Painful thyroid. acute pyogenic or fungal thyroiditis subacute thyroiditis hemorrhage into a cyst Acute hemorrhagic degeneration in a nodule , Hashimotos disease with painful recurrence thyroid malignancy(lymphoma) amiodarone-induced thyroiditis or amyloidosis. Acute Thyroiditis. - PowerPoint PPT Presentation
Painful thyroidacute pyogenic or fungal thyroiditissubacute thyroiditis hemorrhage into a cystAcute hemorrhagic degeneration in a nodule,Hashimotos disease with painful recurrence thyroid malignancy(lymphoma)amiodarone-induced thyroiditis or amyloidosis
Acute ThyroiditisCauses68% Bacterial (S. aureus, S. pyogenes)15% Fungal9% Mycobacterial
May occur secondary toPyriform sinus fistulaePharyngeal space infectionsPersistent Thyroglossal remnantsThyroid surgery wound infections (rare)
More common in HIVAcute ThyroiditisSymptoms
Thyroid pain and tendernessFeverDysphagiaDysphoniaWarm, tender, enlarged thyroid Acute ThyroiditisDiagnosisFNA to drain abscess, obtain cultureRAIU normal&TFT NL (versus decreased in DeQuervains)CT or US if infected TGDC suspected
TreatmentHigh mortality without prompt treatmentIV Antibiotics Nafcillin / Gentamycin or Rocephin for empiric therapySearch for pyriform fistulae (BA swallow, endoscopy)Recovery is usually complete
7Subacute Thyroiditis SubacuteMost common cause of painful thyroiditis
20% of thyrotoxic casesDe Quervains thyroiditisGiant cell thyroiditisPseudogranulomatous thyroiditisSubacute 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 ThyroiditisViral (granulomatous) Mumps, coxsackie, influenza, adeno and echoviruses
Subacute thyroiditis features5:1 female predominanceAge of onset 20-60yProdrome (myalgias, fever, pharyngitis)Seasonal variation (correlation with enterovirus?)Fever/severe neck painDysphagia,odynophagia,hoaresnessThe pain, which is aggravated by turning thehead 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 immunoglobulinsThyroid storm case reportsSubacute thyroiditis featuresOn 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 ThyroiditisDeQuervains, GranulomatousFNA may reveal multinuleated giant cells or granulomatous change.
CoursePain and thyrotoxicosis (3-6 weeks)Asymptomatic euthyroidismHypothyroid period (weeks to months)Recovery (complete in 95% after 4-6 months)
2-9% with recurrent disease5% residual hypothyroidism
Clinical Course of Sub Acute Thyroiditis
Subacute ThyroiditisDeQuervains, GranulomatousDiagnosisElevated ESR usually>100Elevated/NL CBCAnemia (normochromic, normocytic)Low TSH, Elevated T4 > T3, Low anti-TPO/TgbLow RAI uptake (same as silent thyroiditis)
TreatmentNSAIDs and salicylates.Oral steroids in severe casesBeta blockers for symptoms of hyperthyroidism, Iopanoic acid for severe symptomsPTU not indicated since excess hormone results from leak instead of hyperfunctionSymptoms can recur requiring repeat treatment
Treatment: Subacute Thyroiditislarge doses of aspirin (e.g., 600 mg every 46 h) or NSAIDs marked local or systemic symptoms, glucocorticoids usual starting dose is 4060 mg prednisone, depending on severity. The dose is gradually tapered over 68 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 24 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.Patients follow up 11.3.92
T4:5.3T3:81TSH:2.3ESR:4FBS:107Thank You for Your Attention
Williams Text of Endocrinology, Fig 11.50Thyroid noduleRisk factors for cancer:Age 45Male sexHx of radiation ( up to 5% of patients develop Ca)Solitary thyroid nodule + h/o radiation = 40% will have CaFamily Hx or h/o diseases associated with thyroid Ca: Cowdens and Gardner syndromes, FAP, Pheo and HyperparathyroidismSize > 4 cmPrior h/o thyroid Ca
Thyroid noduleSign of malignancy:Rapid growthHard noduleFixatedVocal cord paralysisEnlarged lymph nodesFamily h/o thyroid CaSymptoms of invasionAll - 71% risk of malignancy
Dx of follicular neoplasm on FNA: 20% thyroid Ca
