Friday, 6 March 2015

Diagnosis and management of Goitre.



Goitre
Physical
The general examination for hyperthyroidism, hypothyroidism, and autoimmune stigmata is followed by systematic examination of the goiter.
A retrosternal goiter may not be evident on physical examination.
Examination of the goiter is best performed with the patient upright, sitting or standing. Inspection from the side may better outline the thyroid profile, as shown below. Asking the patient to take a sip of water facilitates inspection. The thyroid should move upon swallowing.

Palpation of the goiter is performed either facing the patient or from behind the patient, with the neck relaxed and not hyperextended. Palpation of the goiter rules out a pseudogoiter, which is a prominent thyroid seen in individuals who are thin. Each lobe is palpated for size, consistency, nodules, and tenderness. Cervical lymph nodes are then palpated. The oropharynx is visualized for the presence of lingular thyroid tissue.
The size of each lobe is measured in 2 dimensions using a tape measure. Some examiners make tracings on a sheet of paper, which is placed in the patient's chart. Suitable landmarks are used and documented to ensure consistent measurement of the thyroid gland.
The pyramidal lobe often is enlarged in Graves disease.
A firm rubbery thyroid gland suggests Hashimoto thyroiditis, and a hard thyroid gland suggests malignancy or Riedel struma.
Multiple nodules may suggest a multinodular goiter or Hashimoto thyroiditis. A solitary hard nodule suggests malignancy, whereas a solitary firm nodule may be a thyroid cyst.
Diffuse thyroid tenderness suggests subacute thyroiditis, and local thyroid tenderness suggests intranodal hemorrhage or necrosis.
Cervical lymph glands are palpated for signs of metastatic thyroid cancer.
Auscultation of a soft bruit over the inferior thyroidal artery may be appreciated in a toxic goiter. Palpation of a toxic goiter may reveal a thrill in the profoundly hyperthyroid patient.
Goiters are described in a variety of ways, including the following:
·         Toxic goiter: A goiter that is associated with hyperthyroidism is described as a toxic goiter. Examples of toxic goiters include diffuse toxic goiter (Graves disease), toxic multinodular goiter, and toxic adenoma (Plummer disease).
·         Nontoxic goiter: A goiter without hyperthyroidism or hypothyroidism is described as a nontoxic goiter. It may be diffuse or multinodular, but a diffuse goiter often evolves into a nodular goiter. Examination of the thyroid may not reveal small or posterior nodules. Examples of nontoxic goiters include chronic lymphocytic thyroiditis (Hashimoto disease), goiter identified in early Graves disease, endemic goiter, sporadic goiter, congenital goiter, and physiologic goiter that occurs during puberty.
Autonomously functioning nodules may present with inability to palpate the contralateral lobe. Unilobar agenesis may also present like a single thyroid nodule with hyperplasia of the remaining lobe.
The Pemberton maneuver raises a goiter into the thoracic inlet when the patient elevates the arms. This may cause shortness of breath, stridor, or distention of neck veins.
Laboratory Studies
·         Initial screening should include TSH. Given the sensitive third-generation assays in the absence of symptoms of hyper or hypothyroidism further testing is not required. An assessment of free thyroxine index or direct measurement of free thyroxine would be the next step in the evaluation.
·         Further laboratory testing is based on presentation and results of screening studies and may include thyroid antibodies (antithyroid peroxidase formerly the antimicrosomal antibodies and antithyroglobulin), thyroglobulin, sedimentation rate and calcitonin in an individual at high risk for medullary carcinoma of the thyroid.
Medical Care
Small benign euthyroid goiters do not require treatment. The effectiveness of medical treatment using thyroid hormone for benign goiters is controversial. Large and complicated goiters may require medical and surgical treatment. Malignant goiters require medical and surgical treatment.
·         The size of a benign euthyroid goiter may be reduced with levothyroxine suppressive therapy. The patient is monitored to keep serum TSH in a low but detectable range to avoid hyperthyroidism, cardiac arrhythmias, and osteoporosis. The patient has to be compliant with monitoring. Some authorities suggest suppressive treatment for a definite time period instead of indefinite therapy. Patients with Hashimoto thyroiditis respond better.
·         Treatment of hypothyroidism or hyperthyroidism often reduces the size of a goiter.
·         Thyroid hormone replacement is often required following surgical and radiation treatment of a goiter. Use of radioactive iodine for the therapy of nontoxic goiter has been disappointing and is controversial.

