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IODIDES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Potassium Iodide is approved for use as a thyroid blocking agent following exposure to radioisotopes of iodine from a nuclear reactor accident. Unapproved use of potassium iodide includes treatment of inflammatory dermatoses or specific dermatological infections.
    B) Radioactive Sodium Iodide (Na I-131) has been used to treat hyperthyroidism and some forms of thyroid carcinoma. Please refer to the RADIOPHARMACEUTICALS management for further information.
    C) Methyl iodide is used as a methylating agent in pharmaceutical and chemical synthesis, in microscopy, as a reagent, as a catalyst in production of organic lead compounds, as an etching agent, as a component in fire extinguishers, and formerly as a soil fumigant. Please refer to the METHYL IODIDE management for further information.
    D) Please refer to the IODINATED CONTRAST MEDIA management for further information.

Specific Substances

    A) POTASSIUM IODIDE
    1) Iodeto de Potassium
    2) Kali Iodidum
    3) Kali Jodidum
    4) Kali Iodetum
    5) Kalium Jodatum
    6) Potassii Iodidum
    7) Potassium (Iodure de)
    8) CAS 7681-11-0
    9) K-I
    CALCIUM IODIDE
    1) CAS 10102-68-8
    2) CaI2
    3) Ca-I2
    SODIUM IODIDE
    1) Sodium (Iodure de)
    2) Sodii Iodidum
    3) Iodeto de Sodio
    4) Natrii Iodetum
    5) Natrii Iodidum
    6) Natrium Iodatum
    7) Natrii Jodidum

    1.2.1) MOLECULAR FORMULA
    1) INDOCYANINE GREEN: C43H47N2NaO6S2

Available Forms Sources

    A) FORMS
    1) POTASSIUM IODIDE (KI):
    a) CONCENTRATED ORAL SOLUTION: Saturated Solution Potassium Iodide (SSKI): 1 gram KI/mL (50 mg/drop) in 30 mL bottles (Prod Info SSKI(R) oral solution, 1999).
    b) ORAL SOLUTION: 65 mg/mL in 30 mL bottles (Prod Info THYROSHIELD(TM) oral solution, 2005)
    c) ORAL TABLET: 130 mg (Prod Info IOSAT(TM) oral tablets, 2005).
    d) POTASSIUM TOXICITY: Each gram of KI contains 6 mEq of Potassium; toxicity can occur at doses as low as 2.5 mEq/kg. Please refer to the POTASSIUM management for further information on potassium toxicity.
    2) Calcium iodide was requested by the FDA to be removed from over-the-counter products due to insufficient evidence proving efficacy (U.S. Food and Drug Administration, 2010).
    3) Sodium iodide is mainly formulated into radiopharmaceuticals (Prod Info sodium iodide I 131 therapeutic oral capsules, 2005; Prod Info sodium iodide I-131 oral solution, 2006)
    B) USES
    1) Calcium iodide was removed from pharmaceutical products due to lack of efficacy at the request of the FDA (Office of the Federal Register, 2010).
    2) Potassium iodide is FDA approved for use as a thyroid blocking agent following exposure to radioisotopes of iodine from a nuclear reactor accident (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005) or for use as an expectorant in the symptomatic treatment of chronic pulmonary disorders (eg, bronchial asthma, bronchitis, and pulmonary emphysema) (Prod Info SSKI(R) oral solution, 1999). Potassium iodide has been utilized in an off-label manner to treat the following disorders: Behcet's syndrome, erythema multiforme, Wegener's granulomatosis, panniculitis, neutrophilic dermatosis or dermatological infections with a bacterial or fungal origin (Sterling & Heymann, 2000; Restrepo, 1994).
    3) Radioactive Sodium Iodide is used to treat hyperthyroidism and some forms of thyroid carcinoma. It is also used as a diagnostic procedure for evaluating thyroid function and/or morphology (Prod Info sodium iodide I 131 therapeutic oral capsules, 2005; Prod Info sodium iodide I-131 oral solution, 2006). See the RADIOPHARMACEUTICALS management for further information about radioactive sodium iodide.
    4) Methyl iodide is used as a methylating agent in pharmaceutical and chemical synthesis, in microscopy, as a reagent, as a catalyst in production of organic lead compounds, as an etching agent, as a component in fire extinguishers, and formerly as a soil fumigant (IARC, 1986). Please refer to the METHYL IODIDE management for further information.
    5) Please refer to the IODINATED CONTRAST MEDIA management for further information.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Iodides have been utilized to treat iodine disorders, hyperthyroidism, bacterial, fungal or protozoal infections, and also were traditionally as expectorants because of their stimulatory effects on bronchial secretions. Potassium iodide is indicated for use as a thyroid blocking agent following exposure to radioisotopes of iodine from a nuclear reactor accident.
    B) PHARMACOLOGY: Iodides are used by the thyroid gland in hormone production. Potassium iodide is taken up by the thyroid gland preventing absorption of radioactive iodide in cases where people are exposed in nuclear emergencies.
    C) EPIDEMIOLOGY: Overdose is rare.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: COMMON: POTASSIUM IODIDE can cause stomach upset, diarrhea, nausea, vomiting, stomach pain, skin rash and salivary gland swelling or tenderness. LESS COMMON: POTASSIUM IODIDE can cause gastrointestinal bleeding, confusion, dysrhythmias, numbness, pain or weakness in hands or feet, unusual fatigue, weakness or heaviness of legs, fever, and edema of neck or throat. Thyroid adenoma, goiter, and myxedema are also possible side effects. RARE: Iodism is a rare occurrence with iodides; however, it may develop during prolonged treatment or with the use of high doses. Symptoms include burning of mouth, severe headache, metallic taste, soreness of teeth and gums, symptoms of head cold, irritation of the eyes with swelling of the eyelids, unusual increase in salivation, acneform skin lesions in the seborrheic areas, and rarely, severe skin eruptions.
    E) WITH POISONING/EXPOSURE
    1) TOXICITY: Overdose of potassium iodide results in angioedema, laryngeal edema, and cutaneous hemorrhage. Very large doses could theoretically cause hyperkalemia and resulting dysrhythmias, but this has not been reported to date.
    0.2.5) CARDIOVASCULAR
    A) WITH THERAPEUTIC USE
    1) Periarteritis nodosa and dysrhythmias may occur with iodides.
    0.2.8) GASTROINTESTINAL
    A) WITH THERAPEUTIC USE
    1) Nausea, vomiting, abdominal pain and parotitis have been reported with potassium iodide use.
    0.2.14) DERMATOLOGIC
    A) WITH THERAPEUTIC USE
    1) Chronic oral administration can produce various cutaneous manifestations, including rash, erythema nodosum, polymorphic eruptions, urticaria, vasculitis, and petechia.
    0.2.16) ENDOCRINE
    A) WITH THERAPEUTIC USE
    1) Chronic iodide therapy has produced goiters, hypothyroidism, and rarely hyperthyroidism.
    0.2.19) IMMUNOLOGIC
    A) WITH THERAPEUTIC USE
    1) Acute hypersensitivity reactions including angioedema, Stevens Johnson syndrome, systemic vasculitis, and serum-sickness-like reactions may occur.
    0.2.20) REPRODUCTIVE
    A) Potassium iodide is classified as FDA pregnancy category D. RADIATION EMERGENCY: In 2001, the FDA issued a guideline for the use of potassium iodide in the event of a nuclear disaster with radioactive iodide. The recommendation from the FDA states pregnant women should be given KI for their own protection and that of the fetus since iodine (radioactive or not) readily crosses the placenta. Excess doses of stable iodide will have an effect on the fetus, therefore, repeat doses are not recommended. Sodium Iodide I-131 is classified as FDA pregnancy category X and sodium iodide I-123 is classified as pregnancy category C. Cretinism and goiter have been reported in children born to mothers chronically taking iodides during pregnancy.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, the manufacturers do not report any carcinogenic potential of potassium iodide. Long term studies to evaluate the carcinogenic potential of iodides have not been preformed.

