Cushing’s Syndrome results from excessive adrenocortical activity, resulting from:

  • Often the use of corticosteroid medications
  • Infrequently secondary to adrenocorticotropic hyperplasia, tumor of the pituitary gland that produces adrenocorticotropic hormone (ACTH).
  • Regardless of the cause, the feedback mechanisms for the adrenal cortex become ineffective, resulting in oversecretion of glucocorticoids, androgens, and possibly mineralocorticoids.
  • Found five times more often in women aged 20 to 40 years old than men.

Assessment Findings

  • Arrested growth, weight gain/obesity, musculoskeletal changes, and glucose intolerance.
  • Classic features: central obesity, buffalo hump (fatty deposit in the neck and supraclavicular areas), a heavy trunk, relatively thin extremities. Thin and fragile skin with ecchymoses and striae.
  • Weakness and lassitude due to affected diurnal cortisone production.
  • Excessive protein catabolism (muscle wasting, osteoporosis, kyphosis, backaches, compression fractures of the vertebrae)
  • Retention of sodium and water, resulting in hypertension and heart failure.
  • Moon-face, oiliness of the skin, and acne formation.
  • Increased susceptibility to infection; slow healing of minor cuts and bruises.
  • Hyperglycemia or overt diabetes.
  • Female Virilization; recession of feminine traits (hirsutism, breast atrophy, amenorrhea, clitoral enlargement, deepened voice) due to excess androgen secretion.
  • Mood and mental changes. Psychosis may develop, distress, and depression are common.
  • If caused by a pituitary tumor, visual disturbances may occur secondary to pressure on the optic chiasm.

Diagnostic Examination

  • Overnight dexamethasone suppression test to measure plasma cortisol levels (stress, obesity, depression, and medications may affect results).
  • Serum Sodium and Potassium, Blood Glucose, 24-hour urinary free cortisol level
  • Imaging Studies (CT, UTZ, MRI) may localize adrenal tissue and detect adrenal tumors.

Medical Management

In many cases, the pituitary gland is the affected site, and not the adrenal cortex.

  • If exogenous corticosteroids are the cause, taper the drug to minimal levels or use alternate-day therapy.
  • Surgical removal of the tumor by transsphenoidal hypophysectomy, which is successful 80% of the time.
  • Radiation may also be used, but takes several months to achieve symptomatic control.
  • If primary adrenal hypertrophy is the cause, then an adrenalectomy may be performed.
  • After surgery, temporary hydrocortisone replacement may be necessary until the adrenal glands respond normally. This may last for several months.
  • If bilateral adrenalectomy is done, lifetime adrenal hormone replacement therapy is required.
  • If ACTH-secreting tumors are the cause, and they cannot be removed, then adrenal enzyme inhibitors may be used. However, the patient should be monitored closely for inadequate adrenal function and other side effects.
    • Metyrapone, Aminoglutethimide, Mitotane, Ketoconazole

Nursing Management

Assessment

  • Focus on the effects of the adrenal cortex hormones on the body
    • Level of activity, ability to perform routine and self-care activity
    • Skin trauma, infection, breakdown, bruising, and edema
    • Changes in appearance, and the patient’s response to it
    • Mental function, mood changes, depression, environmental awareness

Diagnosis and Intervention

  1. Risk for injury r/t weakness
    • Decrease risk of injury: provide a protective environment, assist the patient in ambulating, recommend foods high in protein, calcium, and vitamin D (refer to dietitian)
  2. Risk for infection r/t altered protein metabolism and inflammatory response
    • Decrease risk of infection: avoid exposure to individuals with infections. Assess frequently for subtle signs of infections (corticosteroids may mask the signs of inflammation and infections)
  3. Self-care deficits r/t weakness, fatigue, muscle wasting, and altered sleep patterns
    • Encouraging rest and activity: encourage moderate activity to prevent complications of immobility and promote self esteem. Plan periods of rest throughout the day and provide a relaxing, quiet environment.
  4. Impaired skin integrity r/t edema, impaired healing, and thin fragile skin
    • Promoting skin integrity: meticulous skin care, avoidance of adhesive tape on skin, frequent assessment of skin and bony prominences, and frequent position changes minimize trauma to the skin.
  5. Disturbed body image r/t altered appearance, sexual functioning, and decreased activity level
    • Improving body image: discuss the impact of the disease on the client’s self-concept. Acknowledge that major physical changes can be reversed if the cause of the syndrome is treatable. Diet (low-carbohydrate, low-sodium diet with a high-protein intake) can also reduce some bothersome symptoms.
  6. Disturbed thought processes r/t mood swings, irritability, and depression
    • Improving thought process: explain to the patient and family the causes of emotional instability, and help them cope. Encourage them to verbalize their feelings and concerns. Ask them to report any psychotic (hallucination, delusion, and illusion) behavior.
  7. (Collaborative) Addisonian Crisis:
  8. (Collaborative) Adverse Effects of Adrenocortical Activity
  9. Preparing the patient for surgery: monitor blood glucose levels, and assess stools for blood because diabetes mellitus and peptic ulcers are common problems.
  10. Teaching the patient self-care: present information about the disease (verbal and written).
    • Emphasize the importance of weaning corticosteroid medication instead of abruptly stopping.
    • Emphasize the importance of an adequate supply.
    • Stress dietary modifications (increased calcium, protein) are required in order to counteract effects of the disease e.g. osteoporosis and muscle wasting.
    • Emphasize important of regular medical follow-ups.