Practice nursing care for Clients with Problems of Thyroid and Parathyroid Glands
The thyroid gland is a butterfly-shaped organ located in the lower neck anterior to the trachea. It consists of two lateral lobes connected by an isthmus.
The gland is about
The thyroid gland produces three hormones:
thyroxine (T4),
triiodothyronine (T3),
and calcitonin.
Thyroxine and triiodothyronine are referred to collectively as thyroid hormone.
THYROID FUNCTION AND DYSFUNCTION
Various hormones and chemicals are responsible for normal thyroid function. Key among them are thyroid hormone, calcitonin, and iodine.
Thyroid Hormone
The two separate hormones, thyroxine (T4) and triiodothyronine (T3), that are produced by the thyroid gland and that make up thyroid hormone, are amino acids that have the unique property of containing iodine molecules bound to the amino acid structure. T4 contains four iodine atoms in each molecule, and T3 contains only three. These hormones are synthesized and stored bound to proteins in the cells of the thyroid gland until needed for release into the bloodstream. About 75% of bound thyroid hormone is bound to thyroxine-binding globulin (TBG); the remaining bound thyroid hormone is bound to thyroid-binding prealbumin and albumin.
ROLE OF IODINE
Iodine is essential to the thyroid gland for synthesis of its hormones. In fact, the major use of iodine in the body is by the thyroid, and the major derangement in iodine deficiency is alteration of thyroid function. Iodide is ingested in the diet and absorbed into the blood in the gastrointestinal tract. The thyroid gland is extremely efficient in taking up iodide from the blood and concentrating it within the cells, where iodide ions are converted to iodine molecules, which react with tyrosine (an amino acid) to form the thyroid hormones.
REGULATION OF THYROID HORMONE
The secretion of T3 and T4 by the thyroid gland is controlled by thyroid-stimulating hormone (TSH, or thyrotropin) from the anterior pituitary gland.
TSH controls the rate of thyroid hormone release. In turn, the level of thyroid hormone in the blood determines the release of TSH. If thyroid hormone concentration in the blood decreases, the release of TSH increases, which causes increased output of T3 and T4. This is an example of negative feedback. Thyrotropin-releasing hormone (TRH), secreted by the hypothalamus, exerts a modulating influence on the release of TSH from the pituitary. Environmental factors, such as a decrease in temperature, may lead to increased secretion of TRH, resulting in elevated secretion of thyroid hormones.
FUNCTION OF THYROXINE AND TRIIODOTHYRONINE
The primary function of the thyroid hormone is to control the cellular metabolic activity. T4, a relatively weak hormone, maintains body metabolism in a steady state. T3 is about five times as potent as T4 and has a more rapid metabolic action. These hormones accelerate metabolic processes by increasing the level of specific enzymes that contribute to oxygen consumption and altering the responsiveness of tissues to other hormones. The thyroid hormones influence cell replication and are important in brain development. Thyroid hormone is also necessary for normal growth. The thyroid hormones, through their widespread effects on cellular metabolism, influence every major organ system.
Calcitonin
Calcitonin, or thyrocalcitonin, is another important hormone secreted by the thyroid gland. It is secreted in response to high plasma levels of calcium, and it reduces the plasma level of calcium by increasing its deposition in bone.
Assessment and Diagnostic Findings
The thyroid gland is inspected and palpated routinely on all patients. Inspection begins with identification of landmarks. The lower neck region between the sternocleidomastoid muscles is inspected for swelling or asymmetry. The patient is instructed to extend the neck slightly and swallow. Thyroid tissue rises normally with swallowing. The thyroid is then palpated for size, shape, consistency, symmetry, and the presence of tenderness. The examiner may examine the thyroid from an anterior or a posterior position. In the posterior position, both hands encircle the patient’s neck. The thumbs rest on the nape of the neck, while the index and middle fingers palpate for the thyroid isthmus and the anterior surfaces of the lateral lobes. When palpable, the isthmus is perceived as firm and of a rubber-band consistency. The left lobe is examined by positioning the patient so that the neck flexes slightly forward and to the left. The thyroid cartilage is then displaced to the left with the fingers of the right hand. This maneuver displaces the left lobe deep into the sternocleidomastoid muscle, where it can be more easily palpated. The left lobe is then palpated by placing the left thumb deep into the posterior area of the sternocleidomastoid muscle, while the index and middle fingers exert opposite pressure in the anterior portion of the muscle. Having the patient swallow during the maneuver may assist the examiner to locate the thyroid as it ascends in the neck. The procedure is reversed to examine the right lobe. The isthmus is the only portion of the thyroid that is normally palpable. If a patient has a very thieck, two thin, smooth, nontender lobes may also be palpable. If palpation discloses an enlarged thyroid gland, both lobes are auscultated using the diaphragm of the stethoscope. Auscultation identifies the localized audible vibration of a bruit. This abnormal finding indicates increased blood flow through the thyroid gland and necessitates referral to a physician. Tenderness, enlargement, and nodularity within the thyroid also require referral for additional evaluation.
THYROID FUNCTION TESTS
Assessment measures in addition to palpation and auscultation include thyroid function tests, such as laboratory measurement of thyroid hormones, thyroid scanning, biopsy, and ultrasonography. The most widely used tests are serum immunoassay for TSH and free thyroxine (FT4). Measurement of TSH has a sensitivity and specificity of greater than 95% (Larson, Anderson & Koslawy, 2000). FT4 levels correlate with metabolic status and are elevated in hyperthyroidism and decreased in hypothyroidism.
THYROID-STIMULATING HORMONE
Measurement of the serum TSH concentration is the single best screening test of thyroid function in outpatients because of its high sensitivity. The ability to detect minute changes in serum TSH makes it possible to distinguish subclinical thyroid disease from euthyroid states in patients with low or high normal values. Values above the normal range of 0.4 to 6.15 ?U/mL indicate primary hypothyroidism, and low values indicate hyperthyroidism. When the TSH is normal, there is a 98% chance that the FT4 is also normal. Measurement of TSH is also used for monitoring thyroid hormone replacement therapy and for differentiating between disorders of the thyroid gland itself and disorders of the pituitary or hypothalamus. Current recommendations suggest TSH screening for all adults beginning at age 35, and every 5 years thereafter (Ladenson, Singer, Ain, et al., 2000).
SERUM FREE THYROXINE
The test most commonly used to confirm an abnormal TSH is FT4. FT4 is a direct measurement of free (unbound) thyroxine, the only metabolically active fraction of T4. The range of FT4 in serum is normally 0.9 to 1.7 ng/dL (11.5 to 21.8 pmol/L). When measured by the dialysis method, FT4 is not affected by variations in protein binding and is the procedure of choice for following the changes in T4 secretion during treatment of hyperthyroidism. Measurement of FT4 by the immunoassay technique is less reliable because it may be affected by medication, illness, or changes in protein binding. An estimate (or index) of FT4 can also be calculated by multiplying total T4 by T3 resin uptake.
SERUM T3 AND T4
Measurement of total T3 or T4 includes protein-bound and free hormone levels that occur in response to TSH secretion. T4 is 80% bound to thyroxine-binding globulin (TBG); T3 is bound less firmly. Only 0.03% of T4 and 0.3% of T3 is unbound. Any factor that alters binding proteins also changes the T3 and T4 levels. Serious systemic illnesses, medications (eg, oral contraceptives, corticosteroids, phenytoin, salicylates), and protein wasting as a result of nephrosis and use of androgens may interfere with accurate test results. Normal range for T4 is 4.5 to 11.5 ?g/dL (58.5 to 150 nmol/L). Although serum T3 and T4 levels generally increase or decrease together, the T3 level appears to be a more accurate indicator of hyperthyroidism, which causes a greater rise in T3 than T4 levels. The normal range for serum T3 is 70 to 220 ng/dL (1.15 to 3.10 nmol/L).
T3 RESIN UPTAKE TEST
The T3 resin uptake test is an indirect measure of unsaturated TBG. Its purpose is to determine the amount of thyroid hormone bound to TBG and the number of available binding sites. This provides an index of the amount of thyroid hormone already present in the circulation. Normally, TBG is not fully saturated with thyroid hormone, and additional binding sites are available to combine with radioiodine-labeled T3 added to the blood specimen. The normal T3 uptake value is 25% to 35% (relative uptake fraction, 0.25 to 0.35), which indicates that about one third of the available sites of TBG are occupied by thyroid hormone. If the number of free or unoccupied binding sites is low, as in hyperthyroidism, the T3 uptake is greater than 35% (0.35). If the number of available sites is high, as occurs in hypothyroidism, the test results are less than 25% (0.25). T3 uptake is useful in the evaluation of thyroid hormone levels in patients who have received diagnostic or therapeutic doses of iodine. The test results may be altered by the use of estrogens, androgens, salicylates, phenytoin, anticoagulants, or corticosteroids.
THYROID ANTIBODIES
Autoimmune thyroid diseases include both hypothyroid and hyperthyroid conditions. Results of testing by immunoassay techniques for antithyroid antibodies, specifically antimicrosomal antibodies, are positive in chronic autoimmune thyroid disease (90%), Hashimoto’s thyroiditis (100%), Graves’ disease (80%), and other organ-specific autoimmune disease, such as lupus erythematosus and rheumatoid arthritis. Antithyroid antibody titers are normally present in 5% to 10% of the population and increase with age.
RADIOACTIVE IODINE UPTAKE
The radioactive iodine uptake test measures the rate of iodine uptake by the thyroid gland. The patient is administered a tracer dose of iodine-123 (123I) or another radionuclide, and a count is made over the thyroid gland with use of a scintillation counter, which detects and counts the gamma rays released from the breakdown of 123I in the thyroid. It measures the proportion of the administered dose present in the thyroid gland at a specific time after its administration. It is a simple test and provides reliable results. It is affected by the patient’s intake of iodide or thyroid hormone; therefore, a careful preliminary clinical history is essential in evaluating results. Normal values vary from one geographic region to another and with the intake of iodine. Patients with hyperthyroidism exhibit a high uptake of the 123I (in some patients, up to 90%), whereas patients with hypothyroidism exhibit a very low uptake. This test is also used to determine what dose of 123I should be administered to treat a patient with hyperthyroidism.
FINE-NEEDLE ASPIRATION BIOPSY
Using a small-gauge needle to sample the thyroid tissue for biopsy is a safe and accurate method of detecting malignancy. It is often the initial test for evaluation of thyroid masses. Results are reported as (1) negative (benign), (2) positive (malignant), (3) indeterminate (suspicious), and (4) inadequate (nondiagnostic).
THYROID SCAN, RADIOSCAN, OR SCINTISCAN
In a thyroid scan, a scintillation detector or gamma camera moves back and forth across the area to be studied in a series of parallel tracks, and a visual image is made of the distribution of radioactivity in the area being scanned. Although 123I has been the most commonly used isotope, several other radioactive isotopes, including technetium-99m (99mTc) pertechnetate, thallium, and americium, are also used. Scans are helpful in determining the location, size, shape, and anatomic function of the thyroid gland, particularly when thyroid tissue is substernal or large. Identifying areas of increased function (“hot” areas) or decreased function (“cold” areas) can assist in diagnosis. Although most areas of decreased function do not represent malignancies, lack of function increases the likelihood of malignancy, particularly if only one nonfunctioning area is present. Scanning of the entire body, to obtain the total body profile, may be carried out in a search for a functioning thyroid metastasis.
OTHER DIAGNOSTIC TESTS
Ultrasound, CT scans, and MRI may be used to clarify or confirm the results of other diagnostic studies. Thyroglobulin (Tg), a precursor for T3 and T4, can be measured reliably in the serum by radioimmunoassay. Clinically, it is used to detect persistence or recurrence of thyroid carcinoma.
NURSING IMPLICATIONS
When thyroid tests are scheduled, it is necessary to determine whether the patient has taken medications or agents that contain iodine because these may alter the test results. Iodine-containing medications include contrast agents and those used to treat thyroid disorders. Less obvious sources of iodine are topical antiseptics, multivitamin preparations, and food supplements frequently found in health food stores; cough syrups; and amiodarone, an antiarrhythmic agent. Other medications that may affect test results are estrogens, salicylates, amphetamines, chemotherapeutic agents, antibiotics, corticosteroids, and mercurial diuretics. The nurse asks the patient about the use of these medications and notes their use on the laboratory requisition.
