Canine

Canine Hypoadrenocorticism: Diagnostic Testing

Oct 22, 2026 3 min read
AI-generated clinical reference · Sources and methodology

Bottom line

A low resting cortisol does not diagnose canine hypoadrenocorticism; use ACTH stimulation to establish deficient cortisol reserve. [1] Normal sodium and potassium do not exclude disease. [2] Separate confirmation of glucocorticoid deficiency from classification of its cause, and stabilize an adrenal crisis before completing elective endocrine investigations. [3]

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Which dogs warrant endocrine testing?

Consider hypoadrenocorticism in dogs with recurrent gastrointestinal illness, weight loss, lethargy, or collapse, including patients whose electrolytes remain within reference intervals. [2] Use the illness pattern and competing diagnoses to decide whether to exclude disease with a resting cortisol or proceed directly to ACTH stimulation when suspicion is high. [3]

A practical record should distinguish the presenting problem, current perfusion, sodium and potassium findings, drug exposure, and the question being asked of the test. Do not let a plausible gastrointestinal diagnosis close the endocrine differential before its evidence has been reviewed.

Resting cortisol versus ACTH stimulation

In the absence of glucocorticoid assay interference, a resting serum cortisol above 2 mcg/dL makes hypoadrenocorticism very unlikely. A low result requires confirmatory testing rather than immediate assignment of a lifelong diagnosis. [1]

Interpret the ACTH stimulation test using the performing laboratory's diagnostic cutoff, not the healthy-population reference interval alone. AAHA describes a post-stimulation cortisol below 2 mcg/dL or below laboratory-specific diagnostic cutoffs as confirmatory. [1] Resolve borderline or discordant results with the laboratory and, where appropriate, an internist; this page does not supply a universal cutoff for every assay.

Review all prior systemic and topical glucocorticoids and progestogens. The 2025 ALIVE consensus specifically includes ophthalmic and otic exposure among potential confounders and recommends validated assays with quality control. [4] Document agent, route, last administration, and duration; apply an assay- and drug-specific testing plan.

Classifying primary and secondary disease

The 2025 ALIVE definitions reserve Addison's disease for primary hypoadrenocorticism. Normal sodium and potassium can occur with either primary or secondary disease; the electrolyte phenotype alone cannot establish the site of dysfunction. [4]

Endogenous ACTH assists classification after deficient cortisol reserve is established. Collect it before corticosteroid administration when feasible, and follow the laboratory's handling requirements because ACTH is labile. [2] Keep the cortisol stimulation result, endogenous ACTH result, and medication history distinct in the assessment.

Review trilostane exposure and adrenal monitoring and the prednisone/prednisolone reference when interpreting a treated dog's results.

Adrenal crisis: testing must not delay stabilization

Treat hypovolemic shock immediately. AAHA prioritizes IV fluids to restore perfusion, with specific correction of hyperkalemia, hypoglycemia, or acidosis when indicated, followed by frequent electrolyte monitoring. [3] If urgent glucocorticoid treatment is needed before cortisol testing, AAHA identifies dexamethasone as the option that does not interfere with the cortisol assay. [3]

Record samples already collected and treatments already given. Arrange continued monitoring or transfer according to the patient's support requirements, rather than waiting for a complete diagnostic label.

Frequently Asked Questions

Does a low resting cortisol confirm hypoadrenocorticism?

No. It is an exclusion test when sufficiently high; a low result requires ACTH stimulation to confirm cortisol deficiency. [1]

Can normal electrolytes exclude hypoadrenocorticism?

No. A dog with compatible recurrent illness can have hypoadrenocorticism despite reference-interval sodium and potassium. [2]

Is the sodium-to-potassium ratio diagnostic?

No. Other disorders alter this ratio, so it cannot replace adrenocortical function testing. [1]

Does an ACTH stimulation test distinguish primary from secondary disease?

Not by itself. Endogenous ACTH and the clinical and medication history are needed to classify the cause of deficient cortisol reserve. [4]

When should endogenous ACTH be collected?

Before corticosteroid administration when feasible, using the laboratory's specific collection and transport instructions because ACTH is labile. [2]

Can ear or eye steroids affect the diagnostic assessment?

Yes. ALIVE explicitly includes topical ophthalmic and otic glucocorticoid exposure in the medication history that must be considered before diagnosis. [4]

Should a dog in adrenal crisis wait for endocrine results?

No. Stabilize shock and associated metabolic abnormalities immediately; complete testing around the patient's urgent care needs. [3]

References

  1. AAHA. Canine Hypoadrenocorticism Diagnostic Testing and Monitoring. 2023 Selected Endocrinopathies Guidelines. (2023)
  2. Guzmán Ramos et al. Diagnosis of canine spontaneous hypoadrenocorticism. Canine Medicine and Genetics. (2022)
  3. AAHA. Canine Hypoadrenocorticism Categorical Approach to Diagnosis Based on Clinical Presentation. (2023)
  4. Niessen et al. Agreeing Language in Veterinary Endocrinology (ALIVE): Cushing’s Syndrome and Hypoadrenocorticism—A Modified Delphi-Method-Based System to Create Consensus Definitions. Veterinary Sciences. (2025)

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