Endocrine Emergencies.part2,Adrenal,Thyroid and Parathyroid Disorders

8/14/2019 Endocrine Emergencies.part2,Adrenal,Thyroid and Parathyroid Disorders

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Vol. 19, No. 1 January 1997 HEINZ SYMPOSIUM 1996

Continuing Education Article

FOCAL POINT

KEY FACTS

5Endocrine disorders often causelife-threatening emergencies in

small animals.

EndocrineEmergencies. Part II.

Adrenal, Thyroid, and

Parathyroid DisordersColorado State University

Deborah S. Greco, DVM, PhD

Disorders of the thyroid gland, adrenal glands, and parathyroid glandcan cause life-threatening emergencies in small animals.

ADRENAL DISORDERS

Addisonian CrisisOne of the most well-recognized endocrine emergencies is classic addisoniancrisis.14 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 havea recent history of vague, waxing and waning signs that presaged the onset ofcollapse.14

Hypoadrenocorticism is most commonly diagnosed in young female dogsand 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/orcorticosteroid 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-offsinclude 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 renalfailure, 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

V

s Addisonian tip-offs include a

normal or slow heart rate despite

circulatory shock and the waxing

and waning course before

collapse.

s Endogenous corticotropin

must be measured before any

corticosteroids are given.

s Patients with myxedema

or hypothyroid coma need

intravenousreplacement of

thyroid hormone (5 g/kg

every 12 hours).

s In-house testing can confirm

the diagnosis of hypothyroidism

before emergency treatment

begins.

s Calcitriol (0.25 g orally every

48 hours) can be given for

a short time after surgical

thyroidectomy to prevent

hypocalcemia.


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normal eosinophiland lymphocytecounts in the faceof severe meta-bolic stress. The

anemia of hypo-adrenocorticismhas classically beenattributed to lackof glucocorticoideffects on bonemarrow; however,recent studies sug-gest that hemor-rhagic gastroen-teritis contributessignificantly to

the anemia.

2

Hy-poglycemia ismore common

with secondary oratypical hypoad-renocort ic ism;however, hypo-glycemia is an unusual manifestation of hypoadrenocorti-cism in dogs.2

Diagnosis of primary hypoadrenocorticism is basedon appropriate clinical signs and classic electrolyte im-balances and is confirmed with a corticotropin

(ACTH) response test (see Screening Tests for Hypoad-renocorticism). Intramuscularly injected corticotropin(gel or synthetic) may not be absorbed if the animal isin circulatory shock. Intravenous administration of syn-thetic corticotropin is preferred.2 Furthermore, the gelis no longer available in some parts of the country. En-dogenous corticotropin may be measured to determineif the hypoadrenocorticism is primary (adrenal atrophy)or secondary (corticotropin deficiency); however, thetest sample must be collected before any corticosteroidsare given.

Treatment of the addisonian crisis (see the protocol)

consists of fluid therapy, electrolyte stabilization, gluco-corticoid replacement therapy, treatment of gastroin-testinal hemorrhage, and mineralocorticoid replace-ment therapy.

Normal saline is the fluid of choice for hypoadrenalcrises; in fact, shock doses of normal saline alone areenough to reverse the circulatory shock caused by therenal loss of sodium and chloride resulting from aldos-terone deficiency. Hyperkalemia often resolves with flu-id therapy alone. The article on electrolyte imbalancesin this issue ofCompendiumdescribes treatment of life-threatening hyperkalemia.

Glucocorticoidand mineralo-corticoid therapymust be initiatedonly after diag-

nostics for hy-poadrenocorti-cism have beenperformed. Glu-cocorticoid ther-apy, using ultrashort-acting cor-ticosteroid esters(e.g., dexameth-asone sodiumphosphate andp r e d n i s o l o n e

sodium succi-nate) is indicat-ed. Dexametha-sone does notinterfere withthe cortisol assayand may be pre-

ferred if the animal requires immediate glucocorticoid ad-ministration. Furthermore, a single dose of short-actingcorticosteroid will not suppress the hypothalamichypophysialadrenal axis and therefore will not interfere

with diagnostics.2

Recent studies have emphasized the importance oftreating the gastrointestinal complications of hypoad-renocorticism.2 Some dogs with addisonian crisis die ofgastrointestinal hemorrhage. The cause of the gastroin-testinal hemorrhage is unknown but may be glucocorti-coid deficiency or poor intestinal perfusion caused byshock. Treatment of anemia secondary to severe gas-trointestinal hemorrhage should include blood transfu-sion coupled with gastrointestinal protectants (e.g., su-cralfate, H2 antagonists, and misoprostol).

