This article is educational and is not a substitute for veterinary diagnosis or treatment. A suspected Addisonian crisis is an emergency; do not adjust steroid or electrolyte-replacement medication without the prescribing veterinarian.

Addison's Disease in Dogs: Symptoms, Diagnosis, Crisis, and Treatment

Quick Answer

Addison's disease in dogs, or hypoadrenocorticism, occurs when the body has too little cortisol and sometimes too little aldosterone. These adrenal hormones help maintain circulation, blood glucose, fluid and electrolyte balance, gastrointestinal function, and the response to physical stress. Deficiency can cause intermittent vague illness or a sudden life-threatening Addisonian crisis [1][2].

Common signs include lethargy, reduced appetite, vomiting, diarrhea, weight loss, weakness, shaking, dehydration, and episodes that improve with fluids or steroids and then return. A crisis may cause collapse, severe weakness, slow or abnormal heart rate, pale gums, low blood pressure, low blood sugar, vomiting, diarrhea, and shock. A dog with collapse, repeated vomiting, profound weakness, or known Addison's that cannot keep medication down needs emergency care now.

Routine bloodwork can raise suspicion but does not confirm Addison's. Classic primary Addison's often causes low sodium and high potassium, but normal electrolytes do not exclude the disease. A resting cortisol above a validated cutoff makes Addison's unlikely in most tested populations; a low result is only a screening finding. Confirmation usually requires an ACTH stimulation test showing inadequate cortisol production [1][3][4]. Previous steroid medication can interfere with testing, so the veterinarian needs a complete drug history.

Most dogs have an excellent long-term outlook after stabilization when owners give lifelong prescribed hormone replacement, attend electrolyte and clinical monitoring, and follow a written plan for extra glucocorticoid during illness or physiologic stress [1][2]. Treatment is highly individualized. A dog should never miss or receive an extra mineralocorticoid injection, change prednisone, or substitute a human steroid based on an online schedule.

At a Glance

What the Adrenal Glands Do

Dogs have two small adrenal glands near the kidneys. The adrenal cortex produces several hormones. Cortisol is a glucocorticoid involved in vascular responsiveness, metabolism, blood glucose support, inflammation, gastrointestinal function, and adaptation to physiologic stress. Aldosterone is a mineralocorticoid that helps the kidneys retain sodium and water and excrete potassium [1][2].

In primary hypoadrenocorticism, disease of the adrenal cortex reduces hormone output. Immune-mediated destruction is considered a common cause, although it is not proven in every dog. Less common causes include adrenal hemorrhage, infection or granulomatous disease, neoplasia, and medications that destroy or inhibit adrenal tissue—particularly drugs used to treat hyperadrenocorticism [1][7].

In secondary hypoadrenocorticism, inadequate pituitary ACTH stimulation reduces cortisol production. Aldosterone is regulated largely through other pathways, so sodium and potassium may remain normal. Abrupt withdrawal after prolonged suppressive glucocorticoid therapy can also leave the hypothalamic-pituitary-adrenal axis unable to respond normally. That is one reason prescribed steroids sometimes require a taper rather than sudden discontinuation.

The label “Addison's” is used most often for naturally occurring hypoadrenocorticism. Not every low cortisol measurement means primary immune adrenal destruction, and the cause affects which hormones need replacement.

Addison's Disease Symptoms in Dogs

The Great Imitator

Addison's is called a great imitator because its signs overlap with gastrointestinal disease, kidney injury, pancreatitis, toxin exposure, infection, liver disease, urinary obstruction, and many other conditions. Signs may wax and wane for weeks or months. Fluids, rest, or nonspecific steroid treatment can create temporary improvement without identifying the cause [1][7][8].

Possible signs include:

• reduced appetite or refusal to eat;
• intermittent or repeated vomiting;
• diarrhea, sometimes with blood;
• lethargy and reduced exercise tolerance;
• weakness, wobbliness, or trembling;
• weight loss and loss of muscle;
• dehydration despite drinking;
• abdominal discomfort;
• increased thirst or urination in some dogs;
• slow heart rate despite shock in some classic cases;
• episodic collapse.

