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Cushing’s Syndrome

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Cushing’s syndrome results from excessive adrenocortical activity. It may result from excessive administration of corticosteroids or adrenocorticotropic hormone (ACTH) or from hyperplasia of the adrenal cortex. It may be caused by several mechanism, including a tumor in the pituitary gland or less commonly an ectopic malignancy that produces ACTH. Regardless of the  cause, the negative feedback mechanisms that control the functions of the adrenal cortex  become ineffective, resulting in oversecretion of glucocorticoids, androgens, and possibly mineralocorticoid. Cushing syndrome occurs five times more often in women ages 40 to 60 years than in men.

Clinical Manifestations

  • Arrested growth, weight gain and obesity, musculoskeletal changes, and glucose intolerance
  • Classic features: central-type obesity, with a fatty “buffalo hump” in the neck and supraclavicular area, a heavy trunk, and relatively thin extremities; skin is thin, fragile, easily traumatized, with ecchymoses and striae
  • Weakness and lassitude; sleep is disturbed because of altered diurnal secretion of cortisol.
  • Excessive protein catabolism with muscle wasting and osteoporosis; kyphosis, backache, and compression fractures of the vertebrae are possible
  • Retention of sodium and water, producing hypertension and heart failure
  • “Moon-faced” appearance, oiliness of skin and acne
  • Increased susceptibility to infection; slow healing of minor cuts and bruises
  • Hyperglycemia or overt diabetes
  • Virilization in females (due to excess androgens) with appearance of masculine traits and recession of feminine traits (eg; excessive hair on face, breasts atrophy, menses cease, clitoris enlarges, and voice deepens); libido is lost in males and females
  • Changes occur in mood and mental activity; psychosis may develop and distress and depression are common
  • If Cushing’s syndrome is the result of a pituitary tumor, visual disturbances are possible cause of pressure on the optic chiasm

Assessment and Diagnostic Findings

  • Overnight dexamethasone  suppression test to measure plasma corticol level (stress, obesity, depression, and medications may falsely elevate results)
  • Computed tomography (CT) or magnetic resonance imaging (MRI) scan or ultrasound may localize adrenal tissue and detect adrenal tumors

Medical Management

Treatment is usually directed at the pituitary gland because most cases are due to pituitary tumors rather than tumors of the adrenal cortex.

  • Surgical removal of the tumor (transsphenoidal hypophysectomy) is the treatment of choice (90% success rate.
  • Radiation of the pituitary gland is successful but takes several months for symptom control.
  • Adrenalectomy is performed in  patients with primary adrenal hypertrophy
  • Postoperatively, temporary replacement therapy with hydrocortisone may be necessary until the adrenal glands begin to respond normally (may be several months)
  • If bilateral adrenalectomy was performed, lifetime replacement of adrenal cortex hormones is necessary
  • Adrenal enzyme inhibitors (eg, metyrapone or mitotane) may be used with ectopic ACTH-secreting tumors that cannot be totally removed; monitor closely for inadequate adrenal function and side effects
  • If Cushing’s syndrome results from exogenous corticosteroids, taper the drug to the minimum level or use alternate day therapy to treat the underlying disease.

NURSING PROCESS: The Patient with Cushing’s Syndrome

Assessment

  • Focus on the effects on the body of high concentrations of adrenal cortex hormones
  • Assess patient’s level of activity and ability to carry out routine and self-care activities
  • Observe skin trauma, infection, breakdown, bruising and edema
  • Note changes in appearance and patient’s response to these changes, family is good source of information about patient’s emotional status and changes in appearance
  • Assess patient’s mental function. including mood, response to questions, depression, and awareness of environment

Diagnosis

Nursing Diagnoses

  • Risk for injury related to weakness
  • Risk for infection related to altered protein metabolism and inflammatory response
  • Self-care deficits related to weakness, fatigue, muscle wasting, and altered sleep patterns
  • Impaired skin integrity related to edema, impaired healing, and thin and fragile skin
  • Disturbed body image related to altered appearance, impaired sexual functioning, and decreased activity level
  • Disturbed thought processes related to mood swings, irritability, and depression

Collaborative Problems/Potential Complications

  • Addisonian crisis
  • Adverse effects of adrenocortical activity

Planning and Goals

Major goals include decreased risk for injury, decreased risk for infection, increased ability to carry out self-care activities, impaired skin integrity, improved body image, improved mental function, and absence of complications.