All dogs with hypoadrenocorticism should receivegastrointestinal protectants and immediate glucocorti-

coid therapyafteradrenal testing has been performed.Mineralocorticoid supplementation, using oral fludro-cortisone acetate (0.2 mg per 10 kg orally every 24hours) or desoxycorticosterone pivalate (2 mg/kg intra-muscularly every 25 days), should be initiated only af-ter the results of dynamic adrenal testing have been re-viewed and hypoadrenocorticism confirmed.

Pulmonary ThromboembolismSecondary to Hyperadrenocorticism

Pulmonary thromboembolism is an uncommon re-sult of hyperadrenocorticism but is often fatal.5 Dogs

Small Animal The Compendium January 1997

F L U I D T H E R A P Y s G L U C O C O R T I C O I D s M I N E R A L O C O R T I C O I D s G A S T R O I N T E S T I N A L P R O T E C T A N T S

Screening Tests for Hypoadrenocorticism

Corticotropin (ACTH) Stimulation Test

Protocol: 0.5 U/kg aqueous corticotropin intravenously,serum samples at 0 and 1 hour

Protocol: 2.2 U/kg corticotropin gel intramuscularly(maximum 20 U/dog), serum samples at 0 and 2hours

Normal levels: Baseline 14 mg/dl (28110 mmol/L); aftercorticotropin: < 20 mg/dl (550 mmol/L)

Endogenous Corticotropin

Protocol: Single plasma sample (may be collected beforescreening test and frozen for later analysis); collect

in EDTA vacuum tube (with aprotinin), centrifugeand store in plastic, ship at 4C (or frozen if notcollected in aprotinin)

Normals: 2080 pg/ml (4.48.8 pmol/L)


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undergoing medical or surgical treatment for hyper-adrenocorticism appear to be at increased risk forthromboembolic complications. Recent studies have

shown that Cushings syndrome results in an increase invitamin Kdependent coagulation factors and a de-crease in antithrombin III concentrations.6,7

Clinical signs of acute respiratory distress, includingorthopnea and jugular pulse, are common. Pantingmay occur secondary to hypoxia and/or pleuritic pain.8

Radiographic signs may include hypoperfusion, alve-olar pulmonary infiltrates, pleural effusion, increaseddiameter and blunting of pulmonary arteries, lack ofperfusion of the obstructed pulmonary vasculature, andoverperfusion 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 pulmonarythromboembolism.

Blood gas analysis reveals hypoxemia (50 to 60 mmHg) and hypocapnia (17 to 30 mm Hg), which resultfrom panting. Blood gas analysis following oxygen ad-ministration often reveals a moderate to marked in-crease in arterial blood oxygen content except in thoseanimals with severe pulmonary thrombosis or concur-rent pulmonary disease.9

Treatment of pulmonary thromboembolism sec-ondary to hyperadrenocorticism consists of oxygentherapy and medical treatment to prevent the forma-tion of more blood clots. Medical therapy for pul-monary thromboembolism is best achieved via the use

The Compendium January 1997 Small Animal

C O A G U L A T I O N F A C T O R S s R A D I O G R A P H I C S I G N S s B L O O D G A S s P R E V E N T I N G C L O T S

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 venouspressure

Step 2: Electrolytes Calcium gluconate 515 mg/kg Bradycardia Monitor electrocardiogramif hyperkalemia

Insulin 0.5 U/kgis life-threatening

Dextrose 2 g/U of insulin Hypoglycemia Monitor electrocardiogram

Bicarbonate 12 mmol/kg Alkalosis Monitor blood pHintravenously over515 min

Step 3: Glucocorticoid Dexamethasone 24 mg/kg None Nonesodium phosphate intravenously

