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SELENIOUS ACID

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Selenious acid (H2SeO3) is an inorganic selenium compound used especially as a component of compounds for gun blueing (Ellenhorn & Barceloux, 1988). It is considered the most highly toxic inorganic selenium compound (Normann et al, 1984).

Specific Substances

    A) Selenious acid
    1) Monohydrated selenium dioxide
    2) RCRA WASTE NUMBER: U204
    3) NIOSH/RTECS VS 7175000
    4) Molecular Formula: H2-O3-Se
    5) CAS 7783-00-8
    6) References: RTECS, 1989; EPA, 1985
    Selenium dioxide
    1) Selenium anhydride
    2) Selenium oxide
    3) NIOSH/RTECS VS 8575000
    4) Molecular Formula: 02-Se
    5) CAS 7446-08-4
    6) References: RTECS, 1989; EPA, 1985

    1.2.1) MOLECULAR FORMULA
    1) H2-O3-Se

Available Forms Sources

    A) SOURCES
    1) Selenious acid is prepared by dissolving selenium dioxide in hot water and cooling (Budavari, 1989) or by the action of hot nitric acid on selenium (Lewis, 1993).
    B) USES
    1) GENERAL GUN BLUEING FORMULA (Pentel et al, 1985; Normann et al, 1984; Koppel et al, 1986; Matoba et al, 1986; Carter, 1966; Nantel et al, 1985; Ellenhorn & Barceloux, 1988):
    a) Selenious acid is used as a component of compounds for gun blueing.
    b) Most of these products contain between 1 and 4% selenious acid or selenium dioxide combined with hydrochloric, phosphoric, or nitric acids and either copper sulfate or copper nitrate 1 to 9%. Methanol 10 to 11% is present in some formulations.
    c) The severe toxicity of these agents has generally been ascribed to the selenious acid or selenium dioxide. Toxicity has been reported following the ingestion of selenium dioxide from a bottle of Glass blue, used for stained glass manufacture (Kise et al, 2004).
    2) Selenious acid is used as a reagent for alkaloids, as an oxidizing agent, and as an isotope for labeling radiopharmaceutical compounds (EPA, 1985).

