Vol. 19, No.
1 January 1997 V HEINZ SYMPOSIUM 1996
Continuing Education Article
FOCAL POINT
★Endocrine disorders often cause
life-threatening emergencies in
small animals.
KEY FACTS
■ Addisonian “tip-offs” include a
normal or slow heart rate despite
circulatory shock and the waxing
and waning course before
collapse.
■ Endogenous corticotropin
must be measured before any
corticosteroids are given.
■ Patients with myxedema
or hypothyroid coma need
intravenous replacement of
thyroid hormone (5 µg/kg
every 12 hours).
■ In-house testing can confirm
the diagnosis of hypothyroidism
before emergency treatment
begins.
■ Calcitriol (0.25 µg orally every
48 hours) can be given for
a short time after surgical
thyroidectomy to prevent
hypocalcemia.
Endocrine
Emergencies. Part II.
Adrenal, Thyroid, and
Parathyroid Disorders
Colorado State University
Deborah S. Greco, DVM, PhD
D isorders of the thyroid gland, adrenal glands, and parathyroid gland
can cause life-threatening emergencies in small animals.
ADRENAL DISORDERS
Addisonian Crisis
One of the most well-recognized endocrine emergencies is classic addisonian
crisis.1–4 Brought on by a deficiency of adrenocortical steroids, the classic hy-
poadrenal crisis is manifested as severe, profound shock. Although most affect-
ed dogs and cats are presented in severe cardiovascular collapse, they often have
a recent history of vague, waxing and waning signs that presaged the onset of
collapse.1–4
Hypoadrenocorticism is most commonly diagnosed in young female dogs
and may be immune mediated. Historical findings compatible with hypoad-
renocorticism include intermittent vomiting, diarrhea, weight loss, lethargy,
anorexia, and weakness. These signs often resolve with fluid therapy and/or
corticosteroid treatment. Physical examination of animals in an acute hypoad-
renal crisis reveals weak pulses, bradycardia, prolonged capillary refill time, se-
vere mental depression, and profound muscle weakness. Addisonian “tip-offs”
include a normal or slow heart rate in the face of circulatory shock and the
waxing and waning course of signs prior to collapse.
Electrolyte abnormalities consisting of severe hyponatremia and
hypochloremia associated with hyperkalemia are the hallmarks of hypoadreno-
corticism. Although a sodium:potassium ratio below 1:27 suggests hypoad-
renocorticism, it is not pathognomonic. Gastrointestinal disease, acute renal
failure, and postrenal azotemia may also result in a low sodium:potassium ra-
tio. Azotemia and hyperphosphatemia also attend primary hypoadrenocorti-
cism, thus making it difficult to differentiate from acute renal failure.
Hematologic abnormalities consist of eosinophilia and lymphocytosis or
Small Animal The Compendium January 1997

