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.
Medical treatment
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.
Definitive treatments
Treatment includes RAI and surgery. Both therapies have
advantages and disadvantages and are usually driven by patient choice (Figure
11.1).
Radioactive iodine
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.
Surgery
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 ophthalmopathy
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.
Mild ophthalmopathy
Many patients with Graves’ disease have subtle eye disease,
reporting dryness or grittiness of the eyes when asked directly.
Moderate ophthalmopathy
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 ophthalmopathy
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.
