Acute Adrenal Insufficiency-2 Nursing CEs

Author: Brooke Baldwin-Rodriguez RN MSN WCC

Written: July 10^th, 2007

Updated: September 11, 2009

Course Description

This course is designed to educate the student to the important role critical care nurses play in assessing, diagnosing, treating, and evaluating acute adrenal insufficiency in the critically ill patient. Focus will be placed on identification of adrenal insufficiency. Early identification of adrenal insufficiency is key to performing diagnostic tests that will lead to supportive treatment. Nursing diagnoses will be presented along with nursing related interventions. The final focus of this course will review the desired goals of care.

Course Objectives

• Review general function of the endocrine system
• Review the role of the adrenal glands as a part of the endocrine system
• State the hormones associated with the adrenal glands
• Review the hormones of the adrenal gland
• Discuss the common etiology of acute adrenal insufficiency
• Describe the pathophysiology of acute adrenal insufficiency
• State the hallmark feature of acute adrenal insufficiency
• Associate key symptoms with various body systems
• Review the Cosyntropin Stimulation test for diagnosing acute adrenal insufficiency
• Discuss interpretation of the Cosyntropin stimulation test
• List 6 nursing diagnoses associated with acute adrenal insufficiency
• Review nursing and medical management
• Review the goals and desired outcomes of treatment

The Endocrine System and Adrenal Glands

The Endocrine system communicates by distributing potent hormones throughout the body. When stimulated, the endocrine glands secret hormones into surrounding body fluids and hormones travel to target tissues and exert an effect.  The endocrine system releases hormones into the bloodstream. The circulating blood then delivers hormones to virtually all cells throughout the body. Certain parts of the nervous system stimulate or inhibit the release of hormones. Hormones, in turn, may promote or inhibit the generation of nerve impulses.

The various glands of the endocrine system are capable of synthesizing and releasing hormones.

Hormones have five general functions:

1.      Differentiation of the reproductive and central nervous systems in the developing fetus.

2.      Stimulation of sequential growth and development during childhood and adolescence.

3.      Coordination of the male and female reproductive systems, which makes sexual reproduction possible.

4.      Maintenance of an optimal internal environment throughout the life span.

5.      Initiation of corrective and adaptive responses when emergency demands occur.

During critical illness the main concern is on maintenance of optimal internal environment and initiation of corrective and adaptive responses when emergency demands occur.  Endocrine regulation by way of feedback circuits (systems) is one of the most important ways in which hormonal secretion is maintained within a physiologic range and allows for self regulation. In a positive feedback system low levels of hormone stimulate the release of the controlling hormone. Negative feedback is the most common type of feedback system. Negative feedback systems are important in maintaining hormones within physiologic ranges. The lack of negative-feedback inhibition on hormonal release often results in pathologic conditions.

Role of the Adrenal Gland in the Critically Ill Patient

The adrenal gland, which is retroperitoneal and superior to the kidney, has two separate endocrine tissues that produce hormones:

• Cortical hormones
• Medullary hormones

Cortical hormones include glucocorticoids and mineralcorticoids. Cortisol is the major glucocorticoid and aldosterone is the major mineralcorticoid hormone. The glucocorticoids participate in carbohydrate metabolism, protein metabolism, promotion of lipolysis, and has anti-inflammatory effects. General disorders associated with glucocorticoid dysfunction include Cushing’s syndrome, and adrenal insufficiency. Mineralcorticoids are stimulated by the renin-angiotensin system or when there is hyponatremia or hyperkalemia. Mineralcorticoids act to increase sodium reabsorption which leads to increasing extracellular volume and increases potassium excretion. Disorders of mineralcorticoids include primary aldosteronism and adrenal insufficiency.

Medullary hormones of the adrenal gland are epinephrine and norepinephrine. These hormones are released in states of fear, anxiety, pain, trauma, fluid loss, hemorrhage, extremes of temperature, hypoxia, surgery, hypoglycemia, hypokalemia, hypernatremia, and hypotension. Norepiniphine and epinephrine are active when there is a “fight or flight” response or recovery from insulin-induced or hypoglycemia.

