Hyperthyroidism

Thyrotoxicosis

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.

Diffuse toxic goitre

Graves’ disease a diffuse vascular goitre appearing at the same time as the hyperthyroidism, usually in the younger woman and frequently associated with eye signs. The syndrome is that of primary thyrotoxicosis (Fig. 44.23). The whole of the functioning thyroid tissue is involved, and the hypertrophy and hyperplasia are due to abnormal thyroid-stimulating antibodies (TsAb).

Toxic nodular goitre

A simple nodular goitre is present for a long time before the hyperthyroidism, usually in the middle-aged or elderly and very infrequently associated with eye signs. The syndrome is that of secondary thyrotoxicosis.

In many cases of toxic nodular goitre, the nodules are inactive, and it is the internodular thyroid tissue that is overactive. However, in some toxic nodular goitres, one or more nodules are overactive and here the hyperthyroidism is due to autonomous thyroid tissue as in a toxic adenoma.

Toxic nodule

This 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 TsAb. Because TSH secretion is suppressed by the high level of circulating thyroid hormones, the normal thyroid tissue surrounding the nodule is itself suppressed and inactive.

Histology

The normal thyroid gland (Fig. 44.24) consists of acini lined by flattened cuboidal epithelium and filled with homogeneous colloid. In hyperthyroidism (Fig. 44.25) there is hyperplasia of acini, which are lined by high columnar epithelium. Many of them are empty and others contain vacuolated colloid.

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.

  Symptomatology

Thyrotoxicosis is eight times commoner in females than in males. It may occur at any age. The most significant symptoms are loss of weight in spite of 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.

The goitre in primary thyrotoxicosis is diffuse and vascular, it may be large or small, firm or soft, and a thrill and a bruit may be present. 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 per Se, e.g. orbital proptosis, ophthalmoplegia and pretibial myxoedema, may occur in primary 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.

Cardiac rhythm. A fast heart rate, which persists during sleep, is characteristic. Cardiac arrhythmias are super­imposed on the sinus tachycardia as the disease progresses, and they are commoner in older patients with thyrotoxicosis because of the prevalence of coincidental heart disease. Stages of development of thyrotoxic arrhythmias are:

  multiple extrasystoles;

  paroxysmal atrial tachycardia;

  paroxysmal atrial fibrillation;

  persistent atrial fibrillation, not responsive to digoxin.

  Myopathy. Weakness of the proximal limb muscles is commonly found if looked for. Severe muscular weakness (thyrotoxic myopathy) resembling myasthenia gravis occurs occasionally. Recovery proceeds as hyperthyroidism is controlled.

Eye signs. Some degree of exophthalmos is common (Fig. 44.23). It may be unilateral. True exophthalmos is a proptosis of the eye, caused by infiltration of the retrobulbar tissues with fluid and round cells, with a varying degree of retraction or spasm of the upper eyelid. (Lid spasm occurs because the levator palpebrae superioris muscle is partly innervated by sympathetic fibres.) This results in widening of the palpebral fissure so that the sclera may be seen clearly above the upper margin of the iris and cornea (above the ‘limbus’).

Spasm and retraction usually disappear when the hyperthyroidism is controlled. They may be improved by 3-adrenergic blocking drugs, e.g. guanethidine eye drops. Oedema of the eyelids, conjunctival injection and chemosis are aggravated by compression of the ophthalmic veins (Fig. 44.26). Weakness of the extraocular muscles, particularly the elevators (inferior oblique), results in diplopia. In severe cases, papilloedema and corneal ulceration occur. When severe and progressive, it is known as malignant exophthalmos (Fig. 44.27) and the eye may be destroyed. Graves’ ophthalmopathy is an autoimmune disease in which there are antibody-mediated effects on the ocular muscles.

Exophthalmos tends to improve with time. Sleeping propped up and lateral tarsorrhaphy will help to protect the eye but will not prevent progression. Hypothyroidism increases proptosis by a few millimetres and should be avoided.

Improvement has been reported with massive doses of prednisone. Intraorbital injection of steroids is dangerous because of the venous congestion, and total thyroid ablation has not proved effective. When the eye is in danger, orbital decom­pression may be required (see Dysthyroid exophthalmos). Pretibial myxoedema (Fig. 44.28) is a thickening of the skin by a mucin-like deposit, nearly always associated with true exophthalmos, past or present hyperthyroidism, and high levels of TsAb.