Prednisolone 30 mg/kg None Do not use beforesuccinate intravenously corticotropin response test

Step 4: Restoration Sodium See discussion Alkalosis Monitor pH, bicarbonateof acidbase balance bicarbonate of diabetic

ketoacidosis inPart I

Step 5: Treatment Whole blood Depends on Monitor packed cell volumeof gastrointestinal transfusion packed cell every 4 hourshemorrhage volume, body

weight

Misoprostol 25 g/kg orally threetimes a day

Ranitidine 2 mg/kgintravenously ororally twice a day


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of heparin initially, followed by anticoagulant vitaminK antagonists. The prognosis is very poormost of thedogs die or are euthanatized within a week of a throm-boembolic episode.9

THYROID DISORDERSThyrotoxicosis

Thyrotoxic crisis (thyroid storm) occasionally oc-curs in human patients with hyperthyroidism sec-ondary to Graves disease or toxic multinodular goiter.10

Hyperthyroid cats probably also suffer from thyrotoxiccrises. In fact, feline apathetic hyperthyroidism hasmany of the same clinical features (e.g., anorexia andcongestive heart failure).1113

Thyrotoxic crisis is manifested as severe hyperme-tabolism characterized by fever, tachycardia, pulmonaryedema, or congestive heart failure. Early in the crisis,tremulousness and restlessness may be accompanied byfrank delirium or psychosis.10 Nausea, anorexia, vomit-

ing, and pain may accompany the syndrome. As thedisorder progresses, apathy and stupor may occur asblood pressure falls to hypotensive levels because of cir-culatory failure.10 Clinicians should suspect thyrotoxiccrisis if a cat with a history of thyrotoxicosis or evidenceof previously undiagnosed thyroid disease (goiter) ispresented with pyrexia, tachycardia, or signs of conges-tive heart failure.

Therapy for the crisis consists of efforts to inhibithormone synthesis and release and to antagonize adren-ergically mediated aspects of peripheral thyroid hor-mone action11,14 (Table I). In human medicine, propyl-


H Y P E R T H Y R O I D I S M s T H I A M I N E D E F I C I E N C Y s H Y P O T H Y R O I D I S M

thiouracil is preferable to methimazole as initial therapyfor 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 belimited because of serious side effects.15 Large doses ofdexamethasone may be given to inhibit T4 release fromthe thyroid and peripheral generation of T3.

10

A saturated solution of potassium iodide can be usedto 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-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 alsoimprove after treatment with B vitamins.10,11 Both thi-amine deficiency and hypokalemia are manifested as

ventroflexion of the neck.

Myxedema ComaMyxedema 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 ofthyroid disease (e.g., Doberman pinschers).16,17 Inmyxedema 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.

TABLE IDrugs Used in the Treatment of Thyrotoxicosis

Drug Dose Route and Frequency Mechanism

Propylthiouracil 11 mg/kg Orally three times a day Impairs peripheraldeiodination of T4 to T3

Dexamethasone 24 mg/kg Intravenously, Impairs peripheral

sodium phosphate subcutaneously, or orally deiodination of T4 to T3

Propranolol 2.57.5 mg Orally twice or three times Impairs peripheral

a day deiodination of T4 to T3

Thiamine hydrochloride 12 mg Intramuscularly every 24 hours Reverses thiamine deficiency

Saturated solution One drop in Orally every 24 hours Blocks release of T4of potassium iodide gelatin capsule from thyroid


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In humans and dogs, myxedema coma results frommyxedematous accumulations in the brain and severehyponatremia.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 hydrophilicdeposits in tissue. The hyponatremia occurs despite aconcurrent 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 andpolyradiculoneuritis). Presumptive diagnosis should bebased on signalment (predisposed breed, age), clinicalsigns (weakness, hypothermia, coma, bradycardia), andsupporting clinicopathologic features (i.e., hypercholes-terolemia and hyponatremia).

Therapy should be initiated immediatelywithoutwaiting 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 comafrom other, more common causes of coma.

