As neonatal thyrotoxicosis is known to be associated with neurological impairment in some cases there is a requirement to monitor the fetus rather than wait till birth to diagnose thyroid dysfunction. The use of serial in utero ultrasonographic measurements has been shown to accurately measure fetal thyroid size . If the fetal thyroid does not reduce in size in response to antithyroid drug administration then transplacental passage of TsAb causing fetal hyper-thyroidism should be suspected. A recent comprehensive study by Luton et al.  showed that the sensitivity and specificity of fetal thyroid ultrasound at 32 weeks for the diagnosis of clinically relevant fetal thyroid dysfunction was 92 and 100%, respectively.
Eye symptoms and signs of Graves' hyperthyroidism including excessive watering, pain and irritation as well as chemosis, periorbital oedema, proptosis and ophthalmoplegia may occur before, during or after the onset of hyperthy-roidism and are more common in cigarette smokers. Treatment during pregnancy initially should be symptomatic with topical eye drops and elevation of the head of the bed. Careful monitoring is necessary to check for any signs of optic neuropathy. Oral or intravenous prednisone therapy is indicated in severe congestive ophthalmopathy but should be used sparingly in pregnancy. In line with the Graves' hyperthyroidism, the ophthalmopathy would be expected to improve during gestation.
Subtotal thyroidectomy is indicated if control of the hyperthyroidism is poor on account of poor compliance or inability to take drugs. Patients with a very large goitre may also require surgery because of pressure symptoms. Surgery is preferred in the second trimester as there is a higher risk of associated abortion at an earlier stage of gestation. In general surgery should be avoided if it is considered that medical therapy has a reasonable chance of success.
Management of other causes of hyperthyroidism:
(a) Hyperemesis gravidarum is common and around 5% of cases require hospital admission because of dehydration and ketosis. Thyroid function should be checked in these patients; a correlation has been established between the severity of the hyperemesis and thyroid function with an elevated FT4 and FT3
with suppressed TSH. In those patients who are hyperthyroid antithyroid drugs may be given. The diagnosis of gestational thyrotoxicosis will be confirmed by noting the absence of TSH receptor stimulating antibodies.
(b) Toxic multinodular goitre and toxic adenoma: Radioiodine which may be a treatment of choice is absolutely contraindicated in pregnancy. The conditions may be managed with antithyroid drugs during gestation; if necessary surgery may be performed during the 2nd trimester but if possible it is better to postpone this till the postpartum period.
(c) Subacute thyroiditis: The diagnosis is suggested by the presentation of a painful thyroid in the presence of hyperthyroidism. As radionuclide evaluation (which would demonstrate a low iodine uptake) is contraindicated diagnosis may be made with a fine needle aspiration biopsy of the thyroid associated with an elevation in systemic markers of inflammation. Treatment is firstly with analgesics for pain and oral prednisolone therapy if inflammation is severe. Frequent monitoring of thyroid function is required as a small number of patients will develop hypothyroidism.
The other causes of hyperthyroidism listed are rare and referral to a specialist centre is advised.
Patients with Graves' disease may develop Graves' hyperthyroidism as a post partum phenomenon due to the immune rebound of TSH receptor antibodies. In Graves' disease patients, TSHR Abs have been shown to decrease during late gestation with a significant rebound in the late postpartum . In this situation the hyperthyroidism of Graves' disease may be followed immediately by transient hypothyroidism due to co-existing destructive postpartum thyroiditis during the early postpartum period despite increasing TSAb activity. This may be important when considering postpartum relapse of the disease. Screening for TSAb during pregnancy may detect patients with Graves' disease at risk of postpartum relapse and is also helpful when measured postpartum in diagnosing Graves' disease as the cause of hyperthyroidism as opposed to the hyperthyroid phase of postpartum thyroiditis . The cost benefit of this proposed screening strategy is not available and it is probably not practical in most countries.
The incidence of hypothyroidism during pregnancy is around 2.5% . The aetiology is usually autoimmune thyroiditis characterised by the presence of anti-TPO antibodies. Significant titres of these antibodies are found in about 10% of women at about 14 weeks of gestation. Other causes of hypothyroidism in pregnancy include postoperative thyroid failure and non compliance with existing thyroxine therapy. In areas of iodine deficiency the circulating maternal thyroxine concentrations are low although TSH is usually in the normal range. In this situation the incidence of thyroid abnormalities is higher and in particular thyroid autoimmunity may be associated with diminished thyroid reserve and an increase in spontaneous abortion.
The diagnosis of hypothyroidism is made by noting an elevated TSH accompanied by a low serum FT4. Subclinical hypothyroidism is recognised to be equally as important in its adverse effects, affecting mother and neonate as the full expression of the disease . Maternal hypothyroxinaemia (without increased TSH) is also being increasingly accepted as deleterious to the neu-ropsychological development of the child . Care should be taken in the interpretation of TSH concentrations in early gestation due to the thyrotrophic effects of hCG.
Previous studies have documented the effects of hypothyroidism on maternal and fetal well-being, drawing attention to increased incidence of abortion, obstetric complications and fetal abnormalities in untreated women. Women already receiving thyroxine for hypothyroidism require an increased dose during gestation. This is critical to ensure adequate maternal thyroxine levels for delivery to the fetus especially during the first trimester. The dose should normally be increased by 50-100 |xg/day as soon as pregnancy is diagnosed; subsequent monitoring of TSH and FT4 is then necessary to ensure correct replacement dosage .
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