Thyrotoxicosis
Thyrotoxicosis: Excerpt from Handbook of Diseases
Thyrotoxicosis is a metabolic imbalance that results from thyroid hormone overproduction or thyroid hormone overrelease from the gland. The most common form of thyrotoxicosis is Graves’disease, which increases thyroxine production, enlarges the thyroid gland (goiter), and causes multiple system changes. (See Other forms of thyrotoxicosis.) Its incidence is highest between ages 30 and 40, especially in people with family histories of thyroid abnormalities.
With treatment, most patients can lead normal lives. However, thyroid storm — an acute, severe exacerbation of thyrotoxicosis — is a medical emergency that may lead to life-threatening cardiac, hepatic, or renal consequences.
Causes
Thyrotoxicosis may result from genetic and immunologic factors.
❑ An increased incidence of this disorder in monozygotic twins points to an inherited factor, probably an autosomal recessive gene.
❑ This disease occasionally coexists with other endocrine abnormalities, such as diabetes mellitus, thyroiditis, and hyperparathyroidism.
❑ Thyrotoxicosis may also be caused by the production of autoantibodies (thyroid-stimulating immunoglobulin and thyroid-stimulating hormone [TSH]-binding inhibitory immuno-globulin), possibly because of a defect in suppressor-T-lymphocyte function that allows the formation of autoantibodies.
❑ In latent thyrotoxicosis, excessive dietary intake of iodine and, possibly, stress can precipitate clinical thyrotoxicosis.
❑ In a person with inadequately treated thyrotoxicosis, stress — including surgery, infection, toxemia of pregnancy, and diabetic ketoacidosis — can precipitate thyroid storm.
Signs and symptoms
The classic features of Graves’ disease are an enlarged thyroid (goiter), nervousness, heat intolerance, weight loss despite increased appetite, sweating, frequent bowel movements, tremor, and palpitations. Exophthalmos is considered most characteristic but is absent in many patients with thyrotoxicosis.
Many other signs and symptoms are common because thyrotoxicosis profoundly affects virtually every body system:
❑ Central nervous system: difficulty in concentrating because increased thyroxine secretion accelerates cerebral function; excitability or nervousness due to increased basal metabolic rate; fine tremor, shaky handwriting, and clumsiness from increased activity in the spinal cord area that controls muscle tone; emotional instability and mood swings, ranging from occasional outbursts to overt psychosis
❑ Skin, hair, and nails: smooth, warm, flushed skin (patient sleeps with minimal covers and little clothing); fine, soft hair; premature graying and increased hair loss in both sexes; friable nails and onycholysis (distal nail separated from the bed); pretibial myxedema (dermopathy), producing thickened skin; and accentuated hair follicles, raised red patches of skin that are itchy and sometimes painful, with occasional nodule formation. Microscopic examination shows increased mucin deposits.
❑ Cardiovascular system: tachycardia; full, bounding pulse; wide pulse pressure; cardiomegaly; increased cardiac output and blood volume; visible point of maximal impulse; paroxysmal supraventricular tachycardia and atrial fibrillation (especially in elderly people); and, occasionally, a systolic murmur at the left sternal border
❑ Respiratory system: dyspnea on exertion and at rest, possibly from cardiac decompensation and increased cellular oxygen utilization
❑ GI system: excessive oral intake with weight loss; nausea and vomiting due to increased GI motility and peristalsis; increased defecation; soft stools or, with severe disease, diarrhea; and liver enlargement
❑ Musculoskeletal system: weakness (especially in proximal muscles), fatigue, and muscle atrophy; rare coexistence with myasthenia gravis; possibly generalized or localized paralysis associated with hypokalemia; and occasional acropachy (soft-tissue swelling, accompanied by underlying bone changes where new bone formation occurs)
❑ Reproductive system: in females, oligomenorrhea or amenorrhea, decreased fertility, higher incidence of spontaneous abortions; in males, gynecomastia due to increased estrogen levels; in both sexes, diminished libido
❑ Eyes: exophthalmos (produced by the combined effects of accumulation of mucopolysaccharides and fluids in the retroorbital tissues that force the eyeball outward, and of lid retraction that produces the characteristic staring gaze); occasional inflammation of conjunctivae, corneas, or eye muscles; diplopia; and increased tearing.
