NCP Adrenal Insufficiency (Addison’s Disease)

Adrenal Insufficiency (Addison’s Disease)

Addison’s Disease; Addisonian Crisis

Adrenal insufficiency, or Addison’s disease, is an abnormality of the adrenal glands with the destruction of the adrenal cortex and impairment of glucocorticoid and mineralocorticoid production. This may be caused by an autoimmune condition, tuberculosis, fungal infection, acquired immunodeficiency syndrome (AIDS), metastatic cancer, hemorrhage, infarction, or surgical removal of the adrenal glands. A secondary form can also occur from pituitary suppression, causing decreased levels of adrenocorticotrophic hormone (ACTH), with aldosterone secretion remaining normal. Patients using steroids may also manifest adrenocortical insufficiency if there is abrupt cessation of long-term glucocorticoid therapy because of suppression of endogenous ACTH. Because of widespread steroid use for multiple diseases, secondary adrenocortical insufficiency occurs far more often than the primary form. Addisonian crisis is the most dangerous component of adrenal insufficiency. It is a life-threatening emergency with severe hypotension that may occur during stress, sudden withdrawal of replacement therapy, adrenal surgery, or sudden pituitary gland destruction. This care plan addresses chronic care in an outpatient setting, as well as acute care of Addisonian crisis.

Nursing Diagnosis

Risk for Ineffective Therapeutic Regimen Management

Common Risk Factors

Lack of experience with adrenocortical insufficiency

Complexity of regimen

Knowledge deficits

Common Expected Outcome

Patient verbalizes understanding of adrenal insufficiency and guidelines for replacement therapy.

NOC Outcomes

Knowledge: Disease Process; Knowledge: Medication

NIC Interventions

Teaching: Disease Process; Teaching: Prescribed Medication

Ongoing Assessment



Assess knowledge of adrenal insufficiency, including the need for lifelong medication.

Regardless of the cause of adrenal insufficiency, treatment focuses on replacement with glucocorticoids. The need for lifelong replacement therapy must be addressed because of the serious nature of the disease in order to plan long-term management.

Assess available support systems and the ability to comply with treatment.

The management of adrenal insufficiency is focused on the patient’s ability to avoid risks for crisis and maintain scheduled medication administration. The patient is more likely to be successful adopting these new health behaviors if a strong social support system is available.

Assess ability to identify or verbalize signs and symptoms that require physician consultation: fever, nausea and vomiting, weight loss, diaphoresis, progressive weakness, and/or dizziness.

These are signs of adrenal insufficiency and the patient may be at risk of developing Addisonian crisis, which is a life-threatening emergency.

Therapeutic Interventions



Instruct patient in self-administration of steroids, including expected effects and dosage. The patient with adrenal insufficiency will also require aldosterone replacement (e.g., fludrocortisone acetate [Florinef], a mineralocorticoid), which is taken daily or three times a week.

Knowledge of the disease process and drug regimen will promote compliance. Lifelong glucocorticoid replacement is required in primary Addison’s disease. A patient with secondary adrenocortical insufficiency does not require aldosterone replacement because mineralocorticoid release does not depend on ACTH secretion.

Offer information about the need to adjust corticosteroid dosage when under stress.

The goal of replacement therapy is the return to normal hormone levels. The need for glucocorticoids is proportional to stress levels, because these patients cannot produce endogenous hormone in response to an increase in stress levels. Doses are usually doubled with minor infection or dental work and tripled with major stress such as more extensive surgical procedures or severe infection.

Inform the patient of the availability of injectable cortisol with a sterile syringe.

Patients should carry a readily injectable syringe of cortisol at all times. This syringe may be used by the patient or significant other when the patient is unable to take the oral form and is experiencing symptoms of inadequate replacement therapy.

Emphasize the need for morning or evening dose.

The patient must identify personal stressors and learn to adjust steroidal drugs to compensate for the stress response. Twice-daily dosing is encouraged to prevent crisis. Glucocorticoids are usually given in divided doses with two thirds in the morning and one third in the afternoon. They should not be taken late in the evening because they are stimulating to the central nervous system (CNS) and may cause insomnia. The twice-daily dosing mimics the body’s normal cortisol secretion pattern. However, alternate-day therapy is also common with long-term administration in which the patient is instructed to take twice the usual daily glucocorticoid dose every other morning.

Instruct the patient to take the glucocorticoid after eating.

This reduces gastric irritation.

Stress importance of follow-up health care visits.

Drug levels may be adjusted to the patient’s requirements during visits. With adrenal insufficiency, there is a lifelong need for medical supervision.