normal eosinophil Glucocorticoid

and lymphocyte Screening Tests for Hypoadrenocorticism and mineralo-
counts in the face corticoid therapy
of severe meta- Corticotropin (ACTH) Stimulation Test must be initiated
bolic stress. The only after diag-
anemia of hypo- Protocol: • 0.5 U/kg aqueous corticotropin intravenously, nostics for hy-
adrenocorticism serum samples at 0 and 1 hour poadrenocorti-
has classically been Protocol: • 2.2 U/kg corticotropin gel intramuscularly cism have been
attributed to lack (maximum 20 U/dog), serum samples at 0 and 2 performed. Glu-
of glucocorticoid hours cocorticoid ther-
effects on bone apy, using ultra–
marrow; however, Normal levels: • Baseline 1–4 mg/dl (28–110 mmol/L); after short-acting cor-
recent studies sug- corticotropin: < 20 mg/dl (550 mmol/L) ticosteroid esters
gest that hemor- (e.g., dexameth-
rhagic gastroen- Endogenous Corticotropin asone sodium
teritis contributes Protocol: • Single plasma sample (may be collected before phosphate and
significantly to screening test and frozen for later analysis); collect prednisolone
the anemia.2 Hy- in EDTA vacuum tube (with aprotinin), centrifuge sodium succi-
poglycemia is and store in plastic, ship at 4°C (or frozen if not nate) is indicat-
more common collected in aprotinin) ed. Dexametha-
with secondary or sone does not
Normals: • 20–80 pg/ml (4.4–8.8 pmol/L)
atypical hypoad- interfere with
re n o c o r t i c i s m ; the cortisol assay
however, hypo- and may be pre-
glycemia is an unusual manifestation of hypoadrenocorti- ferred if the animal requires immediate glucocorticoid ad-
cism in dogs.2 ministration. Furthermore, a single dose of short-acting
Diagnosis of primary hypoadrenocorticism is based corticosteroid will not suppress the hypothalamic–
on appropriate clinical signs and classic electrolyte im- hypophysial–adrenal axis and therefore will not interfere
balances and is confirmed with a corticotropin with diagnostics.2
(ACTH) response test (see Screening Tests for Hypoad- Recent studies have emphasized the importance of
renocorticism). Intramuscularly injected corticotropin treating the gastrointestinal complications of hypoad-
(gel or synthetic) may not be absorbed if the animal is renocorticism.2 Some dogs with addisonian crisis die of
in circulatory shock. Intravenous administration of syn- gastrointestinal hemorrhage. The cause of the gastroin-
thetic corticotropin is preferred.2 Furthermore, the gel testinal hemorrhage is unknown but may be glucocorti-
is no longer available in some parts of the country. En- coid deficiency or poor intestinal perfusion caused by
dogenous corticotropin may be measured to determine shock. Treatment of anemia secondary to severe gas-
if the hypoadrenocorticism is primary (adrenal atrophy) trointestinal hemorrhage should include blood transfu-
or secondary (corticotropin deficiency); however, the sion coupled with gastrointestinal protectants (e.g., su-
test sample must be collected before any corticosteroids cralfate, H2 antagonists, and misoprostol).
are given. All dogs with hypoadrenocorticism should receive
Treatment of the addisonian crisis (see the protocol) gastrointestinal protectants and immediate glucocorti-
consists of fluid therapy, electrolyte stabilization, gluco- coid therapy after adrenal testing has been performed.
corticoid replacement therapy, treatment of gastroin- Mineralocorticoid supplementation, using oral fludro-
testinal hemorrhage, and mineralocorticoid replace- cortisone acetate (0.2 mg per 10 kg orally every 24
ment therapy. hours) or desoxycorticosterone pivalate (2 mg/kg intra-
Normal saline is the fluid of choice for hypoadrenal muscularly every 25 days), should be initiated only af-
crises; in fact, shock doses of normal saline alone are ter the results of dynamic adrenal testing have been re-
enough to reverse the circulatory shock caused by the viewed and hypoadrenocorticism confirmed.
renal loss of sodium and chloride resulting from aldos-
terone deficiency. Hyperkalemia often resolves with flu- Pulmonary Thromboembolism
id therapy alone. The article on electrolyte imbalances Secondary to Hyperadrenocorticism
in this issue of Compendium describes treatment of life- Pulmonary thromboembolism is an uncommon re-
threatening hyperkalemia. sult of hyperadrenocorticism but is often fatal.5 Dogs

FLUID THERAPY ■ GLUCOCORTICOID ■ MINERALOCORTICOID ■ GASTROINTESTINAL PROTECTANTS

The Compendium January 1997 Small Animal

PROTOCOL FOR TREATMENT OF HYPOADRENAL CRISIS

Step Drug or Fluid Dosage Side Effects Caution

Step 1: Fluids 0.9% Saline ≤90 ml/kg/hr Overhydration Monitor central venous
pressure

Step 2: Electrolytes Calcium gluconate 5–15 mg/kg Bradycardia Monitor electrocardiogram

if hyperkalemia Insulin 0.5 U/kg
is life-threatening
Dextrose 2 g/U of insulin Hypoglycemia Monitor electrocardiogram
Bicarbonate 1–2 mmol/kg Alkalosis Monitor blood pH
intravenously over
5–15 min

Step 3: Glucocorticoid Dexamethasone 2–4 mg/kg None None

sodium phosphate intravenously
Prednisolone 30 mg/kg None Do not use before
succinate intravenously corticotropin response test

Step 4: Restoration Sodium See discussion Alkalosis Monitor pH, bicarbonate

of acid–base balance bicarbonate of diabetic
ketoacidosis in
Part I

Step 5: Treatment Whole blood Depends on — Monitor packed cell volume

of gastrointestinal transfusion packed cell every 4 hours
hemorrhage volume, body
weight
Misoprostol 2–5 µg/kg —
orally three
times a day
Ranitidine 2 mg/kg
intravenously or
orally twice a day —

