Endocrine surgery

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CHAPTER 11 Endocrine surgery

Thyroid 178
Parathyroids 188
Adrenal gland 189
Multiple endocrine neoplasia (MEN) 193

Thyroid

Congenital

The embryological line of descent of the thyroid gland is from the foramen caecum of the tongue to its normal position in the neck. Occasionally, it may descend lower and even to the superior mediastinum.

Lingual thyroid

This occurs at the foramen caecum of the tongue. It may be asymptomatic or interfere with speech or swallowing. A radio-iodine scan should be performed to confirm the presence of thyroid tissue. Treatment is by suppression of TSH with thyroxine, but surgical excision should be considered if hormonal therapy is ineffective or the patient has obstructive symptoms.

Thyroglossal fistula

This is not congenital but follows rupture, or inadequate excision of a thyroglossal cyst. Recurrent inflammation occurs and the fistula intermittently discharges mucus. Treatment is by excision of the fistula and may require dissection as far as the foramen caecum of the tongue.

Thyroglossal cyst (→ Ch. 8)

Examination of the thyroid gland

Inspection should be carried out initially from the front. Confirm that there is a mass in the neck in the area of the thyroid gland and that it moves up on swallowing. Place a finger in the suprasternal notch and check that the trachea is central. Examine the thyroid from behind. Place the thumbs on the vertebra prominens and the fingers on the anterior part of the neck on either side. Allow the head to tilt forwards slightly to relax the neck muscles. Feel up and down in the area of the thyroid. Applying gentle pressure to one side of the neck over the thyroid facilitates examination of the contralateral lobe. Decide whether there is a single nodule, many nodules or whether there is diffuse enlargement of the thyroid gland.

Give the patient a glass of water to swallow and check again that the gland moves up on swallowing. Palpate up and down the deep cervical chain of lymph nodes to check for lymphadenopathy. Try to get below the lower limit of the thyroid swelling to exclude retrosternal extension. Percussion over the sternum to check for retrosternal extension is inaccurate and outdated. In patients with Graves’ disease auscultate over the gland. Very vascular toxic glands may have a systolic bruit.

Symptoms of thyroid disease

Lump in the neck

• Smooth non-toxic enlargement of the gland. This is characteristic of a physiological goitre, which may occur at puberty or in pregnancy
• A smooth toxic enlargement of the gland associated with Graves’ disease
• A smooth firm enlargement of the gland (occasionally asymmetrical), usually in middle-aged females and often associated with hypothyroidism, e.g. Hashimoto’s disease
• A nodular non-toxic enlargement of the gland. This is characteristic of multinodular goitre
• A solitary nodule in a lobe of the thyroid gland. This may be due to a palpable dominant nodule in a multinodular goitre, a cyst, an adenoma or a carcinoma
• A rapid increase in the size of nodule associated with haemorrhage into a cyst, a rapidly growing carcinoma or thyroiditis, which may be painful
• A hard irregular goitre with infiltration of muscles and lymphadenopathy in the older patient, e.g. anaplastic carcinoma.

Hoarse voice

This is due to pressure on and/or malignant infiltration of one or both recurrent laryngeal nerves.

Dysphagia

This may occur with very large goitres.

Dyspnoea

It is due to tracheal deviation or compression. Stridor may be apparent.

Pain

This may occur with haemorrhage into a nodule, infiltration by carcinoma, subacute thyroiditis or, occasionally, Hashimoto’s disease.

Eye symptoms

Staring or protruding eyes (exophthalmos) in patients with Graves’ disease, double vision, dry ‘gritty’ eyes, difficulty closing eyes. The latter may lead to pain due to corneal ulceration.

Thyrotoxicosis

Palpitations, dyspnoea, nervousness, irritability, tremor of hands, sweating. Increased appetite with weight loss, diarrhoea. Preference for cold weather. Amenorrhoea. Pretibial myxoedema may be found in Graves’ disease.

Myxoedema (hypothyroidism)

Slowness of thought, speech and movement. Weight gain. Cold intolerance, tiredness, lethargy, constipation. Loss of hair. Change of voice (hoarseness). Carpal tunnel syndrome.