NCCN Practice Guidelines 2003J. Hamming. Arch Intern Med 1990R. Wein, Otolaryngology Clinics of NA 2005US signs of malignancyMicrocalcifications 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 thyroidNormal range: ~5-30%Increased RAIUGraves DiseaseToxic Multinodular GoiterThyroid AdenomaDecreased RAIUSubacute or Silent ThyroiditisIodine-InducedFactitious
UltrasonographyFindings suggestive of malignancy:No Presence of haloIrregular borderPresence of cystic componentsPresence of calcificationsHeterogeneous echo patternExtrathyroidal extensionNo findings are definitive27Silent ThyroiditisPost-partum Thyroiditis Postpartum thyroiditis2-21% of pregnanciesCan occur up to one year post partumUsually transient and returns to euthyroid stateTreat HypothyroidismSymptoms with hyperthyroidismPresence of TPO AB increases risk of long term hypothyroidism
Silent ThyroiditisPost-partum ThyroiditisSilent thyroiditis is termed post-partum thyroiditis if it occurs within one year of delivery.ClinicalHyperthyroid symptoms at presentationProgression to euthyroidism followed by hypothyroidism for up to 1 year.Hypothyroidism generally resolvesDiagnosisMay be confused with post-partum Graves relapseTreatmentBeta blockers during toxic phaseNo anti-thyroid medication indicatedIopanoic acid (Telopaque) for severe hyperthyroidismThyroid hormone during hypothyroid phase. Must withdraw in 6 months to check for resolution.Chronic ThyroiditisHashimotosAutoimmuneInitially goiter later very little thyroid tissueRarely associated with painInsidious onset and progressionHashimotosWomen 3.5/1000Men 0.8/1000Frequency increases with ageFamilial historyAssociated with autoimmune diseases
Most common cause of hypothyroidismTPO abs present (90 95%)
Hashimotos ThyroiditisMost common cause of goiter and hypothyroidism in the U.S.PhysicalPainless diffuse goiterLab studiesHypothyroidismAnti TPO antibodies (90%)Anti Thyroglobulin antibodies (20-50%)Acute Hyperthyroidism (5%)TreatmentLevothyroxine if hypothyroidTriiodothyronine (for myxedema coma)Thyroid suppression (levothyroxine) to decrease goiter sizeContraindicationsStop therapy if no resolution notedSurgery for compression or pain.Riedels ThyroiditisRare disease involving fibrosis of the thyroid glandMiddle aged womenInsidious painlessSymptoms due to compressionDense fibrosis develop Usually no thyroid function impairment
DiagnosisThyroid antibodies are present in 2/3Painless goiter woodyOpen biopsy often needed to diagnoseAssociated with focal sclerosis syndromes (retroperitoneal, mediastinal, retroorbital, and sclerosing cholangitis)
TreatmentResection for compressive symptomsChemotherapy with Tamoxifen, Methotrexate, or steroids may be effectiveThyroid 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 autoimmunedisease. Amiodarone IL-2, interferon-, granulocyte/macrophage colony-stimulating factor (GM-CSF) lithiumGnRH agonist leuprolide, but the pathophysiology is obscure.
Thyroiditis has been found in association with the useof a multitargeting kinase inhibitor, sunitinib, in patientswith gastrointestinal stromal tumors or renal cell carcinomaDrug-Associated Thyroiditisexacerbations of Hashimotos disease may be difficult to distinguish from subacute thyroiditis. Lack of elevation of the erythrocyte sedimentation rate and high titers ofthyroid autoantibodies strongly suggest the former condition.Acute pyogenic thyroiditis is distinguished by thepresence 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 ThyroiditisCharacteristicSilent thyroiditisSubacute thyroiditisAge of onset (yr)5-9320-60Sex ratio (F:M)2:15:1EtiologyAutoimmuneViralPathologyLymphocytic infiltrationGiant cells, granulomasProdromePregnancyViral illnessGoiterNon-painfulPainfulFever/malaiseNoYesTPO/thyroglobulin ABHigh and risingLow, absent or transientESRNormalHighRAIU