Canine Hypoadrenocorticism

(Addison Disease)

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Unit: 3

4^th Professional Dr. Anil Kumar

Asst. Professor

Dept. of VCC, BVC, Patna

ADDISON DISEASE

The adrenal glands are essential for life, being responsible for the minute-to-minute regulation of blood pressure, blood volume, and vascular tone.

ADRENAL GLAND

Outer Zone (Cortex)

Inner Zone (Medulla)

The zona glomerulosa,

Zona fasciculate

(70% of the cortex)

Zona reticularis

Mineralocorticoid (Aldosterone)

Glucocorticoid(Cortisol)

Sex steroids

• Ion transport by epithelial cells, resulting in a loss of potassium and retention of sodium.
• A lack of secretion of mineralocorticoids (Addison disease) may result in a lethal retention of potassium and loss of sodium.

• carbohydrate, protein, and lipid metabolism result in sparing of glucose
• Decrease lipogenesis and increase lipolysis in adipose tissue
• suppress inflammatory and immunologic responses
• Favors the spread of infection.
• Negative effect on wound healing (fibroblast proliferation and collagen synthesis )

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• Progesterone, estrogens, and androgens are adrenal sex hormones

• Adrenal hormones are necessary to control salt, sugar and water balance in the body.
• It results from the lack of glucocorticoids, mineralocorticoids, or both
• It is seen most commonly in young to middle-aged female dogs and occasionally in horses.

Etiology:

• Primary—Unknown, but most cases probably result from an autoimmune process and characterized by a lack of glucocorticoids and mineralocorticoids.
• Others :
• Destruction of the adrenal gland by granulomatous disease
• Metastatic tumor,
• Hemorrhage
• Infarction
• Adrenolytic agents (mitotane), or
• adrenal enzyme inhibitors (trilostane)

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FORMS OF HYPOADRENOCORTICISM

Primary Hypoadrenocorticism

• Characterized by a lack of glucocorticoids and mineralocorticoids
• Mostly associated with immune-mediated destruction of adrenal cortical tissue
• Mitotane or trilostane for Hyperadrenocorticism treatment
• Neoplasia, infection, or infarction of the adrenal glands

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Atypical

Hypoadrenocorticism

• Seen in small population of “atypical” dogs
• Adrenal destruction is purported to spare the glomerulosa layer, resulting in an isolated glucocorticoid deficiency and so, do not progress to clinically significant mineralocorticoid deficiency
• Isolated glucocorticoid insufficiency is more commonly seen in older dogs with vague GI signs, weight loss, normal electrolyte concentrations, hypoalbuminemia and hypocholesterolemia.

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Secondary

Hypoadrenocorticism

• It is refers to a central (anterior pituitary) deficiency of ACTH and lead to
• isolated glucocorticoid insufficiency
• Mineralocorticoids are spared because ACTH does not directly influence their release.
• It mainly results from results from abrupt discontinuation of long-term exogenous administration of corticosteroids or progesterone analog
• Rarely, congenital defects of the pituitary gland ( a cystic Rathke’s pouch, neoplasia, or trauma)

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Age, Sex and Breed:

• Dogs of any sex, age, or breed (including mixed breeds) can develop the disease.
• The disease is heritable in certain breeds:

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Clinical Signs:

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• The Addisonian crisis is the life-threatening culmination of combined hormone deficiencies that can be fatal if not appropriately treated

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DIAGNOSIS: The disease is diagnosed on the basis of a:

• Compatible history
• Clinical signs
• Laboratory abnormalities
• Imaging studies and
• ACTH stimulation test results

Note:

The combination of

Na/K ratio with lymphocyte

count is a better screening test

for hypoadrenocorticism

than either variable alone.

• Patients with atypical hypoadrenocorticism are more likely to exhibit hypoalbuminemia, hypocholesterolemia, and anemia on routine blood work.

Diagnostic Imaging:

• Thoracic radiographs may reveal a small heart and caudal vena cava, which indicates hypovolemia
• On abdominal ultrasonography, atrophy of the adrenal glands with thin and short as compared with normal, but in some cases there may benormal size adrenal glands.

ECG: Depending upon the degree of hyperkalemia, the ECG may

• Reveal a bradyarrhythmia with absent P waves
• Tented T waves
• Prolonged QRS complexes, and
• decreased R wave amplitude

ACTH Stimulation Test:

• The gold standard for diagnosis of all forms of hypoadrenocorticism; it should be performed in any patient suspected of having the disease.
• A baseline serum cortisol level > 2 mcg/dL can be used to rule out hypoadrenocorticism, while a cortisol level ≤ 2 mcg/dL necessitates an ACTH stimulation test.

TREATMENT: The main goal of therapy is to:

• Restoration of blood volume
• Correction of electrolyte/acid-base disorders
• Fluid therapy: is always be instituted prior to the use of adrenal steroid replacement therapy and can be performed while the patient is undergoing the ACTH stimulation test.
• Starting with aggressive IV fluid therapy with isotonic crystalloids (0.9% sodium chloride, Ringer’s lactate solution)

To solve an adrenal crisis is an acute medical emergency:

• An infusion with 0.9% saline should be started.
• If the dog is hypoglycemic, the saline should include 2.5%–5% dextrose.
• The hypovolemia is corrected rapidly by administering 0.9% saline (60–70 mL/kg throughout the first 1–2 hours).
• Urine output should be assessed to determine whether the dog is becoming anuric.
• Fluids should be continued, at a rate appropriate to match ongoing losses, until the clinical signs and laboratory abnormalities have resolved.
• If hyperkalemia persists despite fluid resuscitation and mineralocorticoid replacement therapy, suspect renal failure and monitor patient for oliguria or anuria.

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Additionally, to correct life-threatening hyperkalemia:

• Consider treatment with dextrose (10% glucose in 0.9% saline can be given for 30–60 min to increase potassium movement into the cells) and regular insulin (0.25–1 U/Kg, IM, will enhance glucose and potassium uptake), addressing metabolic acidosis, or
• Treatment with a beta-adrenergic drug, such as terbutaline or albuterol.
• Prednisolone sodium succinate (22–30 mg/kg) or dexamethasone sodium phosphate (0.2–1 mg/kg) may be used in the initial management of shock.
• Prednisolone or prednisone should be given at 1 mg/kg, twice a day, for the first few days of therapy and then at 0.25–0.5 mg/kg/day.
• Mineralocorticoid replacement therapy is also begun to help with electrolyte imbalances and hypovolemia.
• Electrolytes, renal function, and glucose should be monitored regularly to assess response to therapy.

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For long term maintenance therapy :

• The mineralocorticoid desoxycorticosterone pivalate (DOCP) is administered at 2.2 mg/kg, IM or SC, every 25–28 days.
• Electrolytes should be measured at 3 and 4 weeks after the first few injections to determine the duration of action.
• Alternatively, fludrocortisone acetate is administered PO at 10–30 mcg/kg/day. Serum electrolytes should be monitored weekly until the proper dose is determined.
• Some dogs (especially dogs on DOCP) also require daily oral glucocorticoid therapy to adequately control clinical signs.
• in ~50% of dogs, replacement doses of prednisone (0.2–0.4 mg/kg/day) are required
• Dogs with atypical Addison disease require only replacement doses of prednisone, although it is recommended that electrolytes be monitored every 3 months for the first year after diagnosis.
• Dogs with chronic hypoadrenocorticism should be re-examined every 3–6 months