eMedicine Specialties > Endocrinology > Thyroid
Subacute Thyroiditis: Treatment & Medication
Updated: Apr 27, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Patients are often dehydrated from thyrotoxicosis; encourage all patients to drink 6-8 cups per day of noncaffeinated fluids.
Subacute thyroiditis - all forms
The treatment of subacute thyroiditis is generally supportive to reduce the symptoms of thyrotoxicosis and to control neck pain in the setting of subacute granulomatous thyroiditis. Because no new hormone is being made, antithyroid medications are not effective in these conditions. Although the abnormal thyroid levels are temporary, emotional support is often necessary.
- Thyroid hormone levels in subacute thyroiditis - The release of preformed hormone cannot be stopped in the destructive phase. In patients with very high levels of thyroid hormone, ipodate (iopanoic acid), better known as Gastrografin, may be administered to inhibit the conversion of T4 to the more active form of thyroid hormone, T3. A dose of 1000 mg in 2 divided doses daily usually provides a rapid reduction in T3 and in thyrotoxic symptoms.
- Pain in lymphocytic thyroiditis - The thyroid pain can be extreme. Nonsteroidal medications are administered. Avoid high-dose aspirin because, in some circumstances, aspirin can competitively displace thyroid hormone from its binding protein and increase the free, or bioactive, fraction of thyroid hormone, which can make patients feel more thyrotoxic. In extreme cases, stronger pain medications, including narcotic analgesics, are indicated for a brief period of 2-3 weeks. In the most extreme cases, high-dose steroids (eg, prednisone 40-60 mg qd) must be administered. The high-dose steroids rapidly and dramatically decrease the pain and thyroid swelling, but the natural course of thyrotoxicosis and pain (ie, 4-6 wk) is not altered, and the glucocorticoid treatment must be continued for this period.
- Peripheral manifestations of thyrotoxicosis - Patients often find great relief from tachycardia, palpitations, anxiety, and tremor with beta-blocker therapy. Propranolol is generally recommended because of its CNS effects. The patient usually titrates the dose depending on the symptoms. Exercise caution with the initial dose; patients may become hypotensive, because they are often dehydrated from the decrease in oral intake of fluids and increased perspiration from thyrotoxicosis.
Surgical Care
Surgical care is almost never recommended for subacute thyroiditis. Surgery is recommended rarely in patients who have frequent recurrences of thyrotoxicosis from lymphocytic thyroiditis or recurrent pain from subacute granulomatous thyroiditis.
Consultations
Generally, all patients with thyrotoxicosis should be referred to an endocrinology specialist. Distinguishing between the causes of thyrotoxicosis is important, because the therapies are very different.
Diet
Avoiding high-dose iodine supplements, such as those found in seaweed tablets, during and after an episode of subacute thyroiditis is important. Inflammation appears to prevent the thyroid from escaping the iodine-induced Wolff-Chaikoff suppression of thyroid hormone synthesis. These patients are likely to become hypothyroid when ingesting large amounts of iodine.
Activity
No limitation in activity is necessary, but patients may experience tachycardia with exercise. Good hydration and beta-blocker therapy should allow patients with subacute thyroiditis – caused thyrotoxicosis to exercise normally.
Medication
Medical treatment for subacute thyroiditis is supportive in general. Thyrotoxicosis can be extreme but temporary (eg, 6-8 wk). The subsequent hypothyroid phase is usually mild and lasts 2-4 months. Therapy is directed toward reducing the signs and symptoms of the hyperthyroidism with beta blockers or iodine agents. Pain is treated with nonsteroidal anti-inflammatory agents (NSAIDs). Rarely, high-dose steroids and narcotic analgesic agents are used for extremely painful or recurrent life-threatening hyperthyroidism.
Nonsteroidal anti-inflammatory drugs
Anti-inflammatory agents are administered to patients with painful subacute thyroiditis. Patients should avoid high-dose aspirin because it can increase free thyroid hormone levels by displacing thyroid hormone from its protein binding sites. Narcotic analgesics can be administered if the pain is extreme and prevents oral hydration. Rarely, high-dose steroids (eg, prednisone 40-60 mg PO qd for 4-6 wk) may be used to decrease the pain, if necessary.
Ibuprofen (Advil, Motrin)
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult
600-800 mg PO tid
Pediatric
4-10 mg/kg per dose PO tid/qid; not to exceed 50 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in CHF, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Naproxen (Aleve, Naprosyn, Naprelan)
For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
Adult
250-500 mg PO bid
Pediatric
10-20 mg/kg PO divided bid
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of the drug
Indomethacin (Indocin)
Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.
Adult
25-50 mg PO tid
Pediatric
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding; renal insufficiency
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, discontinue if patient has persistent leukopenia, granulocytopenia, or thrombocytopenia
Iodinated contrast agents
High iodine levels inhibit the peripheral conversion of T4 to T3. The most effective agents are the iodinated contrast agents, but high levels of iodine provided by SSKI (saturated solution of potassium iodide, 2 drops in full glass of water PO tid) can be substituted.
Iopanoic acid (Telepaque)
PO contrast agent for rapid and significant inhibition of peripheral conversion of T4 to T3. Inorganic iodide released also blocks release of thyroid hormones. Reduction in conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms over a few d.
