Hyperthyroidism

48 Hyperthyroidism




Overview/pathophysiology


Hyperthyroidism is a clinical syndrome caused by excessive circulating thyroid hormone. Because thyroid activity affects all body systems, excessive thyroid hormone exaggerates normal body functions and produces a hypermetabolic state. Lymphocytic (“painless”) and postpartum thyroiditis are autoimmune disorders that result in thyroid inflammation with release of stored thyroid hormone into systemic circulation. Postpartum thyroiditis may ensue several months after delivery and remain active for several months, sometimes followed by hypothyroidism lasting several months. Subacute (granulomatous) thyroiditis is considered a viral syndrome, and it results in a painful, enlarged thyroid with overactive thyroid until the virus is controlled, which may in turn prompt transient hypothyroidism. Hyperthyroid symptoms also result from ingestion of too much thyroid replacement medication.


Graves’ disease (diffuse toxic goiter) accounts for approximately 85% of reported cases of hyperthyroidism. It is characterized by spontaneous exacerbations and remissions that appear to be unaffected by therapy. The cause of Graves’ disease is unknown, but recent advances in diagnostic techniques have isolated an immunoglobulin known as long-acting thyroid stimulator in a majority of patients with this disorder, suggesting that Graves’ disease is an autoimmune response.


The most severe form of hyperthyroidism is thyrotoxic crisis, or thyroid storm, which results from a sudden surge of large amounts of thyroid hormones into the bloodstream, causing an even greater increase in body metabolism. This is a medical emergency. Precipitating factors include infection, trauma, and emotional stress, all of which increase demands on body metabolism. Thyrotoxic crisis also can occur following thyroidectomy because of manipulation of the gland during surgery.



Health care setting


Primary care with possible hospitalization resulting from complications



Assessment




Signs and symptoms:


Nervousness, irritability, alteration in appetite, weight loss or gain, rapid pulse (usually noted by patient), irregular heartbeats, menstrual irregularities, fatigue, heat intolerance, increased perspiration, frequent defecation or diarrhea, anxiety, restlessness, tremor, and insomnia. Patients bordering on thyroid storm may be confused and possibly psychotic.



Physical assessment:


Tachycardia, palpitations, widened pulse pressure, exophthalmos, diplopia, hyperpyrexia, enlargement of the thyroid gland, dependent lower extremity edema, muscle weakness, hyperreflexia, fine tremor, fine hair, thin skin, hypercholesterolemia, impaired glucose tolerance, and stare and/or lid lag. Occasionally males may present with gynecomastia.



Thyrotoxic crisis (thyroid storm):


Acute exacerbation of some or all the above signs, marked tachycardia, hyperpyrexia, central nervous system (CNS) irritability, and sometimes coma or heart failure. Cardiovascular collapse and shock are occasionally how patients present. Various clinical syndromes also produce hyperthyroidism, but thyroid storm is most often associated with Graves’ disease.



History/risk factors:


Family history of hyperthyroidism is a significant factor for development of this disorder. Another important factor is presence of thyroid nodules or nodular toxic goiters in which one or more thyroid adenomas hyperfunction autonomously. Amiodarone use has caused thyroid dysfunction in 14%-18% of individuals taking this commonly used antidysrhythmic drug. Patients should have thyroid studies done before the drug is initiated and be monitored serially afterward. For thyrotoxic crisis, patients with hyperthyroidism resulting from Graves’ disease, thyroid nodules, or toxic goiter may have undergone a recent stressful experience, including severe infection, trauma, major surgery, thromboembolism, diabetic ketoacidosis, preeclampsia, pregnancy, labor, and/or delivery.



Diagnostic tests




Serum thyroid-stimulating hormone (thyrotropin):


Most commonly used test to detect thyroid dysfunction. It is decreased in the presence of disease.



Serum T4 (thyroxine) or free T4:


Elevated in the presence of disease. It may be more accurate than thyroid-stimulating hormone (TSH) if patients have been recently treated for hyperthyroidism or if receiving high doses of thyroid replacement therapy. Thyroxine should be monitored along with TSH for the first year of therapy, especially in older adults.



Serum T3 (thyroxine triiodothyronine) radioimmunoassay or free T3:


Elevated in the presence of disease.



Serum thyroid autoantibodies:


Can detect TSH receptor antibodies and thyroid-stimulating immunoglobulins, which may be present if autoimmune disease is present.



Thyroid binding globulin:


Measures the level of the protein that binds with circulating thyroid hormones. Abnormal T4 or T3 measurements are often caused by binding protein abnormalities rather than abnormal thyroid function.



Thyroid scan 123I (preferably) or 99mTc pertechnetate:


Helps determine the cause of the hyperthyroidism. The scan also may be useful in assessing functional status of any palpable thyroid irregularities or nodules associated with a toxic goiter.



