SELENIUM OXYCHLORIDE

Classification | Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

Specific Substances

1.2.1) MOLECULAR FORMULA
1) Cl2-O-Se

Available Forms Sources

1) Selenium oxychloride is a nearly colorless or yellowish CORROSIVE liquid which fumes on exposure to air (HSDB, 1993; (Budavari, 1989; EPA, 1985). It is miscible with chloroform, carbon tetrachloride, benzene, toluene, and carbon disulfide (HSDB, 1993). It decomposes in water to form HYDROCHLORIC ACID and SELENIOUS ACID (HSDB, 1993; (Budavari, 1989; EPA, 1985; Sax & Lewis, 1989; Sax & Lewis, 1987) AAR, 1987; NIOSH, 1990; (ACGIH, 1986; Finkel, 1983).
2) The toxicity of selenium oxychloride is predicted to be similar to that of SELENIOUS ACID (EPA, 1985). This review is based on the properties of selenious acid. Effects attributed specifically to selenium oxychloride are identified.

1) Selenium oxychloride is used as a solvent for numerous substances, including metals, as a chlorinating agent, and as a plasticizer for resins (Budavari, 1989; Clayton & Clayton, 1981; EPA, 1985; HSDB , 1990).

Overview

Life Support

Clinical Effects

0.2.1)

A) Selenious oxychloride dissociates into HYDROCHLORIC ACID and SELENIOUS ACID on contact with moisture. Its systemic toxicity is thus predicted to be similar to that of SELENIOUS ACID, as reflected in the following discussion. Selenious oxychloride may be absorbed following ingestion, inhalation, or dermal contact.

1) Dermal application has resulted in systemic absorption. Eye contact can result in burns or irritation. Ingestion may result in severe burns of the mouth, esophagus, or gastrointestinal tract.

B) Tachypnea, fever, initial hypertension followed by hypotension and shock, and tachycardia may be noted. Inhalation exposure may result in eye irritation or corneal burns and upper respiratory tract irritation. Pharyngeal edema, erosions, or burns may be noted in selenious acid ingestion exposure.
C) Cardiovascular effects may include ECG abnormalities, dysrhythmias, cardiomyopathy, mild hypertension followed by significant hypotension and shock. Selenium oxychloride releases toxic and irritating fumes of chloride and selenium when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
D) CNS depression or coma may occur following selenious acid ingestion, inhalation, or dermal exposure. Seizures may occur. Restlessness was noted on presentation in a nonfatal case.
E) Nausea, vomiting, diarrhea, and hematemesis may occur. Esophageal, pharyngeal, and gastrointestinal tract burns and erosions have been noted. Congestion and diffuse swelling of the liver and kidney, tubular injury, and small areas of papillary necrosis have been seen in fatal cases.
F) Hematologic effects may include metabolic acidosis, thrombocytopenia, and elevated leukocyte counts. Weakness of skeletal muscles, including the diaphragm, may be severe and lead to respiratory failure requiring mechanical ventilation.
G) Dermal exposures to selenium dioxide (selenium oxide) can produce dermatitis and vesiculation. Precipitation of small amounts of amorphous selenium in the tissues can cause a red staining of the fingers, teeth, and hair. Dermal burns can result from skin contact, and systemic absorption may occur through denuded areas. Necrotizing skin lesions can occur if selenium dioxide gets inside rubber gloves. If this compound penetrates beneath the free edge of the fingernails, excruciating pain may result.
H) TOMES Plus system users may refer to the ACIDS and SELENIOUS ACID MEDITEXT Medical Management FOR MORE INFORMATION.

0.2.3)

A) Tachypnea, fever, initial hypertension followed by hypotension and shock, and tachycardia may be noted.

0.2.4)

A) Vapor exposure may result in eye irritation. Direct contact with the material may cause corneal burns. Selenious acid inhalation exposure may cause irritation of the mucosa of the nose and throat. Pharyngeal edema, erosions, or burns may be noted in selenious acid ingestion exposures.

0.2.5)

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. Cardiac dysrhythmias including sinus tachycardia, frequent premature ventricular contractions, and asystole have been noted in cases of selenious acid poisoning.
B) A toxic cardiomyopathy, with decreased cardiac output contributing to hypotension and shock, has been observed in cases of selenious acid ingestion exposure. Patients ingesting selenious acid may initially develop mild hypertension, but this is followed in serious poisonings by significant hypotension and shock.