ABNORMAL THYROID FUNCTION
Inadequate secretion of thyroid hormone during fetal and neonatal development results in stunted physical and mental growth (cretinism) because of general depression of metabolic activity. In adults, hypothyroidism manifests as lethargy, slow mentation, and generalized slowing of body functions. Oversecretion of thyroid hormones (hyperthyroidism) is manifested by a greatly increased metabolic rate. Many of the other characteristics of hyperthyroidism result from the increased response to circulating catecholamines (epinephrine and norepinephrine). Hypothyroidism and hyperthyroidism are discussed in detail in the following sections of this chapter.
Oversecretion of thyroid hormones is usually associated with an enlarged thyroid gland (goiter).
Goiter also commonly occurs with iodine deficiency. In this latter condition, lack of iodine results in low levels of circulating thyroid hormones, which causes increased release of TSH; the elevated TSH causes overproduction of thyroglobulin and hypertrophy of the thyroid gland. The term euthyroid refers to thyroid hormone production that is withiormal limits.
HYPOTHYROIDISM
Hypothyroidism results from suboptimal levels of thyroid hormone. Thyroid deficiency can affect all body functions and can range from mild, subclinical forms to myxedema, an advanced form.
The most common cause of hypothyroidism in adults is autoimmune thyroiditis (Hashimoto’s disease), in which the immune system attacks the thyroid gland.
Symptoms of hyperthyroidism may later be followed by those of hypothyroidism and myxedema. Hypothyroidism also commonly occurs in patients with previous hyperthyroidism who have been treated with radioiodine or antithyroid medications or who have had surgery. It occurs most frequently in older women. Radiation therapy for head and neck cancer can also cause hypothyroidism in older men; therefore, testing of thyroid function is recommended for all patients who receive such treatment.
Pathophysiology
More than 95% of patients with hypothyroidism have primary or thyroidal hypothyroidism, which refers to dysfunction of the thyroid gland itself. When thyroid dysfunction is caused by failure of the pituitary gland, the hypothalamus, or both, it is known as central hypothyroidism. It may be referred to as pituitary or secondary hypothyroidism if it is caused entirely by a pituitary disorder, and hypothalamic or tertiary hypothyroidism if it is attributable to a disorder of the hypothalamus resulting in inadequate secretion of TSH because of decreased stimulation by TRH. When thyroid deficiency is present at birth, the condition is known as cretinism. In such instances, the mother may also suffer from thyroid deficiency. The term myxedema refers to the accumulation of mucopolysaccharides in subcutaneous and other interstitial tissues. Although myxedema occurs in long-standing hypothyroidism, the term is used appropriately only to describe the extreme symptoms of severe hypothyroidism.
Clinical Manifestations
Early symptoms of hypothyroidism are nonspecific, but extreme fatigue makes it difficult for the person to complete a full day’s work or participate in usual activities. Reports of hair loss, brittle nails, and dry skin are common, and numbness and tingling of the fingers may occur. On occasion, the voice may become husky, and the patient may complain of hoarseness. Menstrual disturbances such as menorrhagia or amenorrhea occur, in addition to loss of libido. Hypothyroidism affects women five times more frequently than men and occurs most often between 30 and 60 years of age. Severe hypothyroidism results in a subnormal temperature and pulse rate. The patient usually begins to gain weight even without an increase in food intake, although severely hypothyroid patients may be cachectic. The skin becomes thickened because of an accumulation of mucopolysaccharides in the subcutaneous tissues (the origin of the term myxedema). The hair thins and falls out; the face becomes expressionless and masklike. The patient often complains of being cold even in a warm environment. At first, the patient may be irritable and may complain of fatigue, but as the condition progresses, the emotional responses are subdued. The mental processes become dulled, and the patient appears apathetic. Speech is slow, the tongue enlarges, and hands and feet increase in size. The patient frequently complains of constipation. Deafness may also occur. Advanced hypothyroidism may produce personality and cognitive changes characteristic of dementia. Inadequate ventilation and sleep apnea can occur with severe hypothyroidism. Pleural effusion, pericardial effusion, and respiratory muscle weakness may also occur. Severe hypothyroidism is associated with an elevated serum cholesterol level, atherosclerosis, coronary artery disease, and poor left ventricular function. The patient with advanced hypothyroidism is hypothermic and abnormally sensitive to sedatives, opioids, and anesthetic agents. Therefore, these medications are administered only with extreme caution. Patients with unrecognized hypothyroidism who are undergoing surgery are at increased risk for intraoperative hypotension and postoperative heart failure and altered mental status. Myxedema coma describes the most extreme, severe stage of hypothyroidism, in which the patient is hypothermic and unconscious. Myxedema coma may follow increasing lethargy, progressing to stupor and then coma. Undiagnosed hypothyroidism may be precipitated by infection or other systemic disease or by use of sedatives or opioid analgesic agents. The patient’s respiratory drive is depressed, resulting in alveolar hypoventilation, progressive CO2 retention, narcosis, and coma. These symptoms, along with cardiovascular collapse and shock, require aggressive and intensive therapy if the patient is to survive. Even with early vigorous therapy, however, mortality is high.
Gerontologic Considerations
Most patients with primary hypothyroidism are 40 to 70 years of age and present with long-standing mild to moderate hypothyroidism. Subclinical disease is common among older women and can be asymptomatic or mistaken for other medical conditions. Subtle symptoms of hypothyroidism, such as fatigue, muscle aches, and mental confusion, may be attributed to the normal aging process by the patient, family, and health care provider. The higher prevalence of hypothyroidism in elderly people may be related to alterations in immune function with age. Regular screening of TSH levels is recommended for people older than 60 because they are at high risk for hypothyroidism (Ladenson et al., 2000). The signs and symptoms of hypothyroidism are often atypical in elderly people; the elderly patient may have few or no symptoms until the dysfunction is severe. Depression, apathy, or decreased mobility or activity may be the major initial symptom. The major symptoms of hypothyroidism may be depression and apathy, and may be accompanied by significant weight loss. One fourth of affected elderly patients experience constipation.
Medical Management
The primary objective in the management of hypothyroidism is to restore a normal metabolic state by replacing the missing hormone.
PHARMACOLOGIC THERAPY
Synthetic levothyroxine (Synthroid or Levothroid) is the preferred preparation for treating hypothyroidism and suppressing nontoxic goiters. The dosage for hormone replacement is based on the patient’s serum TSH concentration. Desiccated thyroid is used less frequently because it often results in transient elevated serum concentrations of T3, with occasional symptoms of hyperthyroidism. If replacement therapy is adequate, the symptoms of myxedema disappear and normal metabolic activity is resumed.
Prevention of Cardiac Dysfunction.
Any patient who has had hypothyroidism for a long period is almost certain to have elevated serum cholesterol levels, atherosclerosis, and coronary artery disease. As long as metabolism is subnormal and the tissues, including the myocardium, require relatively little oxygen, a reduction in blood supply is tolerated without overt symptoms of coronary artery disease. When thyroid hormone is administered, however, the oxygen demand increases, but oxygen delivery cannot be increased unless, or until, the atherosclerosis improves. This occurs very slowly, if at all. The occurrence of angina is the signal that the oxygeeeds of the myocardium exceed its blood supply. Angina or dysrhythmias may occur when thyroid replacement is initiated because thyroid hormones enhance the cardiovascular effects of catecholamines. Obviously, if angina or dysrhythmias occur, thyroid hormone administration must be discontinued immediately. Later, when it can be resumed safely, thyroid hormone replacement should be prescribed cautiously at a lower dosage and under the close observation of the physician and the nurse.
Prevention of Medication Interactions.
Precautions must be taken during the course of therapy because of the interaction of thyroid hormones with other medications. Thyroid hormones may increase blood glucose levels, which may necessitate adjustment in the dosage of insulin or oral antidiabetic agents in patients with diabetes. The effects of thyroid hormone may be increased by phenytoin (Dilantin) and tricyclic antidepressant agents. Thyroid hormones may also increase the pharmacologic effects of digitalis glycosides, anticoagulant agents, and indomethacin, requiring careful observation and assessment by the nurse for side effects. Bone loss and osteoporosis may also occur with thyroid therapy. Even in small doses, hypnotic and sedative agents may induce profound somnolence, lasting far longer than anticipated. Moreover, they are likely to cause respiratory depression, which can easily be fatal because of decreased respiratory reserve and alveolar hypoventilation. If their use is necessary, the dose is one-half or one-third that ordinarily prescribed in patients of similar age and weight with normal thyroid function. If these medications must be used, the patient must be monitored closely for signs of impending narcosis (stupor-like condition) or respiratory failure.
Gerontologic Considerations
In the elderly patient with mild to moderate hypothyroidism, thyroid hormone replacement must be started with low dosages and increased gradually to prevent serious cardiovascular and neurologic side effects. Angina, for example, may occur with rapid thyroid replacement in the presence of coronary artery disease secondary to the hypothyroid state. Heart failure and tachydysrhythmias may worsen during the transition from the hypothyroid state to the normal metabolic state. Dementia may become more apparent during early thyroid hormone replacement in the elderly patient. Elderly patients with severe hypothyroidism and atherosclerosis may also become confused and agitated if their metabolic rates are raised too quickly. Marked clinical improvement follows the administration of hormone replacement; such medication must be continued for life, even though signs of hypothyroidism disappear within 3 to 12 weeks. Myxedema and myxedema coma generally occur exclusively in patients older than 50 years. The high mortality rate of myxedema coma mandates immediate intravenous administration of high doses of thyroid hormone as well as supportive care.
SUPPORTIVE THERAPY
In severe hypothyroidism and myxedema coma, management includes maintaining vital functions. Arterial blood gases may be measured to determine CO2 retention and to guide the use of assisted ventilation to combat hypoventilation. Pulse oximetry may also be helpful in monitoring oxygen saturation levels. Fluids are administered cautiously because of the danger of water intoxication. Application of external heat (eg, heating pads) is avoided because it increases oxygen requirements and may lead to vascular collapse. If hypoglycemia is evident, concentrated glucose may be prescribed to provide glucose without precipitating fluid overload. Thyroid hormone (usually Synthroid) is administered intravenously until consciousness is restored if myxedema has progressed to myxedema coma. The patient is then continued on oral thyroid hormone therapy. Because of an associated adrenocortical insufficiency, corticosteroid therapy may be necessary.
Nursing Management
Nursing care of the patient with hypothyroidism and myxedema is summarized in the Plan of Nursing Care.
MODIFYING ACTIVITY
The patient with hypothyroidism experiences decreased energy and moderate to severe lethargy. As a result, the risk for complications from immobility increases. The patient’s ability to exercise and participate in activities is further limited by the changes in cardiovascular and pulmonary status secondary to hypothyroidism. A major role of the nurse is assisting with care and hygiene while encouraging the patient to participate in activities within established tolerance levels to prevent the complications of immobility.
MONITORING PHYSICAL STATUS
The nurse closely monitors the patient’s vital signs and cognitive level to detect the following:
• Deterioration of physical and mental status
• Signs and symptoms indicating that treatment has resulted in the metabolic rate exceeding the ability of the cardiovascular and pulmonary systems to respond
• Continued limitations or complications of myxedema
PROMOTING PHYSICAL COMFORT
The patient often experiences chilling and extreme intolerance to cold, even if the room feels comfortable or hot to others. Extra clothing and blankets are provided, and the patient is protected from drafts. Use of heating pads and electric blankets is avoided because of the risk of peripheral vasodilation, further loss of body heat, and vascular collapse. Additionally, the patient could be burned by these items without being aware of it because of delayed responses and decreased mental status.
PROVIDING EMOTIONAL SUPPORT
The patient with moderate to severe hypothyroidism may experience severe emotional reactions to changes in appearance and body image and the frequent delay in diagnosis. The nonspecific, early symptoms may produce negative reactions by family members and friends, and the family and friends may have labeled the patient mentally unstable, uncooperative, or unwilling to participate in self-care activities. As hypothyroidism is treated successfully and symptoms subside, the patient may experience depression and guilt as a result of the progression and severity of symptoms that occurred. The nurse informs the patient and family that the symptoms and inability to recognize them are common and part of the disorder itself. The patient and family may require assistance and counseling to deal with the emotional concerns and reactions that result.
