Addison's Disease (Hypoadrenocortism)
What is Addison's Disease?
Addison's disease is an uncommon disease typically affecting young and middle aged dogs. It is usually caused by immune immediated destruction of the adrenal glands.The disease is characterised by deficiency of both mineralocorticoids and glucocorticoids. Mineralocorticoids are produced by the adrenal glands to control the excretion of sodium and potassium. Hence in patients with Addison's disease the lack of mineralocorticoids leads to impaired ability of the kidneys to conserve sodium and excrete potassium. Glucocorticoids are also produced by the adrenal glands and they have an effect on most body tissues. Lack of glucocorticoids that occurs with Addison's disease causes a range of signs, including vomiting, diarrhoea, depression, lethargy, lack of eating, weight loss, slow heart rate and collapse.
The problem in diagnosing and treating Addison's disease is that most of the clinical signs are also frequently seen assoicated with a wide range of more common diseases. Therefore, careful history taking and appropriate blood tests are required to confirm the presence of Addison's disease.
How can Addison's Disease be Diagnosed?
A full blood test must be conducted when Addison's disease is suspected. Classically the blood tests will show a 'stress leucogram' (i.e. high neutrophils, low lymphocytes and eosinophils), together with high potassium and low sodium levels. Electrocardiography can also be helpful in that there will be slow heart rate and a specific pattern present that is characteristic of the high potassium level in blood.
As various tests create a high degree of suspicion of Addison's disease, a special blood test known as ACTH stimulation test is performed to confirm the diagnosis. This test aims to maximally stimulate the adrenal glands, and dogs with the disease typically show a low to negligible response to the test.
What is the Treatment for Addison's Disease?
Acute cases can be life threatening and aggressive treatment is vital. The affected dog must receive aggressive fluid to correct the dehydration (preferably with intravenous saline, or intravenous dextrose when the dog's glucose level in blood is low). Injectable glucocorticoids must also be administered to replace the deficiency. The injectable glucocorticoid is swapped to tablet form once the affected dog returns eating. Mineralocorticoids are also administered (usually in the form of oral tablets). During this treatment program blood tests are regularly taken to monitor the electrolyte (especially sodium and potassium) and glucose levels. The dose of glucocorticoid and mineralocorticoid treatment is adjusted until the blood electrolyte and glucose levels return to normal.
The dog requires long term therapy after his/her condition becomes stable. The therapy includes mineralocorticoid supplementation and in most cases glucocorticoid as well. Salt is also added to the diet. Blood tests looking at electrolyte and kidney enzyme levels are initially tested once every 1 to 2 weeks, and then when the dog is stabilised once every 3 to 4 months. The mineralocorticoid dose will be increased when the sodium level is low and potassium level is high.
The dog can normally be stabilised and live a fairly normal life for quite some years with this sort of treatment regime, so long as the monitoring program is maintained.