Diagnosis of thyrotoxicosis

Most cases are readily diagnosed clinically. Difficulty is most likely to arise in the differentiation of mild hyperthyroidism from an anxiety state when a goitre is present. In these cases, the thyroid status is determined by the diagnostic tests described earlier. 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 are within the normal range. A thyroid scan is essential in the diagnosis of an autonomous toxic nodule.

Thyrotoxicosis should always be considered in:

  children with a growth spurt, behaviour problems or  myopathy;

tachycardia or arrhythmia in the elderly;

unexplained diarrhoea;

  loss of weight.

Principles of treatment of thyrotoxicosis

Nonspecific measures are rest and sedation and, in established thyrotoxicosis, should be used only in conjunction with specific measures the use of antithyroid drugs, surgery and radioiodine.

Antithyroid drugs

Those in common use are carbimazole and propylthiouracil. Beta-adrenergic blockers, such as propranolol and nadolol, may also be used. Iodides, once thought to reduce the vascularity of the thyroid, should only be used as immediate preoperative preparation in the 10 days before surgery. Antithyroid 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 production of TsAb will diminish or cease. It should be noted that antithyroid 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. Recently there has been a trend towards the use of shorter courses (6 months) of these drugs.

It is impossible to predict which patient is likely to go into a remission. [Attempts have been made to predict which patients might relapse after a 6-month course of antithyroid drugs on the basis of human leucocyte antigen (HLA) status and the presence of TsAb production.]

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. In the event of agranulocytosis, the patient should be instructed to discontinue treatment, if a sore throat develops, until the white cell count has been checked.

Initially, 10 mg of carbimazole4 is given three or four times a day, and there is a latent interval of 7—14 days before any clinical improvement is apparent. It is most important to maintain a high concentration of the drug throughout the 24 hours by spacing the doses at 8- or 6-hourly intervals. When the patient becomes euthyroid, a maintenance dose of 5 mg two or three times a day is given for another 12—18 months. If tri-iodothyronine (20 jig up to four times daily) or thyroxine (0.1 mg daily) is given in conjunction with anti-thyroid drugs, there is less danger of producing iatrogenic thyroid insufficiency or an increase in the size of the goitre (‘block and replacement treatment’).

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. This may result in a reduction of TsAb or it may be that circulating TsAb, however high its level, can only produce limited hypertrophy and hyperplasia when the mass of thyroid tissue is small. 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.

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 per cent of cases.

Every operation carries a morbidity but with suitable preparation and an experienced surgeon the mortality is negligible.

Postoperative thyroid insufficiency occurs in 20—45 per cent of cases.

Long-term follow-up is highly desirable as the few patients who develop recurrence may do so at any time in the future. In addition, although it is usually apparent within a year or two, thyroid failure may also he a late development.

•Parathvroid insufficiency: this should he permanent in less than 0.5 per cent.

Radioiodine

Radioiodine5 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. This is due to sublethal damage to those cells not actually destroyed by the initial treatment and this eventually causes failure of cellular reproduction.

Indefinite follow-up is essential.

There is no convincing evidence that radioiodine has been responsible for genetic damage, leukaemia, damage to the foetus if given inadvertently in early pregnancy, or carcinoma in the adult. In some clinics, radioiodine is given to almost all patients over the age of 25, i.e. when development is complete. Follow-up requirements are reduced if a total ablative dose of radioiodine is administered followed by routine replacement treatment with thyroxine. In the UK, reluctance to prescribe radioiodine under the age of 45 has faded. The dose of radioiodine varies between 300 and 600 MBq. Response is slow, but a substantial improvement is to he expected in 8—12 weeks. Accurate dosage is difficult and, should there be no clinical improvement after 12 weeks, a further dose is given. Two or more doses are necessary in 20—3 0 per cent of cases.

Choice of therapeutic agent

Each case must be considered individually. Below are listed guiding principles on the most satisfactory treatment for a particular toxic goitre at a particular age; these must however be modified according to the facilities available and the personality, intelligence and wishes of the individual patient, business or family commitments and any other coexistent medical or surgical condition.

