Note: If dose or dose within range exceeds 1,000 microcuries, dose will be expressed as millicuries. Adhere to radiation safety precautions regarding radioactive iodine treatment. Discontinue antithyroid medications 3 to 4 days prior to administration of sodium iodide I131.
Diagnostic procedures: Oral (based on a 70 kg patient): Note: Consult manufacturer potency tables when applicable. All doses should be individualized; general ranges are listed here:
Thyroid uptake: 5 to 10 microcuries (or 0.185 to 0.37 megabecquerels) 24 hours prior to uptake measurement (ACR/SNMMI/SPR 2019; manufacturer's labeling); maximum: 10 microcuries (0.37 megabecquerels) (ACR/SNMMI/SPR 2019).
Dosage adjustment if used in conjunction with technetium Tc 99m sodium pertechnetate: 4 to 5 microcuries (0.15 to 0.185 megabecquerels) (ACR/SNMMI/SPR 2019).
Thyroid imaging: 50 to 100 microcuries (or 1.85 to 3.7 megabecquerels) 16 to 24 hours prior to imaging. Note: Other agents (eg, sodium iodide I123, technetium-99m pertechnetate) are preferred for routine thyroid scintigraphy for benign disease due to increased thyroid radiation exposure with sodium iodide I131 (ACR/SNMMI/SPR 2019).
Whole-body imaging for thyroid cancer metastases (off label): 1 to 5 millicuries (37 to 185 megabecquerels) 24 to 72 hours prior to imaging (ACR/SNMMI/SPR 2019).
Hyperthyroidism:
Note: Individualize dose based on thyroid uptake and gland size. Manufacturer's labeling recommends 4 to 10 millicuries (or 148 to 370 megabecquerels); however, due to high failure rates, RAI therapy with low activities is generally not recommended (ATA [Ross 2016]).
Graves disease (off-label dosing): Oral: 10 to 15 millicuries (or 370 to 555 megabecquerels) or 150 microcuries/g of tissue corrected for 24-hour radioactive iodine uptake (see dose equation below) (ATA [Ross 2016]).
Note: Radioactive iodine (RAI) therapy is not recommended in patients with active and moderate to severe or sight-threatening Graves orbitopathy. RAI therapy may be considered in patients with active and mild disease; however, if risk factors for worsening of orbitopathy are present (eg, smoking, high thyrotropin receptor antibodies), concomitant use of glucocorticoids is strongly recommended. In the absence of risk factors, concomitant glucocorticoid use may still be considered (ATA [Ross 2016]).
Toxic multinodular goiter (off-label dosing): Oral: 150 to 200 microcuries/g of tissue corrected for 24-hour radioactive iodine uptake (see dose equation below); if hyperthyroidism persists, may repeat after 6 months if needed (ATA [Ross 2016]).
Toxic thyroid adenoma (off-label dosing): Oral: 10 to 20 millicuries (or 370 to 740 megabecquerels) or 150 to 200 microcuries/g of tissue corrected for 24-hour radioactive iodine uptake (see dose equation below); if hyperthyroidism persists, may repeat after 6 months if needed (ATA [Ross 2016]).
Dose equation corrected for 24-hour radioactive iodine uptake: Activity (millicuries) = (gland weight in grams x desired dose in microcuries/gram x [1/24 hour uptake in % of dose])/1,000 (ATA [Ross 2016]).
Thyroid cancer:
Ablation of normal thyroid tissue: Oral: Initial: 30 to 100 millicuries (or 1,100 to 3,700 megabecquerels). Note: If remnant ablation is performed after total thyroidectomy for American Thyroid Association (ATA) low-risk thyroid cancer or intermediate-risk disease with lower risk features, a low administered activity of ~30 millicuries is generally favored over higher administered activities. For initial adjuvant therapy when microscopic residual disease is suspected (in the absence of known distant metastases), up to 150 millicuries has been recommended (ATA [Haugen 2015]).
