Endocrine surgery

Published on 11/04/2015 by admin

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11 Endocrine surgery

Most surgical endocrine disorders are neoplastic, autoimmune or genetic. These conditions may or may not result in endocrine dysfunction depending on whether there is abnormal hormone secretion. The principles of endocrine surgery have been crystallised by John Lynn and are summarised in Table 11.1.

Table 11.1 Principles of endocrine surgery

Principle Example
Be convinced of the biochemical diagnosis In Cushing’s syndrome, is the primary problem of pituitary or adrenal origin?
Make the patient safe Control thyrotoxicosis in Graves’ disease, or hypertension in phaeochromocytoma
Localise the tumour(s) In Conn’s syndrome, which side is the adenoma? CT and renal vein sampling may be necessary
Is an operation necessary? Sometimes medical therapy is more effective, e.g. radioiodine for hyperthyroidism
Decide best technique Open versus laparoscopic adrenalectomy

The thyroid

Surgical anatomy

The thyroid is fixed to the trachea by the pretracheal fascia so it moves up on swallowing. Aberrant thyroid tissues may be found anywhere along the embryological descent of the gland. Blood supply is from the superior and inferior thyroid arteries. Thyroid operations may damage important structures, highlighted in Table 11.2.

Table 11.2 Structures easily damaged during thyroidectomy

Structure Result of injury
Recurrent laryngeal nerve Paresis or paralysis of vocal cord: unilateral – hoarseness bilateral – stridor; change in voice; risk of aspiration
Parathyroid glands Hypocalcaemia – severity depends on amount of tissue that remains
External laryngeal nerve Paresis or paralysis of cricothyroid muscle – inability to achieve high-pitched notes

Thyrotoxicosis

This is a common problem affecting 2% of females and 0.15% of males. The three main causes are:

Graves’ disease

This is the commonest cause of thyrotoxicosis, usually occurring between the ages of 20 and 40 years. Women are affected five times more often than males. Graves’ disease is due to an autoimmune process characterised by abnormal autoantibodies directed against thyroid TSH receptors. The natural history of Graves’ disease is one of intermittent remission and relapse. The thyroid is uniformly enlarged, firm and smooth, not nodular. Eye problems are common (Table 11.3). Thyroid function tests confirm an elevated T3 and T4 and reduced TSH. Anti-thyroglobulin and anti-microsomal antibodies are present when the cause is autoimmune.

Table 11.3 Eye abnormalities in Graves’ disease

Symptoms Signs
Poor sight for both near and distant objects Ophthalmoplegia
Double vision  
Grittiness in the eye Conjunctival oedema (chemosis)
Exophthalmos – protrusion of the globes Exophthalmos
Lid retraction
Lid lag

Management of thyrotoxicosis

The underlying cause must be established since the definitive treatments depend on the underlying diagnosis. However, initial treatment is the same.

First, control the thyrotoxicosis with drugs. A combination of antithyroid drugs and beta-blockade is effective. Carbimazole is the initial antithyroid agent of choice. Agranulocytosis is a complication and the drug must not be used in pregnancy. Beta-blockade with propranolol reduces the effects of T4 on the sympathetic nervous system and controls tachycardia and agitation.

Treat eye complications (seek ophthalmology opinion); see Table 11.4.

Table 11.4 Management of eye complications in Graves’ disease

Problem Treatment
Exposed cornea with drying Methylcellulose eye drops for lubrication
Failure of lid closure in marked exophthalmos Tarsorrhaphy
Inflammation Systemic steroids
Deterioration in sight from compressive optic atrophy Surgical decompression of both orbits
Severe diplopia Corrective surgery to eye muscles

Once the acute thyrotoxic state is controlled, definitive treatment is with radioactive iodine or surgery.

Radioactive iodine (131I) achieves definitive control in most cases and is used for older and younger patients or where surgery is contraindicated. Hypothyroidism may result and replacement therapy must be given if necessary. 131I is effective for toxic nodules since the isotope is concentrated in the diseased hyperactive nodule but not in the suppressed normal gland.

Surgery is preferred for younger patients or when medical therapy has failed. For a solitary toxic nodule, only the affected lobe need be removed. For Graves’ disease and toxic goitre, the options are total thyroidectomy followed by thyroxine replacement therapy, or subtotal thyroidectomy and monitoring for hypothyroidism or recurrent hyperthyroidism. In all cases the patient must be rendered euthyroid by medical means before surgery to avoid a thyrotoxic crisis. Preoperative iodine therapy reduces the vascularity of the gland and makes excision easier.

Thyroid cancer

Carcinoma of the thyroid causes less than 0.5% of all deaths from malignant disease. The aetiology is unknown. Predisposing factors include genetic (medullary carcinoma of the thyroid is familial and associated with neoplasms in other endocrine organs), radiation from external beam radiotherapy, high natural levels or from nuclear explosions (Hiroshima and Nagasaki) or accidents (Chernobyl). Carcinoma is more common in regions where endemic goitre exists. Pathological classification includes:

Thyroiditis

Thyroidectomy

Thyroidectomy is described on page 382. Complications of thyroidectomy are potentially life-threatening and are summarised in Table 11.5.

Table 11.5 Specific complications of thyroidectomy

Complication Clinical features Treatment
Bleeding into the neck Acute airway obstruction with neck swelling, bruising and haematoma. The venous return from the head is also compressed, causing facial congestion and oedema Give oxygen, sit upright, call surgeon and anaesthetist and immediately remove skin and strap muscle sutures to release the haematoma
Hypocalcaemia due to parathyroid gland injury Typically 24–48 hours postoperatively. Paraesthesia round mouth and digits, then muscle spasm and tetany. Tapping the facial nerve below the ear causes facial spasm Oral calcium usually adequate, IV calcium gluconate if necessary
Recurrent laryngeal nerve (RLN) injury Unilateral palsy causes hoarseness of the voice. Bilateral partial RLN palsy causes severe airway obstruction Usually conservative as most will recover
Speech therapy may help
External laryngeal nerve injury Inability to sing, or project voice Conservative
Thyroid crisis (thyrotoxic storm) caused by massive release of thyroxine into circulation during manipulation, e.g. gland in surgery Severe thyrotoxicosis, restlessness, confusion, tachycardia, atrial fibrillation, hypotension, hyperpyrexia, cardiac arrest Control of thyrotoxicosis preoperative is the best way of avoiding the problem. Treatment is urgent using propylthiouracil and beta-blockade, and potassium iodide

Hyperparathyroidism

Hyperparathyroidism is the commonest cause of hypercalcaemia in the community (Box 11.2). Three subtypes are recognised.

Adrenal disorders

The adrenal glands, situated above the kidneys, are derived from two components, the cortex and medulla. The cortex has three zones, each secreting a different hormone (Table 11.6).

Gastrointestinal endocrine tumours

These uncommon tumours cause symptoms due to secreted peptide hormones. Most are malignant apart from insulinomas, which are usually benign.

Pituitary

Pituitary tumours account for 10% of intracranial neoplasms. They are nearly always benign but cause problems due to local expansion (visual field defects due to pressure on the optic chiasma) and consequences of hypersecretion of one of the pituitary hormones (Fig. 11.2).

Acromegaly

Excess growth hormone secretion in adulthood results in acromegaly, the main appearance being overgrowth of the hands and feet and coarse facial features (Fig. 11.3). There are often physiological disturbances including glucose intolerance, osteoporosis and hypertension. Diagnosis is confirmed by elevated plasma growth hormone levels. Treatment is with drugs (octreotide), radiotherapy or surgery.