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adrenal insufficiencyA nonspecific term, referring to either:
(1) Acute adrenocortical insufficiency, see there
(2) Chronic adrenal insufficency, see there; Addison’s disease.
adrenal insufficiencyAdrenal gland insufficiency, adrenocortical insufficency, Addison's disease Endocrinology A condition characterized by a marked ↓ in adrenal function Clinical Weakness, hypotension, easy fatigability, weight loss, N&V, abdominal pain, muscle and joint pain, amenorrhea, bronzing of the skin and hyperpigmentation-especially at skin folds Management Hydrocortisone, fludrocortisone
10 Adrenal insufficiency
- Abrupt onset Adrenal hemorrhage, necrosis, thrombosis, sepsis, coagulopathy, warfarin therapy, antiphospholipid syndrome
- Slow onset Autoimmune disease, TB, adrenomyeloneuropathy, systemic fungal infection, metastatic cancer, AIDS-related-eg Kaposi sarcoma, CMV
- Symptoms shared with 20 adrenal insufficiency Tiredness, weakness, mental depression, anorexia, weight loss, vertigo, orthostatic hypotension, nausea, vomiting, diarrhea, hyponatremia, hypoglycemia, mild anemia, increase WBCs, eosinophilia
- 10 adrenal insufficiency Hyperpigmentation, ↑ K+, vitiligo, autoimmune thyroid disease, CNS Sx if adrenomyeloneuropathy
- Adrenal insufficiency–exclusion of
- Basal cortisol at 8-9 am–≤ 3 µg/dL–normal, 6-24 µg/dL; corticotropin stimulation test-little ↑ after stimulation–normal, plasma cortisol ≥ 20 µg/dL
- 10 adrenal insufficiency Corticotropin stimulation test-no ↑ after stimulation–normal, plasma cortisol ≥ 20 µg/dL; plasma cortisol in low-normal range; plasma corticotropin always ≥ 100 pg/mL
- 20 Adrenal insufficiency
- Abrupt onset Postpartum pituitary necrosis, necrosis or hemorrhage into pituitary adenoma, pituitary or adrenal surgery
- Slow onset Pituitary–1º or metastatic tumor, craniopharyngioma–± accompanied by pituitary surgery or radiation, sarcoidosis, Langerhans cell histiocytosis–histiocytosis X, empty sella syndrome, hypothalamic tumors, long-term glucocorticoid therapy
- Symptoms shared with 10 adrenal insufficiency Tiredness, weakness, mental depression, anorexia, weight loss, vertigo, orthostatic hypotension, nausea, vomiting, diarrhea, hyponatremia, hypoglycemia, mild anemia, increased WBCs, eosinophilia
- 20 adrenal insufficiency Pallor of skin, amenorrhea, ↓ libido, ↓ axillary and pubic hair, small testicles, 2º hyperthyroidism, defect in prepubertal growth, delayed puberty, headache, defects in vision, diabetes insipidus
- Adrenal insufficiency (rule out) Basal cortisol at 8-9 am–≤ 3 µg/dL–normal, 6-24 µg/dL; corticotropin stimulation test-little ↑ after stimulation–normal, plasma cortisol ≥ 20 µg/dL
- 20 adrenal insufficiency Insulin-induced hypoglycemia-little or no ↑ in plasma corticotropin and cortisol in 2º adrenal insufficiency; short metapyrone test–insufficient ↑ in plasma corticotropin and cortisol; low-dose corticotropin stimulation test-little ↑ after stimulation–normal, plasma cortisol ≥ 20 µg/dL
ad·re·nal in·suf·fi·cien·cy(ă-drēnăl in-súfish-en-sē)
Adrenal Insufficiency (Addison’s Disease)
|Mean LOS:||4.9 days|
|Description:||MEDICAL: Endocrine Disorders with CC|
Adrenal insufficiency can be primary or secondary. Addison’s disease, or primary adrenal insufficiency, occurs rarely. Second insufficiency occurs from disorders of the pituitary gland. The adrenal glands consist of the medulla and the cortex. The medulla is responsible for the secretion of the catecholamines epinephrine and norepinephrine; the cortex is responsible for the secretion of glucocorticoids, mineralocorticoids, and androgen. The principal glucocorticoid, cortisol, helps regulate blood pressure, metabolism, anti-inflammatory response, and emotional behavior. The principal mineralocorticoid, aldosterone, is important for regulating sodium levels. Adrenal insufficiency is characterized by the decreased production of cortisol, aldosterone, and androgen. Cortisol deficiency causes altered metabolism, decreased stress tolerance, and emotional lability. Aldosterone deficiency causes urinary loss of sodium, chloride, and water, resulting in dehydration and electrolyte imbalances. Androgen deficiency leads to the loss of secondary sex characteristics. Approximately 8% of people with adrenal insufficiency require hospital treatment each year for adrenal crisis (see acute adrenal crisis).