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: Selenious acid is found in gun blueing, which changes the color of steel from silver-grey to blue-grey. It is also used in the chemical darkening and patination of copper, brass and bronze. Other uses for selenious acid are as a reagent for alkaloids, as an oxidizing agent and as an isotope for labeling radiopharmaceutical compounds.
    B) TOXICOLOGY: The toxicity of selenious acid is thought to be due to inhibition of activity of sulfhydryl-containing enzymes. In addition, it is corrosive, as the pH of several commercial gun blueing solutions containing selenious acid is 1.5. Hepatoxicity, nephrotoxicity, and discoloration of the skin and viscera have been noted in fatal ingestions.
    C) EPIDEMIOLOGY: Reports of selenious acid toxicity are fairly rare but can be fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Ingestion can cause hypersalivation, garlic odor breath, copious vomiting, diarrhea, restlessness, muscle spasms, hypertension and tachycardia. Inhalation of selenious acid fumes has caused bronchospasm, coughing, gagging and syncope. Tachycardia, tachypnea and mild hypotension may also occur. After acute symptoms subside, secondary symptoms may develop over the next 2 to 12 hours, including chills, nausea, vomiting, diarrhea, malaise, headache, fever, cyanosis, respiratory distress, bronchospasm, leukocytosis and a chemical pneumonitis. Dermal exposure to selenious acid can cause a dermatitis and paronychia. Skin contact can cause dermal burns and systemic absorption may occur through denuded areas. Ocular exposures to selenious acid can cause conjunctivitis or corneal burns.
    2) SEVERE TOXICITY: Severe ingestions can cause hematemesis, hypotension, toxic cardiomyopathy, pulmonary edema, seizures and coma. Selenious acid is also corrosive potentially producing esophageal, pharyngeal,and GI tract burns and erosions, as well as liver and kidney injury.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Tachypnea and fever may be noted. Hypertension followed by significant hypotension and shock may be seen.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Institute continuous cardiac monitoring and obtain an ECG.
    C) Monitor serum electrolytes, renal function, liver enzymes, CBC and urinalysis.
    D) Though it is possible to measure selenium concentrations in plasma, it is not readily available or useful for immediate treatment. Selenium blood and urine levels may be useful later to confirm the diagnosis, especially in work-related exposures.
    E) For patients with respiratory symptoms, monitoring pulse oximetry, arterial blood gases, chest x-ray and pulmonary function tests may all be useful.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Basic supportive care is the most important treatment measure. Patients with inhalational exposure should be treated with supplemental oxygen as soon as possible after rescue and have a prolonged period of observation in a controlled setting to monitor for development of a chemical pneumonitis.
    2) INHALATION: Patients should be monitored for respiratory distress and provided treatment as necessary (ie, oxygen, assisted ventilation and inhaled beta adrenergic agonists), if bronchospasm develops. Patients who develop pulmonary edema may benefit from mechanical ventilation and positive-end-expiratory-pressure. Antibiotics are only useful if there is evidence of infection.
    3) DERMAL: Decontamination is the most important initial step with removal of contaminated clothing and washing exposed areas thoroughly with soap and water. Dermal burns should be treated with standard topical therapy. If patients develop dermal hypersensitivity reactions, systemic or topical corticosteroids or antihistamines may be useful. There is no good evidence that washing skin with sodium thiosulfate is better than standard chemical burn therapy.
    4) OCULAR: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature normal saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation or photophobia persists after 15 minutes of irrigation, an ophthalmologic examination should be performed. Serious corneal injuries require ophthalmological consultation.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Patients with severe toxicity need good supportive care as the mainstay of therapy. There is no substantial evidence for the use of chelation, vitamin C or N-acetylcysteine. Standard ACLS measures should be provided to patients that go into shock or cardiopulmonary arrest. If respiratory depression or coma occurs, patients may need endotracheal intubation and assisted ventilation. Seizures should be treated with benzodiazepines, barbiturates and propofol. Endoscopy should be performed to evaluate for gastrointestinal burns following ingestion. Emergent surgery may be needed for patients with gastrointestinal necrosis or perforation.
    C) DECONTAMINATION
    1) PREHOSPITAL: INGESTION: Dilute with small amounts of milk or water if the patient is not vomiting and able to tolerate fluids. DERMAL: Remove contaminated clothing and wash skin with soap and water. OCULAR: Irrigate exposed eyes. INHALATION: Administer oxygen. Treat bronchospasm with inhaled beta agonists.
    2) HOSPITAL: Ingestion has been associated with significant toxicity as well as corrosive injury. Consider insertion of a small, flexible nasogastric tube to suction gastric contents in recent ingestions, the risk of further mucosal injury must be considered. Consider administration of activated charcoal after recent ingestion if the patient can tolerate fluids. DERMAL: Remove contaminated clothing and wash skin with soap and water. OCULAR: Irrigate exposed eyes. INHALATION: Administer oxygen. Treat bronchospasm with inhaled beta agonists.
    D) AIRWAY MANAGEMENT
    1) Airway management may be necessary following exposure, as pulmonary edema, pneumonitis and diaphragmatic weakness may be seen.
    E) ANTIDOTE
    1) There is no known antidote.
    F) ENHANCED ELIMINATION
    1) There is no evidence to support the use of multiple dose activated charcoal or hemoperfusion. Hemodialysis was used after an intentional ingestion (one case) of selenium dioxide with initial decreases in selenium level in both serum and urine, but dialysis clearance was not determined.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild dermal irritation after topical exposure involving a small surface area can be managed at home. Any patient ingesting selenious acid should be referred to a healthcare facility.
    2) OBSERVATION CRITERIA: All patients with a history of ingestion should be sent to a healthcare facility for further observation. Patients who are asymptomatic after 4 to 6 hours of observation may be sent home. All other patients should be observed overnight as secondary symptoms may develop several hours later. Patients may be discharged home after they are clearly improving.
    3) ADMISSION CRITERIA: Patients who develop any symptoms secondary to selenious acid should be admitted for further observation. Depending on the severity of symptoms, a patient may require an intensive care setting. Patients may be discharged home after symptoms are clearly improving after a prolonged period of observation.
    4) CONSULT CRITERIA: Consult a poison center and/or medical toxicologist for any patient with a selenious acid ingestion.
    H) PITFALLS
    1) Even small ingestions may be fatal and patients may quickly become critically ill. Symptoms from an inhalational exposure can have an acute phase of symptoms with improvement, but then develop delayed secondary symptoms that can be quite severe.
    I) PHARMACOKINETICS
    1) Selenious acid is well absorbed by inhalation (97%) and ingestion (87%). Selenious acid and its salts are also capable of penetrating the skin and producing acute poisoning. Selenium is distributed to all soft tissues, but the concentration is especially high in the liver and kidneys. The lungs and milk also contain increased amounts of selenium post administration and it is also transported to the fetus via the placenta. Selenium is drawn to erythrocytes or bound to alpha- or beta-globulin. Dimethylselenide, a volatile compound, is a selenious acid metabolite and selenium dioxide account for the garlic odor noted in the perspiration and on the breath of an exposed individual. The half-life of an absorbed dose of selenium is about 1.2 days, with a terminal half-life of 34 days.
    J) PREDISPOSING CONDITIONS
    1) Patients at extremes of age (very young or very old) are likely to be predisposed to more severe toxicity at lower levels of exposure. In addition, patients with underlying disease (eg, lung disease from smoking or underlying renal or liver disease) may be more sensitive to selenious acid toxicity.
    K) DIFFERENTIAL DIAGNOSIS
    1) Other exposures that can resemble selenious acid include other corrosive acids and substances or medications that can cause severe gastrointestinal symptoms and systemic symptoms (eg, elemental iron).
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: Ingestion of a few drops of selenium acid-containing gun blueing solution may cause illness, and more than 15 mL has been fatal. PEDIATRIC: Ingestion of up to 20 mL of a 2% selenious acid-containing gun blueing compound has been fatal in toddlers. ADULT: Ingestion of 30 to 90 mL of gun blueing solutions containing 2 to 4% selenious acid has been fatal in adults.