Subsequent metastases ablation: Oral: 100 to 200 millicuries (or 3,700 to 7,400 megabecquerels).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in manufacturer's labeling. However, patients with renal impairment may have decreased clearance and increased radiation exposure.
Hemodialysis: Sodium iodide I131 is dialyzable.
There are no dosage adjustments provided in manufacturer's labeling.
Refer to adult dosing.
Empiric dosing for subsequent pulmonary micrometastases ablation for patients ≥70 years: 100 to 150 millicuries (ATA [Haugen 2015])
Graves disease (off-label use): Children ≥5 years of age: Oral: Dose is dependent upon gland size; >150 microcuries/g of thyroid tissue is necessary to induce hypothyroidism; if gland is between 50 to 80 g, higher activities (200 to 300 microcuries/g of thyroid tissue) may be needed. Therapy in children between 5 to 10 years of age is acceptable if the calculated dose is <10 millicuries (ATA [Ross 2016])
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in manufacturer's labeling. However, patients with renal impairment may have decreased clearance and increased radiation exposure.
Hemodialysis: Dialyzable.
There are no dosage adjustments provided in manufacturer's labeling.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Postmarketing:
Cardiovascular: Chest pain, tachycardia
Dermatologic: Erythema of skin, pruritus, skin lesion (iododerma), skin rash, urticaria
Endocrine & metabolic: Goiter, hyperthyroidism, hypoparathyroidism, hypothyroidism (including congenital hypothyroidism), ovarian failure (transient), thyroid storm
Gastrointestinal: Diarrhea, gastritis, nausea, salivary gland disease, sialadenitis, sore throat, vomiting, xerostomia
Genitourinary: Inhibition of testicular function (transient)
Hematologic & oncologic: Anemia, bone marrow depression, hematologic abnormality (including blood dyscrasia), leukemia (can be acute leukemia), leukopenia, malignant solid tumor, neoplasm, thrombocytopenia
Hepatic: Hepatic insufficiency
Hypersensitivity: Hypersensitivity reaction
Local: Local pain (pain on swallowing), local swelling (thyroid or site of iodide avid tumor), localized tenderness
Nervous system: Brain edema (in patients with iodine-avid brain metastases), headache
Ophthalmic: Conjunctivitis, disease of the lacrimal apparatus, epiphora, lacrimal drainage system obstruction (dacryostenosis), xerophthalmia
Respiratory: Bronchospasm, cough, pulmonary fibrosis (in patients with iodine-avid lung metastases), radiation pneumonitis (in patients with iodine-avid lung metastases)
Miscellaneous: Chromosomal abnormality, radiation injury (including radiation sickness)
Preexisting vomiting and diarrhea (treatment); concurrent antithyroid medication; pregnancy; breastfeeding; treatment of thyroid malignancies shown to have no iodide uptake, which include the majority of medullary and anaplastic carcinomas
Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Concerns related to adverse effects:
• Hypersensitivity: Hypersensitivity reactions (including rash and hives) have been reported following sodium iodide I131 administration. Sodium iodide I131 solution may contain sodium bisulfite, a sulfite that may cause allergic-type reactions, including anaphylactic symptoms and life-threatening or less severe asthmatic episodes. The overall incidence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people. During pretherapy assessment, question patients about a history of hypersensitivity to sulfite.
• Radiation-induced thyroiditis: Sodium iodide I131 may cause thyroiditis (with gland enlargement) and thyroid hormone release, particularly if used in the treatment of hyperthyroidism. Thyroiditis may cause or worsen hyperthyroidism and may lead to thyroid storm. When treating hyperthyroidism, consider pretreatment with antithyroid medication to help deplete thyroid hormone content within the gland. Discontinue antithyroid medication at least 3 days prior to sodium iodide I131 administration. Consider beta-blocker therapy prior to sodium iodide I131 administration to minimize the risk of hyperthyroidism and thyroid storm. Thyroiditis may result in gland enlargement with neck tenderness and swelling, pain with swallowing, sore throat, and cough; may require management with anti-inflammatory medications or analgesics.