Primary adrenal insufficiency is caused by the destruction of the adrenal gland. While the disorder is not common, the most typical causes are tuberculosis (TB) or fungal infection, other diseases infiltrating the adrenal glands, and hemorrhage. The most frequent cause is idiopathic atrophy, which is probably autoimmune in origin. Secondary adrenal insufficiency results from hypopituitarism due to hypothalamic-pituitary disease or suppression of the hypothalamic-pituitary axis by steroid therapy.
Idiopathic adrenal atrophy is the most common cause of adrenal insufficiency. It is not known exactly why this occurs, but it is believed to be related to an autoimmune response that results in the slow destruction of adrenal tissue. Tuberculosis, histoplasmosis, AIDS, and hemorrhage into the adrenal glands have all been associated with destruction of the adrenal glands. All patients with adrenal insufficiency or steroid-dependent disorders are at risk for an acute adrenal crisis. Secondary adrenal failure can also occur with adrenocorticotropic hormone (ACTH) deficiency caused by disorders of the pituitary or hypothalamus or suppression because of glucocorticoid therapy. Other causes include physiological stress including surgery, anesthesia, fluid volume loss, trauma, asthma, hypothermia, alcohol abuse, myocardial infarction, fever, hypoglycemia, pain, and depression.
Susceptibility to autoimmune adrenal insufficiency sometimes runs in families. Familial glucocorticoid insufficiency has been reported to have a recessive pattern of transmission. Adrenomyeloneuropathy has been seen to follow an X-linked recessive pattern. X-linked congenital adrenal insufficiency is also associated with mutations in DAX1. DAX1 or mutations also appear to contribute to milder disease or delayed onset. Adrenal insufficiency is often seen in families in association with other autoimmune disorders, most commonly with autoimmune polyendocrine syndrome (APS).
Gender, ethnic/racial, and life span considerations
Addison’s disease, particularly idiopathic autoimmune Addison’s disease, affects females more than males and occurs most often in adults from ages 30 to 50. Ethnicity and race have no known effects on the risk for Addison’s disease.
Global health considerations
In developed countries, the incidence in Western countries is 50 cases per 1 million persons. No data are available on Eastern countries or many developing nations.
Determine if the patient has a history of recent infection, steroid use, or adrenal or pituitary surgery. The patient may describe hyperpigmentation of the skin (particularly on the knuckles, elbows, knees, palmar creases), nailbeds, and mucous membranes that has lasted for months or even years. Establish a history of poor tolerance for stress, weakness, fatigue, and activity intolerance. Ask if the patient has experienced anorexia, nausea, vomiting, or diarrhea as a result of altered metabolism. Some patients have dizziness with orthostasis due to hypotension. Elicit a history of craving for salt or intolerance to cold. Determine presence of altered menses in females and impotence in males.
Assess the patient for signs of dehydration such as tachycardia, altered level of consciousness, dry skin with poor turgor, dry mucous membranes, weight loss, and weak peripheral pulses. Check for postural hypotension—that is, a drop in systolic blood pressure greater than 15 mm Hg when the patient is moved from a lying position to a sitting or standing position.
Inspect the skin for pigmentation changes caused by an altered regulation of melanin, noting if surgical scars, skin folds, and genitalia show a characteristic bronze color. Inspect the patient’s gums and oral mucous membranes to see if they are bluish-black. Take the patient’s temperature to see if it is subnormal. Note any loss of axillary and pubic hair that could be caused by decreased androgen levels.