No item on that list is diagnostic. A dog with one brief soft stool is far more likely to have another explanation than Addison's. Suspicion rises when signs recur, several findings occur together, routine treatment does not hold, laboratory patterns are suggestive, or the dog collapses.

Historical case data describe lethargy, poor appetite, and vomiting among common owner complaints, with weakness and dehydration frequent on examination [8]. Those referral populations contain diagnosed dogs and cannot tell an owner the probability that a vomiting pet has Addison's.

Can Addison's Cause Shaking?

Trembling or shaking can occur with weakness, nausea, abdominal discomfort, low glucose, electrolyte disturbance, or poor circulation. Shaking also occurs with fear, pain, fever, toxin exposure, and neurologic disease. It is a reason for assessment in a sick dog, not a home diagnostic sign.

Does Addison's Cause Excessive Drinking?

Some affected dogs drink or urinate more, particularly when kidney concentration is impaired by electrolyte and circulatory changes. Others drink less because of nausea. Increased thirst also occurs with kidney disease, diabetes mellitus, Cushing's disease, infection, medication, and diet. Measure actual water intake when practical rather than relying on bowl impressions.

Stool and Vomit Changes

Diarrhea can be watery, mucoid, or bloody, and vomiting may be intermittent or severe. Black tarry stool or coffee-ground material can indicate digested blood. Repeated vomiting plus weakness or dehydration warrants prompt veterinary care regardless of the cause. Review the site's emergency-vet or regular-vet guide for general triage, but collapse or inability to keep medication down is an emergency.

Addisonian Crisis in Dogs

An Addisonian crisis is acute decompensation from inadequate corticosteroid support, commonly with severe dehydration, low circulating blood volume, electrolyte abnormalities, low glucose, acid-base disturbance, or shock. It may be the first recognized episode or occur in a diagnosed dog during illness, trauma, surgery, missed treatment, or inadequate stress glucocorticoid [1][2].

Emergency Warning Signs

Go to an emergency veterinary hospital for:

• collapse or inability to stand;
• profound weakness, disorientation, or poor responsiveness;
• repeated vomiting or diarrhea with inability to retain water or medication;
• pale, gray, or very tacky gums;
• cold extremities or abnormal body temperature;
• a very slow, irregular, or weak pulse in a sick dog;
• severe dehydration;
• seizures or suspected severe low blood sugar;
• known Addison's plus missed medication and clinical deterioration.

Do not wait for every classic sign. A dog in shock may have a soft, non-distended abdomen and no dramatic external clue. The dog pale-gums guide explains why abnormal circulation needs urgent attention.

What Happens at the Hospital

The team prioritizes airway, breathing, circulation, vascular access, blood pressure, glucose, electrolytes, kidney values, acid-base status, and electrocardiographic effects of potassium. Intravenous fluids restore circulating volume. Dextrose, anti-nausea treatment, warming, and targeted therapy for dangerous hyperkalemia may be needed. A glucocorticoid compatible with planned cortisol testing can be selected when Addison's is suspected [1][2].

Correcting severe chronic hyponatremia too rapidly can cause neurologic injury, so fluid selection and monitoring require professional calculations and repeated measurements. This is not a condition for oral salt, sports drinks, potassium-binding home remedies, or an old prednisone tablet.

An ACTH stimulation test may be collected before certain steroids if that does not compromise stabilization. Emergency treatment must not be delayed when the dog is unstable. The clinician can often preserve useful samples while beginning life-saving care.

Why Addison's Is Missed

Vague and Intermittent Signs

A dog may be normal between episodes. Gastrointestinal signs can respond temporarily to fluids, antiemetics, dietary changes, or glucocorticoids. Owners may reasonably attribute early lethargy to weather or stress. The disease is uncommon, so more common causes are considered first [1][7].

