There are a number of clinical signs that may lead us to suspect hyperadrenocorticism, and dogs suffering from the disease may show some or all of them. Unfortunately, because Cushing’s disease is a progressive chronic disease, the onset and development of symptoms is often so gradual that many dog owners mistake them for the normal signs of ageing. This is a natural mistake to make but, given how common the disease is in dogs it underlines the importance of ensuring that your dog has a regular annual veterinary check. One study showed that most dogs had been showing at least one symptom for between one and six years before the disease was eventually diagnosed.

Many of the symptoms are also not unique to Cushing’s and may indicate other health issues, making clinical diagnosis more complex. The main signs of the onset of hyperadrenocorticism are:

• Increased or excessive water consumption (polydipsia)
• Increased/excessive urination (polyuria), a by-product of increased water consumption
• Urinary accidents in previously housetrained dogs
• Increased/excessive appetite (polyphagia)
• Sagging, bloated, pot-bellied appearance
• Apparent weight gain, due to fat redistribution
• Loss of muscle mass, giving the appearance of weight loss
• Bony, skull-like appearance of head
• Exercise intolerance, lethargy, general or hind-leg weakness
• Excess panting, seeking cool surfaces to rest on
• Symmetrically thinning hair or baldness (alopecia) on torso
• Other coat changes like dullness, dryness
• Slow regrowth of hair after clipping
• Thin, wrinkled, fragile, and/or darkly pigmented skin
• Easily damaged/bruised skin that heals slowly
• Hard, calcified lumps in the skin (calcinosis cutis)
• Susceptibility to infections (especially skin and urinary)
• Diabetes, pancreatitis and seizures.

The most common reasons owners first bring their dog to the hospital for evaluation are increased water consumption — which affects more than 85% of animals with the disease and can be up to ten times their previous intake — the increased urination that follows higher water consumption, and thinning hair or hair loss.

Increased appetite is seen in around 80% of affected animals. Dogs may beg continually, begin to steal food, and become protective of their food. Often, the owner will assume that the dog is fine because he has a ‘good appetite.’ A pot-bellied appearance is also common, as is hair loss and thin skin, which usually starts around the elbows and spreads to the flanks and abdomen until eventually hair remains only on the head and extremities.

Initially, general blood and urine tests will give us a presumptive diagnosis. However, because most dogs only exhibit some of the signs of the disease, and many signs can also be caused by other metabolic diseases, further confirmatory tests are necessary. These will include a complete blood count (CBC), blood chemistry panel, and urinalysis.

Radiographs (x-rays) of the abdomen and chest may help us further define the cause. Sometimes the tumour has spread from the original site to the lungs; chest x-rays allow us to check for this. As most dogs with Cushing’s are relatively old we also check for other problems at the same time.

An abdominal ultrasound can also be helpful. It is a useful test to evaluate all of the abdominal organs. We can also use it to study the size and shape of the adrenal glands. In pituitary dependent hyperadrenocorticism the adrenal glands are usually normal in size, or enlarged. If a tumor is present however, one adrenal gland is often abnormally large or of uneven shape. Finally, if a tumor is suspected, ultrasound can help identify any metastasis to other organs such as the lungs.

There are a number of different treatment options available. Non-surgical medical management is the most common, and the treatment of choice at Alpine Animal Doctors. There are currently several different oral medications being used to treat canine Cushing’s disease and both pituitary dependent hyperadrenocorticism and adrenal-based hyperadrenocorticism tend to respond effectively to one or other of these treatments. Essentially, the oral medications used act in similar ways to chemotherapy treatments, destroying cells of the adrenal gland that produce the corticosteroid hormones.

Depending on the type of disease, particularly where an adrenal tumor is identified, surgical removal of the affected adrenal gland and the tumour causing the problem is also an option (pituitary tumors are not removed surgically).

In theory, surgical removal of an adrenal tumour will cure adrenal-based Cushing’s disease, and it is true that, once removed, these tumours tend not to recur on the remaining adrenal gland. However, an adrenalectomy is a high risk surgery and, given that most patients are elderly dogs, the risks are compounded for most Cushing’s patients. With the availability of modern oral drug treatments we see little reason to subject a senior dog to surgery when an acceptable outcome can usually be achieved with medication.

The prognosis for dogs treated for Cushing’s disease is generally very good. Symptoms such as excess drinking and urinating normally drop off quite quickly, although it can take several months for hair and skin to improve. Generally, however, patients are much more comfortable once the disease is under control, and usually live happily for a number of years.

However, it should be understood that Cushing’s disease can only be managed. We cannot cure the condition. The objective of treatment is to improve the quality of life and to increase life expectancy. We can usually achieve that but hyperadrenocorticism is a serious condition and maintaining a dog with Cushing’s disease requires vigilance and commitment on the part of the owner.

Cushing’s disease is a complex disorder involving the relationship between a number of different organs. In a normal, healthy dog the hypothalamus — an organ of the brain — ‘directs’ the pituitary gland, located at the base of the brain, to produce adrenocorticotrophic hormones (ACTH). This hormone is released into the bloodstream and stimulates the body’s two adrenal glands, which are located near the kidneys, to secrete another hormone — glucocorticoid (cortisone-like or cortisol)  — into the bloodstream.

Cortisol is necessary for life and affects a wide range of bodily functions in the dog, including blood sugar levels, fat metabolism, skeletal muscles, kidney function, nervous system, cardiovascular system, and immune response. ACTH/cortisol secretion is increased when an animal becomes stressed, from cold, heat, infection, pain, surgery, trauma etc. If blood cortisol levels rise high enough, the pituitary ceases to secrete ACTH. When blood cortisol levels fall, the pituitary secretes more ACTH. The response of the adrenal glands is to secrete glucocorticoid hormones in response to the pituitary, just as the pituitary responds by secreting ACTH in response to the adrenals. The end result is that, in a healthy dog, a balance is achieved.

In Cushing’s disease something goes wrong with this complex feedback loop. The result is a chronic excess of blood cortisol, caused by either a pituitary tumor or an adrenal tumour. Put simply, too much cortisol is poisoning the dog, who can no longer rely on its own feedback mechanism to regulate blood cortisol levels.

In the most common cause of Cushing’s, pituitary dependent hyperadrenocorticism, a tiny (usually less than 3mm in diameter), benign pituitary tumour (microadenoma) secretes an oversupply of ACTH, and ignores the response of the adrenals. The dog’s pituitary continues to pump out ACTH, causing the adrenals to keep producing cortisol, but the pituitary gland does not respond to the elevated blood cortisol levels by stopping its release of ACTH. Dogs with pituitary dependent hyperadrenocorticism are usually found to have two very large adrenal glands, both constantly working to try to keep up production of excess cortisol.

Larger pituitary tumors or macroadenomas (over 1 cm in diameter) are less common but where they do occur they can cause blindness,  seizures,or other neurological problems not directly related to hyperadrenocorticism because of the pressure their size places on brain tissue and nerves.

The less frequently diagnosed adrenal-based hyperadrenocorticism is also caused by a tumour, but located in the adrenal gland and responsible for secreting too much cortisol. The same type of faulty feedback mechanism sees the interaction between pituitary and adrenal messages get ‘lost’, and the tumour continues to secrete too much cortisol regardless of what the brain is telling it. About half of all adrenal tumours are benign (adenomas). The rest are malignant adenocarcinomas and can spread to the lungs and liver.