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Introduction

The chief use of iodine is for its antiseptic property. It is bactericidal, sporicidal, protozoacidal, cysticidal, and virucidal. Liquid formulations of iodine are usually prepared in ethanol (tincture of iodine) to increase solubility and concentration. Lugol solution is 5% iodine and 10% iodide in water. Iodoform is triiodomethane (CHI3). Iodophors such as povidone-iodine (Betadine) consist of iodine linked to a large-molecular-weight molecule. These are usually less toxic owing to the slow release of iodine from the carrier molecule. Radioactive iodine is used in the treatment of thyroid cancer. The antiarrhythmic drug amiodarone releases iodine and may cause either thyrotoxicosis or hypothyroidism after prolonged use. Iodine is also used in the manufacture of dyes and photographic reagents. Table salt is fortified with iodine.

Depends on the product and the route of exposure. Iodophors and iodoform are generally less toxic, as iodine is released more slowly. However, significant systemic absorption can occur in patients receiving povidone-iodine treatment on areas of skin breakdown or when used for internal irrigation of an infected area or as a dye.

  1. Iodine vapor. The ACGIH-recommended workplace ceiling limit (TLV-C) for iodine vapor is 0.1 ppm (1 mg/m3). The air level considered immediately dangerous to life or health (IDLH) is 2 ppm.
  2. Skin and mucous membranes. Strong iodine tincture (7% iodine and 5% potassium iodide in 83% ethanol) may cause burns, but USP iodine tincture (2% iodine and 2% sodium iodide in 50% ethanol) is not likely to produce corrosive damage. Povidone-iodine 10% can also cause burns especially with prolonged exposure (1-8 hours). Systemic absorption of iodine is more likely to occur after an acute application of strong iodine tincture or after chronic applications of less concentrated products; however, it can also occur from internal applications of the 2% povidone-iodine.
  3. Ingestion. Reported fatal doses vary from 200 mg to more than 20 g of iodine; an estimated mean lethal dose is approximately 2-4 g of free iodine. USP iodine tincture contains 100 mg of iodine per 5 mL, and strong iodine tincture contains 350 mg of iodine per 5 mL. Iodine ointment contains 4% iodine. Povidone-iodine 10% contains 1% free iodine. Consider ethanol toxicity with large exposures.

Mechanism of Toxicity

Toxicity can occur through skin or mucosal absorption, ingestion, or inhalation. When ingested, iodine can cause severe corrosive injury to the GI tract owing to its oxidative properties. In the body, iodine is converted rapidly to iodide and stored in the thyroid gland.

Clinical Presentation

The manifestations of acute iodine ingestion are related largely to the corrosive effect on mucous membranes and the GI tract.

  1. Inhalation of iodine vapor can cause severe pulmonary irritation, which can lead to pulmonary edema.
  2. Skin and eye exposures may result in severe corrosive burns.
  3. Ingestion can cause corrosive gastroenteritis with vomiting, hematemesis, and diarrhea, which can result in significant volume loss and circulatory collapse. Pharyngeal swelling and glottic edema have been reported. Mucous membranes are usually stained brown, and the vomitus may be blue if starchy foods are already present in the stomach.
  4. Chronic ingestions or absorption may result in hypothyroidism and goiter, or hyperthyroidism. Systemic absorption has also caused hypernatremia, metabolic acidosis, increased osmolality and hyperchloremia (due to iodine's interference with the chloride assay). Iodides cross the placenta, and neonatal hypothyroidism and death from respiratory distress secondary to goiter have been reported.
  5. Chronic iodine deficiency can lead to hypothyroidism and goiter.

Diagnosis

Is based on a history of exposure and evidence of corrosive injury. Mucous membranes are usually stained brown, and vomitus may be blue.

  1. Specific levels. Blood levels are not clinically useful but may confirm exposure
  2. Other useful laboratory studies for serious corrosive injury include CBC, electrolytes, BUN, and creatinine. For inhalational exposure, arterial blood gases or pulse oximetry and chest radiography are useful.

Treatment

  1. Emergency and supportive measures
    1. Maintain an open airway and perform endotracheal intubation if airway edema is progressive. Treat bronchospasm and pulmonary edema if they occur.
    2. Treat fluid loss from gastroenteritis aggressively with IV crystalloid solutions.
    3. If corrosive injury to the esophagus or stomach is suspected, consult a gastroenterologist to perform endoscopy.
  2. Specific drugs and antidotes. Sodium thiosulfate may convert iodine to iodide and tetrathionate but is not recommended for intravenous use because iodine is converted rapidly to iodide in the body.
  3. Decontamination
    1. Inhalation. Remove the victim from exposure.
    2. Skin and eyes. Remove contaminated clothing and flush exposed skin with water. Irrigate exposed eyes copiously with tepid water or saline for at least 15 minutes.
    3. Ingestion. Do not induce vomiting because of the corrosive effects of iodine. Administer a starchy food (potato, flour, or cornstarch) or milk to lessen GI irritation. Activated charcoal does bind iodine in vitro but is of unknown efficacy.
  4. Enhanced elimination. Since iodine is converted rapidly to iodide once absorbed into the circulation, enhanced drug removal is usually unnecessary. However, hemodialysis was performed (calculated dialysis clearance 120 mL/min) in a patient with hepatic and renal dysfunction and high blood levels (>1,000 mcg/dL) after mediastinal irrigation with povidone-iodine.