THYROID GLAND Dr.Mohanned Alshalah LEC 2 Hyperthyroidism The term thyrotoxicosis is retained because hyperthyroidism, i.e. symptoms due to a raised level of circulating thyroid hormones, is not responsible for all manifestations of the disease. Clinical types are: •diffuse toxic goitre (Graves’ disease) •toxic nodular goitre; •toxic nodule; •hyperthyroidism due to rarer causes. Thyrotoxicosis is eight times more common in women than in men. Clinical features The symptoms are: •tiredness; •emotional lability; •heat intolerance; •weight loss; •excessive appetite; •palpitations. The signs of thyrotoxicosis are: •tachycardia; •hot, moist palms; •exophthalmos; •lid lag/retraction; •agitation; •thyroid goitre and bruit. The most significant symptoms are loss of weight despite a good appetite, a recent preference for cold, and palpitations. The most significant signs are the excitability of the patient, the presence of a goitre, exophthalmos and tachycardia or cardiac arrhythmia. Diffuse toxic goitre (Graves’ disease): A diffuse vascular goitre, a thrill and a bruit may be present. It usually occurs in younger women and is frequently associated with eye signs. 50% of patients have a family history of autoimmune endocrine diseases. 1 THYROID GLAND Dr.Mohanned Alshalah LEC 2 The thyroid tissue is hypertrophy and hyperplasia due to abnormal thyroidstimulating antibodies (TSH-RAbs) that bind to TSH receptor sites and produce a disproportionate and prolonged effect. The onset is abrupt, but remissions and exacerbations are not infrequent. Hyperthyroidism is usually more severe than in secondary thyrotoxicosis but cardiac failure is rare. Manifestations of thyrotoxicosis not due to hyperthyroidism e.g. orbital proptosis, ophthalmoplegia and pretibial myxoedema, may occur in primary thyrotoxicosis. Toxic nodular goitre A simple nodular goitre is present for a long time before the hyperthyroidism, usually in the middle-aged or elderly. The syndrome is that of secondary thyrotoxicosis. In secondary thyrotoxicosis the goitre is nodular. The onset is insidious and may present with cardiac failure or atrial fibrillation. It is characteristic that the hyperthyroidism is not severe. Eye signs other than lid lag and lid spasm (due to hyperthyroidism) are very rare. Toxic nodule A toxic nodule is a solitary overactive nodule, which may be part of a generalised nodularity or a true toxic adenoma. It is autonomous and its hypertrophy and hyperplasia are not due to TSH-RAb. TSH secretion is suppressed by the high level of circulating thyroid hormones and the normal thyroid tissue surrounding the nodule is itself suppressed and inactive. Diagnosis of thyrotoxicosis Most cases are readily diagnosed clinically. Hyperthyroidism is confirmed biochemically by raised level of circulating thyroid hormones and decrease TSH level. A TRH test is rarely indicated. T3 thyrotoxicosis is diagnosed by estimating the free T3. It should be suspected if the clinical picture is suggestive but routine tests of thyroid function reveal a normal T4 but suppressed TSH. A thyroid scan is required to diagnose an autonomous toxic nodule and differentiate it from a dominant swelling in a toxic multinodular goitre. Principles of treatment of thyrotoxicosis Non-specific measures are rest and sedation. 2 THYROID GLAND Dr.Mohanned Alshalah LEC 2 Specific measures: Anti-thyroid drugs Those in common use are carbimazole and propylthiouracil. β- Adrenergic blockers such as propranolol and nadolol are used to block the cardiovascular effects of the elevated T4. Iodides, which may reduce the vascularity of the thyroid, should be used only as immediate preoperative preparation in the 10 days before surgery. Anti-thyroid drugs are used to restore the patient to a euthyroid state and to maintain this for a prolonged period in the hope that a permanent remission will occur, i.e. that the production of TSH-RAbs will diminish or cease. Anti-thyroid drugs cannot cure a toxic nodule. The overactive thyroid tissue is autonomous and recurrence of the hyperthyroidism is certain when the drug is discontinued. Advantages: No surgery and no use of radioactive materials. Disadvantages: •Treatment is prolonged and the failure rate after a course of 1.5—2 years is at least 50 per cent. It is impossible to predict which patient is likely to go into a remission. •Some goitres enlarge and become very vascular during treatment —even if thyroxine is given at the same time. This is probably due to TsAb stimulation during the prolonged course of treatment and not a direct effect of the drug. •Very rarely, there is a dangerous drug reaction, e.g. agranulocytosis or aplastic anaemia. Surgery In diffuse toxic goitre and toxic nodular goitre with overactive internodular tissue, surgery cures by reducing the mass of overactive tissue. Cure is probable if the thyroid tissue can be reduced below a critical mass but there is a risk of both permanent thyroid failure and recurrence of toxicity following subtotal resection. In the autonomous toxic nodule, and in toxic nodular goitre with overactive autonomous toxic nodules, surgery cures by removing all of the overactive thyroid tissue; this allows the suppressed normal tissue to function again. 