Normal Sodium and Potassium

The textbook pattern is hyponatremia and hyperkalemia, often summarized by a low sodium-to-potassium ratio. But dogs with glucocorticoid-deficient disease, secondary disease, early primary disease, or some primary presentations can have normal electrolytes [5][6]. In a study of dogs diagnosed without classic electrolyte changes, some later developed evidence of aldosterone deficiency [5].

The reverse is also important: a low sodium-to-potassium ratio does not equal Addison's. Kidney, gastrointestinal, urinary, hepatobiliary, infectious, and other diseases can produce it. A recent hospital study found multiple nonadrenal mechanisms among dogs and cats with low ratios [9]. The ratio is a clue, not a confirmation.

Steroid Interference

Prednisone, prednisolone, hydrocortisone, topical or injected steroids, and some ear or eye products can suppress the adrenal axis or interfere with cortisol assays. The effect depends on drug, route, dose, duration, and test. Tell the veterinarian about every tablet, injection, cream, drop, supplement, and compounded product. Do not stop a steroid abruptly just to obtain a test.

Diagnostic Process

History and Examination

The clinician reviews the timing and recurrence of gastrointestinal signs, weight, drinking and urination, weakness, collapse, medication exposure, travel, toxins, prior laboratory results, and response to treatment. Temperature, pulse, hydration, blood pressure, abdominal comfort, and perfusion help determine urgency.

No physical finding is unique. A relatively slow heart rate in a collapsed, hyperkalemic dog can be suggestive because shock usually produces tachycardia, but a normal or fast heart rate does not exclude Addison's.

CBC, Chemistry, and Urinalysis

Possible findings include low sodium, high potassium, low chloride, azotemia, low glucose, high calcium, low albumin, low cholesterol, and lack of a typical stress leukogram. Urine may be less concentrated than expected for dehydration. None is diagnostic [1][8].

Azotemia can resemble kidney failure. In Addison's, poor perfusion and sodium loss may reduce kidney filtration, and urine concentration may not look as strong as expected. Values can improve markedly with volume and hormone replacement. Conversely, a dog can have Addison's and intrinsic kidney disease together, so response and follow-up matter.

Resting or Basal Cortisol

A resting cortisol is a useful rule-out test in the right setting. A 2014 study of 450 dogs with nonadrenal illness and 14 affected dogs found that a cutoff of 2 micrograms per deciliter (55 nmol/L) had high sensitivity but modest specificity: values above the cutoff made Addison's unlikely, while values below it occurred in many dogs without Addison's [3]. A large 2025 UK dataset likewise reported a high negative predictive value at that threshold while emphasizing low positive predictive value [4].

Thus:

• a sufficiently high basal cortisol can make Addison's very unlikely;
• a low basal cortisol cannot diagnose Addison's;
• a low result usually leads to ACTH stimulation testing;
• assay, population, illness severity, and steroid exposure affect interpretation.

Do not interpret a number from a different laboratory against an internet reference without units. Micrograms per deciliter and nanomoles per liter are not interchangeable.

ACTH Stimulation Test

The ACTH stimulation test is the standard confirmatory test. Blood cortisol is measured around administration of synthetic ACTH. Healthy adrenal tissue should respond; dogs with hypoadrenocorticism show an inadequate post-stimulation cortisol concentration [1][7]. Protocol and laboratory cutoffs must match the assay.

A flat response confirms inadequate cortisol reserve in the clinical context, but it does not alone distinguish primary from secondary disease or prove aldosterone deficiency. Drug-induced suppression and previous treatment need consideration. Endogenous ACTH, aldosterone evaluation, imaging, and history may be used to classify selected cases.

Endogenous ACTH

In primary Addison's, the pituitary often releases high ACTH because it is trying to stimulate failing adrenal glands. In secondary disease, ACTH is low or inappropriately normal. The sample is technically demanding and must be handled correctly. It is most informative before glucocorticoid treatment alters the axis [8].