PROMOTING HOME AND COMMUNITY-BASED CARE
Teaching Patients Self-Care.
Because most hypothyroidism treatment takes place at home, the patient and family require information and instruction that will enable them to monitor the patient’s condition and response to therapy. The nurse instructs the patient about the desired actions and side effects of medications and about how and when to take prescribed medications. The importance of continuing to take medications as prescribed even after symptoms improve is stressed to the patient. Because of the slowed mental processes that occur with hypothyroidism, it is important that a family member also be informed and instructed about treatment goals, medication schedules, and side effects to be reported to the physician. The nurse provides written instructions and guidelines for the patient and family. Dietary instruction is provided to promote weight loss once medication has been initiated and to promote return of normal bowel patterns. The patient and family are often very concerned about the changes they have observed as a result of the hypothyroid state. It is often reassuring to the patient and family to be informed that many of the symptoms will disappear with effective treatment.
Continuing Care.
The patient with hypothyroidism and myxedema coma needs considerable follow-up and health care. Before hospital discharge, arrangements are made to ensure that the patient returns to an environment that will promote adherence to the prescribed treatment plan. Assistance in devising a schedule or record ensures accurate and complete administration of medications. The nurse reinforces the importance of continued thyroid hormone replacement and periodic follow-up testing and instructs the patient and family members about the signs of overmedication and undermedication. If indicated, a referral is made for home care. The home care nurse assesses the patient’s progress toward recovery and ability to cope with the recent changes, along with the patient’s physical and cognitive status and the patient’s and family’s understanding of the importance of prescribed long-term medication therapy and compliance with the medication schedule and recommended follow-up tests and appointments. The nurse documents, and reports to the patient’s primary health care provider, subtle signs and symptoms that may indicate either inadequate or excessive thyroxine hormone.
Gerontologic Considerations
The elderly patient requires periodic follow-up monitoring of serum TSH levels because poor compliance with therapy may occur or the patient may take the medications erratically. A careful history may identify the need for further teaching about the importance of the medication. Because of the prevalence of hypothyroidism, testing of serum TSH levels in elderly people every 5 years has been recommended (Smallridge, 2000). In addition, the patient is reminded of the importance of participating in general health promotion activities and recommended health screening.
HYPERTHYROIDISM
Hyperthyroidism is the second most prevalent endocrine disorder, after diabetes mellitus.
Graves’ disease, the most common type of hyperthyroidism, results from an excessive output of thyroid hormones caused by abnormal stimulation of the thyroid gland by circulating immunoglobulins. It affects women eight times more frequently than men, with onset usually between the second and fourth decades (Tierney et al., 2001). It may appear after an emotional shock, stress, or an infection, but the exact significance of these relationships is not understood. Other common causes of hyperthyroidism include thyroiditis and excessive ingestion of thyroid hormone.
Clinical Manifestations
Patients with well-developed hyperthyroidism exhibit a characteristic group of signs and symptoms (sometimes referred to as thyrotoxicosis). The presenting symptom is ofteervousness. These patients are often emotionally hyperexcitable, irritable, and apprehensive; they cannot sit quietly; they suffer from palpitations; and their pulse is abnormally rapid at rest as well as on exertion. They tolerate heat poorly and perspire unusually freely. The skin is flushed continuously, with a characteristic salmon color, and is likely to be warm, soft, and moist. Elderly patients, however, may report dry skin and diffuse pruritus. A fine tremor of the hands may be observed.
Patients may exhibit exophthalmos (bulging eyes), which produces a startled facial expression.
Other manifestations include an increased appetite and dietary intake, progressive weight loss, abnormal muscular fatigability and weakness (difficulty in climbing stairs and rising from a chair), amenorrhea, and changes in bowel function. The pulse rate ranges constantly between 90 and 160 beats/min; the systolic, but characteristically not the diastolic, blood pressure is elevated; atrial fibrillation may occur; and cardiac decompensation in the form of heart failure is common, especially in elderly patients. Osteoporosis and fracture are also associated with hyperthyroidism. Cardiac effects may include sinus tachycardia or dysrhythmias, increased pulse pressure, and palpitations; it has been suggested that these changes may be related to increased sensitivity to catecholamines or to changes ieurotransmitter turnover. Myocardial hypertrophy and heart failure may occur if the hyperthyroidism is severe and untreated. The course of the disease may be mild, characterized by remissions and exacerbations and terminating with spontaneous recovery in a few months or years. Conversely, it may progress relentlessly, with the untreated person becoming emaciated, intensely nervous, delirious, and even disoriented; eventually, the heart fails. Symptoms of hyperthyroidism may occur with the release of excessive amounts of thyroid hormone as a result of inflammation after irradiation of the thyroid or destruction of thyroid tissue by tumor. Such symptoms may also occur with excessive administration of thyroid hormone for treatment of hypothyroidism. Long-standing use of thyroid hormone in the absence of close monitoring may be a cause of symptoms of hyperthyroidism. It is also likely to result in premature osteoporosis, particularly in women.
Assessment and Diagnostic Findings
The thyroid gland invariably is enlarged to some extent. It is soft and may pulsate; a thrill often can be palpated, and a bruit is heard over the thyroid arteries. These are signs of greatly increased blood flow through the thyroid gland. In advanced cases, the diagnosis is made on the basis of the symptoms and an increase in serum T4 and an increased 123I or 125I uptake by the thyroid in excess of 50%.
Gerontologic Considerations
Although hyperthyroidism is much less common in elderly people than hypothyroidism, patients older than 60 years account for 10% to 15% of the cases of thyrotoxicosis. Although some older patients develop typical signs and symptoms of thyrotoxicosis, in most an atypical picture is present, which is often subclinical (Toft, 2001). Elderly patients commonly present with vague and nonspecific signs and symptoms, making disorders hard to detect. Symptoms such as tachycardia, fatigue, mental confusion, weight loss, change in bowel habits, and depression can be attributed to age and other illnesses common to elderly people. In addition, the patient may report cardiovascular symptoms and difficulty climbing stairs or rising from a chair because of muscle weakness. New or worsening heart failure or angina is more likely to occur in elderly than in younger patients. The elderly patient may experience a single manifestation, such as atrial fibrillation, anorexia, or weight loss. These signs and symptoms may mask the underlying thyroid disease. Spontaneous remission of hyperthyroidism is rare in elderly patients. Measurement of TSH is indicated in elderly patients with unexplained physical or mental deterioration.
Medical Management
Treatment of hyperthyroidism is directed toward reducing thyroid hyperactivity to relieve symptoms and remove the cause of important complications. Treatment depends on the cause of the hyperthyroidism and may require a combination of therapeutic approaches.
PHARMACOLOGIC THERAPY
Two forms of pharmacotherapy are available for treating hyperthyroidism and controlling excessive thyroid activity:
(1) use of irradiation by administration of the radioisotope 123I or 131I for destructive effects on the thyroid gland and
(2) antithyroid medications that interfere with the synthesis of thyroid hormones and other agents that control manifestations of hyperthyroidism.
Surgical removal of most of the thyroid gland is a nonpharmacologic alternative.
Radioactive Iodine Therapy.
The goal of radioactive iodine therapy (123I or 131I) is to destroy the overactive thyroid cells. Use of radioactive iodine is the most common treatment in elderly patients. Almost all the iodine that enters and is retained in the body becomes concentrated in the thyroid gland. Therefore, the radioactive isotope of iodine is concentrated in the thyroid gland, where it destroys thyroid cells without jeopardizing other radiosensitive tissues. Over a period of several weeks, thyroid cells exposed to the radioactive iodine are destroyed, resulting in reduction of the hyperthyroid state and inevitably hypothyroidism. The patient is instructed about what to expect with this tasteless, colorless radioiodine, which may be administered by the radiologist. A single oral dose of the agent is administered, based on 80 to 160 ?Ci/g estimated thyroid weight. About 70% to 85% of patients are cured by one dose of radioactive iodine. An additional 10% to 20% require two doses; rarely is a third dose necessary. Use of an ablative dose of radioactive iodine initially causes an acute release of thyroid hormone from the thyroid gland and may cause an increase of symptoms.
The patient is observed for signs of thyroid storm; propranolol is useful in controlling these symptoms. After treatment with radioactive iodine, the patient is followed closely until the euthyroid state is reached. In 3 to 4 weeks, symptoms of hyperthyroidism subside. Because the incidence of hypothyroidism after this form of treatment is very high (ie, more than 90% at 10 years), close follow-up is required to evaluate thyroid function. Thyroid hormone replacement is necessary; small doses are usually prescribed, with the dose gradually increased over a period of months (up to about 1 year) until the FT4 and TSH levels stabilize withiormal ranges. Radioactive iodine has been used to treat toxic adenomas and multinodular goiter and most varieties of thyrotoxicosis (rarely permanently successful); it is preferred for treating patients beyond the childbearing years with diffuse toxic goiter. It is contraindicated in pregnancy and iursing mothers because radioiodine crosses the placenta and is secreted in breast milk. A major advantage of treatment with radioactive iodine is that it avoids many of the side effects associated with antithyroid medications. However, many patients and their families fear medications that are radioactive. Because of this fear, many patients elect to take antithyroid medications rather than radioactive iodine.
Gerontologic Considerations
The use of radioactive iodine is generally recommended for treatment of thyrotoxicosis in elderly patients unless an enlarged thyroid gland is pressing on the airway. The hypermetabolic state of thyrotoxicosis must be controlled by antithyroid medications before radioactive iodine is administered because radiation may precipitate thyroid storm by increasing the release of hormone from the thyroid gland. Thyroid storm, if it occurs, has a mortality rate of 10% in elderly patients.
Antithyroid Medications.
The objective of pharmacotherapy is to inhibit one or more stages in thyroid hormone synthesis or hormone release; another goal may be to reduce the amount of thyroid tissue, with resulting decreased thyroid hormone production. Antithyroid agents block the utilization of iodine by interfering with the iodination of thyrosine and the coupling of iodothyrosines in the synthesis of thyroid hormones. This prevents the synthesis of thyroid hormone. The most commonly used medications are propylthiouracil (Propacil, PTU) or methimazole (Tapazole) until the patient is euthyroid (ie, neither hyperthyroid nor hypothyroid). These medications block extrathyroidal conversion of T4 to T3. Because antithyroid medications do not interfere with release or activity of previously formed thyroid hormones, it may take several weeks for relief of symptoms. At this time the maintenance dose is established, followed by a gradual withdrawal of the medication over the next several months. Therapy is determined on the basis of clinical criteria, including changes in pulse rate, pulse pressure, body weight, size of the goiter, and results of laboratory studies of thyroid function. Toxic complications of antithyroid medications are relatively uncommon; nevertheless, the importance of periodic follow-up is emphasized because medication sensitization, fever, rash, urticaria, or even agranulocytosis and thrombocytopenia (decrease in granulocytes and platelets) may develop. With any sign of infection, especially pharyngitis and fever or the occurrence of mouth ulcers, the patient is advised to stop the medication, notify the physician immediately, and undergo hematologic studies. Rash, arthralgias, and fever occur in 5% of patients. Agranulocytosis, the most serious toxic side effect, occurs in 1 of every 200 patients. Its incidence is higher in patients older than 40 years. It generally occurs within the first 3 months of therapy but may occur up to 1 year after it is started.
Patients taking antithyroid medications are instructed not to use decongestants for nasal stuffiness because they are poorly tolerated. Antithyroid medications are contraindicated in late pregnancy because they may produce goiter and cretinism in the fetus. Thyroid hormone is occasionally administered with antithyroid medications to put the thyroid gland at rest. In this approach, hypothyroidism from excess antithyroid medication is avoided, as is stimulation of the thyroid gland by TSH. Thyroid hormone is available as thyroglobulin (Proloid) and levothyroxine sodium (Synthroid). These slow-acting preparations take about 10 days to achieve their full effect. Liothyronine sodium (Cytomel) has a more rapid onset, and its action is of short duration.
Gerontologic Considerations
If antithyroid agents are used in elderly patients, the patient must be monitored closely because elderly patients are more likely to develop granulocytopenia. The dosage of other medications to treat other chronic illnesses in elderly patients may need to be modified because of the altered rate of metabolism in hyperthyroidism.