Clinical Effects

Summary Of Exposure

    A) USES: Selenious acid is found in gun blueing, which changes the color of steel from silver-grey to blue-grey. It is also used in the chemical darkening and patination of copper, brass and bronze. Other uses for selenious acid are as a reagent for alkaloids, as an oxidizing agent and as an isotope for labeling radiopharmaceutical compounds.
    B) TOXICOLOGY: The toxicity of selenious acid is thought to be due to inhibition of activity of sulfhydryl-containing enzymes. In addition, it is corrosive, as the pH of several commercial gun blueing solutions containing selenious acid is 1.5. Hepatoxicity, nephrotoxicity, and discoloration of the skin and viscera have been noted in fatal ingestions.
    C) EPIDEMIOLOGY: Reports of selenious acid toxicity are fairly rare but can be fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Ingestion can cause hypersalivation, garlic odor breath, copious vomiting, diarrhea, restlessness, muscle spasms, hypertension and tachycardia. Inhalation of selenious acid fumes has caused bronchospasm, coughing, gagging and syncope. Tachycardia, tachypnea and mild hypotension may also occur. After acute symptoms subside, secondary symptoms may develop over the next 2 to 12 hours, including chills, nausea, vomiting, diarrhea, malaise, headache, fever, cyanosis, respiratory distress, bronchospasm, leukocytosis and a chemical pneumonitis. Dermal exposure to selenious acid can cause a dermatitis and paronychia. Skin contact can cause dermal burns and systemic absorption may occur through denuded areas. Ocular exposures to selenious acid can cause conjunctivitis or corneal burns.
    2) SEVERE TOXICITY: Severe ingestions can cause hematemesis, hypotension, toxic cardiomyopathy, pulmonary edema, seizures and coma. Selenious acid is also corrosive potentially producing esophageal, pharyngeal,and GI tract burns and erosions, as well as liver and kidney injury.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Tachypnea and fever may be noted. Hypertension followed by significant hypotension and shock may be seen.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) TACHYPNEA may be noted (Carter, 1966).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER has developed as part of the delayed secondary toxicity seen after inhalation of selenium dioxide fumes (Wilson, 1962).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPERTENSION/HYPOTENSION: Patients ingesting selenious acid may initially develop hypertension, but this is followed in serious poisonings by significant hypotension and shock (Carter, 1966).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) TACHYCARDIA has been described in cases of selenious acid poisoning (Hunsaker et al, 2005; Lombeck et al, 1987; Carter, 1966) Matoba, 1986).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CONJUNCTIVITIS has been reported following exposures.
    a) Vapor exposure may result in eye irritation (ACGIH, 1986).
    b) Workers exposed to selenium dioxide dust have developed an allergic type of conjunctivitis (ACGIH, 1986).
    2) CORNEAL BURNS: Direct contact with the material may cause corneal burns (Cerwenka & Cooper, 1961).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Inhalation exposure may cause irritation of the mucosa of the nose and throat (Wilson, 1962).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Inhalation exposure may cause irritation of the mucosa of the nose and throat (Wilson, 1962).
    2) EDEMA/EROSIONS: Pharyngeal edema, erosions or burns may be noted in ingestion exposures (Koppel et al, 1986; Matoba et al, 1986; Schellmann et al, 1986; Nantel et al, 1985).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Ingestion of the less toxic compound, sodium selenite, caused diffuse T-wave flattening, T-wave inversions in the lateral and anterior leads, and a prolonged QT interval (See et al, 2006; Civil & McDonald, 1978). In one case these changes became maximal at three days after exposure and cleared over the following two weeks (Civil & McDonald, 1978).
    b) CASE REPORT: A 24-year-old man ingested an unknown amount of a gun-bluing agent, began vomiting, and subsequently developed hallucinations, persistent tachycardia (114 bpm), and hypotension. An ECG, performed one hour postingestion, revealed sinus tachycardia with nonspecific ST wave changes and a prolonged QTc interval of 498 msec. The patient progressively deteriorated, developing cyanosis, coma, and cardiac arrest. The ECG showed ventricular fibrillation progressing into asystole. Despite aggressive cardiopulmonary resuscitation, including intravenous insertion of a pacemaker, the patient died within 5 hours postingestion. An autopsy revealed cyanosis of the patient's oral mucosa and lips, edematous lungs, and a strong metallic garlic odor emanating from the body cavity. The serum selenium concentration, obtained one hour post ingestion but reported several days later, was 30,000 mcg/L (Hunsaker et al, 2005).
    B) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Cardiac dysrhythmias including sinus tachycardia, frequent premature ventricular contractions, and asystole have been reported (Pentel et al, 1985) (Koppel et al, 1987).
    b) CASE REPORT: After ingesting up to 15 mL of Gun Blue solution (selenious acid), a 22-year-old man developed ventricular fibrillation, and evidence of pulmonary edema. The patient was pronounced dead following unsuccessful resuscitation (Quadrani et al, 2000).