Nursing Interventions

Decreasing Risk for Injury

  • Provide a protective environment to prevent falls, fractures, and other injuries to bones and soft tissues
  • Assist the patient who is weak in ambulating to prevent falls or colliding into furniture
  • Recommend foods high in protein, calcium, and vitamin D to minimize muscle wasting and osteoporosis; refer to dietitian for assistance

Decreasing Risk for Infection

  • Avoid unnecessary exposure to people with infections
  • Assess frequently for subtle signs of infections (corticosteroids mask signs of inflammation and infection)

Promoting Skin Care

  • Use meticulous skin care to avoid traumatizing fragile skin
  • Avoid adhesive tapes, which can tear and irritate the skin
  • Assess skin and bony prominences frequently
  • Encourage and assist patient to change positions ffrequently

Improving Body Image

  • Discuss the impact that changes have had on patient’s self-concept and relationships with others. Major physical changes will disappear  in time if the cause of Cushing’s syndrome can be treated.
  • Weight gain and edema may be modified by a low-carbohydrate, low-sodium diet; a high in protein intake can reduce some bothersome symptoms

Improving Thought Processes

  • Explain to patient and family the cause of emotional instability and help them cope with mood swings, irritability, and depression
  • Report any psychotic behavior
  • Encourage patient and family members to verbalize feelings

Encouraging Rest and Activity

  • Encourage moderate activity to prevent complications of immobility and promote self-esteem
  • Plan rest periods throughout the day and promote a relaxing, quiet environment for rest and sleep

Preparing Patient for Surgery

  • Adrenal hypofunction ans addisonians crisis: monitor for hypotension; rapid, weak pulse, rapid respiratory rate; pallor; and extreme weakness. Note factors that may have led to crisis (eg, stress, trauma, surgery).
  • Administer intravenous fluids and electrolytes  and corticosteroids before, during and after surgery or treatment as indicated.
  • Monitor for circulatory collapse and shock present in addisonian crisis; treat promptly.
  • Assess fluid and electrolyte status by monitoring laboratory values and daily weight.
  • Monitor blood glucose level, and report elevations to physician.

 

Reference:

Joyce Young Johnson et.al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition

Lippincott Wiliams &Wilkins pp; 286-291

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Medical Surgical

Addison’s Disease (Primary Adrenocortical Insufficiency)

Wikipedia

Addison’s disease is caused by a deficiency of cortical hormone. It results when the adrenal cortex function is inadequate to meet the patient’s need for cortical hormones. Autoimmune or idiopathic atrophy of the adrenal glands is responsible for 80% to 90% of cases. Other causes include surgical removal of both adrenal glands or infection (tuberculosis or histoplasmosis) of the adrenal glands. Inadequate secretion of adrenocorticotrophic  hormone (ACTH) from the primary pituitary gland results in adrenal insufficiency. Symptoms may also result from sudden cessation of exogenous adrenocortical hormone therapy, which interferes with normal feedback mechanisms.

Clinical Manifestations:

Clinical manifestations include muscle weakness, anorexia, gastrointestinal symptoms, fatigue, emaciation, dark pigmentation of the skin and mucous membranes, hypotension, low blood glucose, low serum sodium and high serum potassium. The onset usually occurs with nonspecific symptoms. Mental changes (depression, emotional lability, apathy and confusion) are present in 60% to 80% of patients. In severe cases, disturbance of sodium and potassium metabolism may be marked by depletion of sodium and water and severe, chronic dehydration.

