Since myxedema frequently occurs in older persons, it is often associated with underlying coronary artery disease. In this situation, the low levels of circulating thyroid hormone actually protect the heart against increasing demands that could result in angina pectoris, atrial fibrillation, or myocardial infarction. Correction of myxedema must be done cautiously to avoid provoking these cardiac events. If coronary artery surgery is indicated, it should be done first, prior to correction of the myxedema by thyroxine administration.
B. Myxedema Coma
Myxedema coma is an end state of untreated hypothyroidism. It is associated with progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, water intoxication, shock, and death.
Myxedema coma is a medical emergency. The patient should be treated in the intensive care unit, since tracheal intubation and mechanical ventilation may be required. Associated illnesses such as infection or heart failure must be treated by appropriate therapy.
It is important to give all preparations intravenously, because patients with myxedema coma absorb drugs poorly from other routes. Intravenous fluids should be administered with caution to avoid excessive water intake. These patients have large pools of empty T3 and T4 binding sites that must be filled before there is adequate free thyroxine to affect tissue metabolism. Accordingly, the treatment of choice in myxedema coma is to give a loading dose of levothyroxine intravenously—usually 300–400 mcg initially, followed by 50–100 mcg daily. Intravenous T3 5–20 mcg initially, followed by 2.5–10 mcg every 8 hours also can be added but may be more cardiotoxic and more difficult to monitor. Lower T4 and T3 doses should be considered for smaller or older patients, or those with concomitant cardiac disease or arrhythmias. Intravenous hydrocortisone is indicated if the patient has associated adrenal or pituitary insufficiency but is probably not necessary in most patients with primary myxedema. Opioids and sedatives must be used with extreme caution.
C. Hypothyroidism and Pregnancy
Hypothyroid women frequently have anovulatory cycles and are therefore relatively infertile until restoration of the euthyroid state. This has led to the widespread use of thyroid hormone for infertility, although there is no evidence for its usefulness in infertile euthyroid patients. In a pregnant hypothyroid patient receiving thyroxine, it is extremely important that the daily dose of thyroxine be adequate because early development of the fetal brain depends on maternal thyroxine. In many hypothyroid patients, an increase in the thyroxine dose (about 25–30%) is required to normalize the serum TSH level during pregnancy. It is reasonable to counsel women to take one extra dose of their current thyroxine tablet twice a week separated by several days as soon as they are pregnant. Thyroxine should also be administered apart from prenatal vitamins and calcium by at least 4 hours. Because of the elevated maternal TBG levels and, therefore, elevated total T4 levels, adequate maternal thyroxine dosages warrant maintenance of TSH between 0.1 and 3.0 mIU/L (eg, first trimester, 0.1–2.5 mIU/L; second trimester, 0.2–3.0 mIU/L; third trimester, 0.3–3.0 mIU/L) and the total T4 at or above the upper range of normal.
D. Subclinical Hypothyroidism