Levothyroxine should be administered intravenouslyat a dosage of 5 g/kg every 12 hours.11,16 Supportivecare, in the form of assisted ventilation and judiciousfluid therapy with 0.9% saline, may be indicated. Slow,passive rewarming should be consideredbut only af-ter thyroid hormone supplementation because in-creased oxygen requirements and decreased peripheral

vascular tone may exacerbate circulatory failure.17

PARATHYROID DISORDERSHypocalcemic Seizures

Prompt treatment of hypocalcemia is necessary toprevent secondary complications, such as cerebral ede-ma and hyperthermia. Hypocalcemia may be iatrogenic(after thyroidectomy) or may result from chronic oracute renal failure, acute pancreatitis, hypoalbumine-mia, hypoparathyroidism, puerperal tetany, ethyleneglycol intoxication, intestinal malabsorption, and nutri-tional secondary hyperparathyroidism.1821 Early signs


I N - H O U S E T H Y R O I D T E S T I N G s I N T R A V E N O U S L E V O T H Y R O X I N E s F L U I D T H E R A P Y s R E W A R M I N G

TABLE IITreatment of Hypocalcemia

or

or

Drug Dose Administration Comments

Emergency Treatment

Calcium gluconate 1.01.5 ml/kg Slow intravenous bolus to effect Monitor electrocardiogram; if

10% solution bradycardia, ventricular prema-

ture contractions or short Q-T

interval, discontinue briefly. Do

not add to bicarbonate solution.

Calcium chloride 515 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

interval, discontinue briefly. Do

not add to bicarbonate solution.

1.01.5 ml/kg Subcutaneously every 68 hours Used to maintain serum calcium

>8 mg/dl

Vitamin D Therapy

Calcitriol 0.030.06 g/kg Orally every 24 hours Avoid hypercalcemia

Dihydrotachysterol 0.020.03 mg/kg Orally every 24 hours Initial dose; switch to every 48

hours after several days


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of hypocalce-mia are nonspe-cific and includeanorexia (espe-cially in cats);

facial rubbing;ne r vo u sne s s ;and a stiff, stilt-ed gait.18 Later,signs progress toparesthesias, hy-perventilation,and finally gen-era l ized tet -any and/or seiz-ures.18,19

Treatment of

hypocalcemia(Table II) rapid-ly resolves clini-cal signs. Intra-venous calciumchloride or cal-cium gluconateis required im-mediately totreat tetany andseizures. The protocol outlines treatment of hypocal-cemia. Perivascular injection of calcium chloride can re-

sult in calcinosis cutis and severe tissue trauma.

18,20

Calci-um gluconate is less irritating to tissue, but a largervolume must be given to achieve the same effect.18

The most convenient form of supplemental vitaminD is vitamin D3 or calcitriol. If hypercalcemia resultsfrom calcitriol administration, it will resolve within 48hours after the drug is discontinued. A short-termcourse of calcitriol at a dose of 0.25 g can be givenorally every 48 hours after surgical thyroidectomy toprevent hypocalcemia caused by inadvertent damage tothe parathyroid gland.22 Similarly, dogs and cats under-going parathyroidectomy for hyperparathyroidism may

be started on an appropriate dose of vitamin D beforesurgery to prevent severe hypocalcemia after the proce-dure.

Other emergency measures include monitoring bodytemperature and cooling the animal if hyperthermia issevere. Short-acting glucocorticoids can be given ifcerebral edema is suspected.

Hypercalcemic NephropathyHypercalcemic nephropathy has numerous possible

causes, including hypercalcemia of malignancy, hyper-parathyroidism, and hypervitaminosis D.2325 The ini-

tial signs of hy-percalcemia arepolydipsia andpolyuria result-ing from im-

paired responseof distal renaltubules to vaso-pressin.23 List-lessness, depres-sion, and muscle

weakness resultfrom depressedexcitability ofneuromusculartissue. Mild gas-t ro in te s t ina l

signs of hyper-calcemia in-clude inappe-tence, vomiting,and constipa-tion.23

P e r s i s t e n tmild elevationsin serum calci-um (12 to 14

mg/dl) can cause uroliths and signs of urinary tractdisease, such as hematuria and strangury. On the other

hand, severe hypercalcemia (>14 mg/dl) can progressrapidly to acute renal failure when the calcium-phos-phorus product (Ca2+ [mg/dl] PO4

3- [mg/dl]) exceeds60 to 80 because of mineralization of renal tissue.These patients require emergency therapy for hypercal-cemia. Rapid treatment of hypercalcemia is essential topreserve normal renal function and prevent the onsetof renal failure in a patient with treatable underlyingdisease.