Because an acute adrenal crisis may be precipitated by emotional stress, periodic psychosocial assessments are necessary for patients with adrenal insufficiency. Patients with an adrenal insufficiency frequently complain of weakness and fatigue, which are also characteristic of an emotional problem. However, weakness and fatigue of an emotional origin seem to have a pattern of being worse in the morning and lessening throughout the day, while the weakness and fatigue of adrenal insufficiency seem to be precipitated by activity and lessen with rest. Patients with adrenal insufficiency may show signs of depression and irritability from decreased cortisol levels.
General Comments: To determine if a cortisol deficit exists, a plasma cortisol level is drawn in the morning; less than 10 mcg/dL suggests adrenal insufficiency; further testing may be needed to determine if the adrenal glands have a primary deficiency or if the pituitary cannot produce enough ACTH (secondary adrenal failure).
|Test||Normal Result||Abnormality With Condition||Explanation|
|Serum cortisol level||6:00 to 8:00 a.m. levels should be 5–23 mcg/dL||Decreased||Determines the ability of the adrenal gland to produce glucocorticoids|
|Serum electrolytes and chemistries||Sodium 136–145 mEq/L; potassium 3.5–5.1 mEq/L; blood urea nitrogen 5–20 mg/dL; glucose 70–105 mg/dL||Hyponatremia; hyperkalemia; azotemia; hypoglycemia||Values reflect sodium loss from a deficit in mineralocorticoids with loss of fluids and poor glucose control because of decreased gluconeogenesis; most consistent finding is elevated blood urea nitrogen due to hypovolemia, decreased glomerular filtration rate, and decreased renal plasma flow|
|ACTH stimulation test||Within 15–30 min of ACTH infusion, the adrenal cortex releases 2 to 5 times its normal plasma cortisol level and the cortisol value should be above 20 mcg/dL||Level ≤ 20 mcg/dL in 30 or 60 min||Adrenal glands cannot respond to the stimulation from ACTH and demonstrate that they are not functioning normally|
Other Tests: Computed tomography of the abdomen; chest x-ray to determine heart size or presence of tuberculosis or fungal infections; metyrapone suppression test; urine 17-hydroxycorticosteroids (17-OHCS) and 17-ketosteroids (17-KS); thyroid-stimulating hormone; and electrocardiogram (ECG)
Primary nursing diagnosis
DiagnosisAltered nutrition: Less than body requirements related to anorexia, vomiting, and nausea
OutcomesFluid balance; Hydration; Nutritional status: Food and fluid intake; Nutritional status: Energy
InterventionsFluid/electrolyte management; Hypoglycemia management; Nutritional management; Nutritional counseling
Planning and implementation
Collaborative treatment of adrenal insufficiency focuses on restoring fluid, electrolyte, and hormone balances. The fluid used for adrenal insufficiency will most likely be 5% dextrose in 0.9% sodium chloride to replace fluid volume, glucose, and serum sodium. Correct sodium, potassium, calcium, and glucose abnormalities. Patients with adrenal insufficiency will require lifelong replacement steroid therapy. Patients with diabetes mellitus will require insulin adjustments for elevated serum glucose levels.
General Comments: Fludrocortisone promotes kidney reabsorption of sodium and the excretion of potassium. Overtreatment can result in fluid retention and possibly congestive heart failure; therefore, monitor serum potassium and sodium levels frequently during fludrocortisone administration.
|Medication or Drug Class||Dosage||Description||Rationale|
|Glucocorticoids such as hydrocortisone, dexamethasone, and prednisone||Varies by drug||Corticosteroid||Replacement therapy in deficiency state|
|Fludrocortisone||0.1 mg PO daily||Mineralocorticoid||Replacement therapy in deficiency state|
Because of the negative effect of physical and emotional stress on the patient with adrenal insufficiency, promote strategies that reduce stress. Teach the patient to rest between activities to conserve energy and to wear warm clothing to increase comfort and limit heat loss. To limit the risk of infection, encourage the patient to use good hand-washing techniques and to limit exposure to people with infections. To prevent complications, teach the patient to avoid using lotions that contain alcohol to prevent skin dryness and breakdown and to eat a nutritious diet that has adequate proteins, fats, and carbohydrates to maintain sodium and potassium balance.
