chronic suppurative otitis media

318 OTOLARYNGOLOGY
Hashimoto’s thyroiditis. Treatment is with thyroid hormone replacement. The starting dose is usually T4
100 µg/day. In the presence of subclinical hypothyroidism (high TSH > 10 mU/1, normal free T4), then treat
with T4 (100 µg/day) if antibodies are positive, if there are convincing symptoms or a past history of radioiodine
treatment.
2. Toxic goitre (hyperthyroidism). Patients with thyrotoxicosis usually either have Graves disease or a
solitary toxic nodule. Graves disease is caused by circulating thyroid stimulating immunoglobulins (IgG)
which bind to thyroid stimulating hormone receptors (TSH receptor) to increase thyroid hormone
production. These immunoglobulins are usually associated with thyroid eye disease which is caused by a
specific antibody called exophthalmos producing substance (EPS) which targets retro-orbital tissue to cause
oedema of fat and muscle. Graves disease may also be associated with signs of vitiligo, pretibial myxoedema
and other autoimmune disorders such as pernicious anaemia.
Hyperthyroidism is usually treated either medically using tablets (carbimazole or Propylthiouracil) or
with radioiodine. About 50% of patients will relapse following medical treatment. In these patients, together
with those who have significant eye signs or who request surgery, an operation with a ‘near total’ or ‘total’
thyroidectomy is an alternative option. Radioiodine can also be used to treat large multinodular goitres in
the elderly and infirm, when good shrinkage is achievable. Patients who have solitary toxic nodules are
usually best dealt with surgically.
Some patients who have had a multinodular goitre for a long time can develop thyrotoxicosis (Plummer’s
disease). These patients are often elderly with co-existent morbidity such as ischaemic heart disease, and the
rise in T4 is often associated with atrial fibrillation. Because of this, these patients usually have cardiac
signs (and not eye signs) and are usually treated medically. Recurrent thyrotoxicosis is treated on its merits,
but may require further treatment with either the same or another modality. Many patients (whatever their
treatment) will be hypothyroid post-treatment and will be on long-term thyroxine replacement therapy.
3. Inflammatory goitre.
(a) Hashimoto’s thyroiditis. This is most common in late middle-aged women. Antibodies are directed
against thyroglobulin and/or microsomal peroxidase. They cause lymphocyte infiltration, atrophy and
regeneration of the thyroid, and ultimately a goitre. The gland is usually firm, but rubbery. Initially
patients are hyperthyroid, but may become hypothyroid as the disease progresses. Once the diagnosis is
made, patients should be treated with thyroxine suppression and have thyroid function tests once a
year. Rarely surgery may be required for an enlarged gland causing obstructive symptoms or when
there is a fine needle aspiration cytology result that necessitates surgery. These patients are at a high
risk of subsequently developing a thyroid lymphoma.
(b) De Quervain’s thyroiditis is secondary to an acute viral infection. This is a flu-like illness, and
associated with diffuse swelling and tenderness of the gland. There is usually both a transient
hyperthyroidism and production of auto-antibodies.
(c) Riedel’s thyroiditis is rare and associated with a woody hard, sometimes tender, irregular thyroid gland
which histologically shows marked fibrosis. This is thought by some to signify a fibrotic reaction to an
underlying carcinoma or lymphoma.
4. Neoplastic goitre.
This can be a benign adenoma or malignant tumour (see Related topic of interest).
5. Miscellaneous goitres.
For example sarcoidosis, tuberculosis, amyloid, HIV infection.