    c) CASE REPORT: A 24-year-old man ingested an unknown amount of a gun-bluing agent, began vomiting, and subsequently developed hallucinations, persistent tachycardia (HR 114 bpm), and hypotension. An ECG, performed one hour postingestion, revealed sinus tachycardia with nonspecific ST wave changes and a prolonged QTc interval of 498 msec. The patient progressively deteriorated, developing cyanosis, coma, and cardiac arrest. The ECG showed ventricular fibrillation progressing into asystole. Despite aggressive cardiopulmonary resuscitation, including intravenous insertion of a pacemaker, the patient died within 5 hours postingestion. Death was attributable to electromechanical cardiac failure. An autopsy revealed cyanosis of the patient's oral mucosa and lips, edematous lungs, and a strong metallic garlic odor emanating from the body cavity. The serum selenium concentration, obtained one hour post ingestion but reported several days later, was 30,000 mcg/L (Hunsaker et al, 2005).
    d) Following the ingestion of the less toxic compound, sodium selenite, a 75-year-old man developed a prolonged QT interval followed by ventricular tachycardia interspersed with normal complexes with ST depressions prior to cardiac arrest (See et al, 2006).
    C) CARDIOMYOPATHY
    1) WITH POISONING/EXPOSURE
    a) Myocardial depression, with decreased cardiac output contributing to hypotension and shock, has been observed in cases of ingestion exposure (Matoba et al, 1986; Normann et al, 1984; Ellenhorn & Barceloux, 1988; Pentel et al, 1985).
    D) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Patients ingesting selenious acid may initially develop mild hypertension (Carter, 1966).
    E) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Patients ingesting selenious acid may initially develop mild hypertension, but this is followed in serious poisonings by significant hypotension and shock (Carter, 1966).
    b) Hypotension secondary to volume depletion, low peripheral vascular resistance and myocardial depression may occur and the resultant shock may be a cause of early deaths (Hunsaker et al, 2005; Matoba et al, 1986; Normann et al, 1984; Ellenhorn & Barceloux, 1988; Pentel et al, 1985).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) INHALATION EXPOSURE: The initial symptoms following inhalation exposure are a sensation of constriction in the chest, irritation and a burning sensation in the upper respiratory tract, coughing, gagging, tachypnea and a bitter acid taste in the mouth (Wilson, 1962).
    b) The acute phase symptoms may then subside following cessation of exposure, but secondary symptoms may develop over the following two to 12 hour hours consisting of chills, fever, cyanosis, respiratory distress, bronchospasm, leukocytosis and chemical pneumonitis with pulmonary infiltrates and atelectasis (Wilson, 1962).
    c) Those patients who received less first aid in the form of oxygen inhalation immediately after cessation of exposure seemed to develop the worst secondary symptomatology (Wilson, 1962).
    d) Inhalation exposure may result in severe respiratory tract irritation and CHEMICAL PNEUMONITIS (Wilson, 1962). Early treatment with supplemental oxygen may mitigate the severity of the chemical pneumonitis (Wilson, 1962).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Acute lung injury may develop, even in cases of ingestion (Hunsaker et al, 2005; Pentel et al, 1985; Matoba et al, 1986). It is unclear whether the pulmonary edema is cardiogenic or noncardiogenic in origin (Pentel et al, 1985).
    b) CASE REPORT: After ingesting up to 15 mL of Gun Blue solution (selenious acid), a 22-year-old man developed ventricular fibrillation and evidence of pulmonary edema. The patient was pronounced dead following unsuccessful resuscitation (Quadrani et al, 2000).
    C) SEQUELA
    1) WITH POISONING/EXPOSURE
    a) Chronic pulmonary sequelae have NOT been described following acute inhalation injury (Wilson, 1962).
    D) APNEA
    1) WITH POISONING/EXPOSURE
    a) DIAPHRAGMATIC WEAKNESS: Weakness of skeletal muscles including the diaphragm may be severe and could lead to respiratory failure requiring mechanical ventilation (Pentel et al, 1985).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) CNS depression or coma may occur following ingestion, inhalation, or dermal exposure (Hunsaker et al, 2005; Koppel et al, 1986; Nantel et al, 1985; Schellmann et al, 1986).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may occur following ingestion (Koppel et al, 1986).
    C) TOXIC ENCEPHALOPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 40-year-old woman developed violent confusion and restlessness after ingesting 90 mL of gun blueing containing 4% selenious acid and 2.5% copper sulfate (Matoba et al, 1986).
    D) FEELING NERVOUS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Restlessness was noted on presentation in a nonfatal case (Lombeck et al, 1987).
    E) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may develop after inhalation exposure (Wilson, 1962).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) WITH POISONING/EXPOSURE
    a) Nausea is common following selenious acid or selenium dioxide poisoning, regardless of the route of exposure (Nantel et al, 1985; Normann et al, 1984; Pentel et al, 1985; Lombeck et al, 1987; Carter, 1966).
    B) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting is common following selenious acid or selenium dioxide poisoning, regardless of the route of exposure (Hunsaker et al, 2005; Nantel et al, 1985; Normann et al, 1984; Pentel et al, 1985; Lombeck et al, 1987; Carter, 1966).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea is common following selenious acid or selenium dioxide poisoning, regardless of the route of exposure (Nantel et al, 1985; Normann et al, 1984; Pentel et al, 1985; Lombeck et al, 1987; Carter, 1966).