Imaging

Ultrasound may show small adrenal glands in some dogs, but normal-appearing glands do not exclude disease and small glands do not diagnose it alone. Imaging can help investigate hemorrhage, masses, infiltrative disease, or other abdominal causes. Radiographs may show nonspecific low blood volume or a small heart in dehydration.

Typical, Atypical, and Secondary Addison's

“Typical” Primary Addison's

This informal label generally means cortisol and aldosterone deficiency with characteristic electrolyte changes. Dogs often need both glucocorticoid and mineralocorticoid replacement. “Typical” does not mean the clinical signs are obvious or that every sodium and potassium value is identical.

Atypical Addison's

“Atypical” commonly describes confirmed cortisol deficiency without the expected sodium and potassium abnormalities. The term can group different mechanisms: early primary disease, primary disease with retained aldosterone function, secondary disease, or cases that require additional classification [5][6].

Some dogs have gastrointestinal signs, low albumin, or low cholesterol and resemble chronic enteropathy. In a retrospective study of 40 atypical cases, 14% of those with follow-up biochemistry developed electrolyte abnormalities 2 to 51 months after diagnosis [5]. A separate 2024 cohort found evidence that some dogs without electrolyte changes had or later developed aldosterone deficiency [6]. Continued electrolyte monitoring is therefore important.

Equivocal cortisol results should not become a permanent atypical Addison's label without proper confirmation. In the 2017 study, several dogs with borderline results were later diagnosed with inflammatory bowel disease or did not respond as expected [5].

Secondary Hypoadrenocorticism

Pituitary or hypothalamic disease can reduce ACTH and cortisol while mineralocorticoid function remains relatively preserved. Abrupt withdrawal after suppressive exogenous steroids can create a related state. Neurologic or other pituitary hormone signs may prompt additional testing and imaging.

Which Dogs Get Addison's Disease?

Addison's can affect any dog. Historical cohorts often include young to middle-aged adults and more females, with breed clustering in populations such as Standard Poodles, Portuguese Water Dogs, Nova Scotia Duck Tolling Retrievers, Bearded Collies, and others [8][10]. Breed predisposition reflects population genetics and geography; it does not mean an individual is affected.

Genetic architecture is complex and differs by breed. There is no universal DNA test that clears every dog of Addison's risk. A responsible breeder should discuss health in relatives and age and cause of death, not promise that a commercial panel excludes hypoadrenocorticism [10].

Mixed-breed dogs, males, seniors, and dogs outside known breed lists can be diagnosed. Signalment changes pretest suspicion but never replaces testing.

Treatment After Stabilization

Replace the Missing Hormones

Most primary cases need:

1. a glucocorticoid, commonly a low maintenance dose of prednisone or prednisolone; and
2. a mineralocorticoid, commonly injectable desoxycorticosterone pivalate (DOCP) or oral fludrocortisone.

DOCP replaces mineralocorticoid activity but not cortisol, so a glucocorticoid is still necessary. Fludrocortisone has mineralocorticoid and some glucocorticoid activity, but some dogs still need added glucocorticoid [1][2]. Atypical or secondary cases may initially need glucocorticoid alone, with electrolyte monitoring.

The best choice depends on availability, cost, body size, response, caregiver reliability, comorbidities, and monitoring. Product labels differ by country. A compounding or supply change can alter absorption and should be coordinated with the prescriber.

DOCP Monitoring

DOCP is given by injection at an individualized dose and interval. Electrolytes are checked after initial injections and around the expected next dose so the clinician can decide whether dose, interval, or both should change. Clinical signs and hydration matter alongside numbers.

A prospective study of 17 dogs found that a lower starting protocol could control most cases and often required later dose reduction [11]. That research supports thoughtful titration; it does not authorize owners to calculate or reduce injections themselves. Young dogs in that cohort needed different amounts, emphasizing individual response.

Giving DOCP too early or at too high a dose can drive sodium high and potassium low. Waiting too long or underdosing can allow deficiency and crisis. Calendar consistency and laboratory follow-up are central.

