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hyperthyroidism

hyperthyroidism

introduction

  • untreated hyperthyroidism may lead to:
    • loss of weight
    • ophthalmopathy
      • an inflammatory eye disease that develops in the orbit in association with autoimmune thyroid disorders, particularly at risk are smokers
    • thyrotoxic periodic paralysis (similar to familial hypokalaemic periodic paralysis) in genetically susceptible individuals
    • thyroid storm (see below)
  • patients with hyperthyroidism which is not clinically diagnostic of Grave's disease should be considered for a radioactive iodine uptake (RAIU) scan of the neck.
  • patients with nodularity of their thyroid should have a thyroid Technetium scan
  • ultrasonography does not generally contribute to the differential diagnosis of thyrotoxicosis.
  • beta adrenergic blockers should be considered for all patients without contraindications who have hyperthyroidism which is either symptomatic, or in the elderly with resting heart rates > 90/min or coexistent cardiovascular disease.1)
  • methimazole should be used in virtually every child who is treated with antithyroid drug therapy.2)
    • methimazole should be stopped immediately, and white blood counts measured in children who develop fever, arthralgias, mouth sores, pharyngitis, malaise or jaundice.

aetiology of thyrotoxicosis

normal or elevated radioactive iodine uptake over the neck

    • the most common cause of hyperthyroidism in Western countries
    • an autoimmune disorder in which thyrotropin receptor antibodies (TRAbs) stimulate the TSH receptor, increasing thyroid hormone production.
    • 30% remit without Rx
    • once it has been established that the patient is hyperthyroid and the cause is GD, the patient and physician must choose between three effective and relatively safe initial treatment options:
      • 131I therapy (radioactive iodine),
      • antithyroid drugs (ATD), or,
      • thyroidectomy
  • TA or toxic multinodular goitre (TMNG)
  • trophoblastic disease
  • TSH-producing pituitary adenomas
  • resistance to thyroid hormone (T3 receptor mutation)

near absent radioactive iodine uptake over the neck

  • painless (silent) thyroiditis
  • subacute (granulomatous, De Quervain's) thyroiditis
    • presumed viral and associated with fever and thyroid pain
  • iatrogenic thyrotoxicosis
    • iodine-induced hyperthyroidism
      • the thyroid has an instrinsic mechanism to deal with increased iodine - the Wolff-Chaikoff effect which results in a transient decrease in synthesis of thyroid hormone over a period of 24-48hrs.
      • prolonged excess iodine may cause hypothyroidism due to persistence of this effect.
      • failure of this autoregulation (esp. euthyroid pts with nodular goitre or an autonomous thyroid nodule) results in acute thyrotoxosis.
      • the estimated upper limit of tolerable iodine intake is 1.1 mg/day
      • common sources of excess iodine include radiographic contrast agents (320-370mg iodine/ml), amiodarone (75mg iodine per 200mg tablet), topical Betadine (10mg iodine/ml), and dietary supplements such as kelp products
      • susceptible patients include the elderly with nodular goiters (3% risk after iv contrast)
      • beta-adrenergic blocking agents alone or in combination with methimazole should be used to treat overt iodine induced hyperthyroidism.
    • amiodarone induced thyroiditis
      • consider ceasing amiodarone if possible but its long half-life may cause thyrotoxicosis long after it is discontinued
      • methimazole should be used to treat type 1 (iodine-induced) amiodarone induced thyrotoxicosis and corticosteroids should be used to treat type 2 (thyroiditis-induced) amiodarone-induced thyrotoxicosis.
      • patients with amiodarone-induced thyrotoxicosis who are unresponsive to aggressive medical therapy with methimazole and corticosteroids should undergo thyroidectomy.
  • factitious ingestion of thyroid hormone
    • thyroglobulin is released along with thyroid hormone in subacute, painless, and palpation thyroiditis, whereas its release is suppressed in the setting of exogenous thyroid hormone administration. Therefore, if not elucidated by the history, factitious ingestion of thyroid hormone can be distinguished from other causes of thyrotoxicosis by a low serum thyroglobulin level and a near-zero RAIU.
  • struma ovarii
  • acute thyroiditis
  • extensive metastases of follicular thyroid cancer

thyroid storm

  • thyroid storm is a rare acute medical emergency with a high mortality if untreated
  • 80% are women
  • 80% are aged 20-50 years
  • classical signs: fever, cardiac dysfunction (tachycardias, cardiac failure), CNS dysfunction (restlessness, delirium, stupor, coma), and GIT symptoms (nausea, abdominal pain, diarrhoea, and jaundice)
  • precipitating factors in patients with underlying hyperthyroidism include:
    • infections
    • emotional stress
    • surgical manipulation of thyroid gland
    • overdosage of thyroxine
    • administration of iodinated dyes
    • withdrawal of antithyroid drugs
    • administration of radioactive iodide
    • any acute illness, surgical procedure or trauma
  • initial ED Rx of thyroid storm:
    • iv fluids
    • cooling
      • paracetamol
      • cooling blankets, etc
    • beta adrenergic blockers if no bronchospasm present:
      • usually propranolol 40-80mg po 4-6 hrly or 2-10mg iv 3-4hrly (max. rate 1mg/min)
      • alternatively, atenolol 25-100mg po daily or bd, or, metoprolol 25-50mg po qid
      • critically ill patients may be considered for iv infusion of esmolol 50-100 microg/kg/min
      • use with care if cardiac failure present
      • Since there is not sufficient beta-1 selectivity of the available beta-blockers at the recommended doses, these drugs are generally contraindicated in patients with bronchospastic asthma. However, in patients with quiescent bronchospastic asthma in whom heart rate control is essential, or in patients with mild obstructive airway disease or symptomatic Raynaud’s phenomenon, a nonselective beta-blocker such as nadolol can be used cautiously,with careful monitoring of pulmonary status. Calcium channel blockers, both verapamil and diltiazem, when administered orally and not intravenously, have been shown to effect rate control in patients who do not tolerate or are not candidates for beta-adrenergic blocking agents.3)
    • further Mx after endocrinology advice traditionally includes:
      • oral propylthiouracil (PTU) to block production T4
        • 500-1000mg load then 250mg 4hrly
        • NB. PTU now has a black box warning!
      • oral methimazole (MMI) to block hormone production
        • 60-80mg/day
      • followed by iodine 5 drops (0.25ml or 250mg) po 6 hrly at least 1 hour after PTU to block secretion of T4
      • hydrocortisone 300mg iv load then 100mg 8hrly may be considered for Rx of associated adrenal insufficiency