• Radiation toxicities: Radiation-induced toxicities, including dose-dependent fatalities, have been reported following sodium iodide I131 therapy. Postmarketing reports have identified an increased risk for neoplasia (leukemias and solid tumors), as well as a risk of hematopoietic suppression (transient neutropenia/thrombocytopenia; onset 3 to 5 weeks). Salivary and lacrimal gland toxicity is relatively common and may manifest as conjunctivitis, xerophthalmia, epiphora, sialadenitis, and xerostomia.
• Thyroid-stimulating hormone/thyroid enlargement: Enhanced thyroid-stimulating hormone (TSH) secretion (eg, following discontinuation of antithyroid medications, or the administration of TSH to enhance sodium iodide I131 uptake) may cause thyroid enlargement and obstructive complications of the trachea, esophagus, or blood vessels in the neck. Evaluate patients at high risk of obstructive complications prior to preparative treatments known to cause thyroid enlargement.
Disease-related concerns:
• Graves orbitopathy: Radioactive iodine therapy is not recommended in patients with active and moderate to severe or sight-threatening Graves orbitopathy. Radioiodine therapy may be considered in patients with active and mild disease; however, if patients have additional risk factors for worsening orbitopathy (eg, high thyrotropin receptor antibodies, smoking) concomitant glucocorticoid therapy is strongly recommended. In the absence of risk factors for worsening orbitopathy in patients with mild disease, glucocorticoid coverage may still be considered (ATA [Ross 2016]).
• Hyperthyroidism/thyrotoxic cardiac disease: May be aggravated by radiation thyroiditis; consider pre- and post-treatment with antithyroid agents and/or beta-blockers.
• Hypochloremia: May increase thyroid uptake of sodium iodide I131.
• Renal impairment: Sodium iodide I131 is eliminated predominantly renally; patients with renal impairment may have decreased clearance and increased radiation exposure. Sodium iodide I131 is dialyzable and hemodialysis may be used to decrease total body radiation exposure. Evaluate renal function prior to treatment. Nephrosis may increase thyroid uptake of sodium iodide I131.
Concurrent drug therapy issues:
• Iodine/thyroid medications: Concomitant use of iodine, thyroid, or antithyroid medications may interfere with the uptake of radioiodide; medications should be discontinued for an appropriate time prior to dosing.
Special populations:
• Older adult: Older adult patients are more likely to have decreased renal function and comorbid conditions; may require close evaluation, dose selection, and follow-up compared with younger patients. When treating hyperthyroidism in older patients at risk of developing cardiac complications, pre- and post-treatment with antithyroid drugs and/or beta-blockers may minimize the risk of excessive post-treatment hyperthyroidism due to radiation-induced thyroiditis.
• Pediatric: The thyroid gland may be more sensitive to the effects of sodium iodide I131 in pediatric patients; safety and efficacy have not been established.
Special handling:
• Radiopharmaceutical: Use appropriate precautions for handling, disposal, and minimizing exposure to patients and health care personnel. Use only under supervision of individuals with experience/training in the handling of radioactive materials approved by the applicable regulatory authority. Unwanted radiation exposure can occur from handling and administration of radiopharmaceuticals or from contaminated waste products, including urine and feces. Patients must be instructed in measures to minimize exposure of others.
Other warnings/precautions:
• Appropriate use: Patients should be adequately hydrated prior to and for at least 1 week following administration. Frequent voiding is recommended to enhance radioiodide excretion. Stimulate salivary flow (gum or sugar-free candy) to reduce radiation exposure to salivary glands. Avoid close contact with others (especially pregnant women and children) and contamination of other persons or the environment with body fluids.