Toxic nodular goitre
Medical Care
The optimal therapy for treatment of toxic nodular goiter (TNG) remains controversial. Unlike Graves disease, TNG is not an autoimmune disease and rarely, if ever, remits.[9] Therefore, patients who have autonomously functioning nodules should be treated definitely with radioactive iodine or surgery. The American Thyroid Association and American Association of Clinical Endocrinologists have released guidelines for the management of hyperthyroid and other causes of thyrotoxicosis, including the use of radioactive iodine or surgery to treat toxic multinodular goiter.[10]
Patients with subclinical hyperthyroidism should be monitored closely for overt disease. Some suggest that elderly patients, women with osteopenia, and patients with risk factors for atrial fibrillation should be treated, even those who have subclinical disease.
  • Na131 I treatment - In the United States and Europe, radioactive iodine is considered the treatment of choice for TNG. Except for pregnancy, there are no absolute contraindications to radioiodine therapy.  
    • A single dose of radioiodine therapy has a success rate of 85-100% in patients with TNG. Radioiodine therapy may reduce the size of the goiter by up to 40%.[12, 13]
    • Failure of initial treatment with radioactive iodine has been associated with increased goiter size and higher T3 and free T4 levels, which suggests that these factors may present a need for higher doses of Na131 I.
    • A positive correlation exists between radiation dose to the thyroid and decrease in thyroid volume. In patients with uptake of less than 20%, pretreatment with lithium, PTU, or recombinant TSH can increase the effectiveness of iodine uptake and treatment.[14, 15] This treatment may be valuable in elderly patients in whom surgery is considered high risk.
    • Complications
      • Hypothyroidism occurs in 10-20% of patients; this is similar to the incidence rate after surgery and is substantially less than in the treatment of Graves disease.[16]
      • Tracheal compression due to thyroid swelling after radiation therapy is no longer thought to be a risk.[17]
      • Mild thyrotoxic symptoms after radioiodine occur in about one-third of patients, and about 4% of patients develop a clinically significant radiation-induced thyroiditis. These patients should be treated symptomatically with beta blockers.
      • Elderly patients may have exacerbation of congestive heart failure and atrial fibrillation. Pretreat elderly patients with antithyroid drugs.
      • Thyroid storm is a rare complication, particularly in patients with rapidly enlarging goiters or high total T3 levels. Patients with these conditions should receive pretreatment with antithyroid drugs.
  • Pharmacotherapy - Antithyroid drugs and beta blockers are used for short courses in the treatment of TNG; they are important in rendering patients euthyroid in preparation for radioiodine or surgery and in treating hyperthyroidism while awaiting full clinical response to radioiodine. Patients with subclinical disease at high risk of complications (eg, atrial fibrillation, osteopenia) may be given a trial of low dose methimazole (5-15 mg/d) or beta blockers and should be monitored for a change in symptoms or for disease progression that requires definitive treatment.
    • Thioamides - The role of therapy with thioamides (eg, PTU, methimazole) is to achieve euthyroidism prior to definitive treatment with either surgery or radioiodine therapy. Data suggest that pretreated patients have decreased response to radioiodine. The general recommendation is to stop antithyroid agents at least 4 days prior to radioiodine therapy in order to maximize the radioiodine effect.
      • Antithyroid drugs are often administered for 2-8 weeks before radioiodine therapy in order to avoid the risk of precipitating thyroid storm. Although many physicians no longer consider this treatment necessary, the general consensus is that elderly patients or patients with high risk of cardiac complications should receive this treatment.
      • Antithyroid drugs and beta blockers have side effects, the most common being pruritic rash, fever, gastrointestinal upset, and arthralgias. More serious potential side effects include agranulocytosis, drug-induced lupus and other forms of vasculitis, and liver damage..
    • Beta-adrenergic receptor antagonists - These drugs remain useful in the treatment of symptoms of thyrotoxicosis; they may be used alone in patients with mild thyrotoxicosis or in conjunction with thioamides for treatment of more severe disease.
      • Propranolol, a nonselective beta blocker, may help to lower the heart rate, control tremor, reduce excessive sweating, and alleviate anxiety. Propranolol is also known to reduce the conversion of T4 to T3.
      • In patients with underlying asthma, beta-1 selective antagonists, such as atenolol or metoprolol, would be safer options.
      • In patients with contraindications to beta blockers (eg, moderate to severe asthma), calcium channel antagonists (eg, diltiazem) may be used to help control the heart rate

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