subclinical hyperthyroidism (SH)

  • 1% of population
  • important to document that it is a persistent problem by repeating the serum TSH at 3 or 6 months.
  • deleterious effects on the cardiovascular system and the skeleton might be expected in some patients, and subtle symptoms of thyrotoxicosis or altered cognition might also be potential problems.
  • 2.8-fold risk of atrial fibrillation in persons over age 60 years
  • when TSH is persistently <0.1 mU/L, treatment of SH should be strongly considered in:
    • age > 65 years
    • postmenopausal women who are not on oestrogens or bisphosphonates
    • patients with cardiac risk factors, heart disease or osteoporosis
    • those with hyperthyroid symptoms.
  • when TSH is persistently > 0.1 and <0.5 mU/L, treatment of SH should be considered in:
    • age > 65 years
    • postmenopausal women who are not on oestrogens or bisphosphonates
    • patients with cardiac risk factors or heart disease
    • those with hyperthyroid symptoms.

the pregnant patient

  • the diagnosis of hyperthyroidism in pregnancy can be challenging.4)
  • the diagnosis of hyperthyroidism in pregnancy should be made using serum TSH values, and either total T4 and T3 with total T4 and T3 reference range adjusted at 1.5 times the nonpregnant range or free T4 and free T3 estimations with trimester-specific normal reference ranges.
  • serum TSH levels may be below the nonpregnant reference range in the first half of a normal-term pregnancy presumably the result of stimulation of the normal thyroid by high levels of serum hCG
    • therefore, low serum TSH levels with normal free T4 values in early pregnancy do not indicate abnormal thyroid function.
    • transient hCG-mediated thyrotropin suppression in early pregnancy (gestational hyperthyroidism) should not be treated with antithyroid drug therapy.
    • when associated with hyperemesis gravidarum, it is known as transient hyperthyroidism of hyperemesis gravidarum (THHG)
    • it is thought that some people are sensitive to certain isotypes of HCG and this is the cause of this transient hyperthyroidism and may have a direct role in the hyperemesis.
  • the most common cause is Grave's disease
  • hyperthyroidism caused by a human chorionic gonadotropin (hCG)-producing molar pregnancy or a choriocarcinoma presents with a diffuse hyperactive thyroid similar to GD, but without eye signs and without serum TRAb. In these patients, serum hCG will be higher than expected, and the cause can be identified by obstetrical investigation.
  • TRAb levels should be measured when the etiology of hyperthyroidism in pregnancy is uncertain.
  • patients found to have GD during pregnancy should have TRAb levels measured at diagnosis using a sensitive assay and, if elevated, again at 22–26 weeks of gestation.
  • TRAb levels measured at 22–26 weeks of gestation should be used to guide decisions regarding neonatal monitoring.
  • antithyroid drug therapy should be used for hyperthyroidism due to GD that requires treatment during pregnancy. Propylthiouracil should be used when antithyroid drug therapy is started during the first trimester. Methimazole should be used when antithyroid drug therapy is started after the first trimester.
  • when thyroidectomy is necessary for the treatment of hyperthyroidism during pregnancy, the surgery should be performed if possible during the second trimester.

post-partum

  • In women with thyrotoxicosis after delivery, selective diagnostic studies should be performed to distinguish postpartum thyroiditis from postpartum GD.
  • In women with symptomatic postpartum thyrotoxicosis, the judicious use of beta-adrenergic blocking agents is recommended.

levothyroxine overdose

  • an overdose of levothyroxine can lead to thyrotoxicosis or even thrytoid storm
  • toxic effects may not become evident for 5-100 hours and may last several days as levothyroxine must first be converted to T3 and distributed to the tissues.
  • measuring T4 levels maybe useful in verifying the overdose but levels do not correlate well with symptoms

ED Mx of overdose

  • GIT decontamination with multi-dose activated charcoal may be considered in high dose ingestions > 2mg as it binds charcoal well and levothyroxine undergoes enterohepatic circulation.
  • antisynthesis agents such as PTU and MMI are unnecessary
  • consider corticosteroids to block the peripheral conversion to T3
  • beta adrenergic blockers to Mx symptoms if they occur
hyperthyroidism.txt · Last modified: 2018/08/11 02:44 by wh