Finally, the prospect of a chronic disease and the need to avoid stress may lead patients to impaired social interaction and ineffective coping. Discuss with the patient the presence of support systems and coping patterns. Provide emotional support by encouraging the patient to verbalize feelings about an altered body image and anxieties about the disease process. Incorporate the patient’s unique positive characteristics and strengths into the care plan. Encourage the patient to interact with family and significant others. Before discharge, refer patients who exhibit disabling behaviors to therapists, self-help groups, or crisis intervention centers.
Evidence-Based Practice and Health Policy
Lapi, F., Kezouh, A., Suissa, S., & Ernst, P. (2013). The use of inhaled corticosteroids and the risk of adrenal insufficiency. European Respiratory Journal, 42(1), 79–86.
- Investigators have questioned the effects that respiratory medications, particularly inhaled corticosteroids such as fluticasone, have on the risk for adrenal insufficiency.
- Among a sample of more than 350,000 prevalent users of respiratory medications, high doses of inhaled corticosteroids (equal to or higher than the daily equivalent of 2,000 mcg of beclometasone, 1,600 mcg of budesonide, 4,000 mcg of triamcinolone, 1,000 mcg of fluticasone, or 4,000 mcg of flunisolide) nearly doubled the risk of adrenal insufficiency (OR 1.84, 95% CI 1.16 to 2.90).
- Providers caring for patients being treated with inhaled corticosteroids should be sensitive to the risk for and development of symptoms of adrenal insufficiency.
- Physical findings: Cardiovascular status, including blood pressure and heart rate; tissue perfusion status, including level of consciousness, skin temperature, peripheral pulses, and urine output; fluid volume status, including neck vein assessment, daily weights, and fluid input and output
- Laboratory findings: Blood levels of potassium, sodium, hematocrit, and blood urea nitrogen (BUN)
Discharge and home healthcare guidelines
prevention.To prevent acute adrenal crisis, teach patients how to avoid stress. Emphasize the need to take medications as prescribed and to contact the physician if the patient becomes stressed or unable to take medications. Make sure the patient knows to alert the surgeon about adrenal insufficiency prior to all surgical procedures. Parenteral corticosteroids will likely be prescribed during any major procedure or times of major stress or trauma.
medications.Be sure the patient understands the reason for steroids prescribed. (See Box 1 for a full explanation.)
resources.Referrals may be necessary to identify potential physical and emotional problems. Notify the hospital’s social service department before patient discharge if you have identified obvious environmental stressors. Initiate home health nursing to ensure compliance with medical therapy and early detection of complications. If you identify emotional problems, refer the patient to therapists or self-help groups.Patient Teaching for Corticosteroids
- Emphasize the lifetime nature of taking corticosteroids.
- Provide name, dosage, and action of the prescribed medication.
- Explain the common side effects of weight gain, swelling around the face and eyes, insomnia, bruising, gastric distress, gastric bleeding, and petechiae.
- Advise the patient to take the medication with meals to avoid gastric irritation and to take the medication at the time of day prescribed, usually in the morning.
- Suggest the patient weigh self daily, at the same time each day, and call the healthcare provider if weight changes by 5 pounds.
- Emphasize that the patient should always take the medication. Not taking it can cause life-threatening complications. Tell the patient to call the healthcare provider if she or he is unable to take medication for more than 24 hours.
- Explain that periods of stress require more medication. Tell the patient to call the healthcare provider for changes in dose if he or she experiences extra physical or emotional stress. Illness and temperature extremes are considered stressors.
- Explain preventative measures. Tell the patient that to prevent getting ill, she or he should avoid being in groups with people who are ill and environments where temperatures change from very hot to very cold.
- Teach the patient to recognize signs of undermedication: weakness, fatigue, and dizziness. Emphasize the need to report underdosing to the healthcare provider.
- Teach the patient to avoid dizziness by moving from a sitting to a standing position slowly.
- Urge the patient to always wear a medical alert necklace or bracelet to inform healthcare professionals of the diagnosis.