Addisonian Crisis

This medical emergency develops as the disease progresses. Signs and symptoms include:

  • Cyanosis, fever, and classic signs of circulatory shock: pallor, apprehension, rapid and weak pulse, rapid respirations, and low blood pressure
  • Headache, nausea, abdominal pain, diarrhea, confusion and restlessness
  • Slight overexertion, exposure to cold, and acute infections, decrease salt intake and may lead to circulatory collapse, shock and death
  • Stress of surgery or dehydration from preparation for diagnostic tests or surgery may precipitate addisonian or hypotensive crisis
  • Decreased blood glucose and sodium levels, increased serum potassium (hyperkalemia), and leukocytosis.

Assessment and Diagnostic Findings

Primary adrenocortical insufficiency:

  • greatly increased plasma ACTH (>22.0 pmol/L)
  • serum cortisol low normal or lower than normal (<165 nmol/L)
  • decreased blood glucose (hypoglycemia)
  • decreased sodium levels (hyponatremia)
  • increased serum potassium (hyperkalemia)
  • increased white cell count (leukocytosis)

Medical Management

Immediate treatment is directed toward combating shock.

  • Restore blood circulation, administer fluids, monitor vital signs, and place patient in a recumbent position with legs elevated
  • Administer intravenous hydrocortisone, followed by 5% dextrose in normal saline
  • Vasopressor amines may be required if hypotension persists
  • Antibiotics may be prescribed for infection
  • Oral intake may be initiated as soon as tolerated
  • If adrenal gland does not regain function, lifelong replacement of corticosteroids and mineralocorticoids is required
  • Dietary intake should be supplemented with salt during times of gastrointestinal losses of fluids through vomiting and diarrhea

NURSING PROCESS: The Patient with Addison’s Disease

Assessment

Assessment focuses on fluid imbalance and stress

  • Check blood pressure from a lying to standing position; check pulse rate
  • Assess skin color and turgor
  • Assess history of weight changes, muscle weakness, and fatigue
  • Ask patient and family about onset of illness or increased stress that may have precipitated crisis

Diagnosis

Nursing Diagnoses

  • Deficient fluid volume related to inadequate fluid intake and fluid loss secondary to inadequate adrenal hormone secretion
  • Deficient knowledge about need for hormone replacement and dietary modification

Collaborative Problems/Potential Complications

Addisonian crisis

Planning and Goals

Goals may include improving fluid balance, improving response to activity, decreasing stress, increasing knowledge about need for hormone replacement and dietary modifications, and ensuring absence of complications.

Nursing Interventions

Restoring Fluid

  • Record weight changes daily
  • Assess skin turgor and mucous membranes
  • Instruct patient to report increased thirst
  • Monitor lying, sitting, and standing blood pressures frequently
  • Assist patient in selecting, and encouraging patient to consume, food and fluids that assist in restoring and maintaining fluid and electrolyte balance (eg, foods high in sodium during gastrointestinal disturbances and very hot weather). Include a dietitian for added guidance.
  • Assist patient and family in learning to administer hormone replacement and to modify dosage during illness and stress
  • Provide written and verbal instructions about mineralocorticoid and glucocorticoid therapy.

Improving Activity Intolerance

  • Avoid unnecessary activities and stress that might precipitate a hypotensive episode
  • Detect signs of infection or presence of stressors that may have triggered the crisis
  • Provide a quiet, nonstressful environment during acute crises; carry out all activities for patient
  • Explain all procedures to reduce fear and anxiety
  • Explain rationale for minimizing stress during acute crisis

Monitoring and Managing Complications (Addisonian Crisis)

  • Assess for signs and symptoms of crisis: circulatory collapse and shock
  • Avoid physical and psychological stress, including exposure to cold, overexertion, infection, and emotional distress
  • Initiate immediate treatment with intravenous fluid, glucose, and electrolytes, especially sodium; corticosteroid supplements; and vasopressors
  • Avoid patient exertion; anticipate and take measures to meet patient’s needs
  • Monitor symptoms, vital signs, weight, and fluid and electrolyte balance to evaluate return to precrisis state
  • Identify factors that led to crisis

 

Reference:

Joyce Young Johnson et.al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition

Lippincott Williams & Wilkins pp; 21 – 24