    D) HEMATEMESIS
    1) WITH POISONING/EXPOSURE
    a) Hematemesis may be present in some cases (Kise et al, 2004; Nantel et al, 1985; Matoba et al, 1986).
    E) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) EROSIONS/BURNS: Esophageal, pharyngeal, and gastrointestinal tract burns or erosions have been described in cases of ingestion (Koppel et al, 1986; Matoba et al, 1986; Schellmann et al, 1986; Nantel et al, 1985).
    b) CASE REPORT: A 48-year-old schizophrenic woman developed mildly altered consciousness and hematemesis after intentionally ingesting 2000 mg of selenium dioxide (a bottle of glass blue; 10 times the experimental lethal dose in animals). Endoscopy showed mucosal damage throughout the oral cavity, esophagus, and stomach. Necrotic tissue, forming a deep ulcer (classified as grade 3 corrosive gastritis) was observed at the gastric angulus. Following intubation, gastric lavage and hemodialysis, she was discharged approximately 2 weeks postingestion (Kise et al, 2004).
    F) ACUTE BOWEL INFARCTION
    1) WITH POISONING/EXPOSURE
    a) BOWEL INFARCTION: A small bowel infarction occurred in an adult patient who ingested gun blueing solution, but was felt to be due to repeated hypotensive episodes rather than a direct effect of the selenious acid (Pentel et al, 1985).
    G) GASTRIC HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: In a fatal case of Gun Blue ingestion, the autopsy revealed hemorrhagic gastritis, grayish discoloration of the esophagus and gastric mucosa, and presence of grayish creamy fluid in the stomach consistent with the history of ingestion (Quadrani et al, 2000).
    H) BREATH SMELLS UNPLEASANT
    1) WITH POISONING/EXPOSURE
    a) A garlic-like odor has been reported following ingestion of a gun-bluing solution containing selenious acid (Hunsaker et al, 2005).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Transient elevations in liver function tests have been noted (Kise et al, 2004; Pentel et al, 1985). Congestion and diffuse swelling of the liver has been seen in fatal cases (Koppel et al, 1986).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) TOXIC NEPHROPATHY
    1) WITH POISONING/EXPOSURE
    a) Diffuse swelling of the kidneys, tubular injury, and small areas of papillary necrosis have been noted in fatal cases (Quadrani et al, 2000; Koppel et al, 1986; Pentel et al, 1985).
    b) Mild renal insufficiency has been noted as a premorbid condition in fatal cases (Pentel et al, 1985).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) METABOLIC ACIDOSIS has been noted in cases of ingestion (Pentel et al, 1985).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) Thrombocytopenia has been observed in a patient with fatal selenious acid ingestion (Pentel et al, 1985).
    B) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Elevated leukocyte counts were noted in several workers with inhalation exposure to selenium dioxide fumes and chemical pneumonitis (Wilson, 1962).
    b) An elevated leukocyte count of 21.2 x 10(3)/mcL was reported in a 24-year-old man following ingestion of a gun-bluing agent containing selenious acid (Hunsaker et al, 2005).
    C) COAG./BLEEDING TESTS ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Laboratory examination of a 24-year-old man, who ingested an unknown amount of gun-bluing solution containing selenious acid, revealed elevated hemoglobin and hematocrit concentrations of 19.3 g/dL and 57.7%, respectively, and an elevated INR of 7.6 (Hunsaker et al, 2005).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Dermal exposures to selenium dioxide (selenium oxide) can produce dermatitis (Finkel, 1983; Cerwenka & Cooper, 1961).
    B) NAIL FINDING
    1) WITH POISONING/EXPOSURE
    a) Dermal exposures to selenium dioxide (selenium oxide) can produce paronychia (Finkel, 1983; Cerwenka & Cooper, 1961).
    C) TOOTH COLOR - FINDING
    1) WITH POISONING/EXPOSURE
    a) RED STAINING: Precipitation of small amounts of amorphous selenium in the tissues can cause a red staining of the teeth (Finkel, 1983).
    D) DISCOLORATION OF SKIN
    1) WITH POISONING/EXPOSURE
    a) Orange-red staining of the skin and viscera were seen in one fatal ingestion case (Koppel et al, 1986).
    b) RED STAINING: Precipitation of small amounts of amorphous selenium in the tissues can cause a red staining of the fingers and hair (Finkel, 1983).
    E) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Dermal burns can result from skin contact (Finkel, 1983).
    F) SKIN NECROSIS
    1) WITH POISONING/EXPOSURE
    a) Necrotizing skin lesions can occur if selenium dioxide gets inside rubber gloves (Finkel, 1983).
    G) SYSTEMIC DISEASE
    1) WITH POISONING/EXPOSURE
    a) Systemic absorption may occur through denuded areas (Finkel, 1983).
    H) PAIN
    1) WITH POISONING/EXPOSURE
    a) Excruciating pain may result if this agent penetrates beneath the free edge of the fingernails (ACGIH, 1986; Cerwenka & Cooper, 1961).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Weakness of skeletal muscles including the diaphragm may be severe and can lead to respiratory failure requiring mechanical ventilation (Pentel et al, 1985).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7783-00-8 (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):
    1) Not Listed