Laboratory Monitoring

    A) Plasma iodide levels are not clinically useful or readily available.
    B) Monitor thyroid function in cases of severe overdose for decreased serum T4 levels and increased serum TSH levels.
    C) Monitor ECG for signs of potassium toxicity in cases of severe overdose with potassium iodide.
    D) Monitor serum electrolytes and renal function in patients with severe overdose.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treat acute allergic reactions with or without laryngeal edema with epinephrine and antihistamines. Treat serum-sickness-like reactions with antihistamines and corticosteroids. Treat cases of iodism with intravenous sodium chloride. Most symptomatic cases of thyrotoxicosis can be treated with beta-blockers; treatment with propylthiouracil I131 or surgery is rarely necessary. Overdose with potassium iodide can cause dysrhythmias due to potassium toxicity. Treat as necessary in overdose cases where potassium iodide is the suspected agent.
    C) DECONTAMINATION
    1) PREHOSPITAL: Consider using activated charcoal if ingestion was recent, a substantial ingestion, and the patient can protect their airway.
    2) HOSPITAL: Consider using activated charcoal if ingestion was recent, a substantial ingestion, and the patient can protect their airway.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in rare patients with serious toxicity.
    E) ANTIDOTE
    1) There is no antidote for iodide poisoning.
    F) HYPERSENSITIVITY REACTION
    1) MILD/MODERATE: Antihistamines, inhaled beta agonists, corticosteroids. SEVERE: Oxygen, aggressive airway management, antihistamines, epinephrine, corticosteroids, ECG monitoring, and IV fluids.
    G) SERUM SICKNESS DUE TO DRUG
    1) Treat serum-sickness-like reactions with antihistamines. Corticosteroids should be administered if antihistamines are not effective or if severe symptoms persist.
    H) THYROTOXICOSIS
    1) Discontinuing the inciting agent is usually the only therapy necessary in mild cases. Beta blockers may be used in symptomatic patients. RARELY propylthiouracil, I131, or surgery are necessary.
    I) HYPOTHYROIDISM
    1) Short-term administration of thyroid hormone supplements may hasten recovery. Discontinuation of the iodide source will usually result in restoration of normal thyroid function within several weeks.
    J) ENHANCED ELIMINATION
    1) A diuretic such as mannitol should be administered in treatment of chronic iodide poisoning to increase renal excretion of iodide. Fluids and sodium chloride intake will also hasten iodide excretion.
    K) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: All patients with overdose ingestions should be evaluated in a healthcare facility until symptoms are resolved.
    2) ADMISSION CRITERIA: Patient demonstrating acute allergic reaction, thyrotoxicosis, or severe toxicity should be admitted to the hospital.
    3) CONSULT CRITERIA: Consult a medical toxicologist or Poison Center for assistance in managing patients with severe toxicity or in whom the diagnosis is unclear.
    L) PITFALLS
    1) Ingestions involving potassium iodide can cause potassium toxicity.
    M) PHARMACOKINETICS
    1) Iodides are readily absorbed in the GI tract and distribute widely throughout extracellular fluid of the thyroid gland. The majority of excretion is through the kidneys.
    N) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that may cause similar effects, such as iodine, which is more toxic.