Adjunctive Therapy.
Iodine or iodide compounds, once the only therapy available for patients with hyperthyroidism, are no longer used as the sole method of treatment. Such compounds decrease the release of thyroid hormones from the thyroid gland and reduce the vascularity and size of the thyroid. Compounds such as potassium iodide (KI), Lugol’s solution, and saturated solution of potassium iodide (SSKI) may be used in combination with antithyroid agents or beta-adrenergic blockers to prepare the patient with hyperthyroidism for surgery. These agents reduce the activity of the thyroid hormone and the vascularity of the thyroid gland, making the surgical procedure safer. Solutions of iodine and iodide compounds are more palatable in milk or fruit juice and are administered through a straw to prevent staining of the teeth. These compounds reduce the metabolic rate more rapidly than antithyroid medications, but their action does not last as long. Beta-adrenergic blocking agents are important in controlling the sympathetic nervous system effects of hyperthyroidism. For example, propranolol (Inderal) is used to control nervousness, tachycardia, tremor, anxiety, and heat intolerance. The patient continues taking propranolol until the FT4 is within the normal range and the TSH level approaches normal.
Gerontologic Considerations
Use of beta-adrenergic blocking agents (eg, propranolol [Inderal]) may be indicated to decrease the cardiovascular and neurologic signs and symptoms of thyrotoxicosis. These agents must be used with extreme caution in elderly patients to minimize adverse effects on cardiac function that may produce heart failure.
SURGICAL MANAGEMENT
Surgery to remove thyroid tissue was once the primary method of treating hyperthyroidism; today, surgery is reserved for special circumstances—for example, in pregnant women allergic to antithyroid medications, patients with large goiters, or patients unable to take antithyroid agents. Surgery for treatment of hyperthyroidism is performed soon after the thyroid function has returned to normal (4 to 6 weeks). The surgical removal of about five sixths of the thyroid tissue (subtotal thyroidectomy) practically ensures a prolonged remission in most patients with exophthalmic goiter. Its use today is reserved for large goiters, presence of obstructive symptoms, pregnant women, or when there is a need for rapid normalization of thyroid function (Argueta & Whitaker, 2000; Fatourechi, 2000). Before surgery, propylthiouracil is administered until signs of hyperthyroidism have disappeared. A beta-adrenergic blocking agent (propranolol) may be used to reduce the heart rate and other signs and symptoms of hyperthyroidism; however, this does not create a euthyroid state. Iodine (Lugol’s solution or potassium iodide) may be prescribed in an effort to reduce blood loss; however, the effectiveness of this is unknown. Patients receiving iodine medication must be monitored for evidence of iodine toxicity (iodism), which requires immediate withdrawal of the medication. Symptoms of iodism include swelling of the buccal mucosa, excessive salivation, coryza, and skin eruptions.
Recurrent Hyperthyroidism
No treatment for thyrotoxicosis is without side effects, and all three treatments (radioactive iodine therapy, antithyroid medications, and surgery) share the same complications: relapse or recurrent hyperthyroidism and permanent hypothyroidism. The rate of relapse increases in patients who had very severe disease, a long history of dysfunction, ocular and cardiac symptoms, large goiter, and relapse after previous treatment. The relapse rate after radioactive iodine therapy depends on the dose used in treatment. Patients receiving a lower dose of radioactive iodine are more likely to require subsequent treatment than those being treated with a higher dose. Hypothyroidism occurs in almost 80% of patients at 1 year and in 90% to 100% by 5 years for both the multiple low-dose and single high-dose methods. Although rates of relapse and the occurrence of hypothyroidism vary, relapse with antithyroid medications is about 45% by 1 year after completion of therapy and almost 75% by 5 years later (Larson et al., 2000). Discontinuation of antithyroid medications before therapy is complete usually results in relapse within 6 months in most patients. The incidence of relapse with subtotal thyroidectomy is 19% at 18 months; an incidence of hypothyroidism of 25% has been reported at 18 months after surgery. The risk for these complications illustrates the importance of long-term follow-up of patients treated for hyperthyroidism.
NURSING PROCESS: THE PATIENT WITH HYPERTHYROIDISM
Assessment
The health history and examination focus on symptoms related to accelerated or exaggerated metabolism. These include the patient’s and family’s report of irritability and increased emotional reaction and the impact these changes have had on the patient’s interaction with family, friends, and coworkers. The history includes other stressors and the patient’s ability to cope with stress. The nurse assesses the patient’s nutritional status and the presence of symptoms. Symptoms related to excessive nervous system output and changes in vision and appearance of the eyes are noted. The nurse periodically assesses and monitors the patient’s cardiac status, including heart rate, blood pressure, heart sounds, and peripheral pulses. Because emotional changes are associated with hyperthyroidism, the patient’s emotional state and psychological status are evaluated, as are such symptoms as irritability, anxiety, sleep disturbances, apathy, and lethargy, all of which may occur with hyperthyroidism. The family may also provide information about recent changes in the patient’s emotional status.
Diagnosis
NURSING DIAGNOSES
Based on all the assessment data, the major nursing diagnoses of the patient with hyperthyroidism include the following:
• Imbalanced nutrition, less than body requirements, related to exaggerated metabolic rate, excessive appetite, and increased gastrointestinal activity
• Ineffective coping related to irritability, hyperexcitability, apprehension, and emotional instability
• Low self-esteem related to changes in appearance, excessive appetite, and weight loss
• Altered body temperature
COLLABORATIVE PROBLEMS/ POTENTIAL COMPLICATIONS
Based on assessment data, potential complications may include the following:
• Thyrotoxicosis or thyroid storm
• Hypothyroidism
Planning and Goals
The goals for the patient may be improved nutritional status, improved coping ability, improved self-esteem, maintenance of normal body temperature, and absence of complications.
Nursing Interventions
IMPROVING NUTRITIONAL STATUS
Hyperthyroidism affects all body systems, including the gastrointestinal system. The appetite is increased but may be satisfied by several well-balanced meals of small size, even up to six meals a day. Foods and fluids are selected to replace fluid lost through diarrhea and diaphoresis and to control the diarrhea that results from increased peristalsis. Rapid movement of food through the gastrointestinal tract may result iutritional imbalance and further weight loss. To reduce diarrhea, highly seasoned foods and stimulants such as coffee, tea, cola, and alcohol are discouraged. High-calorie, high-protein foods are encouraged. A quiet atmosphere during mealtime may aid digestion. Weight and dietary intake are recorded to monitor nutritional status.
ENHANCING COPING MEASURES
The patient with hyperthyroidism needs reassurance that the emotional reactions being experienced are a result of the disorder and that with effective treatment those symptoms will be controlled. Because of the negative effect these symptoms have on family and friends, they too need reassurance that these symptoms are expected to disappear with treatment. It is important to use a calm, unhurried approach with the patient. Stressful experiences are minimized; therefore, if hospitalized, the patient is not placed in a room with very ill or talkative patients. The environment is kept quiet and uncluttered. Noises, such as loud music, conversation, and equipment alarms, are minimized. The nurse encourages relaxing activities if they do not overstimulate the patient. If thyroidectomy is planned, the patient needs to know that pharmacologic therapy is necessary to prepare the thyroid gland for surgical treatment. The nurse instructs and reminds the patient to take the medications as prescribed. Because of hyperexcitability and shortened attention span, the patient may require repetition of this information and written instructions.
IMPROVING SELF-ESTEEM
The hyperthyroid patient is likely to experience changes in appearance, appetite, and weight. These factors, along with the patient’s inability to cope well with family and the illness, may result in loss of self-esteem. The nurse conveys an understanding of the patient’s concern about these problems and assists the patient to develop effective coping strategies. The patient and family need to know that these changes are a result of the thyroid dysfunction and are, in fact, out of the patient’s control. If changes in appearance are very disturbing to the patient, mirrors may be covered or removed. In addition, the nurse reminds family members and personnel to avoid bringing these changes to the patient’s attention. The nurse explains to the patient and family that most of these changes are expected to disappear with effective treatment. If the patient experiences eye changes secondary to hyperthyroidism, eye care and protection may become necessary. The patient may need instructions about instillation of eye drops or ointment prescribed to soothe the eyes and protect the exposed cornea. The patient may be embarrassed by the need to eat large meals. Therefore, the nurse arranges for the patient to eat alone if desired and avoids commenting on the patient’s large dietary intake while making sure that the patient receives sufficient food.
MAINTAINING
The patient with hyperthyroidism frequently finds a normal room temperature too warm because of an exaggerated metabolic rate and increased heat production. The nurse maintains the environment at a cool, comfortable temperature and changes bedding and clothing as needed. Cool baths and cool or cold fluids may provide relief. The reason for the patient’s discomfort and the importance of providing a cool environment are explained to the family and staff.
MONITORING AND MANAGING POTENTIAL COMPLICATIONS
The nurse closely monitors the patient with hyperthyroidism for signs and symptoms that may be indicative of thyroid storm. Cardiac and respiratory function are assessed by measuring vital signs and cardiac output, ECG monitoring, arterial blood gases, and pulse oximetry. Assessment continues when treatment is initiated because of the potential side effects on cardiac function. Oxygen is administered to prevent hypoxia, to improve tissue oxygenation, and to meet the high metabolic demands. Intravenous fluids may be necessary to maintain blood glucose levels and to replace lost fluids. Antithyroid medications (PTU or methimazole) may be prescribed to reduce thyroid hormone levels. In addition, propranolol and digitalis may be prescribed to treat cardiac symptoms. If shock develops, treatment strategies must be implemented (see Chap. 15). Hypothyroidism is likely to occur with any of the treatments used to treat hyperthyroidism. Therefore, the nurse periodically monitors the patient. Most patients report a greatly improved sense of well-being after treatment of hyperthyroidism, and some fail to continue to take prescribed thyroid replacement therapy. Therefore, part of patient and family teaching is instruction about the importance of continuing therapy indefinitely after discharge and a discussion of the consequences of failing to take medication.
PROMOTING HOME AND COMMUNITY-BASED CARE
Teaching Patients Self-Care
The nurse teaches the patient with hyperthyroidism how and when to take prescribed medication, and provides instruction about the essential role of the medication in the broader therapeutic plan. Because of the hyperexcitability and decreased attention span associated with hyperthyroidism, the nurse provides a written plan for the patient to use at home. The type and amount of information given depend on the patient’s stress and anxiety levels. The patient and family members receive verbal and written information about the actions and possible side effects of the medications. The nurse identifies adverse effects that should be reported if they occur (Chart 42-5). If a total or subtotal thyroidectomy is anticipated, the patient needs information about what to expect. This information is repeated as the time of surgery approaches. The nurse also advises the patient to avoid stressful situations that may precipitate thyroid storm.
Continuing Care
Referral for home care, if indicated, allows the home care nurse to assess the home and family environment and the patient’s and family’s understanding of the importance of adhering to the therapeutic regimen and the recommended follow-up monitoring. The nurse reinforces to the patient and family the importance of long-term follow-up because of the risk for hypothyroidism after thyroidectomy or treatment with antithyroid medications or radioactive iodine. The nurse also assesses the patient for changes indicating return to normal thyroid function and signs and symptoms of hyperthyroidism and hypothyroidism. Further, the nurse reminds the patient and family about the importance of health promotion activities and recommended health screening.
Evaluation
EXPECTED PATIENT OUTCOMES
Expected patient outcomes may include:
1. Improves nutritional status
a. Reports adequate dietary intake and decreased hunger
b. Identifies high-calorie, high-protein foods; identifies foods to be avoided
c. Avoids use of alcohol and other stimulants
d. Reports decreased episodes of diarrhea
2. Demonstrates effective coping methods in dealing with family, friends, and coworkers
a. Explains reasons for irritability and emotional instability
b. Avoids stressful situations, events, and people
c. Participates in relaxing, nonstressful activities
3. Achieves increased self-esteem
a. Verbalizes feelings about self and illness
b. Describes feelings of frustration and loss of control to others
c. Describes reasons for increased appetite
4. Maintains normal body temperature
5. Absence of complications
a. Serum thyroid hormone and TSH levels are withiormal limits
b. Identifies signs and symptoms of thyroid storm and hypothyroidism
c. Vital signs and results of ECG, arterial blood gases, and pulse oximetry are within normal limits
d. States importance of regular follow-up and lifelong maintenance of prescribed therapy
THYROIDITIS
Thyroiditis, inflammation of the thyroid gland, can be acute, subacute, or chronic. Each type of thyroiditis is characterized by inflammation, fibrosis, or lymphocytic infiltration of the thyroid gland.
