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Antiseptics are chemicals that kill bacteria or inhibit growth. Iodine and iodophors like povidone-iodine are commonly used antiseptics but can cause toxicity. Iodine toxicity may cause gastrointestinal irritation, metabolic acidosis, and interference with cellular metabolism. Chronic exposure can also impact thyroid function and cause hypothyroidism or hyperthyroidism. Treatment focuses on supportive care, gastric decontamination, and enhancing elimination of the chemical from the body.
Antiseptics are chemicals that kill bacteria or inhibit growth. Iodine and iodophors like povidone-iodine are commonly used antiseptics but can cause toxicity. Iodine toxicity may cause gastrointestinal irritation, metabolic acidosis, and interference with cellular metabolism. Chronic exposure can also impact thyroid function and cause hypothyroidism or hyperthyroidism. Treatment focuses on supportive care, gastric decontamination, and enhancing elimination of the chemical from the body.
Antiseptics are chemicals that kill bacteria or inhibit growth. Iodine and iodophors like povidone-iodine are commonly used antiseptics but can cause toxicity. Iodine toxicity may cause gastrointestinal irritation, metabolic acidosis, and interference with cellular metabolism. Chronic exposure can also impact thyroid function and cause hypothyroidism or hyperthyroidism. Treatment focuses on supportive care, gastric decontamination, and enhancing elimination of the chemical from the body.
Antiseptics are chemicals that are applied to living tissues to kill
bacteria or inhibit their growth. Free iodine (I2) has significant concentration-dependent tissue and systemic toxicity. Iodide (I-) causes a negative anion gap and is associated with thyroid disorders, salivary gland disorders, and dermal reactions. Most acute exposures to boric acid are benign. Severe toxicity results from chronic exposure or massive exposure. Characteristic symptoms of boric acid toxicity include green- blue vomit and diarrhea, erythroderma with desquamation, and central nervous system (CNS), renal, bone marrow, and hepatic injury. Iodophors, Iodine, and Iodide Iodophors such as povidone-iodine (Betadine) are complex detergent- based solutions of iodide (I-), free iodine (I2), and iodine bound to povidone, a carrier molecule that limits the availability of free iodine. The toxicity of iodine is much greater than that of iodide. Most iodophors contain only 80 to 120 g/100 mL of free iodine, making them much less toxic than older iodine preparations such as tincture of iodine, which contains 2 g of iodine in 100 mL. Nevertheless, severe toxicity after exposures to iodophors have been reported. The iodophors are used as antiseptics and irrigants. Iodine-containing solutions are also used as expectorants, as vaginal irrigants, for contrast studies in radiology, and as therapy for acute hyperthyroidism. Lugols iodine solution, commonly used in the acute treatment of hyperthyroidism, contains 5 % I2 and 10 % potassium iodide (I-). Pathophysiology The antibacterial property of iodide is facilitated by a covalent linkage to bacterial cell surface glycoproteins, which enhances the bactericidal properties of polymorphonucleocytes. The mechanism of iodine toxicity in human poisoning is not well defined. Based on the significant lactic acidosis seen in acute iodine toxicity, the cellular toxicity has been attributed to interference with cellular oxidative metabolism and adenosine triphosphate production. Chronic exposure results in disturbances of thyroid structure and function and may be manifest as hyperthyroidism, hypothyroidism, goiter, or thyroiditis.[ These seemingly paradoxical responses are due to the stimulation of increased thyroid hormone production in some individuals and the blockade of thyroid hormone production in others. The developing fetus is especially susceptible to the thyroid suppressant effects of iodine. Iodine toxicity occurs through ingestion, through absorption during wound irrigation with iodophor-containing solutions, through mucosal exposure, and during topical application to dermal burns. Clinical Presentation Clinical Presentation of Exposure to Antiseptics, Disinfectants, and Sterilizing Agents: Respiratory irritation, distress, or failure Dermal and mucous membrane irritation and burns: Acute ingestion of iodine (I2)-containing solutions results in gastrointestinal irritation, gastrointestinal ulceration, Lethargy, coma, seizures Metabolic acidosis Embolic phenomena (hydrogen peroxide) Erythroderma (boric acid), ioderma (iodides) Hyperchloremia, negative anion gap (iodides) Chronic ingestion of iodine leads to thyroid disorders in some individuals. Large or chronic exposure to iodides results in sensitivity reactions manifest as painful salivary gland enlargement and a variety of dermal eruptions, so-called ioderma. Treatment Stabilize patient and provide supportive care gastric decontamination may be done by aspiration with a small nasogastric tube. Iodine may be converted to less toxic iodide by the administration of starch or milk. Sodium thiosulfate will also convert iodine to iodide. Activated charcoal is indicated unless significant symptoms suggest the need for endoscopic evaluation of caustic injury Decontaminate skin and mucous membranes with water (all) or polyethylene glycolindustrial methylated spirits (phenol) Treat dermal or mucous membrane burns Institute fluid management Perform endoscopy and surgical intervention for gastrointestinal burns Enhance elimination Hemodialysis: formaldehyde, boric acid, iodine (severe poisoning) Hyperbaric oxygen therapy: emboli with hydrogen peroxideSymptomatic
patients with chronic exposure to iodine-containing medications require