a) A 27-year-old man developed undefined visual disturbances, aching in the eyes, and swollen and hyperemic eyelids on postoperative day 1. He experienced central scotoma and visual acuity reduced to perception of hand movements for both eyes on postoperative day 2. At a 2 month follow-up, he improved with 20/25 vision in both eyes; however, the paracentral scotoma persisted. A 38-year-old male developed foggy vision, and red and swollen eyelids on postoperative day 1. He experienced central vision loss and visual acuity reduced to perception of hand movements for both eyes. At a 2 month follow-up, his vision was 20/400 in both eyes. A 16-year-old female complained of flickering vision with visual acuity of 20/800 for the right eye and counting fingers on the left eye on postoperative day 2. One day after high-dose corticosteroid therapy, the visual acuity was 20/25 and 20/20 but with a very small central visual field. After some weeks, the visual acuity stabilized at 20/25 and 20/20, but a paracentral ringscotoma persisted (Wagenfeld, 2007; Wagenfeld et al, 2007).

a) Tachycardia may occur secondary to corrosive gastroenteritis.

a) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis, coagulopathy, hypothyroidism, confusion, metabolic acidosis, hyperkalemia, and hyperchloremia. She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).

a) Circulatory collapse may occur secondary to corrosive gastroenteritis (Edwards et al, 2005; Kurt et al, 1996).
b) CASE REPORT: A 70-year-old woman ingested 200 mL of 10% w/v of iodine and developed multiorgan failure and died 67 hours after exposure from progressive hypotension that failed to respond to inotrope therapy. Autopsy revealed severe corrosive mucosal necrosis in the esophagus and stomach (Edwards et al, 2005).
c) CASE REPORT: A 9-week-old infant with colic was treated with povidone-iodine (50 mL diluted with 250 mL of polyethylene glycol (PEG) bowel prep solution as an enema and 10 mL diluted with 90 mL of PEG solution by feeding tube at 50 mL/hour for 3 hours). Three hours later the child was found in cardiopulmonary arrest and could not be resuscitated. Autopsy revealed severe gastrointestinal burns (Kurt et al, 1996).

a) Inhalation of fumes leads to irritation of the mucous membranes of the respiratory tract, which may result in pulmonary edema. Irritation is similar to that of chlorine and bromine.

a) Edema of the glottis can result in asphyxia. Glottis edema from ingestion was reported in early literature as a frequently mentioned cause of death after ingestion (Finkelstein & Jacobi, 1937).

a) CASE REPORT: A 70-year-old woman ingested 200 mL of 10% w/v of iodine and developed a dry cough and progressive oxygen saturation deterioration. Approximately 36 hours after exposure, endotracheal intubation was required for respiratory distress and hypoxia; laryngeal inflammation was present. The patient died 67 hours after exposure and postmortem examination noted florid patchy pneumonic changes in the lungs consistent with chemical pneumonitis (Edwards et al, 2005).

a) CASE REPORT: Interstitial pulmonary edema, inspiratory rales, and tachypnea have been reported following ingestion of an unspecified large quantity of Lugol's solution (Dyck et al, 1979).
b) CASE REPORT: A 48-year-old chemistry teacher developed reactive airway dysfunction syndrome (RADS) after exposure to irritating fumes of a iodine mixture released from a laboratory experiment (oxidation-reduction reaction) using powdered aluminum, powdered iodine, and water. She continued to have symptoms and 9 months after the incident, a bronchoscopy revealed a mild diffuse redness of bronchial mucous membranes. A biopsy specimen showed a slight chronic inflammation with lymphocytic infiltration. A histamine challenge test showed slight bronchial hyperresponsiveness. Despite supportive therapy, including antibiotics and corticosteroids, she continued to experience cough, dyspnea, hoarseness of voice, and speech problems. On a follow-up visit 7 years after the incidence, spirometry showed mild obstruction with a significant bronchodilatation effect. A histamine challenge test revealed a slight bronchial hyperresponsiveness (Hannu et al, 2009).