0.2.6)

A) Pulmonary edema may develop, even in cases of selenious acid ingestion. Selenious acid inhalation exposure can result in severe respiratory tract irritation and chemical pneumonitis. Chronic pulmonary sequelae have not been described following acute selenious acid inhalation injury. Weakness of skeletal muscles including the diaphragm may be severe and can lead to respiratory failure requiring mechanical ventilation in selenious acid poisoning.
B) Selenium oxychloride releases toxic and irritating fumes of chloride and selenium when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

0.2.7)

A) CNS depression or coma may occur following selenious acid ingestion, inhalation, or dermal exposure. Seizures may occur. Restlessness was noted on presentation in a nonfatal case.

0.2.8)

A) Nausea, vomiting, and diarrhea are common following selenious acid or selenium dioxide poisoning, regardless of the route of exposure. Hematemesis may be present. Esophageal, pharyngeal, and gastrointestinal tract burns or erosions have been described in many cases of ingestion.
B) 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.

0.2.9)

A) Transient elevations in liver function tests have been noted in selenious acid poisoning. Congestion and diffuse swelling of the liver have been seen in fatal cases.

0.2.10)

A) Diffuse swelling of the kidneys, tubular injury, and small areas of papillary necrosis have been noted in fatal cases of selenious acid poisoning. Mild renal insufficiency has been noted as a premorbid condition in fatal cases.

0.2.11)

A) Metabolic acidosis has been noted in cases of selenious acid ingestion.

0.2.12)

A) Some of the hypotension noted in selenious acid poisoning may be due to fluid losses from copious vomiting and diarrhea.

0.2.13)

A) Thrombocytopenia has been observed in a patient with fatal selenious acid ingestion. Elevated leukocyte counts were noted in several workers with inhalation exposure to selenium dioxide fumes and chemical pneumonitis.

0.2.14)

A) Dermal exposures to selenium dioxide (selenium oxide) can produce dermatitis and paronychia. Precipitation of small amounts of amorphous selenium in the tissues can cause a red staining of the fingers, teeth, and hair. Orange-red staining of the skin and viscera were seen in one fatal selenious acid ingestion case. Excruciating pain may result if selenious acid penetrates beneath the free edge of the fingernails.
B) Dermal burns can result from selenious acid skin contact, and systemic absorption may occur through denuded areas. Necrotizing skin lesions can occur if selenium dioxide gets inside rubber gloves. Selenious oxychloride is a strong irritant and vesicant substance, and can destroy skin on contact if not immediately washed off.

0.2.15)

A) Weakness of skeletal muscles including the diaphragm may be severe and can lead to respiratory failure requiring mechanical ventilation in selenious acid poisoning.

0.2.20)

A) Some spontaneous abortions and neonates born with bilateral talipes equinovarus (club foot deformity) have been noted in selenite-exposed female workers, suggesting that occupational exposure to selenium compounds may pose a human reproductive risk.
B) Studies with potassium selenate and sodium selenite in rats, rabbits, mice, and hamsters have failed to produce teratogenic effects; an unspecified selenium salt caused teratogenic effects in sheep.
C) Irregular menses have been reported in Japanese selenium rectifier workers.
D) Selenium may be transferred to the fetus through the placenta.
E) Selenium appears in the breast milk, with the levels depending on dietary intake.
F) No information about possible male reproductive effects was found in available references at the time of this review.

0.2.21)

A) Current evidence indicates that selenium and its compounds are NOT carcinogenic in man.

Laboratory Monitoring

Treatment Overview

0.4.2)

A) Do NOT induce emesis, because of the potential for the rapid development of seizures, coma, and shock with cardiorespiratory arrest following ingestion of selenious acid.
B) Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
D) 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.
E) 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.
F) If shock or cardiopulmonary arrest occur, standard Advanced Cardiac Life Support procedures should be followed, although these have often not been effective. Monitor EKG, vital signs, and urine output carefully.
G) 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.
H) 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.
I) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 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) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 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).

