In this chapter, a few of the important and characteristic complications of Graves' disease have been considered in some detail. When these complications occur, particular therapeutic problems arise and must be dealt with.
Thyroid storm, fortunately, is becoming rare. Formerly a complication appearing frequently after surgery on the incompletely prepared patient, it is now usually seen in patients with severe thyrotoxicosis who have neglected therapy or who have an added medical problem, such as an acute infection. Storm may be looked upon as a sudden and violent exacerbation of the signs and symptoms of thyrotoxicosis. Clinically, it is characterized by fever, extreme tachycardia, varied disorders of heart rhythm, and nervous hyperirritability rapidly progressing to exhaustion and often to coma. Mortality is high. A special form of thyroid storm is characterized by apathy and muscle weakness. It is no less serious.
The treatment of thyroid storm should include use of antithyroid drugs and iodide, and also general supportive measures such as cooling, oxygen, transfusions, repletion of electrolytes, nutritional repletion, antibiotics if indicated sedation, and adrenal corticoids. Control of many of the aspects of thyroid storm, especially tachycardia, may be achieved by the use of propranolol.
The infiltrative ophthalmopathy of Graves' disease (GO) usually occurs during a period of thyrotoxicosis, but may appear when there is no thyrotoxicosis or even when there is hypothyroidism. There is evidence that autoimmune mechanisms in the retroocular muscles stimulate preadipocytes and fibroblasts to production of glycosaminoglycans (Gags) leading to water retention and edema and ultimately fibrosis. The event responsible for retroocular autoimmune reactions is most probably the retrobulbar localized TSH-R as the primary antigen (possibly overexpressed) interacting with T cells directed against this antigen. In these autoimmune reactions circulating antibodies play a role as well. GO presents a therapeutic problem, sometimes of stupendous proportions. If simple local measures fail to halt the progress of the ophthalmopathy, glucocorticoids, surgical decompression of the orbits, or radiotherapy to the orbit may be required, and thyroid ablation may also be useful.
The curious deposits of a material rich in glycosaminoglycans in the skin of the lower legs and sometimes over the phalanges are discussed in some detail. This material is seen only in patients with Graves' disease and usually coincides with infiltrative ophthalmopathy. Its appearance has no direct relationship to the level of thyroid function.
Cardiac insufficiency in the course of toxic goiter is looked upon as the effect, in most instances at least of thyrotoxicosis on an already diseased heart. There may be younger patients who sustain permanent heart damage from severe thyrotoxicosis, and long-continued thyrotoxicosis in older age groups may be the only definable etiologic factor in congestive heart failure. The chief indication for treatment in cardiac insufficiency occurring in thyrotoxicosis is to abolish the thyrotoxicosis, but the usual cardiotonic, diuretic and sometimes vasodilatory measures should be employed as well.