Range Of Toxicity

    A) TOXICITY: A specific toxic dose for iodides has not been established. Up to 10 grams of sodium iodide has been administered IV without toxicity. Doses up to 6 grams/day of potassium iodide have been used for dermatological fungal infections. Children received one half or one third of this dose. THERAPEUTIC DOSES: POTASSIUM IODIDE (RADIATION EMERGENCY) ADULTS: 130 mg once daily. CHILDREN: OVER 12 YEARS TO 18 YEARS, WEIGHING AT LEAST 150 POUNDS: 130 mg once daily. OVER 12 YEARS TO 18 YEARS, WEIGHING LESS THAN 150 POUNDS: 65 mg once daily. OVER 3 YEARS TO 12 YEARS: 65 mg once daily. OVER 1 MONTH TO 3 YEARS: 32.5 mg once daily. AT BIRTH TO 1 MONTH : 16.25 mg once daily.

Clinical Effects

Summary Of Exposure

    A) USES: Iodides have been utilized to treat iodine disorders, hyperthyroidism, bacterial, fungal or protozoal infections, and also were traditionally as expectorants because of their stimulatory effects on bronchial secretions. Potassium iodide is indicated for use as a thyroid blocking agent following exposure to radioisotopes of iodine from a nuclear reactor accident.
    B) PHARMACOLOGY: Iodides are used by the thyroid gland in hormone production. Potassium iodide is taken up by the thyroid gland preventing absorption of radioactive iodide in cases where people are exposed in nuclear emergencies.
    C) EPIDEMIOLOGY: Overdose is rare.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: COMMON: POTASSIUM IODIDE can cause stomach upset, diarrhea, nausea, vomiting, stomach pain, skin rash and salivary gland swelling or tenderness. LESS COMMON: POTASSIUM IODIDE can cause gastrointestinal bleeding, confusion, dysrhythmias, numbness, pain or weakness in hands or feet, unusual fatigue, weakness or heaviness of legs, fever, and edema of neck or throat. Thyroid adenoma, goiter, and myxedema are also possible side effects. RARE: Iodism is a rare occurrence with iodides; however, it may develop during prolonged treatment or with the use of high doses. Symptoms include burning of mouth, severe headache, metallic taste, soreness of teeth and gums, symptoms of head cold, irritation of the eyes with swelling of the eyelids, unusual increase in salivation, acneform skin lesions in the seborrheic areas, and rarely, severe skin eruptions.
    E) WITH POISONING/EXPOSURE
    1) TOXICITY: Overdose of potassium iodide results in angioedema, laryngeal edema, and cutaneous hemorrhage. Very large doses could theoretically cause hyperkalemia and resulting dysrhythmias, but this has not been reported to date.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH THERAPEUTIC USE
    1) FEVER: Iodides may cause transient fevers (Prod Info SSKI(R) oral solution, 1999; Horn & Kabins, 1972; Steffen, 1965). One study reported a case of iodide-induced fever that lasted 15 years (Kurtz & Aber, 1982).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Periarteritis nodosa and dysrhythmias may occur with iodides.
    3.5.2) CLINICAL EFFECTS
    A) POLYARTERITIS NODOSA
    1) WITH THERAPEUTIC USE
    a) Periarteritis nodosa has been associated with the use of iodides (Wahlberg & Wikstroem, 1963; Davies, 1969).
    B) CONDUCTION DISORDER OF THE HEART
    1) WITH THERAPEUTIC USE
    a) Dysrhythmias have been reported with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) SPUTUM ABNORMAL - AMOUNT
    1) WITH THERAPEUTIC USE
    a) Increases in bronchial secretions may be present with use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) ASTHENIA
    1) WITH THERAPEUTIC USE
    a) Asthenia, numbness, and pain in the hands and feet have been reported with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    B) CLOUDED CONSCIOUSNESS
    1) WITH THERAPEUTIC USE
    a) Confusion has been reported with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    C) FATIGUE
    1) WITH THERAPEUTIC USE
    a) Unusual fatigue has been reported with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    D) HEAVY FEELING
    1) WITH THERAPEUTIC USE
    a) Heaviness of legs have been reported with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Nausea, vomiting, abdominal pain and parotitis have been reported with potassium iodide use.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH THERAPEUTIC USE
    a) Nausea and vomiting are reported as adverse effects of potassium iodide(Prod Info SSKI(R) oral solution, 1999).
    B) ABDOMINAL PAIN
    1) WITH THERAPEUTIC USE
    a) Abdominal pain is reported as a common adverse effect of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    C) DIARRHEA
    1) WITH THERAPEUTIC USE
    a) Diarrhea is reported as a common adverse effect of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    D) TASTE SENSE ALTERED
    1) WITH THERAPEUTIC USE
    a) Metallic taste may be noted in cases of iodism, which can occur with iodides(Prod Info SSKI(R) oral solution, 1999).
    E) GASTROINTESTINAL HEMORRHAGE
    1) WITH THERAPEUTIC USE
    a) Gastrointestinal bleeding has been reported with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    F) SWELLING OF SALIVARY GLAND
    1) WITH THERAPEUTIC USE
    a) Tenderness and swelling of salivary glands are reported as common adverse effects with therapeutic use of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    G) PAROTITIS
    1) WITH THERAPEUTIC USE
    a) PAROTITIS has been caused by iodides. Onset of symptoms usually disappears in 12 hours of exposure with a duration of less than 72 hours. There may be involvement of the submandibular (an adenitis) and laryngeal edema (Gilman et al, 1985; Katz et al, 1986).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ANION GAP
    1) CASE REPORT: Negative ion gap with mild renal insufficiency was reported in a patient who had ingested 180 mEq of iodide. No measure of plasma iodide was done (Fischman et al, 1978).