Diffuse toxic goitre

Over 45: radioiodine. Under 45: surgery for the large goitre, antithyroid drugs for the small goitre. As mentioned above, radioiodine is being increasingly used in younger patients, particularly when their families are complete.

Large goitres are uncomfortable and remission with antithyroid drugs is less likely than in the small goitre.

Toxic nodular goitre

Surgery. Toxic nodular goitre does not respond as well or as rapidly to radioiodine or antithyroid drugs as does a diffuse toxic goitre, and the goitre itself is often large and uncomfortable and enlarges still further with antithyroid drugs.

Toxic nodule

Surgery or radioiodine. Resection is easy, certain and without morbidity. Radioiodine is a good alternative over the age of 45 because the suppressed thyroid tissue does not take up iodine and there is thus no risk of delayed thyroid insufficiency.

Recurrent thyrotoxicosis after surgery

In general radioiodine, but antithyroid drugs may be used in young women intending to have children. Further surgery has no place.

Failure of previous treatment with antithyroid drugs or radioiodine. Surgery or thyroid ablation with 123I .In advising treatment, intelligence and compliance are important:

   unintelligent patients cannot be trusted to take drugs regularly if they feel well, and are unlikely to attend follow-up clinics indefinitely, which is essential after radioiodine or surgical therapy.

Special problems in treatment

Pregnancy. Radioiodine is absolutely contraindicated because of the risk to the foetus. The danger of surgery is miscarriage; and that of anti-thyroid drugs is of inducing thyroid insufficiency in the mother, and because both TSH and antithyroid drugs cross the placenta, of the baby being born goitrous (Fig. 44.29) and hypothyroid. The risk of either surgery in the second trimester, in competent hands, or careful admini­stration of antithyroid drugs, is very small and the choice is exactly as in the uncomplicated case.

Postpartum hyperthyroidism. Pregnancy may lead to an exacerbation of a variety of autoimmune diseases in the postpartum period. Postpartum hyperthyroidism may be a problem in a patient previously diagnosed with hyperthyroidism or may occur in a patient without any previous history of thyroid disease.

Children. Radioiodine is contraindicated because of the theoretical risk of inducing thyroid carcinoma. There is an increased risk of recurrence after thyroidectomy because thyroid cells are highly active in the young. Children and adolescents should he treated with antithyroid drugs until the late teens, failing which total or near-total thyroidectomy by an expert surgeon should be undertaken.

The thyrocardiac. This is a patient with severe cardiac damage due wholly or partly to hyperthyroidism. The patient is usually middle aged or elderly with secondary thyrotoxicosis and the hyperthyroidism is not very severe. The cardiac condition is far more significant than the hyperthyroidism, but this must be rapidly controlled to prevent further cardiac damage. Betablockade (propranolol) can assist rapid control of cardiac effects.

Radioiodine is the treatment of choice together with antithyroid drugs started either before or after and continued until the radioiodine has had an effect (usually 6 weeks).

High titres of thyroid antibodies. Their presence indicates lymphatic infiltration of the goitre, i.e. a diffuse or focal thyroiditis, and a liability to spontaneous remission.

These patients are best treated conservatively but if medical treatment fails, definitive treatment by operation or radioiodine is not contra-indicated. Steroids may help to reduce pain and swelling.

Proptosis of recent onset. There is a conventional view that to termi­nate thyrotoxicosis abruptly by thyroidectomy or radioiodine when proptosis is recent may induce malignant exophthalmos. Whilst there is no real proof of this it is reasonable to treat these patients with anti-thyroid drugs until the proptosis has been static for 6 months

Hyperthyroidism due to other causes

Thyrotoxicosis factitia. (Usually seen in health ‘cranks’ or those given thyroid extract as ‘a tonic’.) Hyperthyroidism may he induced by taking thyroxine, but only if the dosage exceeds the normal requirements of 0.15—0.25 mg a day. Doses below the normal requirements simply suppress normal hormone production by the thyroid. cretinism

Jod-Basedow thyrotoxicosis. (Jod = German for iodine + Basedow. In European countries diffuse toxic goitre is often called Basedow’s disease.) Large doses of iodide given to a hyperplastic endemic goitre which is iodine avid may produce temporary hyperthyroidism, and very occasionally persistent hyperthyroidism.

