Hypothyroidism
In hypothyroidism, metabolic processes slow down because of a deficiency of the thyroid hormones triiodothyronine (T3) or thyroxine (T4).
Hypothyroidism is classified as primary or secondary. Primary hypothyroidism stems from a disorder of the thyroid gland. Secondary hypothyroidism is caused by a failure to stimulate normal thyroid function or by a failure of target tissues to respond to normal blood levels of thyroid hormones. Either type may progress to myxedema, which is clinically much more severe and considered a medical emergency. (See What to do in myxedema coma, page 462.)
The disorder is most prevalent in females; in the United States, incidence is rising significantly in persons ages 40 to 50.
Causes
Hypothyroidism results from a variety of abnormalities that lead to insufficient synthesis of thyroid hormones. Common
causes of hypothyroidism include thyroid gland surgery (thyroidectomy), inflammation from irradiation therapy, chronic autoimmune thyroiditis (Hashimoto’s disease), or inflammatory conditions, such as amyloidosis and sarcoidosis.
causes of hypothyroidism include thyroid gland surgery (thyroidectomy), inflammation from irradiation therapy, chronic autoimmune thyroiditis (Hashimoto’s disease), or inflammatory conditions, such as amyloidosis and sarcoidosis.
Life-threatening complicationsWhat to do in myxedema coma
A medical emergency, myxedema coma is commonly fatal. Progression is usually gradual, but when stress aggravates severe or prolonged hypothyroidism, coma may develop abruptly. Examples of severe stress include infection, exposure to cold, and trauma. Other precipitating factors include thyroid medication withdrawal and the use of sedatives, narcotics, or anesthetics.
Signs and symptoms
Patients in myxedema coma have significantly depressed respirations, so their partial pressure of arterial carbon dioxide levels may rise. Decreased cardiac output and worsening cerebral hypoxia may also occur. The patient is stuporous and hypothermic, and his vital signs reflect bradycardia and hypotension.
Emergency interventions
If your patient becomes comatose, notify the physician immediately, and begin these interventions as soon as possible:
Maintain airway patency with ventilatory support if necessary.
Maintain circulation through I.V. fluid replacement.
Provide continuous electrocardiogram monitoring.
Monitor arterial blood gas measurements to detect hypoxia and metabolic acidosis.
Warm the patient by wrapping him in blankets. Don’t use a warming blanket because it might increase peripheral vasodilation, causing shock.
Monitor body temperature until stable with a low–reading thermometer.
Replace thyroid hormone by administering large I.V. levothyroxine doses as ordered. Monitor vital signs because rapid correction of hypothyroidism can cause adverse cardiac effects.
Monitor intake and output and daily weight. With treatment, urine output should increase and body weight decrease; if not, report this to the physician.
Replace fluids and other substances such as glucose. Monitor serum electrolyte levels.
Administer corticosteroids, as ordered.
Check for possible sources of infection, such as blood, sputum, or urine, which may have precipitated coma. Treat infections or any other underlying illness.
The disorder may also result from pituitary failure to produce thyroid–stimulating hormone (TSH), hypothalamic failure to produce thyrotropin–releasing hormone, inborn errors of thyroid hormone synthesis, inability to synthesize thyroid hormones because of iodine deficiency (usually dietary), or the use of antithyroid medications such as propylthiouracil.
Complications
Because thyroid hormones affect almost every organ system in the body, complications of hypothyroidism vary according to the organs involved; the duration and severity of the condition also affect complications.
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