Hicon solution is packaged with capsules containing ~300 mg of dibasic sodium phosphate buffer for preparation of individualized dose.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Generic: 100 mCi (5s)
Solution, Oral:
Hicon: 250 mCi, 500 mCi, 1000 mCi (1 mL) [contains edetate (edta) disodium dihydrate]
May be product dependent
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Draximage: 0.1 mCi, 200 mCi [contains edetate (edta) disodium dihydrate]
Solution, Oral:
Draximage: 200 mCi/mL (1 mL) [contains edetate (edta) disodium dihydrate]
Generic: 1000 mCi/mL (1 mL, 2 mL, 3 mL, 5 mL)
Ensure adequate hydration before and after treatment; instruct patients to void frequently to enhance elimination of radioiodide not absorbed by thyroid. Adhere to radiation safety precautions regarding radioactive iodine treatment.
Hicon: Administer on an empty stomach; patient should fast at least 2 hours before and 2 hours after administration to ensure adequate absorption. Solution must be diluted and prepared prior to administration; do not administer concentrated solution. Provide solution dose in a shielded container with a straw for administration.
Radiopharmaceutical; use appropriate precautions for handling and disposal. Waterproof gloves should be worn while handling and administering sodium iodide I131.
Oral: Radiopharmaceutical; use appropriate precautions for handling and disposal. Waterproof gloves should be worn while handling and administering sodium iodide I131. Ensure adequate hydration before and after treatment; instruct patients to void frequently to enhance elimination of radioiodide not absorbed by thyroid.
Hicon: Solution must be diluted and prepared prior to administration; do not administer concentrated solution. Provide solution dose in a shielded container with a straw for administration. Administer on an empty stomach; fast at least 2 hours before and 2 hours after administration to ensure adequate absorption.
Diagnostic agent: Diagnostic use in performance of radioactive iodide (RAI) uptake test to evaluate thyroid function and for thyroid imaging. Note: Other agents (eg, sodium iodide I123, technetium-99m pertechnetate) are preferred for routine thyroid scintigraphy for benign disease due to increased thyroid radiation exposure with sodium iodide I131 (ACR/SNMMI/SPR 2019).
Therapeutic agent: Treatment of hyperthyroidism and select cases of thyroid carcinomas (if the lesions take up iodide); palliative effects may be observed in patients with advanced thyroid malignancy if the metastatic lesions take up iodide.
Whole body imaging for thyroid cancer metastases
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drugs that have a heightened risk of causing significant patient harm when used in error.
Radiopharmaceutical: Use appropriate precaution for handling, disposal, and minimizing exposure to patients and healthcare personnel. Use under supervision of experienced personnel. Should be stored in original lead container or adequate radiation shield.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Amiodarone: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue amiodarone at least 6 months before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Antithyroid Agents: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue antithyroid medications at least 3 days before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Iodinated Contrast Agents: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue iodinated contrast agents before sodium iodide I-131 administration, and avoid concurrent use. Stop water soluble agents 2 months before, and stop lipophilic agents 6 months before, sodium iodide I-131 administration. Risk X: Avoid combination
Iodine: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue topical iodine at least 3 weeks before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Potassium Iodate: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue potassium iodate at least 3 weeks before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Potassium Iodide: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue potassium iodide at least 3 weeks before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Povidone-Iodine (Topical): May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue topical povidone-iodine at least 3 weeks before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Sodium Iodide: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue sodium iodide supplementation at least 10 days before sodium iodide I-131 administration, and avoid concurrent use. Risk X: Avoid combination
Thyroid Products: May diminish the therapeutic effect of Sodium Iodide I131. Management: Discontinue thyroid products before sodium iodide I-131 administration, and avoid concurrent use. Stop triiodothyronine (T3) 2 weeks before, and stop thyroxine (T4) 4 weeks before, sodium iodide I-131 administration. Risk X: Avoid combination
Evaluate pregnancy status prior to use; a pregnancy test should be done prior to administration in patients who may become pregnant. Pregnancy should be ruled out prior to therapy.