Dermatologic

    3.14.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Chronic oral administration can produce various cutaneous manifestations, including rash, erythema nodosum, polymorphic eruptions, urticaria, vasculitis, and petechia.
    3.14.2) CLINICAL EFFECTS
    A) BULLOUS ERUPTION
    1) WITH THERAPEUTIC USE
    a) Bullous pemphigoid has been reported with therapeutic use of potassium iodide (Sterling & Heymann, 2000).
    b) IODODERMA: Topical administration can produce a nonspecific papulovesicular lesion. Iododerma after chronic oral administration can produce carbuncular lesions, which progress to scarring, erythema nodosum, or vasculitis. Other lesions include polymorphic eruptions, urticaria, and petechia (Burnett, 1989; Prod Info SSKI(R) oral solution, 1999; Sterling & Heymann, 2000).
    B) BLEEDING
    1) WITH POISONING/EXPOSURE
    a) Cutaneous hemorrhage has been reported in cases involving potassium iodide overdose (Prod Info SSKI(R) oral solution, 1999).

Endocrine

    3.16.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Chronic iodide therapy has produced goiters, hypothyroidism, and rarely hyperthyroidism.
    3.16.2) CLINICAL EFFECTS
    A) HYPERTHYROIDISM
    1) WITH THERAPEUTIC USE
    a) Iodides can induce thyrotoxicosis in selected cases, but is probably quite rare, although occurring more commonly in Europe. Onset may be up to 4 months after initiation of potassium iodide therapy and may last from 1 to 6 months (Fradkin & Wolff, 1983; Klein & Levey, 1983; Yoshinari et al, 1988) .
    b) Hyperthyroidism can occur with potassium iodide (Sterling & Heymann, 2000).
    B) GOITER
    1) WITH THERAPEUTIC USE
    a) CASE SERIES: In one study, 47 of 55 patients on long-term daily iodide therapy for cystic fibrosis of the pancreas developed goiters. Onset was after 2 to 3 years of therapy usually but ranged from 3 months to 12 years (Dolan & Gibson, 1971). Goiter can also occur with therapeutic doses of potassium iodide (Prod Info SSKI(R) oral solution, 1999; Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005).
    b) PEDIATRIC: Fetal and neonatal goiter are possible with maternal use of potassium iodide (Sterling & Heymann, 2000; Galina et al, 1962).
    C) HYPOTHYROIDISM
    1) WITH THERAPEUTIC USE
    a) SUMMARY: Hypothyroidism may occur after iodide use (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005; Sterling & Heymann, 2000) .
    b) CASE SERIES: Hypothyroidism was noted in 14 of 55 patients receiving long-term iodide therapy for cystic fibrosis (Dolan & Gibson, 1971), as well as other patients on therapeutic iodides (Gomolin, 1987; Johnson & Rapini, 1988; Bona et al, 1988).
    c) MECHANISM: Hypothyroidism is caused by inhibition of thyroid hormone synthesis at a critical level of iodide administration, called the "Wolff-Chaikoff effect". Normal subjects will adapt or "escape" from this inhibitory effect with continued administration of iodide (Johnson & Rapini, 1988).
    d) RISK FACTORS: Patients who are less likely to adapt to the Wolff-Chaikoff effect and are at risk of developing hypothyroidism include patients with Graves' disease, goiter, or Hashimoto's thyroiditis. Susceptibility correlates with higher baseline TSH serum concentrations (Clark et al, 1990).
    D) THYROID ADENOMA
    1) WITH THERAPEUTIC USE
    a) Thyroid adenoma has been reported as an adverse effect of potassium iodide (Prod Info SSKI(R) oral solution, 1999).
    E) MYXEDEMA
    1) WITH THERAPEUTIC USE
    a) Myxedema has been reported as an adverse effect of potassium iodide (Prod Info SSKI(R) oral solution, 1999).