In sub acute or acute forms of autoimmune thyroiditis or of de Quervain’s thyroiditis (see later), mild hyperthyroidism may occur in the early stages due to liberation of thyroid hormones from damaged tissue.

A large mass of secondary carcinoma will rarely produce sufficient hormone to induce mild hyperthyroidism.

Neonatal thyrotoxicosis occurs in babies horn to hyperthyroid mothers or to euthyroid mothers who have had thyrotoxicosis. High TsAb titres are present in both mother and child because TsAb can cross the placental barrier. The hyperthyroidism gradually subsides after 3—4 weeks’ time as the TsAb titres fall in the baby’s serum.

Surgery for thyrotoxicosis

Preoperative preparation (Fig. 44.30)

Traditional preparation aims to make the patient euthyroid or near euthyroid at operation. The thyroid state is determined by clinical assessment, i.e. by improvement in previous symptoms and by objective signs such as gain in weight and lowering of the pulse rate, and by serial estimations of the thyroid profile.

Preparation is as an out-patient and only rarely is admis­sion to hospital necessary on account of severe symptoms at presentation or failure to control the hyperthyroidism. Failure to control with antithyroid drugs is unusual but may be due to uneven dosage, i.e. not taking the drug at 6- or 8-hourly intervals.

Carbimazole 30—40 mg a day is the drug of choice for preparation. When euthyroid after 8—12 weeks the dose may be reduced to 5 mg 8-hourly and the addition of thyroxine may facilitate maintenance of the euthyroid state. The last dose of carbimazole may he given on the evening before surgery. Iodides6 are not used alone because, if the patient needs preoperative treatment, a more effective drug should be given. Iodides may be given with carbimazole for 10—14 days immediately before operation but their use is of doubtful value and has been given up in many centres.

An alternative method of preparation that appears to be safe is to abolish the clinical manifestations of the toxic state, using beta-blocking drugs. This results in very rapid control and operation may be arranged within a week or two. The appropriate drugs are propranolol 40 mg three times daily or, preferably, the longer acting nadolol 160 mg once daily. Clinical response to beta-blockade is rapid and the patient may be reassessed within days: if clinically euthyroid, an operation date may be arranged; if not, the dose of beta-blocker is increased with early reassessment. Quite often larger doses are necessary.

Beta-blockers act on the target organs and not on the gland itself. Propranolol inhibits the peripheral conversion of 14 to 13. Long-acting betablockers, e.g. nadolol, are now also available and are administered once daily. They do not interfere with synthesis of thyroid hormones, so that 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.

The addition of iodine for 10 days before operation gives an additional measure of safety in case the early morning dose of beta-blocker on the day of operation is mistakenly omitted (Plummer).

Propranolol or nadolol control symptoms very rapidly and have additional value in combination with carbimazole in the immediate treatment of patients with very severe hyper­thyroidism.

Subtotal thyroidectomy

Preoperative investigations to be carried out and recorded are:

  thyroid function tests;

  indirect laryngoscopy it is a matter for local protocols whether this is routine. The outcome should have little impact on the operation because every recurrent laryngeal nerve must be routinely and obsessionally preserved;

thyroid antibodies;

serum calcium estimation;

an isotope scan before preoperative preparation is necessary in patients with toxic nodular goitre if total thyroidectomy is not planned. The surgeon should know which nodules, if any, are autonomous and active in order to ensure their resection. A scan is of no value in diffuse toxic goitre when uptake, for practical purposes, is uniform. The diagnosis of a single toxic nodule can only be made by demonstrating that the nodule is active and the remaining thyroid tissue suppressed.

The extent of the resection depends on the size of the gland, the age of the patient, the experience of the surgeon, the need to minimise the risk of recurrent toxicity and the wish to avoid postoperative thyroid replacement. Thus young patients with small glands are at greatest risk of recurrence even with very small remnant sizes. There is an increasing trend towards total thyroidectomy which simplifies subsequent management and rapidly achieves a perma­nent euthyroid state on thyroxine replacement. In contrast, a patient with a large goitre who wishes to avoid postoperative medication is suitable for subtotal thyroidectomy.

