Hypoadrenocorticism [Addison's Disease]
Learn what the condition is, how it may be detected early, how it is treated or managed, and which breeds or species are linked to it.
Learn what the condition is, how it may be detected early, how it is treated or managed, and which breeds or species are linked to it.
A concise guide to the condition’s pattern, detection, management and urgency.
This snapshot is a general guide, not a diagnosis or treatment plan. New, severe or worsening signs require veterinary assessment.
Hypoadrenocorticism, commonly called Addison’s disease, occurs when the adrenal glands do not produce enough of the hormones needed to help the body respond to stress and maintain normal fluid and electrolyte balance. The two hormones of greatest importance are cortisol and aldosterone. When both are deficient, sodium and potassium levels can become abnormal and the dog may struggle to maintain blood pressure, hydration and normal heart function. Some dogs develop an atypical form in which cortisol is low but electrolyte changes are not initially present. Addison’s disease is seen most often in young to middle-aged dogs and some breeds have a recognised predisposition, although any dog can be affected.
The early signs can be frustratingly vague. A dog may seem tired, lose interest in food, lose weight, vomit, develop diarrhoea or appear weak for a few days and then improve. These episodes can recur, particularly after stress, illness, travel or other changes in routine.
The most serious presentation is an Addisonian crisis. Affected dogs can become profoundly weak, dehydrated, collapse or develop dangerous heart rhythm abnormalities as potassium rises and circulation deteriorates. This is a medical emergency requiring immediate veterinary treatment. Once Addison’s disease is recognised and hormone replacement is stabilised, however, the outlook is generally very good. Most treated dogs can return to normal activity and enjoy a normal quality of life, provided medication and monitoring are maintained consistently.
The key difficulty is inconsistency: mild disease can resemble a stomach upset, while an Addisonian crisis can become life-threatening very quickly. Recurrent, unexplained episodes of gastrointestinal illness or weakness therefore deserve investigation even when the dog seems completely normal between them.
Particular attention is paid to sodium, potassium and the sodium-to-potassium ratio, although these values can remain normal in atypical Addison’s disease.
Routine population screening cannot currently predict which healthy dog will later develop Addison’s disease, so early detection depends on recognising suspicious patterns and investigating them promptly. In predisposed breeds, a veterinarian may choose to establish baseline blood results in a young adult and repeat routine biochemistry periodically. A complete blood count can also provide useful clues when a dog that appears unwell does not show the expected stress response.
Testing should be brought forward whenever a dog has repeated episodes of vomiting, diarrhoea, poor appetite, unexplained weight loss, weakness, shaking or unusual lethargy, especially when signs improve temporarily with fluids or supportive treatment and then return. A resting cortisol measurement may be used to help rule out the disease, while an ACTH stimulation test is the standard test used to confirm inadequate adrenal response.
Once Addison’s disease is diagnosed, thyroid function may also be assessed when clinically appropriate because autoimmune endocrine disorders can occasionally occur together. Treat sudden collapse, marked weakness or severe gastrointestinal illness as urgent rather than waiting for a routine appointment.
Because the signs mimic many gastrointestinal and metabolic conditions, Addison’s disease may remain unrecognised until testing is performed. Routine blood work can raise suspicion when characteristic electrolyte changes are present, but normal electrolytes do not exclude atypical disease.
Treatment depends on whether the dog is stable or experiencing an Addisonian crisis. A crisis requires hospital care with intravenous fluids to restore circulation and correct dehydration, careful management of dangerous electrolyte abnormalities, and glucocorticoid medication to replace deficient cortisol. Heart rhythm and blood chemistry are monitored closely because severe potassium elevation can interfere with normal cardiac function. Once the dog is stable, treatment moves to long-term hormone replacement.
Most dogs require lifelong mineralocorticoid replacement to control sodium and potassium balance. This may be given as a regular injectable medication or, in some cases, an oral mineralocorticoid. A low maintenance dose of a glucocorticoid is also commonly prescribed. Dogs with atypical Addison’s disease may initially need glucocorticoid replacement alone, although electrolytes should still be monitored because mineralocorticoid deficiency can develop later.
Medication doses are adjusted using the dog’s clinical response and repeat electrolyte testing. Additional glucocorticoid is often needed during periods of significant stress, illness, surgery or other events that increase the body’s normal cortisol requirement; owners should follow their veterinarian’s individual “stress dosing” instructions. Consistent medication is essential and should not be stopped abruptly. With appropriate replacement therapy, scheduled blood tests and prompt attention to breakthrough signs, the long-term prognosis is usually excellent.
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