Endocrine surgery

Published on 11/04/2015 by admin

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Last modified 11/04/2015

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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.