undergoing medical or surgical treatment for hyper-
adrenocorticism appear to be at increased risk for
thromboembolic complications. Recent studies have
shown that Cushing’s syndrome results in an increase in
vitamin K–dependent coagulation factors and a de-
crease in antithrombin III concentrations.6,7
Clinical signs of acute respiratory distress, including
orthopnea and jugular pulse, are common. Panting
may occur secondary to hypoxia and/or pleuritic pain.8
Radiographic signs may include hypoperfusion, alve-
olar pulmonary infiltrates, pleural effusion, increased
diameter and blunting of pulmonary arteries, lack of
perfusion of the obstructed pulmonary vasculature, and
overperfusion of the unobstructed pulmonary vascula-
ture.5,9 However, many dogs with pulmonary throm-
boembolism have normal radiographs. Normal radio-
graphs despite severe dyspnea suggest pulmonary
thromboembolism.
Blood gas analysis reveals hypoxemia (50 to 60 mm
Hg) and hypocapnia (17 to 30 mm Hg), which result
from panting. Blood gas analysis following oxygen ad-
ministration often reveals a moderate to marked in-
crease in arterial blood oxygen content except in those
animals with severe pulmonary thrombosis or concur-
rent pulmonary disease.9
Treatment of pulmonary thromboembolism sec-
ondary to hyperadrenocorticism consists of oxygen
therapy and medical treatment to prevent the forma-
tion of more blood clots. Medical therapy for pul-
monary thromboembolism is best achieved via the use

COAGULATION FACTORS ■ RADIOGRAPHIC SIGNS ■ BLOOD GAS ■ PREVENTING CLOTS

Small Animal The Compendium January 1997

TABLE I
Drugs Used in the Treatment of Thyrotoxicosis

Drug Dose Route and Frequency Mechanism

Propylthiouracil 11 mg/kg Orally three times a day Impairs peripheral

deiodination of T4 to T3

Dexamethasone 2–4 mg/kg Intravenously, Impairs peripheral

sodium phosphate subcutaneously, or orally deiodination of T4 to T3

Propranolol 2.5–7.5 mg Orally twice or three times Impairs peripheral

a day deiodination of T4 to T3

Thiamine hydrochloride 1–2 mg Intramuscularly every 24 hours Reverses thiamine deficiency

Saturated solution One drop in Orally every 24 hours Blocks release of T4

of potassium iodide gelatin capsule from thyroid

of heparin initially, followed by anticoagulant vitamin
K antagonists. The prognosis is very poor—most of the
dogs die or are euthanatized within a week of a throm-
boembolic episode.9
THYROID DISORDERS
Thyrotoxicosis
Thyrotoxic crisis (“thyroid storm”) occasionally oc-
curs in human patients with hyperthyroidism sec-
ondary to Grave’s disease or toxic multinodular goiter.10
Hyperthyroid cats probably also suffer from thyrotoxic
crises. In fact, feline apathetic hyperthyroidism has
many of the same clinical features (e.g., anorexia and
congestive heart failure).11–13
Thyrotoxic crisis is manifested as severe hyperme-
tabolism characterized by fever, tachycardia, pulmonary
edema, or congestive heart failure. Early in the crisis,
tremulousness and restlessness may be accompanied by
frank delirium or psychosis.10 Nausea, anorexia, vomit-
ing, and pain may accompany the syndrome. As the
disorder progresses, apathy and stupor may occur as
blood pressure falls to hypotensive levels because of cir-
culatory failure.10 Clinicians should suspect thyrotoxic
crisis if a cat with a history of thyrotoxicosis or evidence
of previously undiagnosed thyroid disease (goiter) is
presented with pyrexia, tachycardia, or signs of conges-
tive heart failure.
Therapy for the crisis consists of efforts to inhibit
hormone synthesis and release and to antagonize adren-
ergically mediated aspects of peripheral thyroid hor-
mone action11,14 (Table I). In human medicine, propyl-
thiouracil is preferable to methimazole as initial therapy
for thyroid storm because it prevents peripheral conver-
sion of T4 to the active form (triiodothyronine [T3]).14
The use of propylthiouracil in cats, however, may be
limited because of serious side effects.15 Large doses of
dexamethasone may be given to inhibit T4 release from
the thyroid and peripheral generation of T3.10
A saturated solution of potassium iodide can be used
to acutely retard the release of hormone from the thy-
roid. However, cats dislike the taste of inorganic iodine,
so it must be enclosed in a capsule for oral administra-
tion.11
Cardiac manifestations should be treated using
β-blockers, such as propranolol.11 Pyrexia, if present,
should be addressed supportively by evaporative cool-
ing. Thiamine deficiency has been observed in apathet-
ic hyperthyroid cats; humans with thyroid storm also
improve after treatment with B vitamins.10,11 Both thi-
amine deficiency and hypokalemia are manifested as
ventroflexion of the neck.
Myxedema Coma
Myxedema coma in dogs is a rare complication of ca-
nine hypothyroidism and is observed in young to mid-
dle-aged dogs in breeds with a high incidence of
thyroid disease (e.g., Doberman pinschers). 16,17 In
myxedema coma, the dog becomes hypothermic, pro-
foundly weak, and exhibits a diminished level of con-
sciousness.17 Secondary signs include nonpitting edema,
mental dullness, depression, unresponsiveness, inappe-
tence, anorexia, and bradycardia.