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Institute continuous cardiac monitoring and obtain an ECG.
    C) Monitor serum electrolytes, renal function, liver enzymes, CBC and urinalysis.
    D) Though it is possible to measure selenium concentrations in plasma, it is not readily available or useful for immediate treatment. Selenium blood and urine levels may be useful later to confirm the diagnosis, especially in work-related exposures.
    E) For patients with respiratory symptoms, monitoring pulse oximetry, arterial blood gases, chest x-ray and pulmonary function tests may all be useful.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitoring selenium blood levels may be useful to confirm the substance and if a laboratory can provide timely assays, to follow the course of the poisoning.
    B) TOXICITY
    1) Selenious acid may produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, acid-base status, fluid status, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Monitoring urine selenium excretion may be useful to confirm the substance and if a laboratory can provide timely assays, to follow the course of the poisoning.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitoring such cardiovascular parameters as central venous pressure, pulmonary wedge pressure, cardiac output, and total peripheral resistance may be valuable in assessing therapeutic interventions when cardiopulmonary toxicity and shock are present.
    b) For patients with respiratory symptoms, monitoring pulse oximetry, arterial blood gases, chest x-ray and pulmonary function tests may all be useful.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Selenium may be measured in biological samples by atomic absorption spectrometry (Lombeck et al, 1987; Schellmann et al, 1986; Matoba et al, 1986; Koppel et al, 1986).