Investigation of thyroid dysfunction/swellings

Patients can be euthyroid, hyperthyroid or hypothyroid. Measure TSH, free T4, free T3, thyroid antibodies. TSH is elevated in hypothyroidism. TSH is suppressed in thyrotoxicosis. Thyroid autoantibodies suggest immune aetiology of disease.

Fine needle aspiration

This will distinguish between a solid lesion and a cyst. If the lesion is solid, cells are sent for cytological examination. This is a safe technique. Usually it is possible to discriminate benign from malignant disease, although some difficulties may be encountered. In particular, cytology cannot distinguish between benign and malignant follicular lesions. Fine needle biopsy should be performed in the investigation of all thyroid nodules. Its reliability can be improved by carrying out the biopsy under ultrasound guidance.

Plain radiograph of chest thoracic inlet

May show tracheal displacement or compression. Retrosternal extension.

Ultrasound scan

It establishes the size and shape of the gland and indicates if nodules are single or multiple and their size. It will also distinguish between cystic and solid lesions.

Radioisotope scans

These are only helpful in some patients with thyrotoxicosis. In Graves’ disease the uptake is increased and diffuse. In toxic nodular goitre the uptake is patchy and multiple or unifocal depending on the pathology.

Goitre

A goitre is an enlargement of the thyroid gland (for Classification → Table 11.1).

TABLE 11.1 Classification of goitres

Simple (non-toxic goitre) Simple hyperplastic goitre Multinodular goitre
Toxic goitre Diffuse (Graves’ disease) Toxic nodule (adenoma) Toxic multinodular goitre
Neoplastic goitre Benign:

• adenoma

Malignant:

• papillary
• follicular
• anaplastic
• medullary
• lymphoma

Inflammatory De Quervain’s thyroiditisRiedel’s thyroiditis Autoimmune Hashimoto’s thyroiditis

Simple hyperplastic goitre

Iodine deficiency is the commonest pathological cause. Physiological causes include puberty and pregnancy. Endemic goitres occur in childhood and are common in areas where the drinking water has a low iodine content. They are rare in the UK where iodide is added to table salt.

Symptoms and signs

The patient is usually euthyroid. Usually a smooth goitre. Iodine deficiency types of goitre may become very large.

Investigations

• Free T4 usually normal
• TSH may be raised
• CXR to exclude tracheal compression or deviation.
• CT scan (→ Fig. 11.1) – retrosternal goitre, tracheal deviation/compression.
image

Figure 11.1 A CT scan of the neck showing a goitre (large mass in the left lobe of the thyroid gland). The trachea (arrow) is slightly deviated to the right.

Treatment

Addition of iodized salt to diet in areas where iodine deficiency occurs. Thyroxine orally daily to suppress TSH. Partial thyroidectomy is indicated only if the gland is very large and causing pressure effects.

Multinodular goitre

This is the commonest cause of goitre in the UK. The gland is enlarged and irregular. The condition develops spontaneously and also in simple colloid goitres. There are areas of hypoplasia and hyperplasia within the gland. The condition is more common in women. With large glands, tracheal deviation and compression may occur. Toxic change may occasionally occur with the symptoms of hyperthyroidism.

Symptoms and signs

In endemic areas, nodular goitre appears at 15–30 years, while sporadic ones occur later at 25–40 years. Occasionally only a solitary nodule is palpable. Dyspnoea, dysphagia may occur if the gland is very large. Pain may occur due to haemorrhage into a cyst.

Investigations

• TSH, free T4
• If thyroid function is normal, isotope scan is not indicated
• CXR/CT if retrosternal extension is suspected.

Treatment

If the patient is clinically euthyroid and the goitre is small, no treatment is required. If the gland is large and unsightly and causes symptoms of compression, or thyrotoxicosis occurs, thyroidectomy is indicated.

