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Painful thyroid. acute pyogenic or fungal thyroiditis subacute thyroiditis hemorrhage into a cyst Acute hemorrhagic degeneration in a nodule , Hashimoto’s disease with painful recurrence thyroid malignancy(lymphoma) amiodarone-induced thyroiditis or amyloidosis. Acute Thyroiditis.
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Painful thyroid • acute pyogenic or fungal thyroiditis • subacute thyroiditis • hemorrhage into a cyst • Acute hemorrhagic degeneration in a nodule, • Hashimoto’s disease with painful recurrence • thyroid malignancy(lymphoma) • amiodarone-induced thyroiditis or amyloidosis
Acute Thyroiditis • Causes • 68% Bacterial (S. aureus, S. pyogenes) • 15% Fungal • 9% Mycobacterial • May occur secondary to • Pyriform sinus fistulae • Pharyngeal space infections • Persistent Thyroglossal remnants • Thyroid surgery wound infections (rare) • More common in HIV
Acute Thyroiditis • Symptoms • Thyroid pain and tenderness • Fever • Dysphagia • Dysphonia • Warm, tender, enlarged thyroid
Acute Thyroiditis • Diagnosis • FNA to drain abscess, obtain culture • RAIU normal&TFT NL (versus decreased in DeQuervain’s) • CT or US if infected TGDC suspected • Treatment • High mortality without prompt treatment • IV Antibiotics • Nafcillin / Gentamycin or Rocephin for empiric therapy • Search for pyriform fistulae (BA swallow, endoscopy) • Recovery is usually complete
Subacute Thyroiditis • Subacute • Most common cause of painful thyroiditis • 20% of thyrotoxic cases • De Quervain’s thyroiditis • Giant cell thyroiditis • Pseudogranulomatous thyroiditis • Subacute painful thyroiditis
characteristic features • well-developed follicular lesion that consists of a central core of colloid surrounded by the multinucleated giant cells, hence the designation giant cell thyroiditis. • Colloid may be found in the interstitium or within the giant cells.
Sub Acute Thyroiditis Viral (granulomatous) Mumps, coxsackie, influenza, adeno and echoviruses
Subacute thyroiditis features • 5:1 female predominance • Age of onset 20-60y • Prodrome (myalgias, fever, pharyngitis) • Seasonal variation (correlation with enterovirus?) • Fever/severe neck pain • Dysphagia,odynophagia,hoaresness • The pain, which is aggravated by turning the head or swallowing, characteristically radiates to the ear, jaw, or occiput and may mimic disorders arising in these areas. • Usually low to absent titer of anti-TPO immunoglobulins • Thyroid storm – case reports
Subacute thyroiditis features • On palpation, at least part of the thyroid is slightly to moderately enlarged, firm, often nodular, and usually exquisitely tender. • One lobe is frequently being more severely affected than the other, and the symptoms may be truly unilateral. • The overlying skin may be warm and erythematous.
Subacute ThyroiditisDeQuervain’s, Granulomatous • FNA may reveal multinuleated giant cells or granulomatous change. • Course • Pain and thyrotoxicosis (3-6 weeks) • Asymptomatic euthyroidism • Hypothyroid period (weeks to months) • Recovery (complete in 95% after 4-6 months) • 2-9% with recurrent disease • 5% residual hypothyroidism
Subacute ThyroiditisDeQuervain’s, Granulomatous • Diagnosis • Elevated ESR usually>100 • Elevated/NL CBC • Anemia (normochromic, normocytic) • Low TSH, Elevated T4 > T3, Low anti-TPO/Tgb • Low RAI uptake (same as silent thyroiditis) • Treatment • NSAID’s and salicylates. • Oral steroids in severe cases • Beta blockers for symptoms of hyperthyroidism, Iopanoic acid for severe symptoms • PTU not indicated since excess hormone results from leak instead of hyperfunction • Symptoms can recur requiring repeat treatment
Treatment: Subacute Thyroiditis • large doses of aspirin (e.g., 600 mg every 4–6 h) or NSAIDs • marked local or systemic symptoms, glucocorticoids usual starting dose is 40–60 mg prednisone, depending on severity. The dose is gradually tapered over 6–8 weeks, in response to improvement in symptoms and the ESR. • If a relapse occurs during glucocorticoid withdrawal, treatment should be started again and withdrawn more gradually. In these patients, it is useful to wait until the radioactive iodine uptake normalizes before stopping treatment. • monitoring every 2–4 weeks using TSH and unbound T4 levels. • Symptoms of thyrotoxicosis improve spontaneously but may be ameliorated by -adrenergic blockers. • antithyroid drugs play no role in treatment of the thyrotoxic phase. Levothyroxine replacement may be needed if the hypothyroid phase is prolonged, but doses should be low enough (50 to 100 g daily) to allow TSH-mediated recovery.
