Addison's disease in dogs: symptoms, crisis and treatment

Overview

The adrenal glands are small organs beside the kidneys. They produce hormones including cortisol and aldosterone. Cortisol is a glucocorticoid, one of the body's own hormones regulating the stress response. Aldosterone is a mineralocorticoid affecting salt and fluid balance.

Cortisol helps maintain metabolism. It also affects the immune system. It is needed for normal digestive tract function too. Hormone deficiency therefore affects several organ systems. The disease is fairly uncommon in dogs. It is sometimes called an imitator of other illnesses because its signs are not distinctive.

Typical Addison's disease involves deficiency of both cortisol and aldosterone. In the atypical form, cortisol deficiency occurs without the usual electrolyte changes. Electrolytes may be normal in as many as 25–30% of patients. Normal sodium and potassium therefore do not rule out the disease.

Causes

The most common mechanism is damage to the adrenal cortex that is suspected to be immune-mediated. The body's defences may destroy the tissue responsible for hormone production. Inherited susceptibility is associated with some cases. This form originating in the adrenal gland is called primary insufficiency.

Less commonly, a tumour or bleeding damages the adrenal cortex. Medicines treating Cushing's disease can sometimes reduce hormone production too far. Abrupt withdrawal of prolonged corticosteroid treatment can also cause hormone deficiency. Do not stop medication yourself.

In the secondary form, the pituitary gland does not produce enough ACTH. ACTH directs the adrenal glands to make cortisol. Aldosterone production is usually preserved in secondary disease. In primary atypical disease, however, aldosterone deficiency may develop later.

Pituitary tumours or inflammation can be involved in the less common secondary hormone deficiency. Pituitary surgery can also affect ACTH production. Infection can occasionally underlie adrenal insufficiency.

Risk factors

Any age or breed can develop the disease. It is often diagnosed in young or middle-aged adults. Diagnosis commonly occurs at 4–6 years of age. Age is nevertheless no reason to leave an older dog with signs uninvestigated.

Females are often affected more than males. However, the effect of sex on risk is not entirely clear. Susceptible breeds include Standard Poodles, Portuguese Water Dogs and Great Danes. Bearded Collies, Rottweilers and West Highland White Terriers are also mentioned in relation to breed susceptibility. Susceptibility has also been described in Labrador Retrievers and Soft Coated Wheaten Terriers. Crossbreeds develop the disease too.

Typical symptoms

Signs can range from mild and temporary to severe illness. They may occur for days, weeks or months before diagnosis. Common signs at home include:

• Loss of appetite or eating less than usual.
• Intermittent vomiting.
• Recurring diarrhoea.
• Weight loss.
• Tiredness and little desire to exercise.
• Trembling or muscle weakness.
• Increased drinking and urination.

Initially, signs may appear only during stressful situations, such as infection, injury or surgery. Muscle weakness can make walking unsteady. Your dog's condition may improve between episodes. Muscle pain can also occur. Abdominal pain is possible too. During a crisis, vomit or diarrhoea may contain blood.

Complications and consequences

In an Addisonian crisis, circulating fluid volume falls and blood pressure drops dangerously. High potassium can cause slow heart rhythm disturbances. Blood glucose may fall markedly because of cortisol deficiency. Without treatment, a crisis can cause unconsciousness and death. Sudden collapse is therefore an emergency even in a dog whose previous signs were mild.

Fluid loss and low blood pressure can raise kidney blood values. These may improve rapidly with fluids without permanent kidney failure. However, the situation can initially resemble kidney disease itself. Appropriate treatment and regular monitoring give a good long-term outlook. There is no curative treatment.

Aldosterone deficiency can also involve metabolic acidosis, or increased acidity in the body. Poor treatment response and concurrent illness such as diabetes can worsen the outlook.

Diagnosis at the vet

The vet asks about the course of signs and previous medicines, and examines general condition. Basic tests include a blood count, blood biochemistry and a urine sample. Typical changes are high potassium and low sodium. A sodium-to-potassium ratio below 27 may raise suspicion. However, it is not specific to this disease.

The blood count may show mild anaemia. White blood cell changes normally associated with stress may be absent with cortisol deficiency. Biochemistry may show low albumin or cholesterol. Ionised blood calcium may also be raised. Heart rhythm and blood pressure are additionally monitored in a crisis.

A resting cortisol above 2 micrograms per decilitre effectively rules out the disease with almost 100% certainty if no corticosteroid medicine interferes with measurement. A low resting cortisol, however, does not confirm diagnosis. An ACTH stimulation test confirms it. This assesses the adrenal gland's ability to increase cortisol production in response to ACTH.

The test requires 2 blood samples. The first is taken before synthetic ACTH. In a standard protocol, another sample is taken after 1 hour. Methods using a 1–2-hour interval also exist. In Addison's disease, cortisol does not rise normally during testing. Results are compared with the laboratory's diagnostic threshold, often below 2 micrograms per decilitre.

