THERAPY FOR TOXIC NODULAR GOITER

Treatment of toxic nodular goiter with RAI is generally satisfactory and will cause a reversion to euthyroid or hypothyroid state. The dose of 131I may be calculated on the basis of uptake determinations and gland weight, as discussed in Chapter 11 on Graves' disease. Multinodular glands, toxic or not, are relatively resistant to 131I, and for this reason some therapists increase the standard dose by 20-50%. (This is done as part of the schedule given in Chapter 11 since dose is increased with weight). It is frequently seen that areas in the thyroid of low functional activity at the time of therapy, may become activated after destruction of the hyperfunctioning. Frequently doses are between 15 and 50 mCi (555 and 1850 MBq). Jensen et al.88a treated their patients with a mean dose of 37 mCi (1370 MBq) range 6.3-150 mCi (233-5550 MBq). After one year of follow-up 16% of patients were hypothyroid. Danaci et al.86 treated multinodular toxic goiters with a fixed dose of 16.6 mCi (631 MBq) 131I and they reported a cumulative relapse rate of 39% at 5 years and a cumulative incidence of hypothyroidism of 24% at 5 years. In a large prospective study involving 130 consecutive patients with toxic multinodular goiter and a mean follow-up of 6 years, 92% of patients were cured after one or two treatments with 131I. Thyroid volume was reduced by a mean value of 43% and side effects were few. Patients were treated with a median dose of 10mCi (370 MBq) (86a). Some authors prefer to administer a standard dose of 400MBq to both patients with Graves' disease and toxic MNG. This patient-friendly and possibly cost-effective regimen proved to be very effective in curing hyperthyroidism 88b.

An acute increase in the severity of thyrotoxicosis after radioiodine treatment may occur due to damage of the thyroid cells and release of stored thyroid hormone. It may sometimes occur months later, due to induction of autoimmune hyperthyroidism with development of thyroid stimulating antibodies, especially in patients presenting with TPO antibodies.88c,88d Therapy with 131I usually reduces the gland to a cosmetically satisfactory size, but rarely to normal dimensions. Even in the case of toxic nodular goiters of large size many thyroidologists use 131I as the first choice of treatment. Careful pre-treatment with antithyroid drugs in these cases is imperative. Therapy can induce worsened thyrotoxicosis with cardiac problems, and death has been reported. If the patient is made euthyroid with antithyroid drugs prior to therapy, this is unlikely to happen. Alternatively multiple smaller doses may be given, or the RAI treatment can be followed promptly by administration of antithyroid drug and then KI, as detailed in Chapter 11. When using large doses, it is important to consider the radiation dose administered and potential effects on neck structures and the body.

Some physicians find that subtotal thyroidectomy is a useful alternative therapy , after preparation with antithyroid drugs and KI. Thyroidectomy is indicated if there is a question of carcinoma. The patient may then be prepared with an antithyroid drug administered until the euthyroid state is achieved. The degree of thyrotoxicosis in this group of patients is usually rather mild. Thus, it is permissible to prepare the patient simply by the administration of propranolol. Thyroid storm occurs only with the greatest rarity after surgical treatment of toxic nodular goiter. When, after operation, airway patentcy is significantly compromised because of tracheomalacia (an extreme rarity!), a tracheotomy tube is often inserted and left in place for several weeks until peritracheal scarring has produced a rigid airway. Alternatively, the trachea is sutured to surrounding tissues, or plastic rings are sutured to the outside of the trachea in order to provide support.

Unfortunately, many patients with toxic nodular goiter first come to the attention of the physician because of cardiac symptoms, such as palpitations due to atrial fibrillation or symptoms of congestive heart failure. These patients need cardio-specific and antithyroid medication simultaneously. After rendering the patient euthyroid and stabilization of the cardiac situation, radioiodine therapy is satisfactory in spite of a slow response in this type of patient.