When thyrotoxicosis escalates to thyroid storm, these symptoms can be accompanied by extreme irritability, hypertension, tachycardia, vomiting, temperature up to 106° F (41.1° C), delirium, and coma.
Clinical tip Consider apathetic thyrotoxicosis in elderly patients who exhibit atrial fibrillation or depression.
Diagnosis
The diagnosis of thyrotoxicosis usually is straightforward and depends on a careful clinical history and physical examination, a high index of suspicion, and routine hormone determinations. The following tests confirm the disorder:
❑ Radioimmunoassay shows increased serum thyroxine (T4) and triiodothyronine (T3) concentrations.
❑ Thyroid scan reveals increased uptake of radioactive iodine 131 (131I) in Graves’ disease, and usually in toxic multinodular goiter and toxic adenoma. Radioactive uptake is low in thyroiditis and thyrotoxic factitia. This test is contraindicated if the patient is pregnant.
❑ TSH levels are decreased.
❑ Thyroid-releasing hormone (TRH) stimulation test indicates thyrotoxicosis if the TSH level fails to rise within 30 minutes after the administration of TRH. TRH testing is rarely necessary due to highly sensitive TSH assays.
❑ Ultrasonography confirms subclinical ophthalmopathy.
Treatment
A number of approaches are utilized for the treatment of thyrotoxicosis. The primary forms of therapy include antithyroid drugs, 131I, and surgery. Appropriate treatment depends on the size of the goiter, the causes, the patient’s age and parity, and how long surgery will be delayed (if the patient is an appropriate candidate for surgery).
Antithyroid therapy
Therapy with antithyroid drugs is used for children, young adults, pregnant women, and patients who refuse surgery or 131I treatment. Antithyroid drugs are also used to correct the thyrotoxic state in preparation for 131I treatment or surgery. Treatment options include the following:
❑ Thyroid hormone antagonists include propylthiouracil and methimazole, which block thyroid hormone synthesis. Although hypermetabolic symptoms subside within 4 to 8 weeks after such therapy begins, the patient must continue the medication for 6 months to 2 years, in an attempt to achieve remission in Graves’disease.
❑ Propranolol may be given concomitantly to manage tachycardia and other peripheral effects of excessive hypersympathetic activity. Propranolol blocks the conversion of T4 to the active T3 hormone.
❑ During pregnancy, antithyroid medication should be kept at the minimum dosage required to keep maternal thyroid function within the high-normal range until delivery and to minimize the risk of fetal hypothyroidism. Propylthiouracil is the preferred agent for the pregnant patient. (See Congenital thyrotoxicosis).
131I
The treatment of choice for patients not planning to have children is a single oral dose of 131I. (Patients of reproductive age must give informed consent for this treatment, since small amounts of 131I concentrate in the gonads.)
During treatment with 131I, the thyroid gland picks up the radioactive element as it would regular iodine. Subsequently, the radioactivity destroys some of the cells that normally concentrate iodine and produce T4, thus decreasing thyroid hormone production and normalizing thyroid size and function.
In most patients, hypermetabolic symptoms diminish from 6 to 8 weeks after such treatment. However, some patients may require a second dose of 131I.
CLINICAL TIP: Patients commonly become permanently hypothyroid after 131I ablation.
Surgery
Near-total thyroidectomy, which decreases the thyroid gland’s capacity for hormone production, is indicated for patients whose thyrotoxicosis has repeatedly relapsed after drug therapy or patients who refuse or aren’t candidates for 131I treatment.
Preoperatively, the patient may receive iodides (Lugol’s solution or saturated solution of potassium iodide), antithyroid drugs, and propranolol to help prevent thyroid storm. If euthyroidism isn’t achieved, surgery should be delayed, and antithyroid drugs and propranolol should be administered to decrease the systemic effects (such as cardiac arrhythmias) caused by thyrotoxicosis.
After surgery, patients require regular medical supervision for the rest of their lives because they usually develop hypothyroidism, sometimes as long as several years after treatment.