ACUTE THYROIDITIS
Acute thyroiditis is a rare disorder caused by infection of the thyroid gland by bacteria, fungi, mycobacteria, or parasites. Staphylococcus aureus and other staphylococci are the most common causes. Infection typically causes anterior neck pain and swelling, fever, dysphagia, and dysphonia. Pharyngitis or pharyngeal pain is often present. Examination may reveal warmth, erythema (redness), and tenderness of the thyroid gland. Treatment of acute thyroiditis includes antimicrobial agents and fluid replacement. Surgical incision and drainage may be needed if an abscess is present.
SUBACUTE THYROIDITIS
Subacute thyroiditis may be subacute granulomatous thyroiditis (deQuervain’s thyroiditis) or painless thyroiditis (silent thyroiditis or subacute lymphocytic thyroiditis). Subacute granulomatous thyroiditis is an inflammatory disorder of the thyroid gland that predominantly affects women between 40 and 50 years old (Smallridge, 2000). The condition presents as a painful swelling in the anterior neck that lasts 1 to 2 months and then disappears spontaneously without residual effect. It often follows a respiratory infection. The thyroid enlarges symmetrically and may be painful. The overlying skin is often reddened and warm. Swallowing may be difficult and uncomfortable. Irritability, nervousness, insomnia, and weight loss—manifestations of hyperthyroidism—are common, and many patients experience chills and fever as well. Treatment aims to control the inflammation. In general, nonsteroidal anti-inflammatory drugs (NSAIDs) are used to relieve neck pain. Acetylsalicylic acid (aspirin) is avoided if symptoms of hyperthyroidism occur because aspirin displaces thyroid hormone from its binding sites and increases the amount of circulating hormone. Beta-blocking agents (eg, propranolol) may be used to control symptoms of hyperthyroidism. Antithyroid agents, which block the synthesis of T3 and T4, are not effective in thyroiditis because the associated thyrotoxicosis results from the release of stored thyroid hormones rather than from their increased synthesis. In more severe cases, oral corticosteroids may be prescribed to reduce swelling and relieve pain; however, they do not usually affect the underlying cause. In some cases, temporary hypothyroidism may develop and may necessitate thyroid hormone therapy. Follow-up monitoring is necessary to document the patient’s return to a euthyroid state. Painless thyroiditis (subacute lymphocytic thyroiditis) often occurs in the postpartum period and is thought to be an autoimmune process. Symptoms of hyperthyroidism or hypothyroidism are possible. Treatment is directed at symptoms, and yearly follow-up is recommended to determine the patient’s need for treatment of subsequent hypothyroidism.
CHRONIC THYROIDITIS (HASHIMOTO’S DISEASE)
Chronic thyroiditis, which occurs most frequently in women between 30 and 50 years old, has been termed Hashimoto’s disease, or chronic lymphocytic thyroiditis; its diagnosis is based on the histologic appearance of the inflamed gland. In contrast to acute thyroiditis, the chronic forms are usually not accompanied by pain, pressure symptoms, or fever, and thyroid activity is usually normal or low rather than increased. Cell-mediated immunity may play a significant role in the pathogenesis of chronic thyroiditis, and there may be a genetic predisposition to it. If untreated, the disease runs a slow, progressive course, leading eventually to hypothyroidism. The objective of treatment is to reduce the size of the thyroid gland and prevent hypothyroidism. Thyroid hormone therapy is prescribed to reduce thyroid activity and the production of thyroglobulin. If hypothyroid symptoms are present, thyroid hormone therapy is prescribed. Surgery may be required if pressure symptoms persist.
THYROID TUMORS
Tumors of the thyroid gland are classified on the basis of being benign or malignant, the presence or absence of associated thyrotoxicosis, and the diffuse or irregular quality of the glandular enlargement. If the enlargement is sufficient to cause a visible swelling in the neck, the tumor is referred to as a goiter. All grades of goiter are encountered, from those that are barely visible to those producing disfigurement. Some are symmetric and diffuse; others are nodular. Some are accompanied by hyperthyroidism, in which case they are described as toxic; others are associated with a euthyroid state and are called nontoxic goiters.
ENDEMIC (IODINE-DEFICIENT) GOITER
The most common type of goiter, encountered chiefly in geographic regions where the natural supply of iodine is deficient (eg, the Great Lakes areas of the
NODULAR GOITER
Some thyroid glands are nodular because of areas of hyperplasia (overgrowth). No symptoms may arise as a result of this condition, but not uncommonly these nodules slowly increase in size, with some descending into the thorax, where they cause local pressure symptoms. Some nodules become malignant, and some are associated with a hyperthyroid state. Thus, the patient with many thyroid nodules may eventually require surgery.
THYROID CANCER
Cancer of the thyroid is much less prevalent than other forms of cancer; however, it accounts for 90% of endocrine malignancies. According to the American Cancer Society (2002), about 20,700 new cases of thyroid cancer are diagnosed each year. Women account for 15,800 of the new cases and men 4,900. About 800 women and 500 men die annually from this malignancy. There are several types of cancer of the thyroid gland; the type determines the course and prognosis. External radiation of the head, neck, or chest in infancy and childhood increases the risk of thyroid carcinoma. Between 1940 and 1960, radiation therapy was occasionally used to shrink enlarged tonsillar and adenoid tissue, to treat acne, or to reduce an enlarged thymus. For people exposed to external radiation in childhood, there appears to be an increased incidence of thyroid cancer 5 to 40 years after irradiation. Consequently, people who underwent such treatment should consult a physician, request an isotope thyroid scan as part of the evaluation, follow recommended treatment of abnormalities of the gland, and continue with annual checkups.
Assessment and Diagnostic Findings
Lesions that are single, hard, and fixed on palpation or associated with cervical lymphadenopathy suggest malignancy. Thyroid function tests may be helpful in evaluating thyroid nodules and masses; however, their results are rarely conclusive. Needle biopsy of the thyroid gland is used as an outpatient procedure to make a diagnosis of thyroid cancer, to differentiate cancerous thyroid nodules from noncancerous nodules, and to stage the cancer if detected. The procedure is safe and usually requires only a local anesthetic. Patients who undergo the procedure are followed closely, however, because cancerous tissues may be missed during the procedure. A second type of aspiration or biopsy uses a largebore needle rather than the fine needle used in standard biopsy; it may be used when the results of the standard biopsy are inconclusive, or with rapidly growing tumors. Additional diagnostic studies include ultrasound, MRI, CT scans, thyroid scans, radioactive iodine uptake studies, and thyroid suppression tests.
Medical Management
The treatment of choice for thyroid carcinoma is surgical removal. Total or near-total thyroidectomy is performed when possible. Modified neck dissection or more extensive radical neck dissection is performed if there is lymph node involvement.
SURGICAL MANAGEMENT
Efforts are made to spare parathyroid tissue to reduce the risk for postoperative hypocalcemia and tetany. After surgery, ablation procedures are carried out with radioactive iodine to eradicate residual thyroid tissue if the tumor is radiosensitive. Radioactive iodine also maximizes the chance of discovering thyroid metastasis at a later date if total-body scans are carried out. After surgery, thyroid hormone is administered in suppressive doses to lower the levels of TSH to a euthyroid state (Thyroid Carcinoma Guidelines, 2001).
If remaining thyroid tissue is inadequate to produce sufficient thyroid hormone, thyroxine is required permanently. Several routes are available for administering radiation to the thyroid or tissues of the neck, including oral administration of radioactive iodine and external administration of radiation therapy. The patient who receives external sources of radiation therapy is at risk for mucositis, dryness of the mouth, dysphagia, redness of the skin, anorexia, and fatigue (see Chap. 16 for a discussion of these side effects of radiation). Chemotherapy is infrequently used to treat thyroid cancer. Patients whose thyroid cancer is detected early and who are appropriately treated usually do very well. Patients who have had papillary cancer, the most common and least aggressive tumor, have a 10-year survival rate greater than 90%. Long-term survival is also common in follicular cancer, a more aggressive form of thyroid cancer (Tierney et al., 2001). Continued thyroid hormone therapy and periodic follow-up and diagnostic testing, however, are important to ensure the patient’s well-being (Thyroid Carcinoma Guidelines, 2001). Postoperatively, the patient is instructed to take exogenous thyroid hormone to prevent hypothyroidism. Later follow-up includes clinical assessment for recurrence of nodules or masses in the neck and signs of hoarseness, dysphagia, or dyspnea. Totalbody scans are performed 2 to 4 months after surgery to detect residual thyroid tissue or metastatic disease. Thyroid hormones are stopped for about 6 weeks before the tests. Care must be taken to avoid iodine-containing foods and contrast agents. A repeat scan is done 1 year after the initial surgery. If measurements are stable, a final scan is obtained in 3 to 5 years. FT4, TSH, serum calcium, and phosphorus levels are monitored to determine whether the thyroid hormone supplementation is adequate and to note whether calcium balance is maintained. Although local and systemic reactions to radiation may occur and may include neutropenia or thrombocytopenia, these complications are rare when radioactive iodine is used. Patients who undergo surgery that is combined with radioiodine have a higher survival rate than those undergoing surgery alone. Patient teaching emphasizes the importance of taking prescribed medications and following recommendations for follow-up monitoring. The patient who is undergoing radiation therapy is also instructed in how to assess and manage side effects of treatment.
Partial or complete thyroidectomy may be carried out as primary treatment of thyroid carcinoma, hyperthyroidism, or hyperparathyroidism. The type and extent of the surgery depend on the diagnosis, goal of surgery, and prognosis. Thyroidectomy may be the treatment of choice for patients with symptomatic hyperparathyroidism (see later discussion), kidney stones, or bone disease. The patient undergoing surgery for treatment of hyperthyroidism is given appropriate medications to return the thyroid hormone levels and metabolic rate to normal and to reduce the risk for thyroid storm and hemorrhage during the postoperative period. Medications that may prolong clotting (eg, aspirin) are stopped several weeks before surgery to minimize the risk for postoperative bleeding.
Nursing Management
Important preoperative goals are to gain the patient’s confidence and reduce anxiety. Often, the patient’s home life has become tense because of his or her restlessness, irritability, and nervousness secondary to hyperthyroidism. Efforts are necessary to protect the patient from such tension and stress to avoid precipitating thyroid storm. If the patient reports increased stress when with family or friends, suggestions are made to limit contact with them. Quiet and relaxing forms of recreation or occupational therapy may be helpful.
PROVIDING PREOPERATIVE CARE
The nurse instructs the patient about the importance of eating a diet high in carbohydrates and proteins. A high daily caloric intake is necessary because of the increased metabolic activity and rapid depletion of glycogen reserves. Supplementary vitamins, particularly thiamine and ascorbic acid, may be prescribed. The patient is reminded to avoid tea, coffee, cola, and other stimulants. The nurse also informs the patient about the purpose of preoperative tests, if they are to be performed, and explains what preoperative preparations to expect. The information should help to reduce the patient’s anxiety about the surgery. In addition, special efforts are made to ensure a good night’s rest before surgery, although many patients are admitted to the hospital on the day of surgery. Preoperative teaching includes demonstrating to the patient how to support the neck with the hands after surgery to prevent stress on the incision. This involves raising the elbows and placing the hands behind the neck to provide support and reduce strain and tension on the neck muscles and the surgical incision.