Fludrocortisone Monitoring

Fludrocortisone is given orally on a consistent schedule. Electrolytes, signs, weight, and glucocorticoid effects guide adjustment. Dose needs can rise over time in some dogs. Vomiting or missed tablets can rapidly undermine coverage.

Never double a missed dose unless the prescribing clinic specifically says to do so. Call for instructions. Owners should maintain an emergency supply without using expired or differently concentrated medication interchangeably.

Glucocorticoid Replacement

The goal is the lowest dose that prevents cortisol-deficiency signs while avoiding chronic excess. Too little can cause poor appetite, vomiting, diarrhea, lethargy, and inadequate stress response. Too much can cause excessive thirst and urination, increased appetite, panting, muscle loss, thin skin, infection risk, and weight gain [1].

Owners should receive written instructions for routine dosing and for temporary stress dosing during events such as significant illness, surgery, injury, or other physiologic stress. What counts as stress and how much to give is patient-specific. A noisy evening or normal walk does not automatically justify repeated high steroid doses. If the dog is vomiting and cannot retain medication, oral stress dosing is not reliable—contact a hospital.

Diet and Salt

Most stabilized dogs can eat a complete and balanced diet appropriate to their other needs. Do not add salt, potassium, electrolyte powders, coconut water, or sports drinks unless the veterinarian prescribes them for a defined reason. Hormone replacement corrects the underlying regulation problem; seasoning food does not substitute for aldosterone.

During a crisis or severe gastrointestinal episode, nutrition and fluid plans are clinical. After recovery, consistent meals can make appetite changes easier to detect.

Living With an Addisonian Dog

Build a Written System

Keep a medication chart with drug, strength, dose, time, refill date, and prescriber. Record DOCP injection dates and laboratory results. Use reminders before supplies run out. Every caregiver should know that the dog has Addison's and where emergency instructions are stored.

Carry a wallet card and add a phone note stating diagnosis, medications, clinic, emergency hospital, and last mineralocorticoid treatment. A tag saying “Addison's—needs steroids in emergency” can help after an accident, though it does not replace records.

Track the Dog, Not Just the Electrolytes

Record appetite, vomiting, stool, energy, water intake, urination, body weight, panting, and exercise tolerance. Trends around the injection interval may reveal underreplacement; persistent thirst, panting, and hunger may suggest glucocorticoid excess. Similar signs can have other causes, so report rather than self-adjust.

Travel and Boarding

Carry more medication than the planned trip, split it between secure locations, preserve label and temperature requirements, and identify a nearby emergency hospital. Time-zone changes should be planned with the clinic. Airlines and borders may require documentation.

Boarding staff need exact dosing, stress-dose instructions, emergency authorization, and permission to seek care. A facility unable to administer critical medication reliably is not appropriate. Consider a trained in-home caregiver for dogs stressed by boarding.

Surgery and Dental Procedures

Tell the veterinary team before any anesthetic procedure. The dog may need perioperative glucocorticoid support, electrolyte assessment, and fluid planning. Do not withhold essential medication because routine pre-anesthetic instructions say “nothing by mouth” without asking. Dental disease still needs treatment; Addison's changes planning, not the value of care.

Vaccination and Preventive Care

Vaccination decisions should consider disease exposure, medication dose, immune status, prior reactions, and local law. Physiologic replacement glucocorticoid is not automatically equivalent to high-dose immunosuppression, but the veterinarian should review the plan. Parasite prevention, dental care, weight management, and routine examinations remain important.

Monitoring Schedule

Monitoring is most intensive after diagnosis, a crisis, a product change, or a dose adjustment. Once stable, visits remain necessary because needs, weight, kidney function, and concurrent disease change. DOCP patients commonly have electrolytes assessed at defined points after treatment and before the next planned dose during titration; stable protocols may later be streamlined by the prescriber [1][2].