Technique. General anaesthesia is administered through an endotracheal tube and good muscle relaxation obtained. The patient is supine on the operating table with the table tilted 15degree at the head end to reduce venous engorgement. A sandbag is placed transversely under the shoulders and the neck extended (with care particularly in the elderly) to make the thyroid gland more prominent. A skin crease incision is made midway between the notch of the thyroid cartilage and the suprasternal notch. Flaps of skin, subcutaneous tissue and platysma are raised upwards to the superior thyroid notch and downwards to the suprasternal notch. The deep cervical fascia is divided in the midline between the sternothyroid muscles down to the plane of the thyroid capsule. The muscles are not divided as a routine but may be if greater exposure is required. The sternothyroid muscle is mobilised off the thyroid lobes. In 30 per cent of patients, middle thyroid veins passing directly into the internal jugular vein require ligation and division. The main blood supply is the superior thyroid artery which must be ligated securely. The lobe is then free to rotate out of its bed. The inferior thyroid arteries are not routinely ligated to preserve parathyroid blood supply. The recurrent laryngeal nerve should be identified in its course in the operative field. It should first he sought below the level of the inferior thyroid artery as it passes obliquely upwards and forwards. This course (Fig. 44.31), oblique to the trachea and oesophagus, is accentuated by mobilisation of the thyroid lobe. If not immediately seen, the nerve can usually be palpated as a taut strand. At a higher level the nerve lies between the branches of the inferior thyroid artery. The nerve passes into the larynx immediately behind the inferior euro of the thyroid cartilage which is therefore a very important landmark. If the right nerve cannot he found in its usual course, an anomalous (nonrecurrent) nerve, present in 1 per cent of cases, should he suspected; this arises from the vagus trunk and usually passes from behind the carotid sheath, curving medially, forwards and upwards, and may be mistaken for the inferior thyroid artery. The parathyroid glands are protected by identification on careful inspection of the goitre before resection and by avoiding ligatures and sutures close to the hilum of identified glands. The use of diathermy in this area should he avoided as heat conduction may devascularise the parathyroids or damage the recurrent laryngeal nerves (Fig. 44.12). If a parathyroid gland is inadvertently excised or devascularised, it should he autotransplanted in several fragments within the sternomastoid muscle. Subtotal resection of each lobe is carried out, leaving a remnant of between 4 and 5 g on each side. Absolute haemostasis is secured by ligation of individual vessels and by suture of the thyroid remnants to the tracheal fascia. The pretracheal muscles amid cervical fascia are sutured and the wound is closed with or without suction drainage to the deep cervical space.

Postoperative complications

Haemorrhage. A tension haematoma deep to the cervical fascia (Fig. 44.33) is usually due to slipping (If a ligature on the superior thyroid artery: occasionally haemorrhage from a thyroid remnant or a thyroid vein may he responsible. It may, on rare occasions, be necessary to re open the wound in the ward to relieve tension before taking the patient to theatre to evacuate the haematoma and to tie off a bleeding vessel.

A small subcutaneous haematoma or collection of serum may form under the skin flaps and should he evacuated or aspirated in the following 72 hours. This should not be confused with the potentially life-threatening deep tension haematoma.

Respiratory obstruction. This is very rarely due to collapse or kinking of the trachea. Most cases are due to laryngeal oedema. The most important cause of laryngeal oedema is a tension haematoma. However, trauma to the larynx by anaesthetic intubation and surgical manipulation is an important contributory factors particularly if the goitre is very vascular and may cause laryngeal oedema without a tension haematoma. Unilateral or bilateral recurrent nerve paralysis will not cause immediate postoperative respiratory obstruction unless laryngeal oedema is also present, but they will aggravate the obstruction.

If releasing the tension haematoma does not immediately relieve airway obstruction, the trachea should he intubated at once. An endotracheal tube can he left in place for several days; steroids are given to reduce oedema and a tracheostomy is rarely necessary. Intubation in the presence of laryngeal oedema may be very difficult and should be carried out by an experienced anaesthetist; repeated unsuccessful attempts may increase obstruction and cause serious cerebral anoxia (Wade). In an emergency, it is far safer for the inexperienced surgeon to perform a needle tracheostomy as a temporary measure; a Medicut 12G needle (diameter 2.3 mm) is highly satisfactory.