a) PREDISPOSING FACTORS

a) CASE REPORT: A 42-year-old spinal cord injured male developed necrotizing fasciitis after sustaining a bruise to his right gluteal region. Iodoform gauze packing was changed daily on the patient following debridement surgery. On the 7th postoperative day, the patient developed restlessness, increased psychomotor activity and disorientation to time and place. His serum iodine concentration was found to be 454 mcg/dL. Iodoform gauze was discontinued, haloperidol was administered and his delirium gradually improved (Shioda et al, 2004).

a) Headache, dizziness, and delirium have been reported in severe intoxications.

a) Altered sensorium (agitation, confusion, hallucinations) have occurred in association with elevated serum iodine concentrations (Alvarez, 1979).

a) CASE REPORT: An 18-year-old man developed seizures followed by several days of mental status depression after receiving 5 days of mediastinal irrigation with 0.5% povidone-iodine at 100 milliliters/hour (Ponn, 1987). He had a complicated medical history which may have predisposed him to seizures, including past surgery for a cerebral artery aneurysm, craniotomy with wound infection, and aortic valve replacement complicated by mediastinitis.

a) Seizure activity was reported in an adult following continuous povidone-iodine mediastinal irrigation (Zec et al, 1992). No other recognized causes were thought to be related to the patient's seizure activity, however, it was suggested that postoperative renal failure or other circumstances may have contributed to seizure activity (Hauben, 1993).

a) CASE REPORT: A 71-year-old man developed fasciitis in both arms after undergoing a laminectomy for an epidural abscess. Iodoform gauze dressing was applied on the wounds and was changed daily following a debridement surgery. Following the second debridement, his consciousness deteriorated gradually and he became unresponsive 2 days later. His plasma iodine concentration was 6,280 mcg/dL 13 days after the application of the iodoform gauze (19 days after laminectomy). Following the discontinuation of iodoform gauze dressing, his symptoms improved gradually over the next 3 months (Araki et al, 2007).

a) CASE REPORT: A 67-year-old woman developed acute toxic gastric mucosal damage following the use of Lugol's iodine spray during chromoendoscopy. After the removal of stagnant iodine in the stomach, intensely edematous and hemorrhagic mucosa with loss of superficial gastric mucosal layer in the greater curve were observed. Acute edema of the lamina propria with loss of the superficial epithelium consistent with an acute toxic gastric mucosal injury were confirmed by gastric biopsies (Sreedharan et al, 2005).

a) SUMMARY: Symptoms of acute poisoning are mainly due to corrosive gastroenteritis. Ingestion of concentrated solutions may result in gastrointestinal irritation, vomiting, and necrosis at various levels of the upper GI tract (Edwards et al, 2005; Kurt et al, 1996).
b) CASE REPORT: A 70-year-old woman ingested 200 mL of 10% w/v of iodine and developed multiorgan failure and died 67 hours after exposure from progressive hypotension. Despite a lack of gastrointestinal symptoms, autopsy revealed severe corrosive mucosal necrosis in the esophagus and stomach, which was thought to be associated with subsequent hypovolemia (Edwards et al, 2005).
c) CASE REPORT: A 9-week-old infant with colic was treated with povidone-iodine (50 mL diluted with 250 mL of polyethylene glycol (PEG) bowel prep solution as an enema and 10 mL diluted with 90 mL of PEG solution by feeding tube at 50 mL/hour for 3 hours). Three hours later the child was found in cardiopulmonary arrest and could not be resuscitated. Autopsy revealed congested gastric mucosa with bloody material and corrosion and necrosis of the intestinal mucosa from the pylorus to the caecum and into the large bowel (Kurt et al, 1996).

a) A blue colored emesis indicates the presence of starch in the stomach and the conversion of iodine to iodide which is relatively innocuous.

a) An abnormal sensation of taste and a slimy feeling on the tongue were reported after 7 days of packing a surgical wound with iodoform gauze. The patient also developed nausea, vomiting and delirium. The serum iodine level was found to be 454 mcg/dL (Shioda et al, 2004).

a) A metallic taste may be noted.

a) Elevated serum transaminases and bilirubin concentrations have been reported occasionally in patients with elevated serum iodine concentrations (Lavelle et al, 1975; Pietsch & Meakins, 1976).