Toxic goitre

This may be a diffuse goitre (Graves’ disease), toxic multinodular goitre or solitary toxic adenoma. In Graves’ disease, TSH receptor antibodies are present. In toxic multinodular goitre, several nodules in a non-toxic goitre begin to function independently of TSH. A solitary toxic nodule functions autonomously. Toxic goitre is six times more common in females.

Symptoms and signs

Hyperthyroidism, tachycardia, palpitations, AF, tremor, increased tendon reflexes. In Graves’ disease – exophthalmos, lid lag, pretibial myxoedema. Occasionally bruit over gland.

Investigations

• Low TSH; free T4 (↑); free T3 (↑)
• Isotope scan may show ‘hot’ nodules.

Treatment

Antithyroid drugs

For the patient with Graves’ disease, carbimazole 40 mg daily as ‘blocking’ dose until euthyroid and then 5 mg t.d.s. for 12–18 months or continue ‘block’ and ‘replace’ with thyroxine. About 50% of patients with Graves’ disease remain euthyroid when the drug is discontinued. Severely toxic patients may require β-blockers until euthyroid. Relapses, if they happen, usually occur within 2 years of stopping treatment. Hypothyroidism may develop. Side-effects of carbimazole include rashes and neutropenia – patients must be warned to report any sore throat or mouth ulcers occurring, especially in the initial stages of carbimazole treatment. Patients with thyrotoxicosis due to toxic multinodular goitre/toxic adenoma, can be rendered euthyroid with antithyroid drugs but require definitive treatment with radio-iodine or surgery.

Radio-iodine

131I is administered orally. It usually takes 8–12 weeks before the patient becomes euthyroid. After the 131I is given, antithyroid drugs need to be taken until the symptoms settle. It is appropriate treatment for most patients with thyrotoxicosis, recurrent hyperthyroidism, and poor-risk patients. It should not be used in children and pregnant women because of potential radiation hazards. There is a high incidence of late myxoedema.

Surgery

This is the treatment of choice for younger patients, children and patients with large goitres. The patient should be rendered euthyroid prior to surgery with antithyroid drugs. Blocking therapy with carbimazole, and replacing endogenous hormone production with thyroxine administration is optimum preparation for surgery. Propranolol may be needed if control is difficult to achieve or when urgent surgery may be indicated. Total thyroidectomy is the preferred procedure. Thyroid lobectomy is the appropriate treatment for a solitary toxic nodule.

Prognosis

Hypothyroidism may occur after radioactive iodine and will occur after surgery. If subtotal resection is performed, about 4% remain toxic and around 8–10% will become toxic again at a later time. 131I treatment is then appropriate. About 4% become hypothyroid immediately and up to 60% may ultimately become hypothyroid. This depends on the dose of radioactive iodine. At the low dose, 10% become hypothyroid at 1 year then cumulatively 3% per year become hypothyroid. With bigger doses (ablative), up to 60% become hypothyroid at 1 year. Lifelong monitoring of thyroid function is required.

Neoplastic goitre

Benign

Adenomas

True follicular adenomas are encapsulated and are usually >2 cm on presentation. They are solid on ultrasound and ‘cold’ on isotope scans. FNAC will not distinguish them from follicular carcinoma. They must be excised. Lobectomy is adequate treatment.

Malignant

The large majority are primary tumours. Aetiological factors include exposure to ionizing radiation in childhood; endemic goitre (iodine deficiency) may be associated with follicular carcinoma but the risk is small. There is also a rare association with adenomatous colonic polyps. Papillary cancer may be associated with an autosomal dominant family history. Family history may be present in patients with medullary carcinoma associated with MEN Type II. Metastatic carcinoma to the thyroid is rare but may spread via the bloodstream from breast, lung, kidney and prostate. The main types of thyroid cancer are as follows.

Differentiated (papillary and follicular)

Papillary (60%)

Papillary occurs at any age with a peak incidence in the third and fourth decades. Usually a slow-growing nodule, which may metastasize early to regional lymph nodes. They are often multicentric within the thyroid gland. The tumour is TSH dependent. The condition of ‘lateral aberrant thyroid’ more correctly represents secondary deposit of papillary carcinoma in lymph nodes.

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