ity of surgical therapy to produce a euthyroid state in many patients over long-term follow-up gives it one advantage over RAI therapy, but this must be weighed against the risk of hypoparathyroidism and recurrent nerve damage.
Course After Surgery —
In the immediate postoperative period, patients should be followed closely. They should ideally have a special duty nurse or family member providing watch during the first 24 hours, and a tracheotomy set and calcium chloride or gluconate for infusion should be at the bedside. During this period, undetected hemorrhage can lead to asphyxiation. Current use of drains with constant suction helps protect against this problem. Transient hypocalcemia is common, resulting from trauma to the parathyroid glands and their blood supply and also possibly to rapid uptake of calcium by the bones, which have been depleted of calcium by the thyrotoxicosis . Oral or intra- venous calcium supplementation suffices in most instances to control the symptoms. The calcium may be given slowly intravenously as calcium gluconate or calcium chloride in a dose ranging from 0.5 to 1.0 g every 4-8 hours, as indicated by clinical observation and determination of Ca2+. Replacement thyroid hormone- If sub-total throidectomy has been performed, thyroid hormeone replacement may not be needed. In 50-70% of patients, the residual gland is able to form enough hormone to prevent even transient clinical hypothyroidism. Serum hormone levels should be determined every two to four months until it is clear that the patient does not need replacement.
Some surgeons give their patients thyroxine for an indefinite period after the operation in an attempt to avoid transient hypothyroidism and to remove any stimulus to regeneration of the gland. If total thyroidectomy has been performed, as is increasingly the case, full replacement doses of thyroxine (1.7 ug/kg BW, or about 1ug/pound of lean body mass) should be instituted immediately, and T4 levels checked in about 2 weeks for adjustment. Patients should be informed that they will need this treatment for life, and that they should re regularly checked, and consistent in their daily dosage.
Long Term Follow-Up
Probably the thyroid remnant is not normal. It has a rapid 131-I turnover rate and a small pool of stored organic iodine. Suppressibility by T3 administration returns within a few months of operation in some patients. TSAb tend to disappear from the blood in the ensuing 3 – 12 months [208-210]. After subtotal thyroidectomy, thyrotoxicosis recurs in 5 – 10% of patients, often many years after the original episode. The long term outcome of thyroid surgery for hyperthyroidism was reviewed by the Department of Surgery at Karolinska Institute. Of 380 patients observed and treated by surgery for thyrotoxicosis, primarily by subtotal thyroidectomy, 1% developed permanent hypoparathyroidism. Recurrent disease occurred in 2%. The operators intended to leave less than two grams of thyroid tissue, which presumably accounts for the low recurrence rate (210.1).
Finally, adequate follow-up must be carried out after any kind of treatment of Graves’ disease. Recurrence is always possible, either early or late, and there is always the threat that the ophthalmopathic problems may worsen when all else in the progress of the patient seems favorable. A surprisingly large proportion of patients who have had subtotal thyroidectomy for Graves’ disease and who are clinically euthyroid can be shown to have an abnormal TRH response (excessive or depressed), and up to a third have elevated serum TSH levels [210, 211]. Some of them are undoubtedly mildly hypothyroid, whereas others are close to euthyroid but require the stimulation of TSH to maintain this state. These patients should have replacement T 4therapy if the elevated TSH persists. Over subsequent years the residual thyroid fails in more patients, due either to reduced blood supply, fibrosis from trauma, or continuing autoimmune thyroiditis. After 10 years, and depending on the extent of the original surgery, 20 – 40% are hypothyroid. Th