a) Renal failure characterized by serum creatinine levels up to 3.5 mg/dL (309 micromol/L) have been reported (Dela Cruz et al, 1987).

a) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis, coagulopathy, hypothyroidism, confusion, metabolic acidosis, hyperkalemia, and hyperchloremia. She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).
b) CASE REPORT: A 70-year-old woman ingested 200 mL of 10% w/v of iodine and developed hypotension and anuric renal failure and required hemodialysis. Despite aggressive supportive care, multiorgan failure occurred, and the patient died 67 hours after exposure from progressive hypotension (Edwards et al, 2005).
c) CASE REPORT: Acute renal failure was reported in a 63-year-old woman who was being treated with continuous povidone-iodine mediastinal irrigation after median sternotomy (Campistol et al, 1988).
d) CASE REPORT: Acute renal failure requiring hemodialysis was reported in a 53-year-old woman following bypass surgery in which continuous povidone-iodine mediastinal irrigation was required for purulent drainage (Ryan et al, 1999). Despite a long hospital course, the patient made a complete recovery.
e) CASE REPORT: A 30-year-old man developed sore throat, epigastralgia, and bilateral flank pain soon after ingesting 200 mL of iodine tincture (containing 60 mg/mL of iodine and 40 mg/mL of potassium iodide in 70% v/v ethanol). He presented to the ED 18 hours after ingestion with acute renal failure. Laboratory results revealed white blood cell count of 35,200 x 10(9)/L with 91% neutrophils, hemoglobin 14 g/dL. serum C-reactive protein 2.09 mg/dL, potassium 5.6 mEq/L, BUN 46 mg/dL, creatinine 3.76 mg/dL, total bilirubin 2.45 mg/dL with conjugated form of 0.56 mg/dL, and plasma free Hb of 222 mg/dL (reference range, 1 to 5 mg/dL). Iodine-related severe intravascular hemolysis was suspected requiring 3 sessions of plasma exchange (PE) with the dose of 2600 mL over 2 hours/day. He also underwent intermittent hemodialysis for persistent anuria after day 3. Tarry stool with Hb decreasing to 7.4 g/dL was observed about 80 hours after ingestion. Two weeks after ingestion, he developed aspiration pneumonia and respiratory failure, necessitating 3 weeks of mechanical ventilation. Following supportive care, his renal function gradually improved and he was discharged 8 weeks after ingestion. Total serum iodine concentrations without protein-bound iodine on presentation, 6 days and 11 days postingestion were 1,155,901 mcg/L (reference range, 30.48 to 80.01 mcg/L), 63,336 mcg/L, and 4849 mcg/L, respectively (Mao et al, 2011).

a) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis, coagulopathy, hypothyroidism, confusion, metabolic acidosis, hyperkalemia, and hyperchloremia. She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).

a) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis, coagulopathy, hypothyroidism, confusion, metabolic acidosis (pH 7.29, pCO2 34 mmHg, bicarbonate 17 mmol/L [24 to 26], anion gap 11 mEq/L), hyperkalemia (6 mmol/L [3.5 to 4.5]), and hyperchloremia (113 mmol/L [95 to 105]). She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).

a) Metabolic acidosis may be associated with iodine toxicity. There is an increased anion gap due to elevated serum lactate levels (Edwards et al, 2005; Dyck et al, 1979; Dela Cruz et al, 1987).

a) Neutropenia has been reported in association with elevated serum iodine concentrations (Alvarez, 1979).

