland. If surgery cannot be performed, clinical symp- Diagnosis and Treatment
VetBooks.ir toms may be managed with trilostane (Vetoryl®) or op‐ The finding of a urine osmolality higher than that of
DDD (Lysodren®). Trilostane is a competitive inhibitor of
serum in the face of hyponatremia is suggestive of
3‐beta‐hydroxysteroid dehydrogenase, thereby reducing
cortisol synthesis from the adrenal gland. The inhibition SIADH. Careful water restriction will improve clinical
symptoms while the cause is elucidated. Water restric-
of steroid production is rapidly reversible and dose tion must be monitored closely to avoid rapid fluctua-
dependent. Effects on cortisol production will wane tions in serum sodium concentrations. SIADH has been
within 10–20 hours after cessation of the drug. Lysodren described rarely with tumors in dogs (such as salivary
is directly cytotoxic to the cells of the zona fasciculata carcinoma). This condition is more common with sys-
and zona reticularis of the adrenal cortex. As approxi- temic diseases, such as cholangiohepatitis, congenital
mately 50% of cortical adrenal tumors are malignant, op‐ hydrocephalus, and meningitis. Therefore, water restric-
DDD is the theoretical medical therapy of choice though tion could lead to dehydration if the patient is clinically
studies evaluating survival and disease‐free interval of ill. With chronic hyponatremia, the serum sodium con-
dogs with adrenocortical carcinoma treated with trilos- centrations should not increase at a rate greater than
tane vs op‐DDD are lacking. 0.5 mEq/L/h or 8–10 mEq/day to avoid cerebral fluid
Management of symptoms may be made easier by the
use of trilostane, as the side‐effects are generally found to shifts. Due to the paucity of reports of this disease in the
veterinary literature, the prognosis is unpredictable and
be less severe. Lysodren may be difficult to administer in dependent on the underlying condition.
a clinically ill animal, as it causes nonselective adrenal
cortical necrosis and could result in a relative hypoad-
renocortical state. This could be difficult to manage in Erythrocytosis
the ill patient due to the length of time needed to recover
from excessive adrenal gland destruction. Trilostane, Etiology/Pathophysiology
however, will have no effect on delaying the progression
of metastatic disease. Erythrocytosis is defined as an increase in red blood cell
Therefore, in the case of nonsurgical metastatic dis- parameters (hematocrit, red blood cell count, hemo-
ease, Lysodren may be more effective at prolonging sur- globin). It may also be referred to as polycythemia. This
vival due to the cytotoxic effects on metastatic tissue. condition may be classified as relative or absolute.
Trilostane has been used successfully to control clinical A relative polycythemia is an apparent increase in red
symptoms of Cushing disease caused by an adrenal blood cell mass that is actually due to a decrease in
tumor in the absence of metastases. The use of trilostane plasma volume. This is commonly noted with dehydra-
or op‐DDD for the medical management of an adrenal tion and may be treated with fluid therapy to offset the
tumor should be carefully considered by the clinician if reduction in plasma volume. A relative polycythemia
surgery is not feasible. would be expected to be associated with normal (or low)
erythropoietin levels.
An absolute polycythemia may be subclassified as pri-
Syndrome of Inappropriate mary or secondary. Primary polycythemia is independ-
Antidiuretic Hormone Secretion ent of erythropoietin influence and arises from
progenitor cells within the bone marrow. The expanded
red blood cell mass appears morphologically normal,
Etiology/Pathophysiology
and bone marrow aspiration suggests erythroid hyper-
Syndrome of inappropriate antidiuretic hormone secre- plasia. Primary polycythemia is classified as a myelopro-
tion (SIADH) is commonly discussed but rarely diag- liferative disease, and is often referred to as polycythemia
nosed in the small animal patient. Much more common vera. It may rarely progress to leukemia.
in human medicine, SIADH is frequently diagnosed in An absolute polycythemia that is classified as second-
patients with pulmonary cancer (oat cell carcinoma). ary is dependent on erythropoietin influence. This may
Excessive production of ADH by the tumor cells results be an appropriate response, as seen with altitude changes,
in inappropriate free water retention. This leads to one of right‐to‐left cardiac shunting disorders and hereditary
the hallmark signs of the disorder, hyponatremia. Due to methemoglobin reductase deficiency. An inappropriate
excessive volume expansion, many elements within the polycythemic response may be seen with certain tumors,
blood may undergo dilutional effects, such as urea nitro- especially of the kidney.
gen and potassium. Serum osmolality is also low, but These tumors may produce erythropoietin ectopically,
urine osmolality may be higher than that of serum as free resulting in a paraneoplastic syndrome of erythrocyto-
water is being retained by the kidneys. sis. Several other mechanisms have been proposed to