Doppler ultrasonography:


To diagnose size of the gland and abnormal densities, which can indicate presence of nodules.



Radioiodine (131I) uptake and thyroid scan:


Clarifies gland size and detects presence of hot or cold nodules.



123I scintiscan/thyroid scintigraphy:


Defines functional characteristics of the gland to help determine cause of hyperthyroidism.





Nursing diagnosis:


Ineffective protection

related to potential for thyrotoxic crisis (thyroid storm) occurring with emotional stress, trauma, infection, or surgical manipulation of the gland


Desired Outcomes: Patient is free of symptoms of thyroid storm as evidenced by normothermia; blood pressure (BP) 90/60 mm Hg or more (or within patient’s baseline range); heart rate (HR) 100 bpm or less; and orientation to person, place, and time. If thyroid storm occurs, it is detected promptly and reported immediately.























































ASSESSMENT/INTERVENTIONS RATIONALES
Assess for hyperthermia and report rectal or core temperature greater than 38.3° C (101° F). An increased temperature often is the first sign of impending thyroid storm.
Assess patient for signs of heart failure. Immediately report significant findings to health care provider, and prepare to transfer patient to intensive care unit if they are noted. Signs of heart failure (jugular vein distention, crackles, decreased amplitude of peripheral pulses, peripheral edema, and hypotension) can occur as an effect of thyroid storm. If not aggressively monitored and managed, thyroid storm can lead to lethal cardiac and hemodynamic compromise.
Assess vital signs hourly in patients in whom thyroid storm is suspected. These assessments may reveal evidence of hypotension and increasing tachycardia and fever, which may reflect increasing severity of heart failure associated with thyroid storm.
Provide a cool, calm, protected environment. Reassure patient and explain all procedures before performing them. Limit the number of visitors. These measures minimize emotional and physical stress, which can precipitate thyroid storm.
Ensure good hand hygiene and meticulous aseptic technique for dressing changes and invasive procedures. Advise visitors who have contracted or been exposed to a communicable disease either not to enter patient’s room or to wear a surgical mask, if appropriate. These measures reduce risk of infection, which is a precipitating factor in development of thyroid storm.
In the Presence of Thyroid Storm  
Assess for hyperthermia, and as prescribed, administer acetaminophen. Acetaminophen will decrease temperature secondary to the fever associated with thyroid storm.
Caution: Avoid giving aspirin. Aspirin is contraindicated because it releases thyroxine from protein-binding sites and increases free thyroxine levels, which would exacerbate symptoms of thyroid storm.
Provide cool sponge baths, or apply ice packs to patient’s axilla and groin area. If high temperature continues, obtain prescription for a hypothermia blanket. These actions will decrease the fever caused by thyroid storm.
Administer thioamides, such as propylthiouracil (PTU) and methimazole as prescribed. Thioamides will prevent further synthesis and release of thyroid hormones. The most severe side effect is leukopenia, which increases the possibility that patient may acquire an infection. PTU is more effective than methimazole in thyroid storm. Patients should discontinue thioamides at the first sign of infection and obtain a complete blood count. If the blood count is normal, medication is promptly resumed. Rash, another side effect, can be treated easily with antihistamines. Methimazole may have a lower rate of these effects.
Administer propranolol as prescribed. Propranolol will block sympathetic nervous system (SNS) effects. It reduces HR and BP, which are elevated as a result of hyperthyroidism.
Administer intravenous (IV) fluids as prescribed. Fluid volume deficit may occur because of increased fluid excretion by the kidneys or excessive diaphoresis. IV fluids will provide adequate hydration and prevent vascular collapse.
Carefully monitor intake and output (I&O) hourly. Hourly assessment of I&O will reveal fluid overload or inadequate fluid replacement, either of which necessitates prompt intervention. Decreasing output with normal specific gravity may indicate decreased cardiac output, whereas decreasing output with increased specific gravity can signal dehydration.
Administer sodium iodide as prescribed, 1 hr after administering PTU. Iodine is necessary for subsequent production of thyroid hormones following resolution of the crisis. Caution: If given before PTU, sodium iodide can exacerbate symptoms in susceptible persons.
Administer small doses of insulin as prescribed. This will help control hyperglycemia. Hyperglycemia can occur as an effect of thyroid storm because of the release of stress hormones as part of the body’s response to the hypermetabolic state. Stress hormones create insulin resistance.
Administer prescribed supplemental O2 as necessary. O2 demands are increased as metabolism increases.
< div class='tao-gold-member'>

Related posts:

  1. Psychosocial support
  2. Care of the renal transplant recipient
  3. Pneumothorax/hemothorax
  4. Bronchiolitis

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 18, 2016 | Posted by in NURSING | Comments Off on Hyperthyroidism

Full access? Get Clinical Tree
Get Clinical Tree app for offline access