Immunologic

    3.19.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Acute hypersensitivity reactions including angioedema, Stevens Johnson syndrome, systemic vasculitis, and serum-sickness-like reactions may occur.
    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH THERAPEUTIC USE
    a) Reactions including angioedema, urticaria, cutaneous and mucosal hemorrhages, serum-sickness-like reaction (fever, arthralgia, lymphadenopathy, eosinophilia), lymphadenitis, and systemic vasculitis may occur when applied topically or administered systemically with potassium iodide(Prod Info SSKI(R) oral solution, 1999; Eeckhout et al, 1987).
    B) STEVENS-JOHNSON SYNDROME
    1) WITH THERAPEUTIC USE
    a) Stevens Johnson Syndrome is associated with the use of iodides (Araugo & Flowers, 1984).
    C) SWELLING
    1) WITH THERAPEUTIC USE
    a) Swelling of the neck and throat may occur with therapeutic use of potassium iodide(Prod Info SSKI(R) oral solution, 1999).
    2) WITH POISONING/EXPOSURE
    a) Angioedema and laryngeal edema may be present in cases involving potassium iodide overdose (Prod Info SSKI(R) oral solution, 1999).

Reproductive

    3.20.1) SUMMARY
    A) Potassium iodide is classified as FDA pregnancy category D. RADIATION EMERGENCY: In 2001, the FDA issued a guideline for the use of potassium iodide in the event of a nuclear disaster with radioactive iodide. The recommendation from the FDA states pregnant women should be given KI for their own protection and that of the fetus since iodine (radioactive or not) readily crosses the placenta. Excess doses of stable iodide will have an effect on the fetus, therefore, repeat doses are not recommended. Sodium Iodide I-131 is classified as FDA pregnancy category X and sodium iodide I-123 is classified as pregnancy category C. Cretinism and goiter have been reported in children born to mothers chronically taking iodides during pregnancy.
    3.20.3) EFFECTS IN PREGNANCY
    A) GOITER
    1) Iodides are readily diffused across the placenta. Neonatal deaths from respiratory distress secondary to goiter have been reported (Galina et al, 1962; Visconti, 1981).
    B) HYPOTHYROIDISM
    1) CRETINISM: Iodides alone should not be used in pregnancy since they are not reliable or effective for long-term management of hyperthyroidism and severe fetal complications such as cretinism and death from obstructive goiter have resulted (Herbst & Selenkow, 1965).
    C) PREGNANCY CATEGORY
    1) POTASSIUM IODIDE: D (Prod Info SSKI(R) oral solution, 1999). RADIATION EMERGENCY: In 2001, the FDA issued a guideline that contains information for the administration of potassium iodide in the event of a nuclear disaster with radioactive iodide. The recommendation states pregnant women should be given KI for their own protection and that of the fetus since iodine (radioactive or not) readily crosses the placenta. Excess doses of stable iodide will have an effect on the fetus, therefore, repeat doses are not recommended (Center for Drug Evaluation and Research, 2001).
    2) SODIUM IODIDE I-131: X (Prod Info Sodium Iodide I-131 oral solution, 2006).
    3) SODIUM IODIDE I-123: C (Prod Info sodium iodide I 123 diagnostic oral capsules, 2007).
    4) INDOCYANINE GREEN: There are no data on the use of indocyanine green in pregnant women and animal studies have not been performed. It is unknown if indocyanine green use during pregnancy can affect reproduction capacity or cause fetal harm. Due to the lack of human safety information, indocyanine green should be used in pregnant women only if necessary (Prod Info IC-GREEN(R) intravenous injection, 2015).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Stable iodine is present in breast milk and poses a risk of hypothyroidism in nursing neonates (Center for Drug Evaluation and Research, 2001). Potassium iodide can also cause skin rash in a nursing infant (Prod Info SSKI(R) oral solution, 1999). RADIATION EMERGENCY: In 2001, the FDA issued a guideline that contains information for the administration of potassium iodide in pregnant and lactating women during a nuclear disaster with radioactive iodide. The recommendation states lactating women should be given KI for their own protection and to potentially reduce the content of radioactive iodide in breast milk. Both mother and child should directly receive KI in an emergency situation. Repeat dosing of KI in a nursing mother should be avoided due to risk of hypothyroidism in the nursing infant; however, during continued exposure to a severe contamination, the nursing infant should be monitored while repeat doses of KI are administered to the mother (Center for Drug Evaluation and Research, 2001).
    2) INDOCYANINE GREEN: It is unknown whether indocyanine green is excreted into human breast milk. Exercise caution when administering to a lactating woman (Prod Info IC-GREEN(R) intravenous injection, 2015).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, the manufacturers do not report any carcinogenic potential of potassium iodide. Long term studies to evaluate the carcinogenic potential of iodides have not been preformed.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, the manufacturers do not report any carcinogenic potential of potassium iodide. (Prod Info IOSAT(TM) oral tablets, 2005; Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info SSKI(R) oral solution, 1999). Long term studies to evaluate the carcinogenic potential of iodides have not been preformed.
    3.21.4) ANIMAL STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, the manufacturers do not report any carcinogenic potential of potassium iodide. (Prod Info IOSAT(TM) oral tablets, 2005; Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info SSKI(R) oral solution, 1999). Long term studies to evaluate the carcinogenic potential of iodides have not been preformed.