a) Hemolysis has been reported (Dyck et al, 1979).
b) CASE REPORT: A 30-year-old man developed sore throat, epigastralgia, and bilateral flank pain soon after ingesting 200 mL of iodine tincture (containing 60 mg/mL of iodine and 40 mg/mL of potassium iodide in 70% v/v ethanol). He presented to the ED 18 hours after ingestion with acute renal failure. Laboratory results revealed white blood cell count of 35,200 x 10(9)/L with 91% neutrophils, hemoglobin 14 g/dL. serum C-reactive protein 2.09 mg/dL, potassium 5.6 mEq/L, BUN 46 mg/dL, creatinine 3.76 mg/dL, total bilirubin 2.45 mg/dL with conjugated form of 0.56 mg/dL, and plasma free Hb of 222 mg/dL (reference range, 1 to 5 mg/dL). Iodine-related severe intravascular hemolysis was suspected requiring 3 sessions of plasma exchange (PE) with the dose of 2600 mL over 2 hours/day. He also underwent intermittent hemodialysis for persistent anuria after day 3. Tarry stool with Hb decreasing to 7.4 g/dL was observed about 80 hours after ingestion. Two weeks after ingestion, he developed aspiration pneumonia and respiratory failure, necessitating 3 weeks of mechanical ventilation. Following supportive care, his renal function gradually improved and he was discharged 8 weeks after ingestion. Total serum iodine concentrations without protein-bound iodine on presentation, 6 days and 11 days postingestion were 1,155,901 mcg/L (reference range, 30.48 to 80.01 mcg/L), 63,336 mcg/L, and 4849 mcg/L, respectively (Mao et al, 2011).
c) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis (serum haptoglobin less than 0.1 [normal range, 0.3 to 2], lactate dehydrogenase 1685 IU/L [220 to 450] without evidence of schistocyte), coagulopathy, hypothyroidism, confusion, metabolic acidosis, hyperkalemia, and hyperchloremia. She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).

a) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis, coagulopathy, hypothyroidism, confusion, metabolic acidosis, hyperkalemia, and hyperchloremia. Another laparotomy showed a hemoperitoneum by diffuse bleeding without evident vascular damage, suggesting coagulopathy. An acute fibrinolysis (prothrombin time 47% [80 to 100], partial thromboplastin time ratio 1.66 [less than 1.2], fibrinogen 1.7 g/L [1.9 to 4]) was observed, necessitating the administration of fresh frozen plasma (11 Units), fibrinogen (6 g), and tranexamic acid (1 g). She also received 10 Units of packed red cells after compatibility testing. She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).

a) Prolonged exposure to tincture of iodine can induce superficial necrosis. At least one death has been reported consequent to extensive skin involvement.

a) DERMAL ABSORPTION: Topical application of solutions of iodine on burn patients, the use of occlusive dressings, and prolonged contact may result in increased iodine/iodide absorption and subsequent development of systemic toxicity (Lavelle et al, 1975).

a) Skin eruptions ranging from urticaria to erythema to exfoliative dermatitis have been reported (Seymour, 1937).

a) Repeated applications of iodophors may cause contact dermatitis (Okano, 1989).
b) INCIDENCE: The incidence of allergic reactions is 12% to 20% (Harvey, 1985; Kudo et al, 1988).

a) Prolonged skin contact with povidone iodine-in-alcohol solution has resulted in dermal burns (White & Joseet, 1990).

a) CASE REPORT: A 22-year-old US customs photographer developed axillary sweat gland dysfunction (purple discoloration of the underarms and clothing) after dermal iodine exposure. One week before the onset of her symptoms, her latex gloves became stained while handling a large container of approximately 100 pounds of crystalline iodine. Her symptoms resolved over several weeks (Munday et al, 2002).

a) Iodides diffuse across the placenta and into the breast milk. Mounting evidence of neonatal harm suggests that iodides, including topical applications and douches, be avoided during pregnancy and lactation.
b) Infant and neonatal death from respiratory distress secondary to goiter has been reported in mothers taking iodides (Parmalee et al, 1940; Galina et al, 1962).
c) CASE SERIES - Use of felsol powders, historically an iodine-containing antitussive, was associated with fetal goiter in eight infants when used by women during various times in pregnancy (Schardein, 1985).
d) Use of potassium iodide or sodium iodide during pregnancy has been associated with goiter, hypothyroidism, respiratory problems, enlarged heart, compression of the trachea, and death in infants (Pennington, 1990).
e) POVIDONE-IODINE - Chronic topical maternal use of povidone-iodine during pregnancy and breast feeding has been associated with clinical and biochemical hypothyroidism in the infant (Danzigen et al, 1987).
f) The International Commission on Radiological Protection has revised its occupational exposure standards for pregnant workers to 1 mSv. For nuclear medicine technicians or nurses performing procedures with I-131, a dose limit of 1.3 mSv to the maternal abdominal surface corresponds to a fetal dose of 1 mSv (Mountford & Steele, 1995).