The Hypothalamic-Pituitary-Adrenal Axis

Physiologic stress caused by critical illness causes a “fight or flight” response that involves a major neurological and endocrine changes.  The hypothalamic-pituitary-adrenal axis, thyroid, and pancreas activate this response. The actions of the hypothalamic-pituitary-adrenal axis provide a normal physiologic function and response to illness. The hypothalamus releases corticotrophin-releasing hormone. Once corticotrophin releasing hormone is activated, the sympathetic nervous system releases both norepinephrine and epinephrine that cause vascular smooth muscle vasoconstriction and provides and inotropic response. Anti-diuretic hormone is released from the posterior pituitary and promotes intravascular fluid retention. The anterior pituitary releases corticotrophin that leads to the release of mineralcorticoid which retains fluid and the release of glucocorticoid that increases metabolism and the immune/inflammatory response. The actions of this response can be seen in two phases of critical illness: acute phase and prolonged critical illness. 

In the acute phase of a critical illness, the adrenal gland releases norepinephrine and epinephrine into the bloodstream. Epinephrine (adrenaline) released from the medulla of the adrenal glands, increases cerebral blood flow, increased cerebral oxygen consumption, and increases heart rate. Cortisol levels may increase six-fold and alter carbohydrate, fat, and protein metabolism to provide energy immediately to vital organs. With prolonged critical illness the initially high hormonal levels are reduced. Adrenal dysfunction is common in prolonged critical illness lasting more that 7 to 10 days. The loss of sufficient adrenal response and a deficiency of cortisol production may lead to hemodynamic instability, volume depletion, and defective energy metabolism. If a critically ill patient remains hypotensive, vasopressor-dependent, and mechanically ventilated adequacy of adrenal function should be suspected.

Etiology/Pathophysiology

Mechanisms that cause adrenal gland hypofunction include:

• Primary hypoadrenalism
• Secondary hypoadrenalism
• Relative adrenal insufficiency
• Peripheral adrenal resistance

Primary hypoadrenalism is caused by an intrinsic failure of the adrenal gland to produce normal endogenous glucocorticosteroid hormones and results in Addison’s disease. Causes of primary adrenal insufficiency:

u     Autoimmune disease

u     Metastatic cancer

u     Hemorrhagic destruction

u     Sepsis

u     AIDS

u     Drugs: ketoconazole, phenytoin, barbiturates

u     Genetic abnormality such as adrenoleukodystrophy

u     Adrenal enzyme deficiency

Secondary hypoadrenalism is caused by administration of therapeutic steroids. The adrenal gland stops production of intrinsic hormones with exogenous glucocorticoosteroids administration. Other causes, those that are most common in the critically ill, include:

u     Sepsis

u     Trauma

u     Surgery

u     Pituitary hypothalamic tumor

u     Pituitary irradiation

u     Pituitary surgery

u     Brain trauma

Relative adrenal insufficiency occurs when the adrenal gland produces glucocorticosteroids but the quantity is insufficient for the disease process. This occurs predominantly with septic shock states and may occur in 50% to 75% of patient’s who experience septic shock.

Peripheral adrenal resistance is a result of inflammatory cytokines that induce cellular resistance to cortisol.

Critically ill patients are at risk for developing secondary adrenal insufficiency and relative adrenal insufficiency due to major surgery, septic shock, coagulopathies, and HIV infections. For example, inflammatory cytokines released during sepsis promote corticosteroid resistance and the normal adrenal responses are suppressed.

Clinical Presentation

Nurses have a key role in identifying acute adrenal insufficiency. The features may be nonspecific and must be distinguished from other medical disorders. The hallmark feature of acute adrenal insufficiency is hypotension that is refractory to vasopressors.