3 THYROID GLAND Dr.Mohanned Alshalah LEC 2 • Advantages: The goitre is removed, the cure is rapid and the cure rate is high if surgery has been adequate. • Disadvantages: Recurrence of thyrotoxicosis occurs in approximately 5% of cases if less than total thyroidectomy is carried out. There is a risk of permanent hypoparathyroidism and nerve injury. Young women tend to have a worse cosmetic result from the scar. Postoperative thyroid insufficiency occurs in 20–45% of cases. Long-term follow-up is necessary as the few patients who develop recurrence may do so at any time in the future. In addition, although it is usually apparent within 1 or 2 years, thyroid failure may also be a late development. Parathyroid insufficiency should be permanent in less than 0.5%. Radioiodine Radioiodine destroys thyroid cells and, as in thyroidectomy, reduces the mass of functioning thyroid tissue to below a critical level. Advantages: No surgery and no prolonged drug therapy. Disadvantages: •Isotope facilities must be available. •There is a high and progressive incidence of thyroid insufficiency which may reach 75—80 per cent after 10 years. •Indefinite follow-up is essential. Choice of therapy; Patients must be considered individually. In advising treatment, compliance, influenced by social and intellectual factors, is important; many patients cannot be trusted to take drugs regularly if they feel well, and indefinite follow-up, which is essential after radioiodine or subtotal thyroidectomy, is a burden for all. Diffuse toxic goitre In patients over 45 years, radioiodine is appropriate. 4 THYROID GLAND Dr.Mohanned Alshalah LEC 2 In those under 45 years, surgery for the large goitre and anti-thyroid drugs or radioiodine for the small goitre is recommended. Toxic nodular goitre Large goitres should be treated surgically because they do not respond as well as rapidly to radioiodine or anti-thyroid drugs as a diffuse toxic goitre. Toxic nodule Surgery or radioiodine treatment is appropriate. Resection is easy, certain and without morbidity. Radioiodine is a good alternative for those over the age of 45 years because the suppressed thyroid tissue does not take up iodine and there is thus no risk of delayed thyroid insufficiency. Recurrent thyrotoxicosis after surgery Radioiodine is the treatment of choice, but antithyroid drugs may be used in young women intending to have children. Further surgery has little place. Problems in treatment of thyrotoxicosis in Pregnancy ?? Surgery for thyrotoxicosis Preoperative preparation Traditional preparation aims to make the patient biochemically euthyroid at operation. The thyroid state is determined by clinical assessment, i.e. by improvement in previous symptoms and by objective signs such as weight gain and lowering of the pulse rate, and by serial estimations of the thyroid profile. Carbimazole 30–40 mg/ day is the drug of choice for preparation. When euthyroid (after 8–12 weeks), the dose may be reduced to 5 mg 8-hourly or a ‘block and replace’ regime used . Iodides are not used alone because if the patient needs preoperative treatment a more effective drug should be given. An alternative method of preparation is to abolish the clinical manifestations of the toxic state using β-blocking drugs. β- Blockers act on the target organs and not on the gland itself. Propranolol inhibits the peripheral conversion of T4 to T3. This result in very rapid control and operation may be arranged within 1 week. 5 THYROID GLAND Dr.Mohanned Alshalah LEC 2 β -Blockers do not interfere with synthesis of thyroid hormones, and hormone levels remain high during treatment and for some days after thyroidectomy. It is therefore important to continue to give the drug for 7 days postoperatively. Iodine may be given with carbimazole or β-blocker for the 10 days before operation. Iodide alone produces a transient remission and may reduce vasularity, thereby marginally improving safety. Propranolol or nadolol controls symptoms very rapidly and has additional value in combination with carbimazole in the immediate treatment of patients with very severe hyperthyroidism. Preoperative investigations to be carried out and recorded are: • Thyroid function tests. • Laryngoscopy. • Thyroid antibodies. • Serum calcium estimation. • An isotope scan before preoperative preparation in toxic nodular goitre if total thyroidectomy is not planned. Postoperative complications Haemorrhage Respiratory obstruction Recurrent laryngeal nerve paralysis and voice change may be unilateral or bilateral, transient or permanent. Thyroid insufficiency (20–45%) Parathyroid insufficiency: The incidence of permanent hypoparathyroidism should be less than 1% and most cases present dramatically 2–5 days after operation. Thyrotoxic crisis (storm): It occurs if a thyrotoxic patient has been inadequately prepared for thyroidectomy. Wound infection Hypertrophic or keloid scar Stitch granuloma Recurrent thyrotoxicosis: (5%) after subtotal thyroidectomy for Graves’ disease 6