a) IODINATED GLYCEROL: X (Briggs et al, 1998)
b) IODINE: D (Briggs et al, 1998)
c) IOPODATE: D (Briggs et al, 1998)
d) POVIDONE-IODINE: D (Briggs et al, 1998)

a) Iodides diffuse across the placenta, and are concentrated in breast milk (Briggs et al, 1998a). Mounting evidence of neonatal harm suggests that iodides, including topical applications and douches, be avoided during pregnancy and lactation.
b) POVIDONE-IODINE use during breast feeding has been associated with hypothyroidism.
c) A case of hypothyroidism has been reported in a 15-day-old male whose mother received an iodine antiseptic. The patient, whose mother used an iodine antiseptic on her episiotomy incision for 10 to 12 days postpartum, presented with a high thyroid stimulating hormone (TSH) level (26.11 milliunits (mU)/L) and low free thyroxine level (fT4)(6.83 picogram (pg)/mL). X-rays revealed bone maturation of 40 weeks and thyroid ultrasonography revealed a thyroid volume of 1.04 mL (normal: 0.79 mL). Urinary iodine levels were 41 mcg/dL (normal: 10 to 20 mcg/dL) and the iodine concentration present in the mother's breast milk was 30 mcg/dL (normal: 10 to 20 mcg/dL). A diagnosis of hypothyroidism attributed to iodine overload was made and the patient was treated with 8 mcg/kg/day of L-T4. Forty-days postpartum, the infant was on the same dose of L-T4 with TSH levels at 3.04 mU/L, fT4 at 9.9 pg/mL, and fT3 at 3.23 pg/mL. Treatment with L-T4 was continued with dose reductions and treatment discontinuation planned according to future thyroid function tests (Kurtoglu et al, 2009).
d) CASE REPORT - One case of severe transient congenital hypothyroidism has been reported in a breastfed infant whose mother performed vaginal douching with povidone-iodine solution twice daily since delivery (20 days).

a) Transient hypothyroidism characterized by elevated urinary iodide concentrations, elevated serum iodine concentrations, elevated TSH concentrations, and low T4 concentrations has been demonstrated in povidone-iodine exposed mothers and their infants (l'Allemand et al, 1983; Clemens & Neumann, 1989).
b) Hypothyroidism has also been described in neonates treated with topical povidone-iodine (Cosman et al, 1988; Smerdely et al, 1989; Newman, 1989; Linder et al, 1995).
c) Infants undergoing continuous cyclic peritoneal dialysis have been reported to develop hypothyroidism secondary to iodine exposure from a cap used to seal the Tenckhoff catheter (Vulsma et al, 1990).
d) Chronic administration of iodinated glycerol therapy may cause hypothyroidism (Geurian & Branam, 1994) and goiter (Gomolin, 1989).
e) CASE REPORT: A 41-year-old woman developed a transient hypotension a few minutes after receiving repeated intrauterine injections of povidone iodine 2% (total amount 350 mL in a few minutes) as a dye during a diagnostic laparoscopy to check the fallopian tube patency. Her hospital course was complicated with anuric renal failure, anemia, hemolysis, coagulopathy, hypothyroidism (mildly elevated TSH (5.82 mcIU/mL; normal 0.2 to 3.6) and low thyroid hormones (fT3: 1.44 pg/mL [normal, 1.35 to 3.5]; fT4: 0.7 ng/dL [normal 0.9 to 2]), confusion, metabolic acidosis, hyperkalemia, and hyperchloremia. She was treated with supportive therapy, including renal replacement therapy (RRT) on the 44th postoperative hour (continuous venovenous hemodiafiltration without hydric loss; blood flow rate of 300 mL/min, hemofiltration and dialysate flow rates of 1.5 to 4 L/hr). Iodine concentration was 6929 mcg/dL (normal, 3.4 to 8 mcg/dL) during the first surgical procedure, 597 mcg/dL 28 hours after the initiation of RRT, and 24 mcg/dL after 6 days of RRT. Urine iodine was 3135 mcg/dL. She underwent another laparotomy and then a total hysterectomy on day 8 because of intense pelvic pain and hemorrhagic massive uterine infarction. A histological analysis of the uterus and the adnexa revealed fibrinoid thrombi and a brown pigmentation. Her condition gradually improved and renal replacement therapy was discontinued on day 11 (Lakhal et al, 2011).