ACTH testing primarily demonstrates cortisol deficiency rather than automatically showing aldosterone deficiency. Measuring the body's own ACTH can help distinguish an adrenal problem from a pituitary one. Endogenous ACTH is often high in primary disease. In secondary disease, it is usually low. X-rays or ultrasound may be needed to exclude other causes of signs.

Medication history includes both oral and topical corticosteroids. Some glucocorticoids can interfere with cortisol measurement through cross-reaction. A laboratory reference range established for healthy dogs differs from the diagnostic threshold for Addison's disease.

Treatment

The vet prescribes treatment and every medication change. Crisis treatment starts with intravenous fluids in emergency care. Fluids correct shock and dehydration. Severe sodium deficiency must be corrected in a controlled way because overly rapid correction can damage the nervous system. Blood pressure and electrolytes are monitored closely during treatment.

Low blood glucose is corrected with intravenous glucose when needed. Dangerously high potassium may require medication protecting the heart. Glucocorticoid replacement starts promptly. Vomiting and nausea are treated with medicines when necessary. Nutritional support is also provided according to circumstances.

Once your dog is stable, missing hormones are replaced with long-term medication. A glucocorticoid such as prednisone or prednisolone treats cortisol deficiency. Aldosterone deficiency requires mineralocorticoid replacement. Options include desoxycortone pivalate, or DOCP, and fludrocortisone. Fludrocortisone also has some glucocorticoid activity.

Medication is adjusted according to condition, response and electrolyte results. The aim is the lowest effective replacement treatment. Early in injection treatment, electrolytes may be checked at 10–14 days and again at 25 days. Once stable, rechecks may be every 3–6 months, for example. Your dog's circumstances may require more frequent monitoring.

Excessive glucocorticoid activity can increase thirst and urination. It can also increase appetite and panting. Prolonged excess may involve muscle wasting or hair loss. Report these changes to the vet treating your dog. Do not stop hormone replacement yourself based on signs.

Hydrocortisone, with both glucocorticoid and mineralocorticoid effects, can also be used in initial crisis care. Fludrocortisone alone does not adequately replace cortisol in every dog. Excessive hormone replacement can also increase infection susceptibility. Secondary insufficiency associated with abrupt corticosteroid withdrawal may sometimes be temporary. This differs from permanent adrenal cortex destruction, where replacement continues throughout life.

Hormone replacement in a stable dog can be started and managed as outpatient care.

Prevention

The exact cause of primary disease is often unknown, and no reliable prevention is known. In a diagnosed dog, prevention focuses on avoiding crises and maintaining treatment. Stress can make your dog unwell more readily than usual. Moving home, fireworks or another predictable stress may require a medication change planned in advance by the vet.

Keep daily life as calm and predictable as possible. Do not change medication without veterinary instructions. Abruptly stopping prolonged corticosteroid treatment can itself cause secondary hormone deficiency. Dogs with atypical disease continue to have electrolytes monitored because aldosterone deficiency may develop.

Important for dog owners

Keep a medicine list and the vet's written stress-management instructions readily available, including during travel and boarding. Put injection visits, blood tests and rechecks in your calendar. Record appetite, vomiting, diarrhoea, weight and changes in drinking or urination. Contact the practice if your dog vomits medication or refuses food. An ordinary good day is no reason to stop medicines, because typical Addison's disease requires lifelong hormone replacement.

Tell a new vet about the diagnosis and every current medicine before investigations or procedures. Topical corticosteroids also belong in the medication history. Establish in advance whom to call in an emergency and what to do if sudden vomiting or weakness starts. Collapse or reduced consciousness needs immediate treatment. The aim is for your dog to continue a normal, enjoyable daily life.

Frequently asked questions

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

Yes. Electrolytes remain normal in as many as 25–30% of affected dogs. Atypical disease can cause vomiting, tiredness and loss of appetite, for example. Based on signs, the vet may investigate cortisol production even when ordinary electrolyte values raise no suspicion.

Does low cortisol confirm the diagnosis?

Not automatically. Most dogs with resting cortisol below 2 micrograms per decilitre do not have Addison's disease. The result therefore requires ACTH stimulation testing when appropriate. The vet interprets it alongside signs, other blood results and medication history.

What happens during an ACTH test?

Your dog has 2 blood samples taken. Synthetic ACTH is given between samples to stimulate cortisol production. Depending on the method, the second sample is taken 1–2 hours later. The practice performing the test provides preparation instructions.

Is medication lifelong?

Typical Addison's disease usually requires lifelong cortisol and aldosterone replacement. Medicine needs and the appropriate amount are assessed from condition and blood tests. If signs return, do not change the amount yourself; ask the vet treating your dog what to do.

Can my dog live a normal life?

Most appropriately treated and monitored dogs have a good outlook and can lead a normal life. Untreated disease, however, can be life-threatening. Continuous medication, agreed rechecks and advance instructions for stressful situations form part of daily care.