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Endocrine Emergencies.part2,Adrenal,Thyroid and Parathyroid Disorders

Endocrine Emergencies.part2,Adrenal,Thyroid and Parathyroid Disorders

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Vol. 19, No. 1January 1997HEINZ SYMPOSIUM 1996Continuing Education Article
FOCAL POINTKEY FACTS
5
Endocrine disorders often causelife-threatening emergencies insmall animals.
EndocrineEmergencies. Part II. Adrenal, Thyroid, andParathyroid Disorders
Colorado State University 
Deborah S. Greco, DVM, PhD
D
isorders of the thyroid gland, adrenal glands, and parathyroid glandcan cause life-threatening emergencies in small animals.
ADRENAL DISORDERSAddisonian Crisis
One of the most well-recognized endocrine emergencies is classic addisoniancrisis.
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 havea recent history of vague, waxing and waning signs that presaged the onset of collapse.
1–4
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-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 andhypochloremia 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 anormal or slow heart rate despitecirculatory shock and the waxingand waning course beforecollapse.
s
Endogenous corticotropinmust be measured before anycorticosteroids are given.
s
Patients with myxedemaor hypothyroid coma need
intravenous 
replacement ofthyroid hormone (5
µ
g/kgevery 12 hours).
s
In-house testing can confirmthe diagnosis of hypothyroidismbefore emergency treatmentbegins.
s
Calcitriol (0.25 µg orally every48 hours) can be given fora short time after surgicalthyroidectomy to preventhypocalcemia.
 
normal eosinophiland lymphocytecounts in the faceof severe meta-bolic stress. Theanemia of hypo-adrenocorticismhas classically beenattributed to lack of glucocorticoideffects on bonemarrow; however,recent studies sug-gest that hemor-rhagic gastroen-teritis contributessignificantly tothe anemia.
2
Hy-poglycemia ismore common with secondary oratypical hypoad-renocorticism;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 corticosteroids are 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 of 
Compendium 
describes treatment of life-threatening hyperkalemia.Glucocorticoidand mineralo-corticoid therapy must be initiatedonly after diag-nostics for hy-poadrenocorti-cism have beenperformed. Glu-cocorticoid ther-apy, using ultra
short-acting cor-ticosteroid esters(e.g., dexameth-asone sodiumphosphate andprednisolonesodium succi-nate) is indicat-ed. Dexametha-sone does notinterfere withthe cortisol assay and may be pre-ferred if the animal requires immediate glucocorticoid ad-ministration. Furthermore, a single dose of short-actingcorticosteroid will not suppress the hypothalamic
hypophysial
adrenal axis and therefore will not interfere with diagnostics.
2
Recent studies have emphasized the importance of treating the gastrointestinal complications of hypoad-renocorticism.
2
Some dogs with addisonian crisis die of gastrointestinal hemorrhage. The cause of the gastroin-testinal hemorrhage is unknown but may be glucocorti-coid deficiency or poor intestinal perfusion caused by shock. Treatment of anemia secondary to severe gas-trointestinal hemorrhage should include blood transfu-sion coupled with gastrointestinal protectants (e.g., su-cralfate, H
2
antagonists, and misoprostol). All dogs with hypoadrenocorticism should receivegastrointestinal protectants and immediate glucocorti-coid therapy 
after 
adrenal 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
FLUID THERAPY
s
GLUCOCORTICOID
s
MINERALOCORTICOID
s
GASTROINTESTINAL PROTECTANTS
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 1
4 mg/dl (28
110 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); collectin EDTA vacuum tube (with aprotinin), centrifugeand store in plastic, ship at 4
°
C (or frozen if notcollected in aprotinin)
Normals:
 20
80 pg/ml (4.4
8.8 pmol/L)
 
undergoing medical or surgical treatment for hyper-adrenocorticism appear to be at increased risk forthromboembolic complications. Recent studies haveshown that Cushing
s syndrome results in an increase invitamin K 
dependent 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 of perfusion 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 pulmonary thromboembolism.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 1997Small Animal
COAGULATION FACTORS
s
RADIOGRAPHIC SIGNS
s
BLOOD GAS
s
PREVENTING CLOTS
PROTOCOL FOR TREATMENT OF HYPOADRENAL CRISIS
StepDrug or FluidDosageSide EffectsCautio
Step 1: Fluids
0.9% Saline
90 ml/kg/hrOverhydrationMonitor central venouspressure
Step 2: Electrolytes
Calcium gluconate5
15 mg/kgBradycardiaMonitor electrocardiogram
if hyperkalemia 
Insulin0.5 U/kg
is life-threatening 
Dextrose2 g/U of insulinHypoglycemiaMonitor electrocardiogramBicarbonate1
2 mmol/kgAlkalosisMonitor blood pHintravenously over5
15 min
Step 3: Glucocorticoi
Dexamethasone2
4 mg/kgNoneNonesodium phosphateintravenouslPrednisolone 30 mg/kg NoneDo not use beforesuccinateintravenouslycorticotropin response test
Step 4: Restoration
SodiumSee discussionAlkalosisMonitor pH, bicarbonate
of acid–base balance
bicarbonateof diabeticketoacidosis inPart I
Step 5: Treatment 
 Whole bloodDepends on
Monitor packed cell volume
of gastrointestinal
transfusionpacked cellevery 4 hours
hemorrhage
volume, body  weightMisoprostol2
5 µg/kg
orally threetimes a day Ranitidine2 mg/kgintravenously ororally twice a day 

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