a) Mild elevations in thyroid stimulating hormone and depression of total triiodothyronine, thyroxine and response to thyrotropin releasing hormone developed in volunteers after 7 days treatment with water purification tablets (32 milligrams free iodine/day) (Georgitis & McDermott, 1993).
b) CASE REPORT: A 13-day-old neonate developed iodine overload and severe hypothyroidism after an iodine-containing antiseptic was applied 3 times a day for umbilical care since birth. His thyrotropin (TSH) concentration were 42.9 mUnits/L, and 120 mUnits/L (normal, 0.5 to 6.5 mUnits/L) on 4th and 8th days of life. Thyroxine (T4) concentration was 6.08 mcg/dL (normal, 8.2 to 17.2 mcg/dL) on 8th day of life. Laboratory results from the 13th day of life revealed free triiodothyronin (fT3) level 1.79 pg/mL (normal: 2.5 to 3.9 pg/mL), fT4 4.69 pg/mL (normal, 9 to 26 pg/mL), TSH 66.11 mUnits/L (normal: 0.5 to 6.5 mUnits/L) and thyroglobulin 2.36 ng/mL (normal: 2 to 106 ng/mL). Following supportive care, including L-T4 therapy (13 mcg/kg/day), his thyroid function tests gradually normalized (Kurtoglu et al, 2009).

a) Iodine-induced thyrotoxicosis (jodbasedow) is a condition that may develop in older patients with long-standing iodine deficiencies who receive high doses of iodine (Kobberling et al, 1985; Fradkin, 1983; Klein & Levey, 1983; Shetty & Duthie, 1990).
b) CASE SERIES: Two euthyroid adult patients with burns over 45% to 80% of the body surface developed hyperthyroidism after 3 to 6 weeks' topical treatment with 1% povidone-iodine (Rath & Meissl, 1988).
c) CASE REPORT: An infant developed iodine-induced hyperthyroidism after mediastinal irrigation with full strength povidone-iodine (10%) at 3 mL/hr for 4 days (Bryant & Zimmerman, 1995). Thyroid function returned to normal one month after therapy was discontinued.
d) CASE REPORT: A 22-month-old burn patient (burns over 80% of body surface area) developed thyrotoxicosis after alternate-day povidone-iodine (Betadine) washes. He developed tachycardia, hypertension, fever, sweating, agitation, diarrhea, and neutropenia. Thyroid function tests showed low levels of thyrotropin (less than 0.1 mIU/L) and high free thyroxine (36.1 pmol/L, normal 10 to 24), and normal free triiodothyronine (3.7 pmol/L). Marked elevated levels of iodine were observed in plasma (9.6 mcmol/L; normal 0.32 to 0.63) and urine (60.6 mcmol/L; normal 0.39 to 1.97). Following the discontinuation of povidone-iodine and treatment with propranolol and carbimazole, his thyroid function returned to normal by day 42. However, one week later his thyroid function tests revealed hypothyroidism and he required long term thyroid supplementation (Robertson et al, 2002).

a) PUBLIC HEALTH IMPLICATIONS: Thirty-three (29%) peace corps volunteers developed thyroid dysfunction; 44 (46%) had enlarged thyroids related to an iodine-resin two stage water purification system used for volunteers in Niger, West Africa (Khan et al, 1998).
b) Iodine supplementation programs in Zimbabwe have resulted in an increase in Graves disease, toxic nodular goiter, and thyrotoxicosis (Todd et al, 1995).

