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.
Hy-poglycemia ismore common with secondary oratypical hypoad-renocorticism;however, hypo-glycemia is an unusual manifestation of hypoadrenocorti-cism in dogs.
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.
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
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
adrenal axis and therefore will not interfere with diagnostics.
Recent studies have emphasized the importance of treating the gastrointestinal complications of hypoad-renocorticism.
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
antagonists, and misoprostol). All dogs with hypoadrenocorticism should receivegastrointestinal protectants and immediate glucocorti-coid therapy
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.
Screening Tests for Hypoadrenocorticism
Corticotropin (ACTH) Stimulation Test
0.5 U/kg aqueous corticotropin intravenously,serum samples at 0 and 1 hour
2.2 U/kg corticotropin gel intramuscularly (maximum 20 U/dog), serum samples at 0 and 2hours
4 mg/dl (28
110 mmol/L); aftercorticotropin: < 20 mg/dl (550 mmol/L)
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)
80 pg/ml (4.4