An atypical dog needs periodic sodium and potassium checks because mineralocorticoid deficiency may develop [5][6]. All dogs need assessment for underreplacement, glucocorticoid excess, medication adherence, and new illness.

Home sodium or potassium devices are not a substitute for validated laboratory analysis and clinical examination. A normal electrolyte panel does not prove cortisol replacement is correct.

Prognosis and Life Expectancy

With timely diagnosis and appropriate replacement, long-term prognosis is generally excellent [1][2][7]. Many dogs return to ordinary family life, exercise, travel, and normal activities. The disease usually shortens neither joy nor function when it is well controlled, but no article can promise a specific lifespan.

Risk comes from an unrecognized first crisis, missed or vomited medication, inadequate stress coverage, delayed emergency care, monitoring failure, or unrelated disease. Financial and logistical access to lifelong prescriptions and testing should be planned from diagnosis.

Addison's is usually managed rather than cured. Rare drug-induced or secondary suppression scenarios may recover under specialist supervision, but owners should never taper replacement to “test” recovery without an endocrine plan.

Common Myths

“Normal Electrolytes Rule It Out”

False. Dogs with glucocorticoid-deficient, secondary, early, or some primary disease can have normal sodium and potassium [5][6].

“A Low Sodium-to-Potassium Ratio Diagnoses Addison's”

False. Many other diseases lower the ratio [9]. Confirmation requires adrenal function testing in context.

“A Low Resting Cortisol Proves Addison's”

False. Many ill dogs have low basal cortisol. A sufficiently high value is useful to rule out; a low value usually calls for an ACTH stimulation test [3][4].

“Once Electrolytes Are Normal, Prednisone Is Optional”

False for a cortisol-deficient dog treated with DOCP. DOCP does not replace glucocorticoid. Stopping prednisone can permit gastrointestinal illness or crisis even with normal sodium and potassium.

“More Steroid Is Safer”

Not chronically. Excess causes predictable harm. The maintenance goal is the lowest effective replacement, with temporary increases only under the written stress plan [1].

“Addison's Can Be Managed With Salt Water”

False. Salt does not replace cortisol or controlled aldosterone activity and may worsen another undiagnosed condition. Crisis requires IV support and hormone treatment.

When to Call the Veterinarian

Call the same day for new poor appetite, one or more vomiting episodes, diarrhea, unusual lethargy, shaking, increased thirst, medication mistakes, or a change in exercise tolerance in a diagnosed dog. The team can decide whether the stress plan, examination, electrolytes, or emergency care is needed.

Go to emergency care for collapse, inability to stand, repeated vomiting, inability to keep medication down, severe weakness, pale gums, altered consciousness, seizures, breathing difficulty, or rapidly worsening illness. Do not drive long distances past an open capable hospital just to reach the usual clinic.

For an undiagnosed dog with recurrent gastrointestinal illness, bring previous laboratory results and a full steroid history. Ask whether Addison's is among the differentials; do not insist on the diagnosis or start borrowed medication.

Frequently Asked Questions

What are the first signs of Addison's disease in dogs?

Early signs are often nonspecific and intermittent: reduced appetite, vomiting, diarrhea, lethargy, weakness, trembling, weight loss, or poor exercise tolerance. They may improve temporarily and recur. No single sign confirms Addison's [1][8].

What does an Addisonian crisis look like?

A crisis can cause collapse, profound weakness, repeated vomiting or diarrhea, dehydration, pale gums, abnormal heart rate, low blood pressure, low glucose, and shock. It requires immediate emergency treatment.

How is Addison's disease diagnosed in dogs?

History, examination, CBC, chemistry, electrolytes, and urinalysis create suspicion. A resting cortisol can help rule it out when sufficiently high. Confirmation usually uses an ACTH stimulation test showing inadequate cortisol response [1][3][4].

Can a dog have Addison's with normal sodium and potassium?

Yes. Atypical, secondary, early, and some primary cases can have normal electrolytes. Some later develop aldosterone deficiency, so ongoing monitoring is important [5][6].