Initial treatment of hypercalcemia includes fluid di-uresis using sodium-containing fluids2325 (Table III).Once the animal has been rehydrated and extracellular

fluid volume has been expanded by 3% to 5% usingfluid therapy, pharmacologic diuresis may be inducedwith furosemide.25 Thiazide diuretics enhance calciumresorption in distal tubules and are therefore contra-indicated.25 Once the cause of the hypercalcemia isidentified, corticosteroids (2 mg/kg twice a day) may beused to increase renal excretion of calcium.

Although hypercalcemia of malignancy respondsto corticosteroid therapy, other causes of hypercalce-mia (e.g., hyperparathyroidism) do not.23 Furthermore,use of corticosteroids before a definitive diagnosis isestablished may obscure the cause of hypercalcemia.


T H Y R O I D E C T O M Y s V I T A M I N D s U R O L I T H S s F L U I D D I U R E S I S s C O R T I C O S T E R O I D S

TABLE III

Emergency Treatment of Hypercalcemia

Fluid/Drug Dosage Comments

0.9% saline 120180 ml/kg/day Increases renal calcium excretionintravenously

Furosemide 5 mg/kg/hr Volume expansion must precedeintravenously furosemide administration

Etridonate 7.5 mg/kg For 37 days or until serum calciumintravenously over normalizes; based on human dose4 hours

EDTA 2575 mg/kg hourly Chelator, nephrotoxic

Calcitonin 4 U/kg intramuscularly Until serum calcium normalizesevery 12 hours (cats)

8 U/kg subcutaneously Until serum calcium normalizesevery 24 hours (dogs)

Bicarbonate 14 mEq/kg intravenously Decreases ionized fraction ofevery 4 hours calcium, may cause alkalosis


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corticism in ten cats.J Vet Intern Med3(2):5558, 1989.5. LaRue MJ, Murtaugh RJ: Pulmonary thromboembolism in

dogs: 47 cases (19861987).JAVMA197:13681373, 1990.6. Feldman BF: Hemostatic abnormalities in canine Cushings

syndrome. Res Vet Sci41:228, 1986.7. Ortega TM, Feldman EC, Ownings JT, et al: Hypercoagu-

lopathy in dogs with hyperadrenocorticism. J Vet InternMed10(3):185, 1996.

8. Burns MG, Kelly AB, Hornof WJ, Howerth EW: Pul-monary artery thrombosis in three dogs with hyperadreno-corticism.JAVMA178:388392, 1981.

9. Johnson LR, Lappin MR: Clinical features of fatal pul-monary thromboembolism: 19851995. J Vet Intern Med10(3):162, 1996.

10. Ingbar SH: The thyroid gland, in Wilson JD, Foster DW(eds): Textbook of Endocrinology. Philadelphia, WB SaundersCo, 1985, pp 682815.

11. Feldman EC, Nelson RW: Canine and Feline Endocrinologyand Reproduction. Philadelphia, WB Saunders Co, 1996, pp163165.

12. Peterson ME: Hyperthyroidism, in Ettinger SJ, Feldman EC

(eds): Textbook of Veterinary Internal Medicine, ed 4.Philadelphia, WB Saunders Co, 1995, p 1466.

13. Peterson ME, Kintzer PP, Cavanagh PG, et al: Feline hyper-thyroidism: Pretreatment clinical and laboratory evaluationof 131 cases.JAVMA183:103110, 1983.