Genotoxicity

    A) At the time of this review, the manufacturer does not report any mutagenic potential of potassium iodide(Prod Info IOSAT(TM) oral tablets, 2005; Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info SSKI(R) oral solution, 1999). Long term studies to evaluate the mutagenic potential of iodides have not been preformed.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma iodide levels are not clinically useful or readily available.
    B) Monitor thyroid function in cases of severe overdose for decreased serum T4 levels and increased serum TSH levels.
    C) Monitor ECG for signs of potassium toxicity in cases of severe overdose with potassium iodide.
    D) Monitor serum electrolytes and renal function in patients with severe overdose.
    4.1.2) SERUM/BLOOD
    A) Monitor serum electrolytes and renal function in patients with severe overdose.
    B) ENDOCRINE
    1) Monitor thyroid function in cases of severe overdose for decreased serum T4 levels and increased serum TSH levels.
    2) Protein bound iodine (PBI) will be elevated for up to three weeks after ingestion of pharmacologic doses of inorganic iodides while more specific measures of circulating thyroxine may not be affected.
    C) LABORATORY INTERFERENCE
    1) Some laboratory chloride determinations are performed with the Technicon Station System, a potentiometric measurement. This system may give an extremely high serum chloride reading and negative anion gap in the presence of high serum iodides (Fischman et al, 1978).
    4.1.4) OTHER
    A) OTHER
    1) ECG
    a) Monitor ECG for signs of potassium toxicity in cases of severe overdose with potassium iodide.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patient demonstrating acute allergic reaction, thyrotoxicosis, or severe toxicity should be admitted to the hospital.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or Poison Center for assistance in managing patients with severe toxicity or in whom the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) All patients with overdose ingestions should be evaluated in a healthcare facility until symptoms are resolved.