1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

J) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
K) 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.
L) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
M) If esophageal or GI tract burns are suspected or present, surgical consultation is advisable.
N) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenious acid.
O) An in-vitro study showed that hemoperfusion might have only a "moderate effect" on selenium blood levels in selenious acid poisoning. This procedure has not been utilized in human poisoning cases and cannot be recommended at this time. No mention of early exchange transfusion for the treatment of selenious acid poisoning has been made in the literature.
P) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

0.4.3)

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) Initial respiratory tract irritation may appear to improve, but can then worsen between 2 and 12 hours after exposure. Severe chemical pneumonitis may then develop over the following one to three days.

1) Early administration of supplemental oxygen seemed to mitigate the degree of chemical pneumonitis that developed in one incident. 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.

C) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
D) 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.
E) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
F) If shock or cardiopulmonary arrest occur, standard Advanced Cardiac Life Support procedures should be followed, although these have often not been effective. Monitor EKG, vital signs, and urine output carefully.
G) 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.
H) 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.
I) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 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) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 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).

J) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
K) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenious acid.
L) An in-vitro study showed that hemoperfusion might have only a "moderate effect" on selenium blood levels in selenious acid poisoning. This procedure has not been utilized in human poisoning cases and cannot be recommended at this time. No mention of early exchange transfusion for the treatment of selenious acid poisoning has been made in the literature.
M) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
N) 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.

0.4.4)

A) DECONTAMINATION: 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, the patient should be seen in a healthcare facility.
B) Because of the potential for serious corneal burns following direct eye contact with this agent, prolonged initial flushing and early ophthalmologic consultation are advisable.

0.4.5)

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).
2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
3) Washing exposed skin with a 10 percent aqueous solution of sodium thiosulfate followed by topical application of a 10 percent sodium thiosulfate cream has been previously recommended. There is, however, no scientific evidence that the use of sodium thiosulfate is actually as good or better than standard topical chemical burn therapy.
4) Following selenium dioxide dermal burns, increased systemic absorption may take place through denuded areas of skin.

a) 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.
b) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Range Of Toxicity

Clinical Effects

Summary Of Exposure

1) Dermal application has resulted in systemic absorption. Eye contact can result in burns or irritation. Ingestion may result in severe burns of the mouth, esophagus, or gastrointestinal tract.

Vital Signs

3.3.1)

A) Tachypnea, fever, initial hypertension followed by hypotension and shock, and tachycardia may be noted.

3.3.2)

A) TACHYPNEA may be noted in selenious acid poisoning (Carter, 1966).

3.3.3)

A) FEVER has developed as part of the delayed secondary toxicity seen after inhalation of selenium dioxide fumes (Wilson, 1962).

3.3.4)

A) 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)

A) TACHYCARDIA - An elevated pulse has been described in cases of selenious acid poisoning (Lombeck et al, 1987; Carter, 1966).

Heent

3.4.1)

3.4.3)

A) CONJUNCTIVITIS - Vapor exposure may result in eye irritation (ACGIH, 1986).

1) Eye contact with selenium oxychloride can result in burns or irritation (EPA, 1985; Sittig, 1991).

B) CORNEAL BURNS - Direct contact with the material may cause corneal burns (Cerwenka & Cooper, 1961; Sittig, 1991).

1) Eye contact with selenium oxychloride can result in burns or irritation (EPA, 1985; Sittig, 1991; ILO, 1998).

C) ROSE EYE - Exposure may result in a pinkish allergic condition of the eyelids, often accompanied by a conjunctivitis of the palpebral conjunctiva (Zenz, 1994).

3.4.5)

A) IRRITATION - Selenious acid inhalation exposure may cause irritation of the mucosa of the nose and throat (Wilson, 1962).

3.4.6)

A) IRRITATION - Selenious acid inhalation exposure may cause irritation of the mucosa of the nose and throat (Wilson, 1962).
B) EDEMA/EROSIONS - Pharyngeal edema, erosions, or burns may be noted in selenious acid ingestion exposures (Koppel et al, 1986; Matoba et al, 1986; Schellmann et al, 1986; Nantel et al, 1985).