HYPERTHYROIDISM ■ THIAMINE DEFICIENCY ■ HYPOTHYROIDISM

Small Animal The Compendium January 1997

TABLE II
Treatment of Hypocalcemia

Drug Dose Administration Comments

Emergency Treatment
Calcium gluconate 1.0–1.5 ml/kg Slow intravenous bolus to effect Monitor electrocardiogram; if
10% solution bradycardia, ventricular prema-
ture contractions or short Q-T
or interval, discontinue briefly. Do
not add to bicarbonate solution.

Calcium chloride 5–15 mg/kg Intravenously to effect Never give subcutaneously (causes
perivasculitis); monitor as above

To Maintain Serum Calcium

Calcium gluconate 60 mg/kg/day Constant-rate infusion Monitor electrocardiogram; if
10% solution bradycardia, ventricular prema-
ture contractions or short Q-T
or interval, discontinue briefly. Do
not add to bicarbonate solution.

1.0–1.5 ml/kg Subcutaneously every 6–8 hours Used to maintain serum calcium
>8 mg/dl

Vitamin D Therapy
Calcitriol 0.03–0.06 µg/kg Orally every 24 hours Avoid hypercalcemia
Dihydrotachysterol 0.02–0.03 mg/kg Orally every 24 hours Initial dose; switch to every 48
hours after several days

In humans and dogs, myxedema coma results from
myxedematous accumulations in the brain and severe
hyponatremia.10,16,17 Hyponatremia results from an in-
crease in total body water because of impaired renal ex-
cretion of water and retention of water by hydrophilic
deposits in tissue. The hyponatremia occurs despite a
concurrent decrease in plasma volume.10 Early recogni-
tion and aggressive therapy are crucial to survival.
Diagnostic differentials include metabolic abnormali-
ties (e.g., hypoglycemia, electrolyte imbalances, hypo-
adrenocorticism, and hepatoencephalopathy) and neu-
romuscular diseases (e.g., myasthenia gravis and
polyradiculoneuritis). Presumptive diagnosis should be
based on signalment (predisposed breed, age), clinical
signs (weakness, hypothermia, coma, bradycardia), and
supporting clinicopathologic features (i.e., hypercholes-
terolemia and hyponatremia).
Therapy should be initiated immediately—without
waiting for results of serum total thyroxine (T4) analy-
sis. With the advent of in-house thyroid testing units,
however, emergency total T4 analysis may be possible
and is recommended to differentiate myxedema coma
from other, more common causes of coma.
Levothyroxine should be administered intravenously
at a dosage of 5 µg/kg every 12 hours.11,16 Supportive
care, in the form of assisted ventilation and judicious
fluid therapy with 0.9% saline, may be indicated. Slow,
passive rewarming should be considered—but only af-
ter thyroid hormone supplementation because in-
creased oxygen requirements and decreased peripheral
vascular tone may exacerbate circulatory failure.17
PARATHYROID DISORDERS
Hypocalcemic Seizures
Prompt treatment of hypocalcemia is necessary to
prevent secondary complications, such as cerebral ede-
ma and hyperthermia. Hypocalcemia may be iatrogenic
(after thyroidectomy) or may result from chronic or
acute renal failure, acute pancreatitis, hypoalbumine-
mia, hypoparathyroidism, puerperal tetany, ethylene
glycol intoxication, intestinal malabsorption, and nutri-
tional secondary hyperparathyroidism.18–21 Early signs