Explain how to obtain a medical identification tag and the importance of wearing it.

This tag may be lifesaving for the patient with adrenal insufficiency in the case of unexpected trauma, accident, or crisis.

Discuss signs or symptoms requiring physician consultation. Patients should be taught signs and symptoms of glucocorticoid deficiency and excess.

Recognition of early signs and symptoms may prevent Addisonian crisis.

Nursing Diagnosis

Risk for Imbalanced Nutrition: Less Than Body Requirements

Common Risk Factors

Decreased gastrointestinal (GI) enzymes, causing loss of appetite and decreased oral intake tolerance

Decreased gastric acid production

Nausea, vomiting, diarrhea

Common Expected Outcome

Patient’s nutritional status is optimized as evidenced by maintenance of weight and adequate dietary intake.

NOC Outcome

Nutritional Status: Nutrient Intake

NIC Intervention

Nutrition Management

Ongoing Assessment



Assess appetite and for the presence of nausea, vomiting, or diarrhea.

Cortisol deficit can impair GI function, causing anorexia, nausea, and vomiting.

Monitor trends in weight.

This provides documentation of weight loss trends. Weight loss is a common manifestation of adrenal insufficiency.

Assess foods that patient can tolerate.

Appetite may increase with preferred and tolerable foods.

Monitor serum glucose levels.

Patients with adrenal insufficiency are likely to experience hypoglycemia.

Assess for salt cravings.

Aldosterone deficiency causes increased renal excretion of sodium.

Therapeutic Interventions



Encourage high-protein, low-carbohydrate, high-sodium diet.

The patient tires because of inadequate production of hepatic glucagon; the recommended diet prevents fatigue, hypoglycemia, and hyponatremia. The patient with primary Addison’s disease needs to increase salt intake 5 g if any activity causes an increase in diaphoresis (e.g., activities in warm weather).

Suggest need for frequent small meals.

Inadequate caloric intake in meals may precipitate hypoglycemia. Promotion of oral intake maintains adequate blood glucose levels and nutrition.

Encourage rest periods after eating.

This is important to facilitate digestion.

Nursing Diagnosis

Risk for Deficient Fluid Volume

Common Risk Factors

Increase in sodium and water excretion with potassium retention

GI disturbances (e.g., nausea, vomiting, diarrhea, which can be manifestations of Addison’s disease).

Common Expected Outcome

Patient experiences adequate fluid volume and electrolyte balance as evidenced by urine output greater than 30 mL/hr, normotensive blood pressure (BP), heart rate (HR) less than 100 beats/min, consistent weight, and normal skin turgor.

NOC Outcomes

Fluid Balance; Electrolyte and Acid-Base Balance

NIC Interventions

Fluid Monitoring; Fluid Management; Electrolyte Management

Ongoing Assessment



Assess skin turgor and mucous membranes for signs of dehydration.

The patient will have dry skin and mucous membranes. Tenting of the skin will occur. The tongue may have longitudinal furrows.

Assess vital signs, especially noting BP and HR for orthostatic changes.

A BP drop of more than 15 mm Hg when changing from supine to sitting position, with a concurrent elevation of 15 beats/min in HR, indicates reduced circulating fluids.

Assess color, concentration, and amount of urine.

Urine volume will decrease, urine specific gravity will increase, and color will be darker.

Assess trends in weight.

Rapid weight loss will occur with fluid volume deficit.

Assess for fatigue, sensory deficits, or muscle weakness, which may progress to paralysis.

These are signs of hyperkalemia. Aldosterone deficiency leads to potassium retention by the kidneys.

Assess electrocardiogram rhythm, as available, for signs of hyperkalemia.

Signs of hyperkalemia are sharp peaked T wave and widened QRS complex.

Assess additional indicated laboratory tests.

Abnormal laboratory findings include hyperkalemia (related to aldosterone deficiency and decreased renal perfusion), hyponatremia (related to decreased aldosterone and impaired free water clearance), and increase in blood urea nitrogen (related to decreased glomerular filtration from hypotension).

Therapeutic Interventions



Encourage oral fluids as the patient tolerates.

As sodium loss increases, extracellular fluid volume decreases. These interventions are necessary to prevent fluid volume deficit because the kidneys are unable to conserve sodium.

Instruct the patient to ingest salt additives in conditions of excess heat or humidity.

Sweating increases sodium loss.

If Addisonian crisis occurs:

· Refer or admit the patient to an acute care setting.

Immediate hospital admission and treatment are needed because of the high mortality with Addisonian crisis.