Adult
2 g PO, then 0.5 g PO bid
Pediatric
Not established
Coadministration with lithium may result in hypothyroid effects
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Possibility of hypotension increases with increased dosage; anuria may develop if agents are administered to patients with combined hepatic and renal disease or severe renal impairment; prolonged iodine storage in tissues may lead to rebound thyrotoxicosis with potential to cause ethionamide resistance
Ipodate (Oragrafin)
One of the most effective inhibitors of deiodinase, which converts T4 to the more biologically active T3. Reduction in conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms.
Adult
2 g PO, then 0.5 g PO bid
Pediatric
Not established
Coadministration with lithium may result in hypothyroid effects
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Risk of hypotension increases with increased dose; anuria may develop if agents are administered to patients with combined hepatic and renal disease or severe renal impairment; prolonged iodine storage in tissues may lead to rebound thyrotoxicosis with potential to cause ethionamide resistance
Thyroid hormones
Most patients with subacute thyroiditis experience a hypothyroid phase following thyrotoxicosis. Asymptomatic patients do not need to be treated if TSH is mildly elevated (<15 µIU/mL), but they should be tested q4wk to confirm that hypothyroidism is not worsening or becoming permanent. Thyroid hormone is generally administered (usually 50 mcg/d) to normalize TSH. After 6 months, when 90-95% of patients have returned to normal thyroid function, thyroid hormone is discontinued and the TSH level is checked 4 wk after discontinuation of therapy. If the TSH level is within the reference range, no further treatment is necessary. If the TSH level is elevated, the patient has permanent hypothyroidism, and therapy should be continued indefinitely.
Levothyroxine (Levoxyl, Synthroid)
In active form, influences growth and maturation of tissues. Involved in normal growth, metabolism, and development. L-thyroxine supplementation only during the hypothyroid phase of subacute thyroiditis. The goal of therapy is a TSH level within the reference range for 6 mo; then discontinue therapy. TSH should be checked 4 wk later, and, if TSH is elevated, L-thyroxine therapy must be reinstituted and continued indefinitely.
Adult
50 mcg/d PO; after 6 wk, if TSH level is abnormal, adjust dose
Pediatric
1-2 mcg/kg/d PO; after 6 wk, if TSH level is abnormal, adjust dose
Cholestyramine may decrease L-thyroxine absorption; concomitant administration with calcium or iron supplements may decrease L-thyroxine absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; effect of anticoagulants is increased when administered with liothyronine; activity of some beta-blockers may decrease when hypothyroid patient is converted to a euthyroid state
Documented hypersensitivity; uncorrected adrenal insufficiency; coronary artery disease; atrial arrhythmia
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in angina pectoris or cardiovascular disease; monitor thyroid status periodically
Beta-adrenergic blocking agents
Beta blockers reduce many of the symptoms of thyrotoxicosis, including tachycardia, tremor, and anxiety. Propranolol is usually recommended because of CNS penetration, but some patients prefer the longer-acting beta blockers.
Propranolol (Inderal)
DOC in treating cardiac arrhythmia resulting from hyperthyroidism. Controls cardiac and psychomotor manifestations within minutes.
Adult
20-40 mg PO q4-8h
Pediatric
2-4 mg/kg PO divided q6-8h
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol
Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely
Atenolol (Tenormin)
Selectively blocks beta1-receptors with little or no effect on beta2 types.
Adult
50-100 mg PO qd
Pediatric
1-2 mg/kg/d PO
Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity of atenolol
Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and may mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during an IV administration, carefully monitor BP, heart rate, and ECG
Corticosteroids
If thyroid pain is extreme, high-dose steroids rapidly reduce thyroid hormone levels and swelling. Generally, therapy must be continued for 4-6 wk before tapering.
Prednisone (Deltasone, Orasone, Sterapred)
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Adult
40-60 mg PO qd for 4-6 wk; taper as symptoms resolve
Pediatric
Not established
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
More on Subacute Thyroiditis |
| Overview: Subacute Thyroiditis |
| Differential Diagnoses & Workup: Subacute Thyroiditis |
 Treatment & Medication: Subacute Thyroiditis |
| Follow-up: Subacute Thyroiditis |
| Multimedia: Subacute Thyroiditis |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
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Omori N, Omori K, Takano K. Association of the ultrasonographic findings of subacute thyroiditis with thyroid pain and laboratory findings. Endocr J. Jul 2008;55(3):583-8. [Medline]. [Full Text].
Nishimaki M, Isozaki O, Yoshihara A, Okubo Y, Takano K. Clinical characteristics of frequently recurring painless thyroiditis: contributions of higher thyroid hormone levels, younger onset, male gender, presence of thyroid autoantibody and absence of goiter to repeated recurrence. Endocr J. Feb 18 2009;[Medline]. [Full Text].
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Further Reading
Clinical guidelines:
Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline.
Clinical trials:
Generic vs. Name-Brand Levothyroxine
Maternal Hypothyroidism in Pregnancy
Keywords
subacute thyroiditis, thyroid, hypothyroidism, thyroid disease, hyperthyroidism, hypothyroid, thyroid symptoms, thyroiditis, hyperthyroid, thyroid hormone, symptoms of thyroid, symptoms of thyroid problems, thyroid disorder, thyroxine, thyroid disorders, thyroid tests, thyroid hormones, T3 thyroid, T4 thyroid, thyrotoxicosis, postpartum thyroiditis, triiodothyronine, lymphocytic thyroiditis, de Quervain's, silent thyroiditis, de Quervain thyroiditis, subacute painless thyroiditis, subacute lymphocytic thyroiditis, subacute postpartum thyroiditis, subacute granulomatous thyroiditis, subacute painful thyroiditis, de Quervain's thyroiditis