Monitoring

    A) Plasma iodide levels are not clinically useful or readily available.
    B) Monitor thyroid function in cases of severe overdose for decreased serum T4 levels and increased serum TSH levels.
    C) Monitor ECG for signs of potassium toxicity in cases of severe overdose with potassium iodide.
    D) Monitor serum electrolytes and renal function in patients with severe overdose.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL:
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) There is little or no information concerning how well iodides are adsorbed by activated charcoal. Iodine is absorbed in vitro (Mitchell et al, 1989; Rausch, 1935).
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Plasma iodide levels are not clinically useful or widely available.
    2) Monitor thyroid function in cases of severe overdose for decreased serum T4 levels and increased serum TSH levels.
    3) Monitor ECG for signs of potassium toxicity in cases of severe overdose with potassium iodide.
    4) Monitor serum electrolytes and renal function in patients with severe overdose.
    B) ACUTE ALLERGIC REACTION
    1) SUMMARY
    a) Mild to moderate allergic reactions may be treated with antihistamines with or without inhaled beta adrenergic agonists, corticosteroids or epinephrine. Treatment of severe anaphylaxis also includes oxygen supplementation, aggressive airway management, epinephrine, ECG monitoring, and IV fluids.
    2) BRONCHOSPASM
    a) ALBUTEROL
    1) ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007). CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 mg/kg (up to 10 mg) every 1 to 4 hours as needed, or 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    3) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm.
    b) PREDNISONE: ADULT: 40 to 80 milligrams/day. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 to 2 divided doses divided twice daily (National Heart,Lung,and Blood Institute, 2007).
    4) MILD CASES
    a) DIPHENHYDRAMINE
    1) SUMMARY: Oral diphenhydramine, as well as other H1 antihistamines can be used as indicated (Lieberman et al, 2010).
    2) ADULT: 50 milligrams orally, or 10 to 50 mg intravenously at a rate not to exceed 25 mg/min or may be given by deep intramuscular injection. A total of 100 mg may be administered if needed. Maximum daily dosage is 400 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    3) CHILD: 5 mg/kg/24 hours or 150 mg/m(2)/24 hours. Divided into 4 doses, administered intravenously at a rate not exceeding 25 mg/min or by deep intramuscular injection. Maximum daily dosage is 300 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    5) MODERATE CASES
    a) EPINEPHRINE: INJECTABLE SOLUTION: It should be administered early in patients by IM injection. Using a 1:1000 (1 mg/mL) solution of epinephrine. Initial Dose: 0.01 mg/kg intramuscularly with a maximum dose of 0.5 mg in adults and 0.3 mg in children. The dose may be repeated every 5 to 15 minutes, if no clinical improvement. Most patients respond to 1 or 2 doses (Nowak & Macias, 2014).
    6) SEVERE CASES
    a) EPINEPHRINE
    1) INTRAVENOUS BOLUS: ADULT: 1 mg intravenously as a 1:10,000 (0.1 mg/mL) solution; CHILD: 0.01 mL/kg intravenously to a maximum single dose of 1 mg given as a 1:10,000 (0.1 mg/mL) solution. It can be repeated every 3 to 5 minutes as needed. The dose can also be given by the intraosseous route if IV access cannot be established (Lieberman et al, 2015). ALTERNATIVE ROUTE: ENDOTRACHEAL ADMINISTRATION: If IV/IO access is unavailable. DOSE: ADULT: Administer 2 to 2.5 mg of 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube. CHILD: DOSE: 0.1 mg/kg to a maximum of 2.5 mg administered as a 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube (Lieberman et al, 2015).
    2) INTRAVENOUS INFUSION: Intravenous administration may be considered in patients poorly responsive to IM or SubQ epinephrine. An epinephrine infusion may be prepared by adding 1 mg (1 mL of 1:1000 (1 mg/mL) solution) to 250 mL D5W, yielding a concentration of 4 mcg/mL, and infuse this solution IV at a rate of 1 mcg/min to 10 mcg/min (maximum rate). CHILD: A dosage of 0.01 mg/kg (0.1 mL/kg of a 1:10,000 (0.1 mg/mL) solution up to 10 mcg/min (maximum dose 0.3 mg) is recommended for children (Lieberman et al, 2010). Careful titration of a continuous infusion of IV epinephrine, based on the severity of the reaction, along with a crystalloid infusion can be considered in the treatment of anaphylactic shock. It appears to be a reasonable alternative to IV boluses, if the patient is not in cardiac arrest (Vanden Hoek,TLet al,null).
    7) AIRWAY MANAGEMENT
    a) OXYGEN: 5 to 10 liters/minute via high flow mask.
    b) INTUBATION: Perform early if any stridor or signs of airway obstruction.
    c) CRICOTHYROTOMY: Use if unable to intubate with complete airway obstruction (Vanden Hoek,TLet al,null).
    d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
    e) ALBUTEROL: ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007).
    f) ALBUTEROL: CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    8) MONITORING
    a) CARDIAC MONITOR: All complicated cases.
    b) IV ACCESS: Routine in all complicated cases.
    9) HYPOTENSION
    a) If hypotensive give 500 to 2000 milliliters crystalloid initially (20 milliliters/kilogram in children) and titrate to desired effect (stabilization of vital signs, mentation, urine output); adults may require up to 6 to 10 L/24 hours. Central venous or pulmonary artery pressure monitoring is recommended in patients with persistent hypotension.
    1) VASOPRESSORS: Should be used in refractory cases unresponsive to repeated doses of epinephrine and after vigorous intravenous crystalloid rehydration (Lieberman et al, 2010).
    2) DOPAMINE: Initial Dose: 2 to 20 micrograms/kilogram/minute intravenously; titrate to maintain systolic blood pressure greater than 90 mm Hg (Lieberman et al, 2010).
    10) H1 and H2 ANTIHISTAMINES
    a) SUMMARY: Antihistamines are second-line therapy and are used as supportive therapy and should not be used in place of epinephrine (Lieberman et al, 2010).
    1) DIPHENHYDRAMINE: ADULT: 25 to 50 milligrams via a slow intravenous infusion or IM. PEDIATRIC: 1 milligram/kilogram via slow intravenous infusion or IM up to 50 mg in children (Lieberman et al, 2010).
    b) RANITIDINE: ADULT: 1 mg/kg parenterally; CHILD: 12.5 to 50 mg parenterally. If the intravenous route is used, ranitidine should be infused over 10 to 15 minutes or diluted in 5% dextrose to a volume of 20 mL and injected over 5 minutes (Lieberman et al, 2010).
    c) Oral diphenhydramine, as well as other H1 antihistamines, can also be used as indicated (Lieberman et al, 2010).
    11) DYSRHYTHMIAS
    a) Dysrhythmias and cardiac dysfunction may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine) (Vanden Hoek,TLet al,null). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.
    12) OTHER THERAPIES
    a) There have been a few reports of patients with anaphylaxis, with or without cardiac arrest, that have responded to vasopressin therapy that did not respond to standard therapy. Although there are no randomized controlled trials, other alternative vasoactive therapies (ie, vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in patients in cardiac arrest secondary to anaphylaxis that do not respond to epinephrine (Vanden Hoek,TLet al,null).
    C) SERUM SICKNESS DUE TO DRUG
    1) DIPHENHYDRAMINE/ADULT
    a) DOSE: 10 to 50 mg intravenously at a rate not exceeding 25 mg/minute or deep intramuscularly; maximum dose: 100 mg/dose; maximum daily dose: 400 mg/day (Prod Info diphenhydramine hcl injection, 2006).
    2) DIPHENHYDRAMINE/PEDIATRIC
    a) DOSE: 5 mg/kg/day or 150 mg/m(2)/day intravenously divided into 4 doses at a rate not exceeding 25 mg/minute, or deep intramuscularly; maximum daily dose: 300 mg/day. Not recommended in premature infants and neonates (Prod Info diphenhydramine hcl injection, 2006).
    3) Corticosteroids should be administered if antihistamines are not effective or if severe symptoms persist.
    D) DIURESIS
    1) A diuretic such as mannitol should be administered in treatment of chronic iodide poisoning to increase renal excretion of iodide. Fluids and sodium chloride intake will also hasten iodide excretion.
    E) THYROTOXICOSIS
    1) Discontinuing the inciting agent is usually the only therapy necessary in mild cases. Beta blockers may be used in symptomatic patients. RARELY propylthiouracil, I131, or surgery are necessary.
    F) HYPOTHYROIDISM
    1) Discontinuation of the iodide source will usually result in restoration of normal thyroid function within several weeks (Gomolin, 1987). Short-term administration of thyroid hormone supplements may hasten recovery (Johnson & Rapini, 1988).

Enhanced Elimination

    A) DIURESIS
    1) A diuretic such as mannitol should be administered in treatment of chronic iodide poisoning to increase renal excretion of iodide. Fluids and sodium chloride intake will also hasten iodide excretion. (Prod Info SSKI(R) oral solution, 1999).