Cardiovascular

3.5.1)

3.5.2)

A) ELECTROCARDIOGRAM ABNORMAL

1) 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, all of which became maximal at three days after exposure and cleared over the following two weeks (Civil & McDonald, 1978).

B) CONDUCTION DISORDER OF THE HEART

1) Cardiac dysrhythmias including sinus tachycardia, frequent premature ventricular contractions, and asystole have been noted in cases of selenious acid poisoning (Pentel et al, 1985) Koppel et al, 1987).

C) CARDIOMYOPATHY

1) A toxic cardiomyopathy, with decreased cardiac output contributing to hypotension and shock, has been observed in cases of selenious acid ingestion exposure (Matoba et al, 1986; Normann et al, 1984; Ellenhorn & Barceloux, 1988; Pentel et al, 1985).

D) HYPOTENSIVE EPISODE

1) Patients ingesting selenious acid may initially develop mild hypertension, but this is followed in serious poisonings by significant hypotension and shock (Carter, 1966).
2) Hypotension secondary to both low peripheral vascular resistance and toxic cardiomyopathy can occur and the resultant shock may be a cause of early deaths (Matoba et al, 1986; Normann et al, 1984; Ellenhorn & Barceloux, 1988; Pentel et al, 1985).

Respiratory

3.6.1)

3.6.2)

A) ACUTE LUNG INJURY

1) Pulmonary edema may develop, even in cases of selenious acid ingestion (Pentel et al, 1985). It is unclear whether the pulmonary edema is cardiogenic or noncardiogenic in origin (Pentel et al, 1985).

B) PNEUMONITIS

1) Selenious acid inhalation exposure can 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).
2) Chronic pulmonary sequelae have not been described following acute selenious acid inhalation injury (Wilson, 1962).

C) APNEA

1) Weakness of skeletal muscles including the diaphragm may be severe and can lead to respiratory failure requiring mechanical ventilation in selenious acid poisoning (Pentel et al, 1985).

D) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS

1) Selenium oxychloride releases toxic and irritating fumes of chloride and selenium when heated to decomposition (Lewis, 1996; EPA, 1985). Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

Neurologic

3.7.1)

A) CNS depression or coma may occur following selenious acid ingestion, inhalation, or dermal exposure. Seizures may occur. Restlessness was noted on presentation in a nonfatal case.

3.7.2)

A) COMA

1) CNS depression or coma may occur following selenious acid ingestion, inhalation, or dermal exposure (Koppel et al, 1986; Nantel et al, 1985; Schellmann et al, 1986).

B) SEIZURE

1) Seizures may occur following selenious acid ingestion (Koppel et al, 1986).

C) FEELING NERVOUS

1) Restlessness was noted on presentation in a nonfatal case selenious acid poisoning (Lombeck et al, 1987).

Gastrointestinal

3.8.1)

3.8.2)

A) NAUSEA, VOMITING AND DIARRHEA

1) Nausea, vomiting, and diarrhea are 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).
2) Nausea and abdominal cramps may occur following ingestion of selenium oxychloride (ILO, 1998).
3) Hematemesis may be present in some cases (Nantel et al, 1985).

B) CHEMICAL BURN

1) Esophageal, pharyngeal, and gastrointestinal tract burns or erosions have been described in many cases of ingestion (Koppel et al, 1986; Matoba et al, 1986; Schellmann et al, 1986; Nantel et al, 1985).
2) Ingestion of selenium oxychloride may result in severe burns of the mouth, esophagus, or gastrointestinal tract (EPA, 1985; Sittig, 1991).

C) VASCULAR INSUFFICIENCY OF INTESTINE

1) 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).

Hepatic

3.9.1)

A) Transient elevations in liver function tests have been noted in selenious acid poisoning. Congestion and diffuse swelling of the liver have been seen in fatal cases.

3.9.2)

A) LIVER DAMAGE

1) Transient elevations in liver function tests have been noted in selenious acid poisoning (Nantel et al, 1985). Congestion and diffuse swelling of the liver have been seen in fatal cases (Koppel et al, 1987).

Genitourinary

3.10.1)

3.10.2)

A) TOXIC NEPHROPATHY

1) Diffuse swelling of the kidneys, tubular injury, and small areas of papillary necrosis have been noted in fatal cases of selenious acid poisoning (Koppel et al, 1987; (Pentel et al, 1985). Mild renal insufficiency has been noted as a premorbid condition in fatal cases (Pentel et al, 1985).