Recurrent laryngeal nerve paralysis may be unilateral or bilateral, transient or permanent (Chapter 43). Transient paralysis occurs in about 3 per cent of nerves at risk and recovers in 3 weeks to 3 months. Permanent paralysis is extremely rare if the nerve has been identified at operation.

Thyroid insufficiency. This usually occurs within 2 years, but it is sometimes delayed for 5 years or more. It is often insidious and difficult to recognise. The incidence is considerably higher than used to he thought and figures of 20—45 per cent have been reported after opera­tions on diffuse toxic goitres and toxic nodular goitres with internodular hyperplasia. It represents a change in the autoimmune response from stimulation to destruction of thyroid cells. There is, however, a definite relationship between the estimated weight of the thyroid remnant and the development of thyroid failure after subtotal thyroidectomy for Graves’ disease. Thyroid insufficiency is rare after surgery for a toxic adenoma because there is no autoimmune disease present.

Parathyroid insufficiency is due to removal of parathyroid glands, or infarction through damage to the parathyroid end-artery; often both factors occur together. Vascular injury is probably far more important than inadvertent removal. The incidence of this condition should be less than 0.5 per cent and most cases present dramatically 2—5 days after operation, but very rarely the onset is delayed for 2—3 weeks or a patient with marked hypocalcaemia is asymptomatic.

Thyrotoxic crisis (storm) is an acute exacerbation of hyperthyroidism. It occurs if a thyrotoxic patient has been inadequately prepared for thyroidectomy, and is now extremely rare. Very rarely, a thyrotoxic patient presents in a crisis amid this may follow an unrelated operation. Symptomatic and supportive treatment is for dehydration, hyperpyrexia and restlessness. This requires the administration of intravenous fluids, cooling the patient with ice packs, administration of oxygen, diuretics for cardiac failure, digoxin for uncontrolled atrial fibrillation, sedation and intra­venous hydrocortisone. Specific treatment is by carbimazole 10—20 mg 6-hourly, Lugol’s iodine 10 drops 8-hourly by mouth or sodium iodide 1 g intravenously (i.v.). Propranolol 40 mg 6-hourly orally will block adverse beta-adrenergic effects. This agent may be given by careful intravenous administration (1—2 mg) under precise electrocardiographic control.

Wound infection. A subcutaneous or deep cervical abscess should he drained.

Hypertrophic or keloid scar is more likely to form if the incision overlies the sternum. Intradermal injections (If corticosteroid should he given at once and repeated monthly if necessary.

Stitch granuloma. This may occur with or without sinus formation and is seen after the use of nonabsorbable suture material. Absorbable ligatures and sutures must be used throughout thyroid surgery. Some surgeons use a subcuticular absorbable skin suture rather than the traditional skin clips or staples. Skin staples should be removed in less than 48 hours.

Postoperative care

Indirect laryngoscopy has been advised as a routine before leaving hospital. Alternatively, it may he avoided when the voice is normal and the cough occlusive. About 25 per cent of patients develop transient hypocalcaemia and, if associated symptoms are severe, intravenous calcium gluconate or oral calcium may be necessary, although this is unusual. To screen for parathyroid insufficiency, the serum calcium should be measured at the first review attendance 4—6 weeks after operation

After operation, stability in terms of thyroid function takes time. It is important that biochemical (subclinical) thyroid failure should not he aim indication for treatment during the first year as the majority of patients with early subclinical failure, which is common, ultimately regains normality. Even when there are clinical features of failure, thyroxine should he withheld if possible during the first 6 months. Most patients who develop thyroid failure do so within the first 2 years, but there is a continiuing incidence thereafter. Recurrent thyrotoxicosis may occur at any time after operation. Follow-up should therefore he for life.

Once a stable situation has been achieved, follow-up after thyroid surgery may be carried out by an automated computer-activated system. Such systems in Scotland and Wales have been shown to be extremely cost-effective and dramatically reduce the number of patient attendances at the thyroid clinic.

The incidences quoted for thyroid failure (20—45 per cent) and recurrent thyrotoxicosis (5 per cent) after subtotal thyroidectomy for Graves’ disease refer to UK experience arid may be different elsewhere in the world. In iceland, for example, an area of high dietary iodine intake, the incidence of thyroid failure is much lower amid that of recurrent toxicity much higher than in the UK.