Basics

DEFINITION

An endocrine disorder resulting from deficient production of glucocorticoids and/or mineralocorticoids in the adrenal glands. Most often, the cause is unknown. It is as if the adrenal glands have “used up” their supply of cortisol. Cortisol's most important job is to help the body respond to stress.

Breed Predilections

• Great Danes, Rottweilers, Portuguese Water Dogs, Standard Poodles, West Highland White Terriers, and Wheaten Terriers have increased relative risk.
• No predilection in cats. All breeds and mixes are affected equally.

Mean Age and Range

• Dogs—range, < 1 to > 12 years; median, 4 years
• Cats—range, 1–9 years; most are middle-aged

Predominant Gender

Female dogs are at an increased relative risk; no predilection in cats.

SIGNS

General Comments

Vary from mild and few in some patients with chronic hypoadrenocorticism to severe and life-threatening in an acute addisonian crisis

Historical Findings

• Dogs—lethargy, anorexia, vomiting, weight loss, waxing/waning course, diarrhea, previous response to therapy, shaking, PU/PD
• Cats—lethargy, anorexia, vomiting, PU/PD, weight loss

Physical Examination Findings

• Dogs—depression, weakness, dehydration, collapse, hypothermia, black, tarry feces, weak pulse, slow pulse, painful abdomen, hair loss
• Cats—dehydration, weakness, weak pulse, slow pulse

CAUSES

• Primary hypoadrenocorticism—Most cases are caused by the gradual destruction of the adrenal cortex, the outer layer of the adrenal glands, by the body's own immune system. About 70 percent of reported cases of Addison's disease in humans are caused by autoimmune disorders, in which the immune system makes antibodies that attack the body's own tissues or organs and slowly destroy them.
• Secondary hypoadrenocorticism—This form of adrenal insufficiency is much more common than primary adrenal insufficiency and can be traced to a lack of ACTH from the pituitary gland. Without ACTH to stimulate the adrenals, the adrenal glands' production of cortisol drops. The pituitary gland may stop producing ACTH because of:
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      • tumors or infections of the area
      • loss of blood flow to the pituitary
      • radiation for the treatment of pituitary tumors
      • surgical removal of parts of the hypothalamus
      • surgical removal of the pituitary gland

Diagnosis

DIFFERENTIAL DIAGNOSIS

• Signs are nonspecific and are seen in other, more common medical disorders, particularly gastrointestinal and renal diseases.
• Although no signs are characteristic of Addison’s disease, a waxing and waning course and previous response to nonspecific medical intervention (“fluids and steroids”) should alert your veterinarian to consider the diagnosis.

CBC/BIOCHEMISTRY/URINALYSIS

• A blood sample taken from your pet may indicate anemia, high white cell count, and lymph cells, indicating infection or inflammation.
• The blood sample might also indicate abnormalities in electrolytes.
• Urinalysis often reveals impaired urine-concentrating ability.
• Note: some patients with hypoadrenocorticism exhibit normal electrolyte levels.

OTHER LABORATORY TESTS

Definitive diagnosis is by demonstration of undetectable-to-low serum cortisol concentrations that fail to increase after administration of ACTH gel. Your pet will spend several hours with us while we perform two blood tests. We will draw blood when you first bring him or her in with an empty stomach. Then we will inject ACTH, wait a few hours for it to circulate in the blood, then draw more blood and send both samples to the laboratory. Results will be available the next day.

IMAGING

Occasionally, ultrasound of the adrenal glands might be done to determine if they have shrunk in size (relative to “normal.”) Treatment

APPROPRIATE HEALTH CARE

• Treatment of chronic hypoadrenocorticism depends on replacing what the body is no longer making. Prednisone is used to replace glucocorticoids and often times can be discontinued once the body stabilizes.
• A drug known as Percotin V is now available to replace mineralocorticoids, which makes living with this disease entirely possible. You will bring your pet to the clinic about once a month where we will recheck the blood levels and determine if, and how much of, an injection is needed.

ACTIVITY

No alteration necessary

DIET

No need to alter

CLIENT EDUCATION

• Lifelong replacement therapy is required.
• Increased dosages of replacement cortisol are required during periods of stress such as travel, hospitalization, and surgery.

Follow-Up

PATIENT MONITORING

PREVENTION/AVOIDANCE

• Continue hormonal replacement therapy for the lifetime of the patient. • Increase the dosage of replacement glucocorticoid during periods of stress such as travel, hospitalization, and surgery. POSSIBLE COMPLICATIONS
• PU/PD may occur from prednisone administration, necessitating decreasing or discontinuing the drug. EXPECTED COURSE AND PROGNOSIS

Except for patients with primary hypoadrenocorticism caused by granulomatous or metastatic disease and secondary hypoadrenocorticism caused by a pituitary mass, the vast majority of patients carry a good to excellent prognosis following proper stabilization and treatment.