· Administer parenteral fluids as prescribed. Anticipate the need for an intravenous (IV) fluid challenge with immediate infusion of fluids for patients with abnormal vital signs.

Normal saline is infused initially to restore fluid volume.

· Administer Kayexalate.

This ion exchange resin can be given orally or by enema to reduce potassium levels.

· Instruct the patient to wear a medical alert bracelet and carry a wallet card.

In the event of trauma or injury, it is important to initiate appropriate therapy immediately.

· Administer replacement medications as prescribed or indicated: oral cortisone (Cortone), hydrocortisone (Cortef), prednisone, or fludrocortisone (Florinef).

Cortisone and prednisone replace cortisol deficits, which will promote sodium resorption. Fludrocortisone is a mineralocorticoid for patients who require aldosterone replacement to promote sodium and water replacement. Acute adrenal insufficiency is a medical emergency requiring immediate fluid and corticosteroid administration. If treated for adrenal crisis, the patient requires IV hydrocortisone initially; usually by the second day, administration can be converted to an oral form of replacement.

Nursing Diagnosis

Risk for Decreased Cardiac Output

Common Risk Factor

Any situations requiring increased corticosteroids (e.g., stress, infection, GI upsets) may lead to shock or vascular collapse

Common Expected Outcome

Patient achieves adequate cardiac output (CO) as evidenced by strong peripheral pulses, normal vital signs, urine output greater than 30 mL/hr, warm and dry skin, and alert responsive mentation.

NOC Outcomes

Cardiac Pump Effectiveness; Circulation Status

NIC Interventions

Hemodynamic Regulation; Shock Management

Ongoing Assessment



Assess skin warmth and peripheral pulses.

Peripheral vasoconstriction causes cool, pale, diaphoretic skin.

Assess level of consciousness.

Early signs of cerebral hypoxia are restlessness and anxiety, leading to agitation and confusion.

Monitor vital signs with frequent monitoring of BP. Include assessment for orthostatic hypotension. Anticipate direct intraarterial monitoring of pressure for a continuing shock state.

Sudden development of profound hypotension may indicate Addisonian crisis. Auscultatory BP may be unreliable secondary to vasoconstriction.

Monitor for dysrhythmias.

Cardiac dysrhythmias may result from the low perfusion state, acidosis, hypoxia, or electrolyte imbalance. Hyperkalemia is present in Addison’s disease. Hyperkalemia is usually responsive to fluid and adrenocorticoid replacement and does not require further intervention.

Monitor urine output.

Oliguria is a classic sign of inadequate renal perfusion.

Monitor oxygen saturation through pulse oximetry or arterial blood gas results, as appropriate.

The patient will have decreased oxygen saturation.

Monitor temperature.

Hyperpyrexia can result from the hormonal and fluid imbalance and may be an early sign of crisis if accompanied by a sudden drop in BP.

If hemodynamic monitoring is in place, assess central venous pressure (CVP), pulmonary artery diastolic pressure (PAD), pulmonary capillary wedge pressure (PCWP), and CO.

CVP provides information on filling pressures of right side of the heart; PAD and PCWP reflect left-sided fluid volumes.

Therapeutic Interventions



Minimize stressful situations and promote a quiet environment.

The patient’s normal response to stress is not functioning because he or she cannot produce corticosteroids. Stress can result in a life-threatening situation with Addisonian crisis.

Provide rest periods.

This prevents overexertion.

Assist the patient with activities, as needed.

The patient in crisis should be helped with all activities (e.g., turning, feeding, cleansing) to prevent overexertion.

If hypotension develops with signs of decreased CO, administer IV fluids rapidly. Administer glucocorticoid (e.g., IV hydrocortisone [Solu-Cortef]).

Fluids restore the patient’s circulating blood volume. Circulatory collapse does not respond to usual treatment (inotropes and vasopressors), and ultimately these patients require glucocorticoids to correct the shock state. Glucocorticoid therapy improves BP by potentiating the vasoconstrictor effect of norepinephrine. Glucocorticoids also cause the renal tubules to increase reabsorption of sodium and water, thus increasing blood volume. In acute situations, it is better to err on the side of overtreatment with glucocorticoids than to inadequately dose the patient with adrenal hypofunction, which could result in adrenal crisis. It is important to be aware of the patient’s risk for adrenal crisis and for adrenal insufficiency, including patients with Addison’s disease or patients with a history of ongoing glucocorticoid treatment, in which an illness or stressful experience could trigger a crisis if replacement therapy is not increased.

Administer antipyretics as needed for fever.

This helps reduce the continuing sodium and water losses from the fever.