Patient’s follow up 11.3.92 • T4:5.3 • T3:81 • TSH:2.3 • ESR:4 • FBS:107
Thyroid nodule Risk factors for cancer: • Age <15, > 45 • Male sex • Hx of radiation ( up to 5% of patients develop Ca) • Solitary thyroid nodule + h/o radiation = 40% will have Ca • Family Hx or h/o diseases associated with thyroid Ca: Cowden’s and Gardner syndromes, FAP, Pheo and Hyperparathyroidism • Size > 4 cm • Prior h/o thyroid Ca
Thyroid nodule Sign of malignancy: • Rapid growth • Hard nodule • Fixated • Vocal cord paralysis • Enlarged lymph nodes • Family h/o thyroid Ca • Symptoms of invasion • All - 71% risk of malignancy • Dx of follicular neoplasm on FNA: 20% thyroid Ca NCCN Practice Guidelines 2003 J. Hamming. Arch Intern Med 1990 R. Wein, Otolaryngology Clinics of NA 2005
US signs of malignancy Benign nodule • Microcalcifications • Solid nodule / marked hypoechogenicity • Irregular margins • Absence of a hypoechoic halo around the nodule • Lymphadenopathy and local invasion of adjacent structures • High vascularity on Doppler flow
Radioactive Iodine Uptake (RAIU) • A small amount of 131I is given orally, and 4 & 24 hr dosimetry readings are taken from the thyroid • Normal range: ~5-30% • Increased RAIU • Graves Disease • Toxic Multinodular Goiter • Thyroid Adenoma • Decreased RAIU • Subacute or Silent Thyroiditis • Iodine-Induced • Factitious
Ultrasonography • Findings suggestive of malignancy: • No Presence of halo • Irregular border • Presence of cystic components • Presence of calcifications • Heterogeneous echo pattern • Extrathyroidal extension • No findings are definitive
Silent ThyroiditisPost-partum Thyroiditis • Postpartum thyroiditis • 2-21% of pregnancies • Can occur up to one year post partum • Usually transient and returns to euthyroid state • Treat • Hypothyroidism • Symptoms with ‘hyperthyroidism’ • Presence of TPO AB increases risk of long term hypothyroidism
Silent ThyroiditisPost-partum Thyroiditis • Silent thyroiditis is termed post-partum thyroiditis if it occurs within one year of delivery. • Clinical • Hyperthyroid symptoms at presentation • Progression to euthyroidism followed by hypothyroidism for up to 1 year. • Hypothyroidism generally resolves • Diagnosis • May be confused with post-partum Graves’ relapse • Treatment • Beta blockers during toxic phase • No anti-thyroid medication indicated • Iopanoic acid (Telopaque) for severe hyperthyroidism • Thyroid hormone during hypothyroid phase. Must withdraw in 6 months to check for resolution.
Chronic Thyroiditis Hashimoto’s • Autoimmune • Initially goiter later very little thyroid tissue • Rarely associated with pain • Insidious onset and progressionHashimoto’s • Women 3.5/1000 • Men 0.8/1000 • Frequency increases with age • Familial history • Associated with autoimmune diseases • Most common cause of hypothyroidism • TPO abs present (90 – 95%)
Hashimoto’s Thyroiditis • Most common cause of goiter and hypothyroidism in the U.S. • Physical • Painless diffuse goiter • Lab studies • Hypothyroidism • Anti TPO antibodies (90%) • Anti Thyroglobulin antibodies (20-50%) • Acute Hyperthyroidism (5%) • Treatment • Levothyroxine if hypothyroid • Triiodothyronine (for myxedema coma) • Thyroid suppression (levothyroxine) to decrease goiter size • Contraindications • Stop therapy if no resolution noted • Surgery for compression or pain.
Riedel’s Thyroiditis • Rare disease involving fibrosis of the thyroid glandMiddle aged women • Insidious painless • Symptoms due to compression • Dense fibrosis develop • Usually no thyroid function impairment • Diagnosis • Thyroid antibodies are present in 2/3 • Painless goiter “woody” • Open biopsy often needed to diagnose • Associated with focal sclerosis syndromes (retroperitoneal, mediastinal, retroorbital, and sclerosingcholangitis) • Treatment • Resection for compressive symptoms • Chemotherapy with Tamoxifen, Methotrexate, or steroids may be effective • Thyroid hormone only for symptoms of hypothyroidism
Drug-Associated Thyroiditis • Most cases of thyroiditis associated with various therapeutic agents appear to be caused by drug-induced exacerbation of underlying autoimmune • disease. • Amiodarone • IL-2, interferon-α, • granulocyte/macrophage colony-stimulating factor (GM-CSF) • lithium • GnRH agonist leuprolide, but the pathophysiology is obscure. • Thyroiditis has been found in association with the use • of a multitargeting kinase inhibitor, sunitinib, in patients • with gastrointestinal stromal tumors or renal cell carcinoma
exacerbations of Hashimoto’s disease may be difficult to distinguish from subacute thyroiditis. Lack of elevation of the erythrocyte sedimentation rate and high titers of • thyroid autoantibodies strongly suggest the former condition. • Acute pyogenic thyroiditis is distinguished by the • presence of a septic focus elsewhere,bygreaterinflammatoryreaction in the tissues adjacent to the thyroid, andby much greater leukocytic and febrile responses .The RAIU and thyroid function are usually preserved in acute pyogenic thyroiditis. Rarely, widespread infiltrating cancer of the thyroid can manifest with aclinical and laboratory picture almost indistinguishable from that of subacute thyroiditis. Ultrasonography and fine-needle aspiration should be performed if this is a consideration