Treatment for ophthalmopathy
Therapy includes local application of topical medications but may require high doses of corticosteroids. A patient with severe exophthalmos that causes pressure on the optic nerve may require external-beam radiation therapy or surgical decompression to lessen pressure on the orbital contents.
Treatment for thyroid storm
This includes administration of an antithyroid drug, propranolol I.V. or by mouth, to block sympathetic effects and conversion of T4 to T3. Corticosteroids also inhibit the conversion of T4 to T3, and an iodide is used to block release of thyroid hormone.
Supportive measures include administration of nutrients, vitamins, fluids, and sedatives.
Special considerations
Patients with thyrotoxicosis require vigilant care to prevent acute exacerbations and complications.
❑ Monitor serum electrolytes, and check periodically for hyperglycemia and glycosuria.
❑ Carefully monitor cardiac function if the patient is elderly or has coronary artery disease. If the heart rate is more than 100 beats/minute, check blood pressure and pulse rate often.
❑ Check the patient’s level of consciousness and urine output.
❑ If the patient is pregnant, tell her to watch closely during the first trimester for signs of spontaneous abortion (spotting, occasional mild cramps) and report such signs immediately.
❑ The patient with dyspnea will be most comfortable sitting upright or in high Fowler’s position.
❑ Remember, severe thyrotoxicosis may produce bizarre behavior. Reassure the patient and his family that such behavior will probably subside with treatment. Provide sedatives as necessary, and encourage the patient to verbalize his feelings about body image changes.
❑ If iodide is part of the treatment, mix it with milk, juice, or water to prevent GI distress, and administer it through a straw to prevent tooth discoloration.
CLINICAL TIP: Administer preparations containing iodine only after antithyroid drugs have been initiated. Otherwise, the iodine will be utilized by the already overactive gland to make more thyroid hormone and worsen the toxic state.
❑ Watch for signs of thyroid storm (tachycardia, hyperkinesis, fever, vomiting, hypertension).
❑ Check intake and output carefully to ensure adequate hydration and fluid balance.
❑ Closely monitor blood pressure, cardiac rate and rhythm, and temperature. If the patient has a high fever, reduce it with appropriate hypothermic measures. Maintain an I.V. line and give drugs as needed.
❑ If the patient has exophthalmos or another ophthalmopathy, suggest eye patches to protect his eyes from dryness at night. Moisten the conjunctivae often with isotonic eyedrops. Instruct him to report signs of decreased visual acuity.
❑ Avoid excessive palpation of the thyroid to avoid precipitating thyroid storm.
After thyroidectomy:
❑ Check often for respiratory distress, and keep a tracheotomy tray at bedside.
❑ Watch for evidence of hemorrhage into the neck such as a tight dressing with no blood on it. Change dressings and perform wound care; check the back of the dressing for drainage. Keep the patient in semi-Fowler’s position, and support his head and neck with sandbags to ease tension on the incision.
❑ Check for dysphagia or hoarseness from possible laryngeal nerve injury.
❑ Watch for signs of hypoparathyroidism (tetany, numbness), a complication that results from accidental removal of the parathyroid glands during surgery.
❑ Stress the importance of regular medical follow-up after discharge because hypothyroidism may develop from 2 to 4 weeks postoperatively.
Drug therapy and 131I therapy require careful monitoring and comprehensive patient teaching as follows:
❑ After 131I therapy, tell the patient not to allow people close to his neck because the radiation is concentrated there. Also, tell patients to keep people away from his bladder area, where unabsorbed 131I accumulates before excretion. These cautions should be maintained for several days. Stress the need for repeated measurement of serum thyroxine levels.
❑ Instruct the patient to take medications with meals to minimize GI distress, and to avoid over-the-counter cough preparations because many contain iodine.
❑ Tell him to report signs of hypersensitivity — fever, enlarged cervical lymph nodes, sore throat, mouth sores, and other signs of blood dyscrasias, and any rash or skin eruptions. He should also watch for signs of liver dysfunction, such as jaundice or dark urine.
❑ Watch the patient taking propranolol for signs of hypotension (dizziness, decreased urine output). Tell him to rise slowly after sitting or lying down to prevent orthostatic hypotension.
❑ Instruct the patient receiving antithyroid drugs or 131I therapy to report any symptoms of hypothyroidism.
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Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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