Page 1039 - Cote clinical veterinary advisor dogs and cats 4th
P. 1039
514 Hypoadrenocorticism
highly unlikely. If low, ACTH stimulation ○ If severely ill, dehydrated, and/or hypoten- (e.g., travel, new pet or child, veterinary
visit, other illness).
test is required for confirmation. sive, give one-third of the shock volume ○ Prednisone doses < 0.1 mg/kg q 24h are
VetBooks.ir Advanced or Confirmatory Testing 90 mL/kg for dogs, 60 mL/kg for cats) often adequate and may be better toler-
(that is, ≈20 mL/kg bolus repeated up to
• ACTH stimulation test is the definitive
IV bolus, then reassess and administer
ated, especially in larger dogs. Monitor
diagnostic test for hypoadrenocorticism.
Basal serum cortisol concentration will be more if necessary. For maintenance and for clinical signs of hypoadrenocorticism
closely in these cases.
to correct dehydration, additional fluids
low and cortisol fails to increase after ACTH should be given as needed over the next ○ Patients receiving fludrocortisone acetate
administration (p. 1300). few days. may not require additional daily gluco-
• Dogs • Fluid therapy is the primary treatment for corticoid therapy long term, but those
○ 1) Collect blood sample for pre-ACTH hyperkalemia and acidosis. receiving deoxycorticosterone pivalate
cortisol level; 2) administer synthetic ○ If hyperkalemia is life-threatening (DOCP) always do.
ACTH (cosyntropin/tetracosactide) (>8.5 mEq/L and/or electrocardiographic • Mineralocorticoid supplementation: DOCP
5 mcg/kg, up to 250 mcg/DOG IV; 3) abnormalities present), treat specifically injection or oral fludrocortisone
collect blood sample 60 minutes later (p. 495). ○ DOCP
(post-ACTH cortisol level). ○ Bicarbonate is rarely needed to treat ■ Initial dose 2.2 mg/kg SQ or IM q
○ ACTH gel is not recommended due to acidosis because fluids are almost always ≈25 days
variability in intramuscular absorption. adequate. ❏ 1.5 mg/kg SQ or IM is effective in
If intramuscular gel is used, postcortisol • Glucocorticoid administration most dogs and is used by the author
samples should be obtained at 1 and 2 ○ Dexamethasone sodium phosphate (pre- as an off-label starting dose.
hours due to inconsistent results. ferred by the author): rapid acting and ■ Measure electrolytes on days 14 and
• Cats is not detected by cortisol assay (ACTH 25 after treatment, and adjust dosing
○ 1) Collect blood sample for pre-ACTH stimulation test). Initially administer based on results.
cortisol level; 2) administer cosyntropin 0.25 mg/kg IV, then 0.1 mg/kg q 12h. ■ If hyperkalemic or hyponatremic on day
125 mcg/CAT IV; 3) collect blood sample ○ Alternatively, hydrocortisone (continuous- 14, increase the next dose by 5%-10%.
60 minutes later (post-ACTH cortisol rate infusion) 0.5-0.625 mg/kg/h has both If electrolytes are normal at 14 days but
level). glucocorticoid and mineralocorticoid abnormal at 25 days, shorten the dosing
• Endogenous ACTH can be measured to properties. However, it interferes with interval by 48 hours. If electrolytes are
differentiate secondary (decreased ACTH) the cortisol assay and should not be normal at each recheck, dosing interval
from primary hypoadrenocorticism (increased administered until after completion of may be increased by several days. In one
ACTH) if electrolyte values are normal. The the ACTH stimulation test. report, dose intervals of as long as 60
difference can be important for prognosis • Hypoglycemia: add dextrose to isotonic days were effective for some dogs.
and monitoring. Secondary hypoadrenocorti- IV fluids to make a 2.5%-5% dextrose ■ If hypokalemic or hypernatremic
cism never becomes typical with electrolyte concentration. If hypoglycemia is severe or on day 14, decrease the next dose
abnormalities; patients with primary atypical the patient has clinical signs of hypoglycemia, by 10%.
hypoadrenocorticism can later develop boluses of 25% dextrose solution, 1 mL/kg ■ After dosage and dosing interval are
electrolyte abnormalities. in 0.9% saline, may be given. determined, clients can be taught to
• After life-saving treatment has been initiated, give DOCP at home.
TREATMENT perform ACTH stimulation test as above ○ Fludrocortisone acetate
(p. 1300). ■ Dogs: 0.01 mg/kg PO q 12h initially;
Treatment Overview • Monitor urine production. dose often needs to be increased based
Initial therapy depends on severity of clinical • Monitor electrolytes and glucose after initial on serum electrolyte concentrations
signs. For animals in an Addisonian crisis, fluid resuscitation and then q 8-12h until over first 6-18 months to maintain
initial therapy is directed at correcting life- normal. normal electrolyte concentrations.
threatening conditions (hypotension, hypovo- • Maintain fluid therapy until patient is ■ Cats: 0.05-0.1 mg/CAT PO q 12h ini-
lemia, hyperkalemia, acidosis, hypoglycemia). eating. tially; adjust based on serum electrolyte
The cornerstone of treatment is IV fluid • Use injectable glucocorticoids until oral concentrations.
therapy. Patients with severe, typical clinical prednisone can be instituted at 1 mg/kg PO ■ Prednisone should be given with fludro-
and laboratory abnormalities should be treated q 24h until the patient goes home. Then cortisone initially but may be tapered
as if they have hypoadrenocorticism; delaying taper the dose as below. after normalization of electrolytes.
treatment until ACTH stimulation results are • Mineralocorticoid administration can be
available may result in death of the patient. initiated after the diagnosis is confirmed. Possible Complications
Chronic, lifelong therapy involves physiologic • With Addisonian crises, death can occur if
replacement of deficient hormones. Chronic Treatment treatment is not prompt and intensive.
• Lifelong supplementation with glucocor- • Overly rapid correction of hyponatremia can
Acute General Treatment ticoids and mineralocorticoids (typical result in demyelination (p. 518).
• Isotonic replacement crystalloids hypoadrenocorticism) or with glucocorticoids • Side effects of prolonged, excessive pred-
○ Traditionally, 0.9% NaCl has been rec- alone (atypical hypoadrenocorticism) is nisone and/or fludrocortisone treatment
ommended because of the high sodium required. include PU/PD and other signs of iatrogenic
content and lack of potassium. However, • Glucocorticoid supplementation: prednisone hyperadrenocorticism. In animals receiving
some clinicians prefer Plasma-Lyte A or 0.25-0.5 mg/kg PO q 12h initially, then taper fludrocortisone, if PU/PD cannot be resolved
lactated Ringer’s solution because they to 0.1-0.25 mg/kg PO q 24h, depending on by tapering prednisone (to lowest dose
correct the acidosis more quickly, and individual needs. needed to prevent signs of hypocortisolism),
their low potassium content still allows ○ Increase dose if signs of hypoadrenocor- switching to DOCP is recommended.
for correction of hyperkalemia. ticism persist, and decrease if signs of
○ Hyponatremia should not be corrected too glucocorticoid excess are present. Recommended Monitoring
quickly or neurologic deficits can develop ○ Increased prednisone (2-3 times normal • With fludrocortisone or prednisone, monitor
(p. 518). dose) is required during times of stress serum biochemistry, including electrolytes,
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