PROVIDING POSTOPERATIVE CARE
The nurse periodically assesses the surgical dressings and reinforces them wheecessary. When the patient is in a recumbent position, the nurse observes the sides and the back of the neck as well as the anterior dressing for bleeding. In addition to monitoring the pulse and blood pressure for any indication of internal bleeding, it is also important to be alert for complaints of a sensation of pressure or fullness at the incision site. Such symptoms may indicate hemorrhage and hematoma formation subcutaneously and should be reported. Difficulty in respiration occurs as a result of edema of the glottis, hematoma formation, or injury to the recurrent laryngeal nerve. This complication requires that an airway be inserted. Therefore, a tracheostomy set is kept at the bedside at all times, and the surgeon is summoned at the first indication of respiratory distress. If the respiratory distress is due to hematoma, surgical evacuation is required. The intensity of pain is assessed and analgesic agents are administered as prescribed for pain. The nurse should anticipate apprehension in the patient and should inform him or her that oxygen will assist breathing. When moving and turning the patient, the nurse carefully supports the head and avoids tension on the sutures. The most comfortable position is the semi-Fowler’s position, with the head elevated and supported by pillows. Intravenous fluids are administered during the immediate postoperative period. Water may be given by mouth as soon as nausea subsides. Usually, there is a little difficulty in swallowing; initially, cold fluids and ice may be taken better than other fluids. Often, patients prefer a soft diet to a liquid diet in the immediate postoperative period. The patient is advised to talk as little as possible to reduce edema to the vocal cords, but when the patient does speak, any voice changes are noted because they might indicate injury to the recurrent laryngeal nerve, which lies just behind the thyroid next to the trachea. An overbed table may be used to provide easy access to items that are needed frequently, such as paper tissues, water pitcher and glass, and a small emesis basin. These are kept within easy reach so that the patient will not need to turn the head to reach for them. It is also convenient to use this table when vapor-mist inhalations are prescribed for the relief of excessive mucous secretions. The patient is usually permitted out of bed as soon as possible and is encouraged to eat foods that are easily eaten. A well-balanced, high-calorie diet may be prescribed to promote weight gain. Sutures or skin clips are usually removed on the second day. The patient is usually discharged from the hospital the day of surgery or soon afterward if the postoperative course is uncomplicated.
MONITORING AND MANAGING POTENTIAL COMPLICATIONS
Hemorrhage, hematoma formation, edema of the glottis, and injury to the recurrent laryngeal nerve are complications that have been reviewed previously in this chapter. Occasionally in thyroid surgery the parathyroid glands are injured or removed, producing a disturbance in calcium metabolism. As the blood calcium level falls, hyperirritability of the nerves occurs, with spasms of the hands and feet and muscle twitching. This group of symptoms is termed tetany, and the nurse must immediately report its appearance because laryngospasm, although rare, may occur and obstruct the airway. Tetany of this type is usually treated with intravenous calcium gluconate. This calcium abnormality is usually temporary after thyroidectomy.
PROMOTING HOME AND COMMUNITY-BASED CARE
Teaching Patients Self-Care.
The patient may be discharged the evening of surgery or within 1 or 2 days. Therefore, the patient and family need to be knowledgeable about the signs and symptoms of the complications that may occur and those that should be reported. Strategies are suggested for managing postoperative pain at home and for increasing humidification. The nurse explains to the patient and family the need for rest, relaxation, and nutrition. The patient is permitted to resume his or her former activities and responsibilities completely once recovered from surgery.
Continuing Care.
If indicated, a referral to home care is made. The home care nurse assesses the patient’s recovery from surgery. The nurse also assesses the surgical incision and reinforces instruction about limiting activities that put strain on the incision and sutures. Family responsibilities and factors relating to the home environment that produce emotional tension have often been implicated as precipitating causes of thyrotoxicosis. A home visit provides an opportunity to evaluate these factors and to suggest ways to improve the home and family environment. The nurse gives specific instructions regarding follow-up visits to the physician or the clinic, which are important for monitoring the thyroid status.
Management of Patients With Parathyroid Disorders
The parathyroid glands (normally four) are situated in the neck and embedded in the posterior aspect of the thyroid gland (Fig. 42-5). These small glands are easily overlooked and can be removed inadvertently during thyroid surgery. Inadvertent surgical removal is the most common cause of hypoparathyroidism.
PARATHYROID FUNCTION
Parathormone, the protein hormone from the parathyroid glands, regulates calcium and phosphorus metabolism. Increased secretion of parathormone results in increased calcium absorption from the kidney, intestine, and bones, thereby raising the blood calcium level. Some actions of this hormone are increased by the presence of vitamin D. Parathormone also tends to lower the blood phosphorus level. Excess parathormone can result in markedly elevated levels of serum calcium, a potentially life-threatening situation. When the product of serum calcium and serum phosphorus (calcium ? phosphorus) rises, calcium phosphate may precipitate in various organs of the body and cause tissue calcification. The serum level of ionized calcium regulates the output of parathormone. Increased serum calcium results in decreased parathormone secretion, creating a negative feedback system.
HYPERPARATHYROIDISM
Hyperparathyroidism, which is caused by overproduction of parathyroid hormone by the parathyroid glands, is characterized by bone decalcification and the development of renal calculi (kidney stones) containing calcium. Primary hyperparathyroidism occurs two to four times more often in women than in men and is most common in patients between 60 and 70 years of age. About 100,000 new cases of hyperparathyroidism are detected each year in the United States. The disease is rare in children younger than 15 years, but the incidence increases tenfold between the ages of 15 and 65 years. Half of the patients diagnosed with hyperparathyroidism do not have symptoms. Secondary hyperparathyroidism, with manifestations similar to those of primary hyperparathyroidism, occurs in patients with chronic renal failure and so-called renal rickets as a result of phosphorus retention, increased stimulation of the parathyroid glands, and increased parathyroid hormone secretion.
Clinical Manifestations
The patient may have no symptoms or may experience signs and symptoms resulting from involvement of several body systems. Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension, and cardiac dysrhythmias may occur; all are attributable to the increased concentration of calcium in the blood. Psychological manifestations may vary from irritability and neurosis to psychoses caused by the direct effect of calcium on the brain and nervous system. An increase in calcium produces a decrease in the excitation potential of nerve and muscle tissue. The formation of stones in one or both kidneys, related to the increased urinary excretion of calcium and phosphorus, is one of the important complications of hyperparathyroidism and occurs in 55% of patients with primary hyperparathyroidism. Renal damage results from the precipitation of calcium phosphate in the renal pelvis and parenchyma, resulting in renal calculi (kidney stones), obstruction, pyelonephritis, and renal failure. Musculoskeletal symptoms accompanying hyperparathyroidism may result from demineralization of the bones or bone tumors composed of benign giant cells resulting from overgrowth of osteoclasts. The patient may develop skeletal pain and tenderness, especially of the back and joints; pain on weight bearing; pathologic fractures; deformities; and shortening of body stature. Bone loss attributable to hyperparathyroidism increases the risk for fracture. The incidence of peptic ulcer and pancreatitis is increased with hyperparathyroidism and may be responsible for many of the gastrointestinal symptoms that occur.
Assessment and Diagnostic Findings
Primary hyperparathyroidism is diagnosed by persistent elevation of serum calcium levels and an elevated level of parathormone. Radioimmunoassays for parathormone are sensitive and differentiate primary hyperparathyroidism from other causes of hypercalcemia in more than 90% of patients with elevated serum calcium levels. An elevated serum calcium level alone is a nonspecific finding because serum levels may be altered by diet, medications, and renal and bone changes. Bone changes may be detected on x-ray or bone scans in advanced disease. The double antibody parathyroid hormone test is used to distinguish between primary hyperparathyroidism and malignancy as a cause of hypercalcemia. Ultrasound, MRI, thallium scan, and fine-needle biopsy have been used to evaluate the function of the parathyroids and to localize parathyroid cysts, adenomas, or hyperplasia.
Complications: Hypercalcemic Crisis
Acute hypercalcemic crisis can occur with extreme elevation of serum calcium levels. Serum calcium levels higher than 15 mg/dL (3.7 mmol/L) result ieurologic, cardiovascular, and renal symptoms that can be life-threatening. Treatment includes rehydration with large volumes of intravenous fluids, diuretic agents to promote renal excretion of excess calcium, and phosphate therapy to correct hypophosphatemia and decrease serum calcium levels by promoting calcium deposit in bone and reducing the gastrointestinal absorption of calcium. Cytotoxic agents (mithramycin), calcitonin, and dialysis may be used in emergency situations to decrease serum calcium levels quickly. A combination of calcitonin and corticosteroids has been administered in emergencies to reduce the serum calcium level by increasing calcium deposition in bone. Other agents that may be administered to decrease serum calcium levels include bisphosphonates (eg, etidronate [Didronel], pamidronate). The patient requires expert assessment and care to minimize complications and reverse the life-threatening hypercalcemia. Medications are administered with care, and attention is given to fluid balance to promote return of normal fluid and electrolyte balance. Supportive measures are necessary for the patient and family.
Medical Management
The insidious onset and chronic nature of hyperparathyroidism and its diverse and commonly vague symptoms may result in depression and frustration. The family may have considered the patient’s illness to be psychosomatic. An awareness of the course of the disorder and an understanding approach by the nurse may help the patient and family to deal with their reactions and feelings. The recommended treatment of primary hyperparathyroidism is the surgical removal of abnormal parathyroid tissue. In some patients without symptoms and with only mildly elevated serum calcium levels and normal renal function, surgery may be delayed and the patient followed closely for worsening of hypercalcemia, bone deterioration, renal impairment, or the development of kidney stones.
HYDRATION THERAPY
Because kidney involvement is possible, patients with hyperparathyroidism are at risk for renal calculi. Therefore, a fluid intake of 2,000 mL or more is encouraged to help prevent calculus formation. Cranberry juice is suggested because it may lower the urinary pH. It can be added to juices and ginger ale for variety. The patient is instructed to report other manifestations of renal calculi, such as abdominal pain and hematuria. Thiazide diuretics are avoided because they decrease the renal excretion of calcium and further elevate serum calcium levels. Because of the risk of hypercalcemic crisis, the patient is instructed to avoid dehydration and to seek immediate health care if conditions that commonly produce dehydration (eg, vomiting, diarrhea) occur. MOBILITY Mobility of the patient, with walking or use of a rocking chair for those with limited mobility, is encouraged as much as possible because bones subjected to normal stress give up less calcium. Bed rest increases calcium excretion and the risk for renal calculi. Oral phosphates lower the serum calcium level in some patients. Longterm use is not recommended because of the risk for ectopic calcium phosphate deposits in soft tissues.
DIET AND MEDICATIONS
Nutritional needs are met, but the patient is advised to avoid a diet with restricted or excess calcium. If the patient has a coexisting peptic ulcer, prescribed antacids and protein feedings are necessary. Because anorexia is common, efforts are made to improve the appetite. Prune juice, stool softeners, and physical activity, along with increased fluid intake, help to offset constipation, which is common postoperatively.
Nursing Management
The nursing management of the patient undergoing parathyroidectomy is essentially the same as that of a patient undergoing thyroidectomy. However, the previously described precautions about dehydration, immobility, and diet are particularly important in the patient awaiting and recovering from parathyroidectomy. Although not all parathyroid tissue is removed during surgery in an effort to control the calcium–phosphorus balance, the nurse closely monitors the patient to detect symptoms of tetany (which may be an early postoperative complication). Most patients quickly regain function of the remaining parathyroid tissue and experience only mild, transient postoperative hypocalcemia. In patients with significant bone disease or bone changes, a more prolonged period of hypocalcemia should be anticipated. The nurse reminds the patient and family about the importance of follow-up to ensure return of serum calcium levels to normal (Chart 42-7).
HYPOPARATHYROIDISM
The most common cause of hypoparathyroidism is inadequate secretion of parathyroid hormone after interruption of the blood supply or surgical removal of parathyroid gland tissue during thyroidectomy, parathyroidectomy, or radical neck dissection. Atrophy of the parathyroid glands of unknown cause is a less common cause of hypoparathyroidism.
Pathophysiology
Symptoms of hypoparathyroidism are caused by a deficiency of parathormone that results in elevated blood phosphate (hyperphosphatemia) and decreased blood calcium (hypocalcemia) levels. In the absence of parathormone, there is decreased intestinal absorption of dietary calcium and decreased resorption of calcium from bone and through the renal tubules. Decreased renal excretion of phosphate causes hypophosphaturia, and low serum calcium levels result in hypocalciuria.