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) Patients who develop any symptoms secondary to selenious acid should be admitted for further observation. Depending on the severity of symptoms, a patient may require an intensive care setting. Patients may be discharged home after symptoms are clearly improving after a prolonged observation.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild dermal irritation after topical exposure involving a small surface area can be managed at home. Any patient ingesting selenious acid should be referred to a healthcare facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center and/or medical toxicologist for any patient with a selenious acid ingestion.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) All patients with a history of ingestion should be set to a healthcare facility for further observation. Patients who are asymptomatic after 4 to 6 hours of observation may be sent home. All other patients should be observed overnight as secondary symptoms may develop several hours later. Patients may be discharged home after they are clearly improving.
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients with inhalation exposure should be treated with supplemental oxygen beginning as soon as possible after rescue and should have a prolonged period of observation in a controlled setting with careful monitoring for the development of chemical pneumonitis.

Monitoring

    A) Monitor vital signs and mental status.
    B) Institute continuous cardiac monitoring and obtain an ECG.
    C) Monitor serum electrolytes, renal function, liver enzymes, CBC and urinalysis.
    D) Though it is possible to measure selenium concentrations in plasma, it is not readily available or useful for immediate treatment. Selenium blood and urine levels may be useful later to confirm the diagnosis, especially in work-related exposures.
    E) For patients with respiratory symptoms, monitoring pulse oximetry, arterial blood gases, chest x-ray and pulmonary function tests may all be useful.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS SHOULD NOT BE INDUCED because of the potential for the rapid development of seizures, coma, and shock with cardiorespiratory arrest following ingestion of selenious acid.
    2) Because small amounts of selenious acid can be fatal and there is no antidote, consider insertion of a small, flexible nasogastric tube to suction gastric contents in recent ingestions.
    B) MUCOSAL DECONTAMINATION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
    C) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.
    D) 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) EMESIS/NOT RECOMMENDED
    1) Emesis SHOULD NOT be induced because of the potential for the rapid development of seizures, coma, and shock with cardiorespiratory arrest following ingestion of selenious acid.
    B) ACTIVATED CHARCOAL
    1) 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.
    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).
    C) NASOGASTRIC SUCTION
    1) Because small amounts of selenious acid can be fatal and there is no antidote, consider insertion of a small, flexible nasogastric tube to suction gastric contents in recent ingestions.
    2) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    3) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Basic supportive care is the most important treatment measure.
    2) Move victims of inhalation exposure from the toxic environment and administer 100% humidified supplemental oxygen with assisted ventilation as required. Exposed skin and eyes should be copiously flushed with water.
    3) In ingestion exposures, the potential for early development of shock, coma, and seizures as well as the potential for erosive lesions of the esophagus and gastrointestinal tract mandate that emesis should NOT be induced and gastric lavage done only with caution.
    4) Shock may develop very rapidly following ingestion and intensive supportive therapy should be provided as soon as possible. The prognosis is poor when more than a small amount of selenious acid is ingested.
    5) Patients with inhalation exposure to selenium dioxide fumes may develop a mild initial illness which is followed in 2 to 12 or more hours by development of fever, chills, malaise, leukocytosis, and chemical pneumonitis. Early administration of supplemental oxygen and prolonged observation in a controlled setting are indicated.
    B) MONITORING OF PATIENT
    1) If shock or cardiopulmonary arrest occur, standard Advanced Cardiac Life Support procedures should be followed, although these have often not been effective (Normann et al, 1984).
    2) Monitor ECG, vital signs, and urine output carefully.
    3) Monitoring such cardiovascular parameters as central venous pressure, pulmonary wedge pressure, cardiac output, and total peripheral resistance may be valuable in assessing therapeutic interventions when cardiopulmonary toxicity and shock are present.
    4) If coma and respiratory depression occur, ensure airway patency and adequacy of respirations and oxygenation. Endotracheal intubation, administration of supplemental oxygen, and assisted ventilation may be required.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    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.
    2) DOPAMINE
    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).
    3) NOREPINEPHRINE
    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
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    F) CHELATION THERAPY
    1) SUMMARY
    a) In general, chelation or antagonist therapy with available agents has NOT been recommended in cases of poisoning with selenious acid.
    2) CALCIUM DISODIUM EDTA
    a) Experimental animal studies have shown that while calcium disodium EDTA decreased selenium toxicity if given within 15 minutes of ingestion, after that time period administration of the chelating agent actually INCREASED selenium toxicity (Civil & McDonald, 1978). Both the chelating agent and its selenium chelate product are nephrotoxic (Civil & McDonald, 1978).
    b) Administration of calcium disodium EDTA is NOT recommended in human poisoning cases.
    3) BAL (DIMERCAPROL)
    a) In experimental animal studies, administration of BAL INCREASED the toxicity of selenium (Civil & McDonald, 1978).
    b) Administration of BAL is NOT recommended in human poisoning cases.
    4) ASCORBIC ACID
    a) Experimental animal studies have shown that although ascorbic acid administration increases the excretion of selenium, it also INCREASES selenium toxicity (Civil & McDonald, 1978).
    b) Administration of ascorbic acid is NOT recommended in human poisoning cases.
    5) OTHERS
    a) Glutathione has been suggested as an antagonist in experimental animals but has not been tried for the treatment of human poisoning (Lombeck et al, 1987).
    b) Methionine was ineffective in treating experimental selenium poisoning (Lombeck et al, 1987).
    c) Bromobenzene may hasten selenium excretion in some experimental animals, but has NOT been recommended for treatment of human poisonings because of its toxicity and high incidence of severe adverse reactions (Finkel, 1983). It was not effective when administered orally to selenium-poisoned rats.
    d) Apparently no studies have been done using d-penicillamine or DMSA for the treatment of selenium poisoning. Severe gastrointestinal symptoms and early development of seizures, coma, or shock would limit the administration of these oral agents. The fact that other chelating agents increase selenium toxicity in experimental animals would argue against their administration.
    G) ENDOSCOPIC PROCEDURE
    1) There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of concentrated selenious acid ingestion. The following information is derived from experience with other corrosives.
    2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    3) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (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; Nuutinen et al, 1994)
    5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    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).
    6) GRADING
    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.
    7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    H) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    I) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, 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).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Initial respiratory tract irritation may appear to improve, but can then worsen between 2 and 12 hours after exposure (Wilson, 1962). Severe chemical pneumonitis may then develop over the following one to three days (Wilson, 1962).
    2) Early administration of supplemental oxygen seemed to mitigate the degree of chemical pneumonitis that developed in one incident (Wilson, 1962).
    3) Patients with inhalation exposure should be treated with supplemental oxygen beginning as soon as possible after rescue and should have a prolonged period of observation in a controlled setting with careful monitoring for the development of chemical pneumonitis.
    B) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    C) PULMONARY EDEMA
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) CONSULTATION
    1) Because of the potential for serious corneal burns following direct eye contact with this agent, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) SODIUM THIOSULFATE
    1) Washing exposed skin with a 10% aqueous solution of sodium thiosulfate followed by topical application of a 10% sodium thiosulfate cream has been previously recommended (Cerwenka & Cooper, 1961). There is, however, no scientific evidence that the use of sodium thiosulfate is actually as good or better than standard topical chemical burn therapy.
    C) SKIN ABSORPTION
    1) Following selenium dioxide dermal burns, increased systemic absorption may take place through denuded areas of skin (Finkel, 1983).
    2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) There is no evidence to support the use of multiple dose activated charcoal or hemoperfusion. Hemodialysis was used after an intentional ingestion (one case) of selenium dioxide with initial decreases in selenium level in both serum and urine, but dialysis clearance was not determined.
    B) HEMOPERFUSION
    1) An in-vitro study showed that hemoperfusion might have only a "moderate effect" on selenium blood levels in selenious acid poisoning (Koppel et al, 1986). This procedure has not been utilized in human poisoning cases and cannot be recommended at this time.
    C) EXCHANGE TRANSFUSION
    1) No mention of early exchange transfusion for the treatment of selenious acid poisoning has been made in the literature.
    D) HEMODIALYSIS
    1) CASE REPORT: A 48-year-old schizophrenic woman developed deep gastric ulcer after ingesting 2000 mg of selenium dioxide (a bottle of glass blue; 10 times the experimental lethal dose in animals) in a suicide attempt. Following intubation and gastric lavage, hemodialysis was initiated. Initially, both the serum and urine selenium levels decreased. However, urinary selenium levels increased later followed by eventual gradual decrease. Dialysis clearance of selenium was not determined. The patient was discharged approximately 2 weeks postingestion (Kise et al, 2004).

