Page 39 Complete Your CE Test Online - Click Here Since nontoxic goiter does not adversely alter the patient’s metabolic state, clinical manifestations of the disease develop solely due to thyroid gland enlargement[5] . Symptoms of nontoxic goiter include [5,11] : ● ● Dysphagia. ● ● Respiratory distress. ● ● Stridor. There is swelling and neck distention and, if the goiter is large enough, obstruction of venous return that causes venous engorgement. Rarely, large goiters may prompt the development of collateral venous circulation in the chest. Venous obstruction may make the patient dizzy or trigger syncope when the arms are raised above the head [5,11] . Diagnostic tests show[5,11] : ● ● Normal or elevated levels of TSH. ● ● Normal levels of thyroid hormones. Diagnostic alert! Abnormalities in T3, T4, and TSH rule out a diagnosis of nontoxic goiter[11] . ● ● Thyroid antibody titers are generally normal. Increases in thyroid antibody titers suggest chronic thyroiditis. ● ● Radioactive iodine uptake is usually normal. However, results may increase if the patient has an iodine deficiency or a biosynthetic defect. ● ● Urinalysis results may show low urinary excretion of iodine. Ultrasound of the thyroid or radioisotope scanning may be used to identify malignancies or nodules that need to be biopsied[5,11] . Treatment and nursing considerations Treatment focuses on reduction of thyroid hyperplasia. The treatment of choice for nontoxic goiter is thyroid hormone replacement therapy with levothyroxine dessicated thyroid or liothyronine. Such treatment inhibits secretion of TSH and allows the thyroid gland to rest[5,11] . Small doses of iodine in the form of Lugol’s solution or potassium solution are given to patients whose goiter is caused by iodine deficiency[5,11] . Patients must be cautioned to take medication exactly as prescribed. Patients’ and families’ knowledge of how to administer medication, dose, route, action, and side effects must be assessed. Patients must inform their HCPs of any and all medications they are taking in conjunction with drugs used to treat goiter including prescription, OTC, herbs, vitamins, minerals, and any other supplements[5,14] . Other treatment initiatives include[5,11] : ● ● Diet: Patients who have sporadic goiters must be taught to avoid goitrogenic foods and medications. Patients who are taking such medications should be cautioned not to discontinue such drugs without approval of the prescribing physician or nurse practitioner. Patients must inform these providers about goiter development and what medications have been prescribed to treat the goiter. Patients with endemic goiters should be instructed to use iodized salt to include necessary amounts of iodine in their diet. ● ● Radiation: Radioiodine ablation therapy to the thyroid gland is administered to destroy cells that concentrate iodine for the production of thyroid hormone. ● ● Surgery: Patients who have large goiters that do not respond to other treatment measures may need surgery. Partial removal of the thyroid gland (subtotal thyroidectomy) may relieve pressure on adjacent structures. Patients with large goiters may experience embarrassment because of their appearance and fear permanent disfigurement. Nurses and other HCPs should provide emotional support and the importance of adhering to prescribed treatment initiatives. Hypoparathyroidism Jane has recently undergone a thyroidectomy as part of the treatment for thyroid cancer. Following surgery Jane develops tremors triggered by voluntary movement, paresthesia, headaches, and severe anxiety. Diagnostic evaluation shows electrolyte imbalances indicative of hypoparathyroidism. It seems that during surgery to remove the thyroid gland, parathyroid tissue had also been removed. Hypoparathyroidism is an uncommon condition caused by a deficiency of PTH. Since PTH is essential to the regulation and maintenance of calcium and phosphorus, hypoparathyroidism is characterized by hypocalcemia and neuromuscular hyper-excitability[6,23] . Etiology and pathophysiology Hypoparathyroidism can be acute or chronic, and is categorized as idiopathic or acquired[5,23] . The most common cause of hypoparathyroidism is due to accidental removal or destruction of parathyroid tissue or circulation to such tissue during thyroidectomy or radical neck dissection[5,6] . EBP alert! Research shows that hypoparathyroidism is most often due to the accidental removal or destruction of parathyroid tissue or circulation to such tissue. Therefore, nurses caring for patients who have undergone thyroid surgery or radical neck dissection must be vigilant in monitoring for signs and symptoms of hypoparathyroidism. Rarely, acquired hypoparathyroidism is caused by massive thyroid irradiation, ischemic infarction of the parathyroid glands during surgery, or from tuberculosis, neoplasms, trauma, sarcoidosis, or hemochromatosis[5] . Acquired hypoparathyroidism may be reversible if the cause is hypomagnesemia (causing impairment of hormone synthesis), suppression of normal gland functioning because of hypercalcemia, or from delayed maturation of parathyroid functioning[5] . Idiopathic hypoparathyroidism may be linked to autoimmune disease or the congenital absence of the parathyroid glands[5,23] . Research shows the following statistics as they relate to hypoparathyroidism[5] : ● ● The incidence is 4 out of 100,000 people. ● ● Incidence of idiopathic and reversible forms is highest in children. ● ● Incidence of the irreversible acquired form is highest in older patients who have undergone surgery for hyperthyroidism or other pathology of the head and neck. Hypoparathyroidism can cause a myriad of effects that lead to severe hypocalcemia and hyperphosphatemia. Recall that PTH is not regulated by either the pituitary or hypothalamus. This hormone maintains blood calcium levels by increasing bone resorption and GI absorption of calcium. PTH maintains an inverse relationship between serum calcium and phosphate levels[5] . Insufficient PTH secretion leads to decreased resorption of calcium from the renal tubules, decreased absorption of calcium in the GI tract, and decreased resorption of calcium from bone. Serum calcium falls to below normal levels triggering signs and symptoms of hypocalcemia such as neuromuscular irritability, increased deep tendon reflexes, and tremors[6] . Since calcium and phosphate have an inverse relationship serum phosphate levels increase, and excretion of phosphate by the kidneys decreases[5,6] . A number of complications are associated with hypoparathyroidism. These include[5] : ● ● Arrhythmias. ● ● Cataracts. ● ● Delayed mental development in children. ● ● Loss of consciousness. ● ● Osteoporosis. ● ● Tetany.