IN-HOUSE THYROID TESTING ■ INTRAVENOUS LEVOTHYROXINE ■ FLUID THERAPY ■ REWARMING

The Compendium January 1997 Small Animal

of hypocalce- TABLE III tial signs of hy-

mia are nonspe- percalcemia are
Emergency Treatment of Hypercalcemia
cific and include polydipsia and
anorexia (espe- Fluid/Drug Dosage Comments polyuria result-
cially in cats); ing from im-
facial rubbing; 0.9% saline 120–180 ml/kg/day Increases renal calcium excretion paired response
ner v o u s n e s s ; intravenously of distal renal
and a stiff, stilt- tubules to vaso-
ed gait.18 Later, Furosemide 5 mg/kg/hr Volume expansion must precede pressin.23 List-
signs progress to intravenously furosemide administration lessness, depres-
paresthesias, hy- sion, and muscle
perventilation, Etridonate 7.5 mg/kg For 3–7 days or until serum calcium weakness result
and finally gen- intravenously over normalizes; based on human dose from depressed
eralized tet- 4 hours excitability of
any and/or seiz- neuromuscular
ures.18,19 EDTA 25–75 mg/kg hourly Chelator, nephrotoxic tissue. Mild gas-
Treatment of trointestinal
hypocalcemia Calcitonin 4 U/kg intramuscularly Until serum calcium normalizes signs of hyper-
(Table II) rapid- every 12 hours (cats) calcemia in-
ly resolves clini- clude inappe-
cal signs. Intra- 8 U/kg subcutaneously Until serum calcium normalizes tence, vomiting,
venous calcium every 24 hours (dogs) and constipa-
chloride or cal- tion.23
cium gluconate Bicarbonate 1–4 mEq/kg intravenously Decreases ionized fraction of Pe r s i s t e n t
is required im- every 4 hours calcium, may cause alkalosis mild elevations
mediately to in serum calci-
treat tetany and um (12 to 14
seizures. The protocol outlines treatment of hypocal- mg/dl) can cause uroliths and signs of urinary tract
cemia. Perivascular injection of calcium chloride can re- disease, such as hematuria and strangury. On the other
sult in calcinosis cutis and severe tissue trauma.18,20 Calci- hand, severe hypercalcemia (>14 mg/dl) can progress
um gluconate is less irritating to tissue, but a larger rapidly to acute renal failure when the calcium-phos-
volume must be given to achieve the same effect.18 phorus product (Ca2+ [mg/dl] × PO43- [mg/dl]) exceeds
The most convenient form of supplemental vitamin 60 to 80 because of mineralization of renal tissue.
D is vitamin D3 or calcitriol. If hypercalcemia results These patients require emergency therapy for hypercal-
from calcitriol administration, it will resolve within 48 cemia. Rapid treatment of hypercalcemia is essential to
hours after the drug is discontinued. A short-term preserve normal renal function and prevent the onset
course of calcitriol at a dose of 0.25 µg can be given of renal failure in a patient with treatable underlying
orally every 48 hours after surgical thyroidectomy to disease.
prevent hypocalcemia caused by inadvertent damage to Initial treatment of hypercalcemia includes fluid di-
the parathyroid gland.22 Similarly, dogs and cats under- uresis using sodium-containing fluids23–25 (Table III).
going parathyroidectomy for hyperparathyroidism may Once the animal has been rehydrated and extracellular
be started on an appropriate dose of vitamin D before fluid volume has been expanded by 3% to 5% using
surgery to prevent severe hypocalcemia after the proce- fluid therapy, pharmacologic diuresis may be induced
dure. with furosemide.25 Thiazide diuretics enhance calcium
Other emergency measures include monitoring body resorption in distal tubules and are therefore contra-
temperature and cooling the animal if hyperthermia is indicated.25 Once the cause of the hypercalcemia is
severe. Short-acting glucocorticoids can be given if identified, corticosteroids (2 mg/kg twice a day) may be
cerebral edema is suspected. used to increase renal excretion of calcium.
Although hypercalcemia of malignancy responds
Hypercalcemic Nephropathy to corticosteroid therapy, other causes of hypercalce-
Hypercalcemic nephropathy has numerous possible mia (e.g., hyperparathyroidism) do not.23 Furthermore,
causes, including hypercalcemia of malignancy, hyper- use of corticosteroids before a definitive diagnosis is
parathyroidism, and hypervitaminosis D.23–25 The ini- established may obscure the cause of hypercalcemia.

THYROIDECTOMY ■ VITAMIN D ■ UROLITHS ■ FLUID DIURESIS ■ CORTICOSTEROIDS

Small Animal The Compendium January 1997

Phosphonates (etridonate, pamidronate), calcitonin, corticism in ten cats. J Vet Intern Med 3(2):55–58, 1989.
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complete line of VLS books, journals, and videos.
VLS
VE T E R I N A RY
BOOKS
L E A R N I N G SYS T E M S 1982.
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