Hyperthyroidism Management and Ophthalmopathy
Management options for hyperthyroidism include anti-thyroid medication, surgery and radioactive iodine (RAI) (Figure 11.1). Medical treatment is usually the first line approach, especially in Graves’ disease, with definitive options (surgery or RAI) chosen later on.
Thionamides (carbimazole and propylthiouracil) block thyroid peroxidase enzymes, thereby reducing the synthesis of T3 and T4. It takes 4–6 weeks for patients to become euthyroid after initiation of anti-thyroid drugs. Beta-blockers can be used to control symptoms until thyroid function returns to normal.
Thionamides can cause agranulocyotisis (bone marrow suppression) and patients should be warned of this potential rare side effect before commencing treatment. If unexplained fever or sore throat occur, an urgent full blood count is required to exclude pancytopaenia, and the drug should be stopped if bone marrow suppression is confirmed. A more common side effect is generalised rash, which disappears after cessation of the drug.
Anti-thyroid treatment regimes
Graves’ disease has a relapsing–remitting natural history, whereas nodular thyroid disease does not tend to go into remission. Definitive options are therefore used earlier in nodular thyroid disease. A 12- to 18-month course of carbimazole or propylthiouracil is generally used first line in Graves’ disease. The relapse rate is approximately 50% upon treatment cessation. Relapse is more likely in patients with high thyroid hormone levels and antibody titres at presentation.
‘Titration’ versus ‘block and replace’
The two approaches to medical treatment with thionamides include the ‘titration’ and ‘block and replace’ regimens. There are advantages and disadvantages to each. Dose titration involves altering the thionamide dose in response to thyroid hormone response. The ‘block and replace’ approach uses high dose thionamide in combination with thyroxine (e.g. 40 mg carbimazole + 100 µg thyroxine). The ‘block and replace’ regimen should not be used in pregnancy as thyroxine crosses the placenta less well than anti-thyroid medication, putting the fetus potentially at risk of hypothyroidism.
Treatment includes RAI and surgery. Both therapies have advantages and disadvantages and are usually driven by patient choice (Figure 11.1).
RAI is a straightforward treatment, and involves the administration of a single dose of 131I. It is contraindicated in pregnancy and can lead to a flare of eye disease in patients with pre-existing ophthalmopathy.
It commonly causes hypothyroidism, which requires lifelong thyroxine replacement. Patients emit a small amount of radiation after administration of 131I and are therefore advised to avoid close contact with young children and pregnant women for a few weeks after treatment.
Thyroidectomy is an effective definitive treatment for hyperthyroidism, particularly when patients cannot easily comply with radiation restriction guidance (e.g. mothers with young children).
Thyroid function should be optimally controlled pre- operatively to avoid anaesthetic problems. This is usually achieved by thionamides alone, but lithium or iodine can be used in refractory cases. Beta-blockade can be used during anaesthetic induction if thyroid function is not optimal, to prevent peri-operative AF.
Complications of thyroid surgery include bleeding, infection, damage to the recurrent laryngeal nerve and temporary or permanent hypocalcaemia, but these risks are low if the procedure is undertaken by an experienced surgeon.
Thyroid eye disease (ophthalmopathy) can occur at the same time as, or within several years either side of thyroid dysfunction in patients with Graves’ disease. It can be mild, moderate or severe.
Many patients with Graves’ disease have subtle eye disease, reporting dryness or grittiness of the eyes when asked directly.
Patients can present with significant inflammatory changes, including eyelid swelling, chemosis and peri-orbital oedema. Proptosis and lid retraction can lead to a ‘staring’ appearance (Figure 11.2), which may be socially debilitating.
Severe proptosis can lead to exposure keratopathy and compressive optic neuropathy, which may be sight-threatening. Diplopia is caused by inflammation of the extraocular muscles.
Management of ophthalmopathy
Thyroid ophthalmopathy is most commonly mild and improves with time (Figure 11.2). Management of mild disease involves simple measures such as sitting up in bed, lubricant eye drops and cessation of smoking (an independent risk factor for ophthalmopathy), in addition to maintenance of euthyroidism. Selenium supplementation can also have a role.
In moderate and severe eye disease, patients may need high dose pulsed intravenous methylprednisolone. Surgical orbital decompression is performed for sight-threatening disease. If diplopia is severe, squint surgery to the retro-ocular muscles may be needed after orbital decompression. Patients with severe lid retraction may need lid-lengthening surgery. Orbital d immunosuppressant agents can be used if other measures fail to improve symptoms.