Other symptoms may include:

u     Electrolyte abnormalities: Hyponatremia, Hyperkalemia

u     Weakness

u     Hyperpigmentation

u     Confusion, altered mental status

u     Vomiting

u     Petechiae

u     Tachycardia

u     Craving for salt

The signs and symptoms of acute adrenal insufficiency result from lack of cortisol production. Lack of cortisol production leads to:

u     Decreased production of glucose, metabolism of protein and fat which may exhibit as hypoglycemia, fatigue, weakness, confusion, listlessness, lethargy, apathy, and tachycardia;

u     Decreased intestinal motility/digestion which may result in abdominal pain and nausea and vomiting; and

u     Decreased vascular tone leads to hypotension.

o       Low filling pressures

o       Low cardiac output, or high cardiac output is the patient is “hyperdynamic”

o       High systemic vascular resistance

The role of nurses in a high level of suspicion may be key to the next step, diagnostic evaluation.

Evaluation of Adrenal Function

Diagnosis of adrenal insufficiency is done by evaluating plasma cortisol levels. A decreased plasma cortisol level is indicative of adrenal insufficiency but does not differentiate between primary and secondary adrenal insufficiency. If the plasma cortisol level is within normal limits in a stressed patient, the cortisol level may be too low to maintain bodily demands of cortisol and is considered abnormally low. Cosyntropin Stimulation tests are performed to detect adrenal insufficiency. The rapid adrenocorticotropic hormone (ACTH) stimulation test is the most common method for determining adrenal insufficiency. It can be performed at anytime of the day or night.

1. Obtain baseline serum cortisol level
2. A synthetic ACTH (250 micrograms) is injected intravenously
3. A post-ACTH plasma cortisol level is obtained at 30 and 60 minutes after the ACTH injection

Once the baseline level is established, the plasma cortisol levels at 30 and 60 minutes post ACTH stimulation can be interpreted. The interpretation of the ACTH stimulation test is as follows:

Nursing Diagnoses

Nursing diagnosis commonly identified with acute adrenal insufficiency is related to the clinical signs and symptoms of the syndrome and the desire to reduce the risk of complications:

u     Deficient fluid volume related to deficiency of aldosterone hormone (mineralocorticoid) and decreased sodium and water retention

u     Ineffective tissue perfusion related to cortisol deficiency, resulting in decreased vascular tone and decreased effectiveness of catecholamines

u     Disturbed thought processes related to decreased glucose levels, decreased protein metabolism, decreased perfusion, and decreased sodium

u     Imbalanced nutrition (less than body requirements) related to cortisol deficiency and resultant decreased metabolism of protein and fats, decreased appetite, and decreased intestinal motility and digestion

u     Deficient knowledge: proper long-term corticosteroid management

u     Activity intolerance related to use of endogenous protein for energy needs and loss of skeletal muscle mass

Nursing and Medical Interventions

Goals of treatment include identifying the patient and treating the precipitating cause, replacing fluid and electrolytes, replacing hormones, and educating the patient and family.

Fluid replacement

Rapid administration of intravenous fluids and electrolytes helps support the blood pressure. Normally, 0.9% of NaCl and glucose 5%, is used for fluid replacement. Initially, 5 liters of fluid may need to be replaced in the first 12 to 24 hours of treatment in order to maintain hemodynamic stability. Acidemia is usually corrected with volume expansion. However, if pH is < 7.1 and bicarbonate level is <10 mEq/L sodium bicarbonate may be given.

Hormone replacement

Both glucocorticoid (such as hydrocortisone) and mineralocorticoids (such as fludrocortisones) may be used to manage adrenal insufficiency. Dexamethasone phosphate (Decadron), 4 milligrams by intravenous bolus is given, followed by 4 milligrams every 8 hours as an initial treatment since it will not interfere with plasma cortisol assay and can be given during the ACTH stimulation test.  Once the ACTH stimulation test has been completed hydrocortisone is typically used.

Hydrocortisone has anti-inflammatory and immunosuppressive effect along with salt-retaining effects in high doses. Once the patient improves, the dose of hydrocortisone is decreased 20% to 40% daily until a maintenance dose is achieved. Short-term, low-dose hydrocortisone is used for patients with depleted cortisol levels who do not demonstrate a rise in cortisol level following corticotrophin stimulation and have a diagnosis of septic shock.

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