Effective contraception is recommended by the manufacturer for females and males during treatment for thyroid disease and for at least 6 months following administration. Practice guidelines advise against planning a pregnancy for 6 to 12 months following use as a diagnostic or therapeutic agent (ACR/ACNM/ASTRO/SNMMI/SPR 2019; IAEA 2018).
Transient infertility may occur (dose related). Transient amenorrhea and ovarian insufficiency have been reported. Transient testicular function impairment has been observed; consider sperm banking prior to therapeutic use.
Sodium iodide I131 crosses the placenta.
Fetal exposure to sodium iodide I131 may cause severe and irreversible hypothyroidism in neonates. A delayed diagnosis following in utero exposure may lead to decreased mental capacity and delayed skeletal maturation. Monitor thyroid function of infants born following inadvertent in utero exposure.
Use as either a diagnostic or therapeutic agent is contraindicated in pregnancy.
Health care providers who are pregnant should avoid direct patient care, and pregnant persons should also limit close contact with patients undergoing treatment with sodium iodide I131 for thyroid disease (ACR/ACNM/ASTRO/SNMMI/SPR 2019).
Sodium iodide I131 is present in breast milk.
Sodium iodide I131 concentrations may be equal to or greater than maternal plasma concentrations. Infant exposure to sodium iodide I131 via breast milk may lead to hypothyroidism in the breastfeeding infant. Radioiodine uptake has been reported in breast tissue for 5 to 32 weeks following the cessation of breastfeeding.
Use as a therapeutic agent is contraindicated in patients who are breastfeeding and the complete cessation of breastfeeding is recommended if sodium iodide I131 is administered. To minimize the radiation dose absorbed into breast tissue, breastfeeding and pumping should be discontinued at least 4 to 6 weeks prior to sodium iodide I131 administration. This also reduces the risk of contaminating clothing if milk leakage of radioactive iodine occurs. Breastfeeding may be resumed with the birth of another child (if no sodium iodide I131 is administered in that postpartum period) (ABM [Mitchell 2019]).
Complete cessation of breastfeeding is also recommended following use as a diagnostic agent (IAEA 2018). Elective diagnostic procedures should be delayed until breastfeeding has stopped (SNM [Parker 2010]).
The manufacturer recommends maintaining a low iodide diet two weeks before administration and to continue for several days during the uptake and imaging process.
In the treatment of Graves disease, it has been recommended that a special diet prior to RAI therapy is not required, but nutritional supplements containing excess iodine and seaweeds be avoided for at least 7 days; a low-iodine diet may benefit those with relatively low RAI uptake to increase the proportion of RAI trapped (ATA [Ross 2016])
Some dietary sources of iodine include cow's milk and dairy products, fish, seaweed, eggs, chocolate, and iodized salt.
Thyroid function tests (TSH, free T4, total T3) within 1 to 2 months post-treatment and at 4 to 6 week intervals for 6 months, or until hypothyroid and stable on thyroid hormone replacement (Graves disease, toxic multinodular goiter, toxic adenoma) (ATA [Ross 2016]); renal function tests in patients with history of renal impairment; CBC within 1 month of therapy.
Evaluate pregnancy status prior to use; a negative human chorionic gonadotropin (hCG) pregnancy test should be done within 24 hours prior to administration in patients who may become pregnant (ACR/ACNM/ASTRO/SNMMI/SPR 2019).
Oral sodium iodide I131 is rapidly absorbed and distributed within the extracellular fluid of the body. Iodide is concentrated in the thyroid via the sodium/iodide symporter, and subsequently oxidized to iodine. Beta emission of sodium iodide I131 destroys thyroid tissue.
Absorption: Oral: Rapidly (90% within 60 minutes)
Distribution: Extracellular space; primarily trapped by the thyroid
Protein binding: None
Metabolism: Iodide is rapidly oxidized to iodine in the thyroid
Excretion: Urine (37% to 75%); feces ~10%
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