Clinical Manifestations
Hypocalcemia causes irritability of the neuromuscular system and contributes to the chief symptom of hypoparathyroidism—tetany. Tetany is a general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movements. Symptoms of latent tetany are numbness, tingling, and cramps in the extremities, and the patient complains of stiffness in the hands and feet. In overt tetany, the
signs include bronchospasm, laryngeal spasm, carpopedal spasm (flexion of the elbows and wrists and extension of the carpophalangeal joints), dysphagia, photophobia, cardiac dysrhythmias, and seizures. Other symptoms include anxiety, irritability, depression, and even delirium. ECG changes and hypotension also may occur.
Assessment and Diagnostic Findings
A positive Trousseau’s sign or a positive Chvostek’s sign suggests latent tetany.
Trousseau’s sign is positive when carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes with a blood pressure cuff.
Chvostek’s sign is positive when a sharp tapping over the facial nerve just in front of the parotid gland and anterior to the ear causes spasm or twitching of the mouth, nose, and eye (see Chap. 14). The diagnosis of hypoparathyroidism often is difficult because of the vague symptoms, such as aches and pains. Therefore, laboratory studies are especially helpful. Tetany develops at serum calcium levels of 5 to 6 mg/dL (1.2 to 1.5 mmol/L) or lower. Serum phosphate levels are increased, and x-rays of bone show increased density. Calcification is detected on x-rays of the subcutaneous or paraspinal basal ganglia of the brain.
Medical Management
The goal of therapy is to raise the serum calcium level to 9 to 10 mg/dL (2.2 to 2.5 mmol/L) and to eliminate the symptoms of hypoparathyroidism and hypocalcemia. When hypocalcemia and tetany occur after a thyroidectomy, the immediate treatment is to administer calcium gluconate intravenously. If this does not decrease neuromuscular irritability and seizure activity immediately, sedative agents such as pentobarbital may be administered. Parenteral parathormone can be administered to treat acute hypoparathyroidism with tetany. The high incidence of allergic reactions to injections of parathormone, however, limits its use to acute episodes of hypocalcemia. The patient receiving parathormone is monitored closely for allergic reactions and changes in serum calcium levels. Because of neuromuscular irritability, the patient with hypocalcemia and tetany requires an environment that is free of noise, drafts, bright lights, or sudden movement. Tracheostomy or mechanical ventilation may become necessary, along with bronchodilating medications, if the patient develops respiratory distress. Therapy for the patient with chronic hypoparathyroidism is determined after serum calcium levels are obtained. A diet high in calcium and low in phosphorus is prescribed. Although milk, milk products, and egg yolk are high in calcium, they are restricted because they also contain high levels of phosphorus. Spinach also is avoided because it contains oxalate, which would form insoluble calcium substances. Oral tablets of calcium salts, such as calcium gluconate, may be used to supplement the diet. Aluminum hydroxide gel or aluminum carbonate (Gelusil, Amphojel) also is administered after meals to bind phosphate and promote its excretion through the gastrointestinal tract. Variable dosages of a vitamin D preparation—dihydrotachysterol (AT 10 or Hytakerol), ergocalciferol (vitamin D), cholecalciferol (vitamin D)—are usually required and enhance calcium absorption from the gastrointestinal tract.
Nursing Management
Nursing management of the patient with possible acute hypoparathyroidism includes the following:
• Care of postoperative patients having thyroidectomy, parathyroidectomy, and radical neck dissection is directed toward detecting early signs of hypocalcemia and anticipating signs of tetany, seizures, and respiratory difficulties.
• Calcium gluconate is kept at the bedside, with equipment necessary for intravenous administration. If the patient has a cardiac disorder, is subject to dysrhythmias, or is receiving digitalis, calcium gluconate is administered slowly and cautiously.
• Calcium and digitalis increase systolic contraction and also potentiate each other; this may produce potentially fatal dysrhythmias. Consequently, the cardiac patient requires continuous cardiac monitoring and careful assessment.
An important aspect of nursing care is teaching about medications and diet therapy. The patient needs to know the reason for high calcium and low phosphate intake and the symptoms of hypocalcemia and hypercalcemia; he or she should know to blood flow to tissues that are important for effective fight or flight, such as cardiac and skeletal muscle. Catecholamines also induce the release of free fatty acids, increase the basal metabolic rate, and elevate the blood glucose level.
Adrenal Cortex
A functioning adrenal cortex is necessary for life; adrenocortical secretions make it possible for the body to adapt to stress of all kinds. The three types of steroid hormones produced by the adrenal cortex are glucocorticoids, the prototype of which is hydrocortisone; mineralocorticoids, mainly aldosterone; and sex hormones, mainly androgens (male sex hormones). Without the adrenal cortex, severe stress would cause peripheral circulatory failure, circulatory shock, and prostration. Survival in the absence of a functioning adrenal cortex is possible only with nutritional, electrolyte, and fluid replacement and appropriate replacement with exogenous adrenocortical hormones.
GLUCOCORTICOIDS
The glucocorticoids are so named because they have an important influence on glucose metabolism: increased hydrocortisone secretion results in elevated blood glucose levels. However, the glucocorticoids have major effects on the metabolism of almost all organs of the body. Glucocorticoids are secreted from the adrenal cortex in response to the release of ACTH from the anterior lobe of the pituitary gland. This system represents an example of negative feedback. The presence of glucocorticoids in the blood inhibits the release of corticotropin-releasing factor from the hypothalamus and also inhibits ACTH secretion from the pituitary. The resultant decrease in ACTH secretion causes diminished release of glucocorticoids from the adrenal cortex. Glucocorticoids (in the form of corticosteroids) are administered frequently to inhibit the inflammatory response to tissue injury and suppress allergic manifestations. Their side effects include the development of diabetes mellitus, osteoporosis, peptic ulcer, increased protein breakdown resulting in muscle wasting and poor wound healing, and redistribution of body fat. Large amounts of exogenously administered glucocorticoids in the blood inhibit the release of ACTH and endogenous glucocorticoids. Because of this, the adrenal cortex can atrophy. If exogenous glucocorticoid administration is discontinued suddenly, adrenal insufficiency results because of the inability of the atrophied cortex to respond adequately.
MINERALOCORTICOIDS
Mineralocorticoids exert their major effects on electrolyte metabolism. They act principally on the renal tubular and gastrointestinal epithelium to cause increased sodium ion absorption in exchange for excretion of potassium or hydrogen ions. ACTH only minimally influences aldosterone secretion. It is primarily secreted in response to the presence of angiotensin II in the bloodstream. Angiotensin II is a substance that elevates the blood pressure by constricting arterioles. Its concentration is increased when renin is released from the kidney in response to decreased perfusion pressure. The resultant increased aldosterone levels promote sodium reabsorption by the kidney and the gastrointestinal tract, which tends to restore blood pressure to normal. The release of aldosterone is also increased by hyperkalemia. Aldosterone is the primary hormone for the long-term regulation of sodium balance.
ADRENAL SEX HORMONES (ANDROGENS)
Androgens, the third major type of steroid hormones produced by the adrenal cortex, exert effects similar to those of male sex hormones. The adrenal gland may also secrete small amounts of some estrogens, or female sex hormones. ACTH controls the secretion of adrenal androgens. When secreted iormal amounts, the adrenal androgens probably have little effect, but when secreted in excess, in certain inborn enzyme deficiencies, masculinization may result. This is termed the adrenogenital syndrome.
PHEOCHROMOCYTOMA
Pheochromocytoma is a tumor that is usually benign and originates from the chromaffin cells of the adrenal medulla. In 80% to 90% of patients (O’Connell, 1999), the tumor arises in the medulla; in the remaining patients, it occurs in the extra-adrenal chromaffin tissue located in or near the aorta, ovaries, spleen, or other organs. Pheochromocytoma may occur at any age, but its peak incidence is between ages 40 and 50 years (Rakel & Bope, 2001). It affects men and women equally. Because of the high incidence of pheochromocytoma in family members, the patient’s family members should be alerted and screened for this tumor. Ten percent of the tumors are bilateral, and 10% are malignant. Pheochromocytoma is the cause of high blood pressure in 0.2% of patients with new onset of hypertension (O’Connell, 1999). Although it is uncommon, it is one form of hypertension that is usually cured by surgery; without detection and treatment, it is usually fatal. Pheochromocytoma may occur in the familial form as part of multiple endocrine neoplasia type 2; therefore, it should be considered a possibility in patients with medullary thyroid carcinoma and parathyroid hyperplasia or tumor.
Clinical Manifestations
The nature and severity of symptoms of functioning tumors of the adrenal medulla depend on the relative proportions of epinephrine and norepinephrine secretion. The typical triad of symptoms comprises headache, diaphoresis, and palpitations (Matthews et al., 1999). Hypertension and other cardiovascular disturbances are common. The hypertension may be intermittent or persistent. Only half of patients with pheochromocytoma, however, have sustained or persistent hypertension. If the hypertension is sustained, it may be difficult to distinguish from other causes of hypertension. Other symptoms may include tremor, headache, flushing, and anxiety. Hyperglycemia may result from conversion of liver and muscle glycogen to glucose by epinephrine secretion; insulin may be required to maintaiormal blood glucose levels. The clinical picture in the paroxysmal form of pheochromocytoma is usually characterized by acute, unpredictable attacks lasting seconds or several hours. During these attacks, the patient is extremely anxious, tremulous, and weak. The patient may experience headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea. Other symptoms include polyuria, nausea, vomiting, diarrhea, abdominal pain, and a feeling of impending doom. Palpitations and tachycardia are common. Blood pressures exceeding 250/150 mm Hg have been recorded. Such blood pressure elevations are life-threatening and may cause severe complications, such as cardiac dysrhythmias, dissecting aneurysm, stroke, and acute renal failure. Postural hypotension occurs in 70% of patients with untreated pheochromocytoma.
Assessment and Diagnostic Findings
Pheochromocytoma is suspected if signs of sympathetic nervous system overactivity occur in association with marked elevation of blood pressure. These signs can be associated with the “five Hs”: hypertension, headache, hyperhidrosis (excessive sweating), hypermetabolism, and hyperglycemia. The presence of these signs has a 93.8% specificity and a 90.9% sensitivity for pheochromocytoma. Absence of hypertension excludes pheochromocytoma with a 99% certainty. Paroxysmal symptoms of pheochromocytoma commonly develop in the fifth decade of life. Measurements of urine and plasma levels of catecholamines are the most direct and conclusive tests for overactivity of the adrenal medulla. Measurements of urinary catecholamine metabolites (metanephrines [MN] and vanillylmandelic acid [VMA]) or free catecholamines are the standard diagnostic tests used in the diagnosis of pheochromocytoma. Levels can be as high as three times normal limits (O’Connell, 1999). A 24-hour specimen of urine is collected for determining free catecholamines, MN, and VMA; the use of combined tests increases the diagnostic accuracy of testing. A number of medications and foods (eg, coffee, tea, bananas, chocolate, vanilla, aspirin) may alter the results of these tests; therefore, careful instructions to avoid restricted items must be given to the patient. Urine collected over a 2- or 3-hour period after an attack of hypertension can be assayed for catecholamine content. Total plasma catecholamine (epinephrine and norepinephrine) concentration is measured with the patient supine and at rest for 30 minutes. To prevent elevation of catecholamine levels by the stress of venipuncture, a butterfly needle, scalp veieedle, or venous catheter may be inserted 30 minutes before the blood specimen is obtained. Factors that may elevate catecholamine levels must be controlled to obtain valid results; these factors include consumption of coffee or tea, use of tobacco, emotional and physical stress, and use of many prescription and over-the-counter medications (eg, amphetamines, nose drops or sprays, decongestant agents, and bronchodilators). Normal plasma values of epinephrine are 100 pg/mL (590 pmol/L); normal values of norepinephrine are generally less than 100 to 550 pg/mL (590 to 3,240 pmol/L). Values of epinephrine greater than 400 pg/mL (2,180 pmol/L) or norepinephrine values greater than 2,000 pg/mL (11,800 pmol/L) are considered diagnostic of pheochromocytoma. Values that fall betweeormal values and those diagnostic of pheochromocytoma indicate the need for further testing. A clonidine suppression test may be performed if the results of plasma and urine tests of catecholamines are inconclusive.