Abstracts

Case Reports

    A) ADULT
    1) ACUTE EFFECTS
    a) An adult industrial worker suffered fatal selenious acid poisoning during an explosion. Approximately 450 L of selenious acid exploded. The patient had dermal burns from the heated material as well as inhalation of fumes and possible ingestion of some of the agent. Death occurred 90 minutes after exposure, despite the fact that protective clothing was worn and the material was immediately washed off. Hypotension, pulmonary edema, cardiomyopathy, and moderate renal tubular injury were noted during resuscitation attempts and at autopsy. Dermal burns covered less than 10% of the total body area (Schellmann et al, 1986).
    B) PEDIATRIC
    1) A 3-year-old child who ingested a 1.8% selenious acid containing gun blueing solution died approximately 1.5 hours after ingestion (Carter, 1966). In a similar case, a 22-month-old child died 1.5 hours after ingestion of 20 mL of a gun-blueing compound containing selenious acid (Normann et al, 1984).
    2) A 17-year-old boy died approximately 2 hours after ingesting an unknown amount of selenium dioxide. The patient presented with asystole and apnea. Findings at autopsy included congestion of lungs and kidneys, diffuse swelling of the heart, brain edema, and orange-brown discoloration of the skin and all viscera (Koppel et al, 1986).

Range Of Toxicity

Summary

    A) TOXICITY: Ingestion of a few drops of selenium acid-containing gun blueing solution may cause illness, and more than 15 mL has been fatal. PEDIATRIC: Ingestion of up to 20 mL of a 2% selenious acid-containing gun blueing compound has been fatal in toddlers. ADULT: Ingestion of 30 to 90 mL of gun blueing solutions containing 2 to 4% selenious acid has been fatal in adults.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) PEDIATRIC
    a) Ingestion of up to 20 mL of a 2% selenious acid-containing gun blueing compound by 3 children (a 2-year-old child and two 22-month-old children) were fatal (Quadrani et al, 2000; Ellenhorn & Barceloux, 1988; Normann et al, 1984).
    b) In a similar case, a 3-year-old child who ingested a 1.8% selenious acid containing gun blueing solution died approximately 1.5 hours after ingestion (Carter, 1966).
    B) ADULT
    1) A 40-year-old woman died after ingestion of nearly 90 mL of a 4% selenious acid gun blueing solution (Matoba et al, 1986).
    2) A 17-year-old patient died after ingestion of approximately 10 g of selenium dioxide (Koppel et al, 1986).
    3) A 30 to 60 mL ingestion of a 2% selenious acid-containing gun blueing compound caused death in an adult (Ellenhorn & Barceloux, 1988).
    C) OCCUPATIONAL
    1) An adult industrial worker suffered fatal selenious acid poisoning during an explosion. Approximately 450 L of selenious acid exploded. The patient had dermal burns from the heated material as well as inhalation of fumes and possible ingestion of some of the agent. Death occurred 90 minutes after exposure, despite the fact that protective clothing was worn and the material was immediately washed off. Hypotension, pulmonary edema, cardiomyopathy, and moderate renal tubular injury were noted during resuscitation attempts and at autopsy. Dermal burns covered less than 10% of the total body area (Schellmann et al, 1986).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) PEDIATRIC
    a) Ingestion of as much as 2.9 g of selenium (11 mL of a selenious acid gun blueing compound) caused moderately severe symptoms in a 2-year-old child. This child fully recovered with supportive therapy. The lack of esophageal injury on esophagoscopy lead the authors to speculate that only a few drops of the material may actually have been ingested (Lombeck et al, 1987).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) Selenium concentration in plasma 5 hours following an ingestion of up to 2.9 grams was 1,580 nanograms/milliliter in a 2-year-old child (Lombeck et al, 1987).
    b) Serial plasma selenium levels in this case were (in nanograms Se/milliliter):
    1) 5 hours postingestion - 1,580 ng/mL
    2) 17 hours postingestion - 560 ng/mL
    3) 36 hours postingestion - 180 ng/mL
    4) Over the following 2 months - 95 to 110 ng/mL
    2) CASE REPORTS
    a) ADULT
    1) A worker fatally poisoned with selenious acid by the dermal and inhalation routes had a postmortem plasma selenium level of 18.4 milligrams Se/liter and a urine level of 2.11 milligrams Se/liter, respectively 250 and 90 times the concentrations normally found (Schellmann et al, 1986).
    2) Serum selenium levels obtained on the fourth and fifth days following ingestion from a 52-year-old patient who ingested 30 to 60 milliliters of a gun blueing solution containing 2% selenious acid were 2435 and 2765 nanograms/milliliter respectively (normals: 86 to 125 nanograms/milliliter) (Pentel et al, 1985).
    3) A 22-month-old male fatally poisoned with 15 milliliters of Gun Blue solution (selenious acid) had a postmortem plasma selenium level of 12 micrograms/milliliter, and gastric content of 270 micrograms/milliliter (Guadrani et al, 2000).
    4) A 48-year-old schizophrenic woman developed deep gastric ulcer after ingesting 2000 mg of selenium dioxide (a bottle of glass blue; 10 times the experimental lethal dose in animals) in a suicide attempt. Plasma levels, obtained 3 to 6 hours after ingestion, was above 2000 mcg/L. Endoscopy showed mucosal damage throughout the oral cavity, esophagus, and stomach. Necrotic tissue, forming a deep ulcer (classified as grade 3 corrosive gastritis) was observed at the gastric angulus. Following intubation, gastric lavage, and hemodialysis, she was discharged approximately 2 weeks postingestion (Kise et al, 2004).
    5) A 24-year-old man ingested an unknown quantity of gun-bluing solution, containing selenious acid, and subsequently developed cyanosis, coma, cardiac arrest, and death. Postmortem selenium fluid and tissue concentrations were as follows (Hunsaker et al, 2005):
    Sample Case Report Normal Values
    Blood (mcg/L) 30,000 (Antemortem Serum) 13,000 (Postmortem whole blood) 66 to 104 serum 80 to 130 whole blood
    Gastric contents (mcg/L) 52,000 .
    Bile (mcg/L) 15,000 .
    Vitreous fluid (mcg/L) 31 .
    Kidney (mcg/g) 7.8 0.89
    Liver (mcg/g) 10 0.35 to 0.65
    Brain (mcg/g) 1.7 0.11 to 0.17
    Heart (mcg/g) 110.33
    Spleen (mcg/g) Not done 0.37
    Lung (mcg/g) Not done 0.30
    Skeletal muscle (mcg/g) 1.7 0.4
    Hair (mcg/g) Not done 0.64

Workplace Standards

    A) ACGIH TLV Values for CAS7783-00-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7783-00-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7783-00-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Selenious acid
    a) D : Not classifiable as to human carcinogenicity.
    3) 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
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7783-00-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Pharmacology Toxicology

Toxicologic Mechanism

    A) The toxicity of selenious acid is thought to be due to inhibition of the activity of sulfhydryl-containing enzymes (Normann et al, 1984).

Physicochemical

Physical Characteristics

    A) Selenium dioxide or selenium oxide (SeO2) is a white crystalline solid that readily decomposes in water, forming selenious acid (H2SeO3) (Ellenhorn & Barceloux, 1988; Koppel et al, 1986).
    B) deliquescent, hexagonal prisms (Budavari, 1989)
    C) transparent, colorless crystals (Lewis, 1992)
    D) colorless (Lewis, 1992)

Ph

    A) The pH of several commercial gun blueing solutions containing selenious acid or selenium dioxide is 1.5.

Molecular Weight

    A) 128.98 (Budavari, 1989)

References

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