Range Of Toxicity

Summary

    A) TOXICITY: A specific toxic dose for iodides has not been established. Up to 10 grams of sodium iodide has been administered IV without toxicity. Doses up to 6 grams/day of potassium iodide have been used for dermatological fungal infections. Children received one half or one third of this dose. THERAPEUTIC DOSES: POTASSIUM IODIDE (RADIATION EMERGENCY) ADULTS: 130 mg once daily. CHILDREN: OVER 12 YEARS TO 18 YEARS, WEIGHING AT LEAST 150 POUNDS: 130 mg once daily. OVER 12 YEARS TO 18 YEARS, WEIGHING LESS THAN 150 POUNDS: 65 mg once daily. OVER 3 YEARS TO 12 YEARS: 65 mg once daily. OVER 1 MONTH TO 3 YEARS: 32.5 mg once daily. AT BIRTH TO 1 MONTH : 16.25 mg once daily.

Therapeutic Dose

    7.2.1) ADULT
    A) POTASSIUM IODIDE: The recommended dose of potassium iodide for thyroid protection 130 mg once daily (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005). Doses up to 6 grams/day of potassium iodide have been used for dermatological fungal infections (Restrepo, 1994).
    B) INDOCYANINE GREEN: The recommended dose for indicator dilution studies is 5 mg IV. For hepatic function studies, the dose is 0.5 mg/kg of body weight. For ophthalmic angiography studies, the recommended dose is 40 mg in 2 mL of Sterile Water for Injection USP; not to exceed 2 mg/kg body-weight; doses are usually injected in a mL volume (Prod Info IC-GREEN(R) intravenous injection, 2015).
    7.2.2) PEDIATRIC
    A) POTASSIUM IODIDE (RADIATION EMERGENCY):
    1) OVER 12 YEARS TO 18 YEARS, WEIGHING AT LEAST 68 KG: 130 mg once daily (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005).
    2) OVER 12 YEARS TO 18 YEARS, WEIGHING LESS THAN 68 KG: 65 mg once daily (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005).
    3) OVER 3 YEARS TO 12 YEARS: 65 mg once daily (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005).
    4) OVER 1 MONTH TO 3 YEARS: 32.5 mg once daily (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005).
    5) AT BIRTH TO 1 MONTH : 16.25 mg once daily (Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005).
    B) Doses up to 6 grams/day of potassium iodide have been used for dermatological fungal infections. Children received one half or one third of this dose (Restrepo, 1994).
    C) INDOCYANINE GREEN
    1) CHILDREN: The recommended dose for indicator dilution studies is 2.5 mg (Prod Info IC-GREEN(R) intravenous injection, 2015).
    2) INFANTS: The recommended dose for indicator dilution studies is 1.25 mg (Prod Info IC-GREEN(R) intravenous injection, 2015).

Minimum Lethal Exposure

    A) CASE REPORTS
    1) At least one fatal case of periarteritis nodosa due to iodide ingestion has been described (Wahlberg & Wikstroem, 1963).

Maximum Tolerated Exposure

    A) Up to 10 grams of sodium iodide has been administered IV without toxicity (Bouchard, 2006).
    B) Doses up to 6 grams per day of potassium iodide have been used for dermatological fungal infections(Restrepo, 1994).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) POTASSIUM IODIDE
    B) SODIUM IODIDE
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 430 mg/kg ((RTECS, 2000))
    2) LD50- (ORAL)MOUSE:
    a) 1 g/kg ((RTECS, 2000))
    3) LD50- (ORAL)RAT:
    a) 4340 mg/kg ((RTECS, 2000))

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Potassium iodide prevents the absorption of radioactive iodide (I-131) in the thyroid gland after exposure (Weiss & Landauer, 2009; Prod Info THYROSHIELD(TM) oral solution, 2005; Prod Info IOSAT(TM) oral tablets, 2005). Potassium iodide has been utilized in an off-label manner to treat the following dermatological disorders: Behcet's syndrome, erythema multiforme, Wegener's granulomatosis, panniculitis, neutrophilic dermatosis or dermatological infections with a bacterial or fungal origin. The precise mechanism of action for efficacy against inflammatory dermatoses or dermatological infections is unknown (Sterling & Heymann, 2000).
    B) Iodides in small quantities (about 150 mg/day) are ingested normally and plasma inorganic iodide concentration is normally less than 10 mg/L (about 10 to 20% of total plasma iodine concentration). Distribution is throughout extracellular body water with concentration in the thyroid gland and salivary secretions.
    C) Iodides are also used to increase the solubility of iodines such as in iodine tinctures.

Physicochemical

Physical Characteristics

    A) INDOCYANINE GREEN is a water-soluble, green powder (Prod Info IC-GREEN(R) intravenous injection, 2015). It is also soluble in methanol and essentially insoluble in other organic solvents (Reynolds, 1990).
    B) POTASSIUM IODIDE is a colorless, opaque, or white crystals or crystalline powder with no odor, is slightly hydroscopic.
    C) SODIUM IODIDE is a colorless, odorless, crystal or whitish powder that is deliquescent in moist air. Sodium iodide develops a brownish color upon decomposition.

Ph

    A) INDOCYANINE GREEN: Approximately 6.5 (Prod Info IC-GREEN(R) intravenous injection, 2015)

Molecular Weight

    A) INDOCYANINE GREEN: 774.96 (Prod Info IC-GREEN(R) intravenous injection, 2015)
    B) POTASSIUM IODIDE: 166.0
    C) SODIUM IODIDE: 149.9

References

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