Clonidine (Catapres) is a centrally acting, antiadrenergic medication that suppresses the release of neurogenically mediated catecholamines. The suppression test is based on the principle that catecholamine levels are normally increased through the activity of the sympathetic nervous system. In pheochromocytoma, increased catecholamine levels result from the diffusion of excess catecholamines into the circulation, bypassing normal storage and release mechanisms. Therefore, in patients with pheochromocytoma, clonidine does not suppress the release of catecholamines. The results of the test are considered normal if 2 to 3 hours after a single oral dose of clonidine, the total plasma catecholamine value decreases at least 40% from baseline. Patients with pheochromocytoma exhibit no change in catecholamine levels. False-positive results, however, may occur in patients with primary hypertension. Imaging studies, such as CT scans, MRI, and ultrasound, may also be carried out to localize the pheochromocytoma and to determine whether more than one tumor is present. Use of 131I-metaiodobenzylguanidine (MIBG) scintigraphy may be required to determine the location of the pheochromocytoma and to detect metastatic sites outside the adrenal gland. MIBG is a specific isotope for catecholamine-producing tissue. It has been helpful in identifying tumors not detected by other tests or procedures. MIBG scintigraphy is a noninvasive, safe procedure that has increased the accuracy of diagnosis of adrenal tumors. Other diagnostic studies may focus on evaluating the function of other endocrine glands because of the association of pheochromocytoma in some patients with other endocrine tumors.
Medical Management
During an episode or attack of hypertension, tachycardia, anxiety, and the other symptoms of pheochromocytoma, the patient is placed on bed rest with the head of the bed elevated to promote an orthostatic decrease in blood pressure.
PHARMACOLOGIC THERAPY
The patient may be moved to the intensive care unit for close monitoring of ECG changes and careful administration of alphaadrenergic blocking agents (eg, phentolamine [Regitine]) or smooth muscle relaxants (eg, sodium nitroprusside [Nipride]) to lower the blood pressure quickly. Phenoxybenzamine (Dibenzyline), a long-acting alpha-blocker, may be used when the blood pressure is stable to prepare the patient for surgery. Beta-adrenergic blocking agents, such as propranolol (Inderal), may be used in patients with cardiac dysrhythmias or those not responsive to alpha-blockers. Alphaadrenergic and beta-adrenergic blocking agents must be used with caution because patients with pheochromocytoma may have increased sensitivity to them. Still other medications that may be used preoperatively are catecholamine synthesis inhibitors, such as alpha-methyl-p-tyrosine (metyrosine). These are occasionally used when adrenergic blocking agents do not reduce the effects of catecholamines.
SURGICAL MANAGEMENT
The definitive treatment of pheochromocytoma is surgical removal of the tumor, usually with adrenalectomy. Bilateral adrenalectomy may be necessary if tumors are present in both adrenal glands. Patient preparation includes control of blood pressure and blood volumes; usually this is carried out over 7 to 10 days. Phentolamine or phenoxybenzamine (Dibenzyline) may be used safely without causing undue hypotension. Other medications (metyrosine [Demser] and prazosin [Minipress]) have been used to treat pheochromocytoma. The patient needs to be well hydrated before, during, and after surgery to prevent hypotension. Manipulation of the tumor during surgical excision may cause release of stored epinephrine and norepinephrine, with marked increases in blood pressure and changes in heart rate. Therefore, use of sodium nitroprusside (Nipride) and alpha-adrenergic blocking agents may be required during and after surgery. Exploration of other possible tumor sites is frequently undertaken to ensure removal of all tumor tissue. As a result, the patient is subject to the stress and effects of a long surgical procedure, which may increase the risk of hypertension postoperatively. Corticosteroid replacement is required if bilateral adrenalectomy has beeecessary. Corticosteroids may also be necessary for the first few days or weeks after removal of a single adrenal gland. Intravenous administration of corticosteroids (methylprednisolone sodium succinate [Solu-Medrol]) may begin the evening before surgery and continue during the early postoperative period to prevent adrenal insufficiency. Oral preparations of corticosteroids (prednisone) will be prescribed after the acute stress of surgery diminishes. Hypotension and hypoglycemia may occur in the postoperative period because of the sudden withdrawal of excessive amounts of catecholamines. Therefore, careful attention is directed toward monitoring and treating these changes. Blood pressure is expected to return to normal with treatment; however, one third of patients continue to be hypertensive after surgery. This may result if not all pheochromocytoma tissue was removed, if pheochromocytoma recurs, or if the blood vessels were damaged by severe and prolonged hypertension. Several days after surgery, urine and plasma levels of catecholamines and their metabolites are measured to determine whether surgery was successful.
Nursing Management
The patient who has undergone surgery to treat pheochromocytoma has experienced a stressful preoperative and postoperative course and may remain fearful of repeated attacks. Although it is usually expected that all pheochromocytoma tissue has been removed, there is a possibility that other sites were undetected and that attacks may recur. The patient is monitored for several days in the intensive care unit with special attention given to ECG changes, arterial pressures, fluid and electrolyte balance, and blood glucose levels. Several intravenous lines are inserted for administration of fluids and medications.
PROMOTING HOME AND COMMUNITY-BASED CARE
Teaching Patients Self-Care.
During the preoperative and postoperative phases of care, the nurse informs the patient about the importance of follow-up monitoring to ensure that pheochromocytoma does not recur undetected. After adrenalectomy, use of corticosteroids may be needed. Therefore, the nurse instructs the patient about their purpose, the medication schedule, and the risks of skipping doses or stopping their administration abruptly. It is important to teach the patient and family how to measure the patient’s blood pressure and when to notify the physician about changes in blood pressure. Additionally, the nurse provides verbal and written instructions about the procedure for collecting 24-hour urine specimens to monitor urine catecholamine levels.
Continuing Care.
A follow-up visit from a home care nurse may be indicated to assess the patient’s postoperative recovery, surgical incision, and compliance with the medication schedule. This may help to reinforce previous teaching about management and monitoring. The home care nurse also obtains blood pressure measurements and assists the patient in preventing or dealing with problems that may result from long-term use of corticosteroids. Because of the risk of recurrence of hypertension, periodic checkups are required, especially in young patients and in patients whose families have a history of pheochromocytoma. The patient is scheduled for periodic follow-up appointments to observe for return of normal blood pressure and plasma and urine levels of catecholamines.
ADRENOCORTICAL INSUFFICIENCY (ADDISON’S DISEASE)
Pathophysiology
Addison’s disease, or adrenocortical insufficiency, results when 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% of cases (Rakel & Bope, 2001). Other causes include surgical removal of both adrenal glands or infection of the adrenal glands. Tuberculosis and histoplasmosis are the most common infections that destroy adrenal gland tissue. Although autoimmune destruction has replaced tuberculosis as the principal cause of Addison’s disease, tuberculosis should be considered in the diagnostic workup because of its increasing incidence. Inadequate secretion of ACTH from the pituitary gland also results in adrenal insufficiency because of decreased stimulation of the adrenal cortex. Therapeutic use of corticosteroids is the most common cause of adrenocortical insufficiency (Coursin & Wood, 2002). The symptoms of adrenocortical insufficiency may also result from the sudden cessation of exogenous adrenocortical hormonal therapy, which suppresses the body’s normal response to stress and interferes with normal feedback mechanisms. Treatment with daily administration of corticosteroids for 2 to 4 weeks may suppress function of the adrenal cortex; therefore, adrenal insufficiency should be considered in any patient who has been treated with corticosteroids.
Clinical Manifestations
Addison’s disease is characterized by muscle weakness, anorexia, gastrointestinal symptoms, fatigue, emaciation, dark pigmentation of the skin, knuckles, knees, elbows, and mucous membranes, hypotension, and low blood glucose levels, low serum sodium levels, and high serum potassium levels. Mental status changes such as depression, emotional lability, apathy, and confusion are present in 60% to 80% of patients. In severe cases, the disturbance of sodium and potassium metabolism may be marked by depletion of sodium and water and severe, chronic dehydration. With disease progression and acute hypotension, the patient develops addisonian crisis, which is characterized by cyanosis and the classic signs of circulatory shock: pallor, apprehension, rapid and weak pulse, rapid respirations, and low blood pressure. In addition, the patient may complain of headache, nausea, abdominal pain, and diarrhea and show signs of confusion and restlessness. Even slight overexertion, exposure to cold, acute infections, or a decrease in salt intake may lead to circulatory collapse, shock, and death if untreated. The stress of surgery or dehydration resulting from preparation for diagnostic tests or surgery may precipitate an addisonian or hypotensive crisis.
Assessment and Diagnostic Findings
Although the clinical manifestations presented appear specific, the onset of Addison’s disease usually occurs with nonspecific symptoms. The diagnosis is confirmed by laboratory test results. Laboratory findings include decreased blood glucose (hypoglycemia) and sodium (hyponatremia) levels, an increased serum potassium (hyperkalemia) level, and an increased white blood cell count (leukocytosis). The diagnosis is confirmed by low levels of adrenocortical hormones in the blood or urine and decreased serum cortisol levels. If the adrenal cortex is destroyed, baseline values are low, and ACTH administration fails to cause the normal rise in plasma cortisol and urinary 17-hydroxycorticosteroids. If the adrenal gland is normal but not stimulated properly by the pituitary, a normal response to repeated doses of exogenous ACTH is seen, but no response follows the administration of metyrapone, which stimulates endogenous ACTH.
Medical Management
Immediate treatment is directed toward combating circulatory shock: restoring blood circulation, administering fluids and corticosteroids, monitoring vital signs, and placing the patient in a recumbent position with the legs elevated. Hydrocortisone (Solu-Cortef) is administered intravenously, followed with 5% dextrose iormal saline. Vasopressor amines may be required if hypotension persists. Antibiotics may be administered if infection has precipitated adrenal crisis in a patient with chronic adrenal insufficiency. Additionally, the patient is assessed closely to identify other factors, stressors, or illnesses that led to the acute episode. Oral intake may be initiated as soon as tolerated. Gradually, intravenous fluids are decreased when oral fluid intake is adequate to prevent hypovolemia. If the adrenal gland does not regain function, the patient needs lifelong replacement of corticosteroids and mineralocorticoids to prevent recurrence of adrenal insufficiency. The patient will require additional supplementary therapy with glucocorticoids during stressful procedures or significant illnesses to prevent addisonian crisis (Coursin & Wood, 2002). Additionally, the patient may need to supplement dietary intake with added salt during times of gastrointestinal losses of fluids through vomiting and diarrhea.
Nursing Management
ASSESSING THE PATIENT
The health history and examination focus on the presence of symptoms of fluid imbalance and on the patient’s level of stress. To detect inadequate fluid volume, the nurse monitors the blood pressure and pulse rate as the patient moves from a lying to a standing position. The nurse assesses the skin color and turgor for changes related to chronic adrenal insufficiency and hypovolemia. Other key assessments include checking for weight changes, muscle weakness, and fatigue and investigating any illness or stress that may have precipitated the acute crisis.
MONITORING AND MANAGING ADDISONIAN CRISIS
The patient at risk is monitored for signs and symptoms indicative of addisonian crisis. These symptoms are often the manifestations of shock: hypotension; rapid, weak pulse; rapid respiratory rate; pallor; and extreme weakness. The patient with addisonian crisis is at risk for circulatory collapse and shock (see Chap. 15 for management of the patient in shock); therefore, physical and psychological stressors must be avoided. These include exposure to cold, overexertion, infection, and emotional distress. The patient with addisonian crisis requires immediate treatment with intravenous administration of fluid, glucose, and electrolytes, especially sodium; replacement of missing steroid hormones; and vasopressors. During acute addisonian crisis, the patient must avoid exertion; therefore, the nurse anticipates the patient’s needs and takes measures to meet them. Careful monitoring of symptoms, vital signs, weight, and fluid and electrolyte status is essential to monitor the patient’s progress and return to a precrisis state. To reduce the risk of future episodes of addisonian crisis, efforts are made to identify and reduce the factors that may have led to the crisis.
RESTORING FLUID BALANCE
To provide information about fluid balance and the adequacy of hormone replacement, the nurse assesses the patient’s skin turgor, mucous membranes, and weight while instructing the patient to report increased thirst, which may indicate impending fluid imbalance. Lying, sitting, and standing blood pressures also provide information about fluid status. A decrease in systolic pressure (