14. Davis LE: Propylthiouracil in the treatment of feline hyper-thyroidism.JAVMA179:485487, 1981.

15. Meric SM: Diagnosis and management of feline hyperthy-roidism. Compend Contin Educ Pract Vet11(9):10531062,1989.

16. Kelly MJ, Hill JR: Canine myxedema stupor and coma.Compend Contin Educ Pract Vet6(12):10491057, 1984.

17. Bichsel P, Jacobs G, Oliver JE: Neurologic manifestationsassociated with hypothyroidism in four dogs. JAVMA192:17451747, 1988.

18. Feldman EC, Nelson RW: Hypocalcemia and primary hy-poparathyroidism, in Feldman EC, Nelson RW (eds): Ca-nine and Feline Endocrinology and Reproduction. Philadel-phia, WB Saunders Co, 1996, pp 497516.

19. Kornegay JN: Hypocalcemia in dogs. Compend Contin EducPract Vet4(2):103110, 1982.

20. Schick MP: Calcinosis cutis secondary to percutaneous pen-etration of calcium chloride in dogs.JAVMA191:207, 1987.

21. Peterson ME: Hypoparathyroidism and other causes ofhypocalcemia in cats, in Kirk RW, Bonagura JA (eds): Cur-rent Veterinary Therapy. XI. Philadelphia, WB Saunders Co,1992, p 376.

22. Graves T: Complications of treatment and concurrent illnessassociated with hyperthyroidism in cats, in Kirk RW,

Bonagura JA (eds): Current Veterinary Therapy. XII.Philadelphia, WB Saunders Co, 1994, pp 369372.

23. Feldman EC, Nelson RW: Hypercalcemia and primary hy-perparathyroidism, in Feldman EC, Nelson RW (eds): Ca-nine and Feline Endocrinology and Reproduction. Philadel-phia, WB Saunders Co, 1996, pp 455493.

24. Chew DJ, Capen CC: Hypercalcemic nephropathy and asso-ciated disorders, in Kirk RW (ed): Current Veterinary Thera-

py. VII. Philadelphia, WB Saunders Co, 1980, pp 1067.25. Chew DJ, Meuten DJ: Disorders of calcium and phosphorus

metabolism. Vet Clin North Am Small Anim Pract 12:411,1982.

26. Fleisch H: Bisphosphonates: A new class of drug in diseaseof bone and calcium metabolism. Recent Results Cancer Res


Phosphonates (etridonate, pamidronate), calcitonin,plicamycin, EDTA, and bicarbonate may also be usedin refractory cases as emergency treatment of hypercal-cemia.2630

About the AuthorDr. Greco is affiliated with the Department of Clinical Sci-

ences, College of Veterinary Medicine and Biomedical

Sciences, Colorado State University, Fort Collins, Col-

orado, and is a Diplomate of the American College of Vet-

erinary Internal Medicine.

REFERENCES1. Hardy RM: Hypoadrenal gland disease, in Ettinger SJ, Feld-

man EC (eds): Textbook of Veterinary Internal Medicine, ed4. Philadelphia, WB Saunders Co, 1995, pp 15791593.

2. Peterson ME, Kintzer P: Pretreatment clinical and laborato-ry findings in 225 dogs with hypoadrenocorticism. JAVMA208:8591, 1996.

3. Willard MD, Schall WD, McCaw DE, Nachreiner RF: Ca-nine hypoadrenocorticism: Report of 37 cases and review of39 previously reported cases. JAVMA180:5962, 637640,1982.

4. Peterson ME, Greco DS, Orth DN: Primary hypoadreno-

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116:1, 1989.27. Percival RC, et al: Role of glucocorticoids in the manage-

ment of malignant hypercalcemia. Br Med J289:287, 1984.28. Bilezikian JP: Management of acute hypercalcemia. N Engl J

Med326:1196, 1992.29. Parfitt AM, Kleerkoper M: Clinical disorders of calcium,

phosphorus, and magnesium metabolism, in Maxwell MH,Kellman CR (eds): Clinical Disorders of Fluid and ElectrolyteMetabolism. New York, McGraw-Hill, 1980, p 947.

30. Kruger JM, Osborne CA: Canine and feline hypercalcemicnephropathy. Part I. Causes and consequences. CompendContin Educ Pract Vet16(10):12991315, 1994.


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Endocrine Emergencies.part2,Adrenal,Thyroid and Parathyroid Disorders