a) CASE REPORT: A 9-week-old infant with colic was treated with povidone-iodine (50 mL diluted with 250 mL of polyethylene glycol (PEG) bowel prep solution as an enema and 10 mL diluted with 90 mL of PEG solution by feeding tube at 50 mL/hour for 3 hours). Three hours later the child was found in cardiopulmonary arrest and could not be resuscitated. Serum glucose was 613 mg/dL (Kurt et al, 1996).

a) SUMMARY: Reactions to iodine may occur acutely or after chronic use and may be characterized as coryza, headache, salivary gland pain, conjunctivitis, fever or skin reactions (urticaria, acneform, erythema, bullous, ioderma).
b) CONTRAST MEDIA: Oral and IV iodine containing radio-contrast media (eg, Telepaque(R); I-125; I-131) may also cause iodine hypersensitivity reaction as well as anaphylactic type reactions (Crocker & Vandam, 1963; Gluck & Mitty, 1990).

a) Starch forms a purple-colored iodine complex which is highly visible and less toxic than iodine (Block et al, 1974).

a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.

a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).

a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
b) DOSE

a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992)

a) Advancing across the cricopharynx under direct vision
b) Gently advancing with minimal air insufflation
c) Never retroverting or retroflexing the endoscope
d) Using a pediatric flexible endoscope
e) Using extreme caution in advancing beyond burn lesion areas
f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).

a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
b) Grade 0 - Normal examination
c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.

a) ANIMAL
b) HUMAN

a) STUDY - In a study of 11 children with deep circumferential esophageal burns after caustic ingestion, insertion of a silicone rubber nasogastric tube for 5 to 6 weeks without steroids or antibiotics was associated with stricture formation in only one case (Wijburg et al, 1989).

a) STUDY - In a retrospective study of patients with extensive transmural esophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (esophagoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).

a) Therapeutic dosage range is 50 to 150 mg/day but up to 500 mg of iodide per day is often used (Haynes & Murad, 1985).

a) TOXIC LEVELS
b) TOPICAL APPLICATION
c) INTRAUTERINE INJECTIONS
d) WOUND IRRIGATION
e) GASTROINTESTINAL IRRIGATION
f) INGESTION

1) Iodine and iodides, iodine
b) Adopted Value

1) Listed as: Iodine
2) REL:
3) IDLH:

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Iodine and iodides, iodine
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Iodine and iodides, iodides
3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Iodine
6) MAK (DFG, 2002): Not Listed
7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

1) Listed as: Iodine
2) Table Z-1 for Iodine:

a) 22 g/kg

a) >8650 mg/kg (RTECS, 1997)

a) 14 g/kg

a) 10,500 mg/kg (RTECS, 1997)

a) HORSE
b) CATTLE
c) SWINE
d) POULTRY

1) GENERAL TREATMENT

a) Probably due to body size, iodine reactions in large animals are uncommon. Treatment protocols for small animals can be adapted for the rare large animal reaction.

a) Concentrated iodines can cause dermal burns due to their corrosive or caustic effects.

a) Upon inhaling iodine vapors, animals have experienced respiratory distress secondary to soft tissue swelling of the larynx and glottis.

a) Ingestion of iodines causes gastrointestinal irritation and occasionally mucosal damage. Delayed complications may include pyloric stenosis, sloughing of the gastric mucosa, peritonitis and sepsis.

a) Few adverse reactions to iodine have been described; the signs might include swelling, urticaria, shivering, salivation, tachycardia, and renal failure.

a) DERMAL -
b) INHALANT -
c) ORAL/PARENTERAL -

a) MAINTAIN VITAL FUNCTIONS - as necessary.

a) After removal of all iodine solutions from the animal and instituting life support, begin intravenous fluid diuresis (small animals 66 to 132 milliliters/kilogram/24 hours); monitor carefully for pulmonary or laryngeal edema.

a) Antibiotics and corticosteroids may be used in the event of mucosal damage. Steroids should be used within 48 hours of exposure and are contraindicated in the presence of perforation; when used, they are continued for several weeks (Beasley et al, 1989).

a) Survey radiographs may be taken of the thorax and abdomen.

a) Analgesics are necessary to alleviate pain with burns.