Presentation on theme: "Painful thyroid acute pyogenic or fungal thyroiditis subacute thyroiditis hemorrhage into a cyst Acute hemorrhagic degeneration in a nodule, Hashimoto’s."— Presentation transcript:
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 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 Thyroiditis DeQuervain’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
Clinical Course of Sub Acute Thyroiditis
Subacute Thyroiditis DeQuervain’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 T4:5.3 T3:81 TSH:2.3 ESR:4 FBS:107
Thank You for Your Attention
Thyroiditis Time Course Williams Text of Endocrinology, Fig 11.50
Thyroid nodule Risk factors for cancer: Age 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 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 Benign nodule
Radioactive Iodine Uptake (RAIU) A small amount of 131 I 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 27
Silent Thyroiditis Post-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 Thyroiditis Post-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 ab s 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 gland Middle 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 sclerosing cholangitis) Treatment Resection for compressive symptoms Chemotherapy with Tamoxifen, Methotrexate, or steroids may be effective Thyroid hormone only for symptoms of hypothyroidism
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 Drug-Associated Thyroiditis
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
Comparison of Thyroiditis Characteristic Silent thyroiditis Subacute thyroiditis Age of onset (yr) Sex ratio (F:M) 2:15:1 EtiologyAutoimmuneViral Pathology Lymphocytic infiltration Giant cells, granulomas ProdromePregnancy Viral illness GoiterNon-painfulPainful Fever/malaiseNoYes TPO/thyroglobulin AB High and rising Low, absent or transient ESRNormalHigh RAIU<5%<5% RelapseCommonRare Permanent hypothyroidism CommonInfrequent