Is a sodium-to-potassium ratio diagnostic?

No. A low ratio can occur with many kidney, gastrointestinal, urinary, liver, infectious, and other diseases [9]. It is a clue that may prompt testing, not proof.

Is Addison's disease curable?

Most naturally occurring primary Addison's is not cured, but it is usually managed very successfully with lifelong hormone replacement and monitoring. Some drug-induced or secondary suppression may behave differently under specialist care.

What medications do Addisonian dogs take?

Dogs need glucocorticoid replacement, often prednisone or prednisolone. Dogs lacking aldosterone also need a mineralocorticoid such as injectable DOCP or oral fludrocortisone. Exact dose and interval are individualized [1][2].

Why does a dog on DOCP still need prednisone?

DOCP replaces mineralocorticoid activity but does not replace cortisol. Prednisone or another prescribed glucocorticoid supplies that missing function.

Can I give extra prednisone when my dog seems tired?

Follow the written stress-dose plan. Tiredness has many causes, and repeated extra steroid can cause harm. If vomiting prevents medication retention or the dog is weak or collapsing, seek emergency care rather than repeatedly dosing by mouth.

What happens if an Addison's dog misses medication?

Risk depends on which drug, timing, and the dog's condition. Call the prescribing clinic immediately for instructions; do not double a dose automatically. Clinical illness, vomiting, weakness, or a missed critical injection may require urgent assessment.

How long can dogs live with Addison's disease?

Many treated dogs have an excellent prognosis and normal quality of life [1][2]. Individual lifespan depends on treatment consistency, crisis prevention, concurrent disease, and access to care; a fixed number cannot be guaranteed.

Is Addison's disease inherited?

Genetic susceptibility exists in some breeds, but inheritance is complex and population-specific [10]. There is no universal DNA clearance test. A family history raises awareness but does not diagnose an individual.

Key Takeaways

• Addison's disease causes cortisol deficiency and, in many primary cases, aldosterone deficiency.
• Signs can be intermittent and mimic gastrointestinal, kidney, and other diseases.
• Collapse, profound weakness, repeated vomiting, pale gums, or inability to retain medication is an emergency.
• Normal sodium and potassium do not exclude Addison's, and a low sodium-to-potassium ratio does not confirm it.
• A sufficiently high basal cortisol helps rule out disease; a low basal cortisol requires confirmation rather than assumption.
• The ACTH stimulation test is the standard confirmatory test, interpreted with steroid history and laboratory cutoffs.
• Long-term therapy replaces glucocorticoid and, when needed, mineralocorticoid; dose changes require veterinary monitoring.
• Atypical cases still need electrolyte surveillance because some progress.
• Most correctly treated dogs have an excellent long-term outlook.

References

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3. Bovens C, Tennant K, Reeve J, Murphy KF. Basal serum cortisol concentration as a screening test for hypoadrenocorticism in dogs. Journal of Veterinary Internal Medicine. 2014;28(5):1541-1545. PMID: 25066405; PMCID: PMC4895569.
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9. Gold AJ, et al. Prevalence, associated disease mechanisms, and outcome of dogs and cats with low blood sodium-to-potassium ratio. Journal of Veterinary Internal Medicine. 2026. PMID: 41934435.
10. Boag AM, Catchpole B. A review of the genetics of hypoadrenocorticism. Topics in Companion Animal Medicine. 2014;29(4):96-101. PMID: 25813849.
11. Sieber-Ruckstuhl NS, Reusch CE, Hofer-Inteeworn N, et al. Evaluation of a low-dose desoxycorticosterone pivalate treatment protocol for long-term management of dogs with primary hypoadrenocorticism. Journal of Veterinary Internal Medicine. 2019;33(3):1266-1271. PMID: 30865322; PMCID: PMC6524388.
12. Chalifoux NV, Larson MM, Panciera DL. Canine hypoadrenocorticism: insights into the Addisonian crisis. Frontiers in Veterinary Science. 2023. PMID: 37138712.