Acid-Base

3.11.1)

A) Metabolic acidosis has been noted in cases of selenious acid ingestion.

3.11.2)

A) ACIDOSIS

1) Metabolic acidosis has been noted in cases of selenious acid ingestion (Pentel et al, 1985).

Hematologic

3.13.1)

3.13.2)

A) THROMBOCYTOPENIC DISORDER

1) Thrombocytopenia has been observed in a patient with fatal selenious acid ingestion (Pentel et al, 1985).

B) LEUKOCYTOSIS

1) Elevated leukocyte counts were noted in several workers with inhalation exposure to selenium dioxide fumes and chemical pneumonitis (Wilson, 1962).

Dermatologic

3.14.1)

3.14.2)

A) DERMATITIS

1) Dermal exposures to selenium dioxide (selenium oxide) can produce dermatitis and paronychia (Finkel, 1983; Cerwenka & Cooper, 1961).

B) DISCOLORATION OF SKIN

1) RED STAINING - Precipitation of small amounts of amorphous selenium in the tissues can cause a red staining of the fingers, teeth, and hair (Finkel, 1983).
2) Orange-red staining of the skin and viscera were seen in one fatal selenious acid ingestion case (Koppel et al, 1987).

C) CHEMICAL BURN

1) Dermal burns can result from selenious acid skin contact, and systemic absorption may occur through denuded areas (Finkel, 1983). Necrotizing skin lesions can occur if selenium dioxide gets inside rubber gloves (Finkel, 1983).
2) Selenious oxychloride is a strong irritant and vesicant substance, and can destroy skin on contact if not immediately washed off (Budavari, 1996; Clayton & Clayton, 1993; Proctor et al, 1988; ACGIH, 1986; ILO, 1998; HSDB , 1999).
3) Less than 0.005 mL applied to the arm of a man caused a painful burn and swelling. Healing required 1 month (Clayton & Clayton, 1993).

D) PAIN

1) Excruciating pain may result if selenious acid penetrates beneath the free edge of the fingernails (ACGIH, 1986; Cerwenka & Cooper, 1961).

E) SKIN ULCER

1) Application of 0.01 mL of selenium oxychloride to the skin of a rabbit resulted in acute vesication and death in less than 24 hours (HSDB , 1999).

Carcinogenicity

3.21.1)

A) IARC Carcinogenicity Ratings for CAS7791-23-3 (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

3.21.2)

A) Current evidence indicates that selenium and its compounds are NOT carcinogenic in man.

3.21.3)

A) LACK OF EFFECT

1) Current evidence indicates that selenium and its compounds are NOT carcinogenic in man (HSDB , 1999).

Genotoxicity

Musculoskeletal

3.15.1)

A) Weakness of skeletal muscles including the diaphragm may be severe and can lead to respiratory failure requiring mechanical ventilation in selenious acid poisoning.

3.15.2)

A) MUSCLE WEAKNESS

1) Weakness of skeletal muscles including the diaphragm may be severe and can lead to respiratory failure requiring mechanical ventilation in selenious acid poisoning (Pentel et al, 1985).

Reproductive

3.20.1)

3.20.2)

A) ABORTION

1) Some spontaneous abortions and neonates born with bilateral talipes equinovarus (club foot deformity) have been noted in selenite-exposed female workers, suggesting that occupational exposure to selenium compounds may pose a human reproductive risk (Council on Scientific Affairs, 1985).

B) ANIMAL STUDIES

1) Studies with sodium selenite in rats, rabbits, mice, hamsters, pigs, and cats have failed to produce teratogenic effects; an unspecified selenium salt caused teratogenic effects in sheep (Schardein, 1993).

3.20.3)

A) MENSTRUAL DISORDER

1) Irregular menses have been reported in Japanese selenium rectifier workers (HSDB , 1999).

B) PLACENTAL BARRIER

1) Selenium may be transferred to the fetus through the placenta (HSDB , 1999).

3.20.4)

A) BREAST MILK

1) Selenium appears in the breast milk, with the levels depending on dietary intake (HSDB , 1999).

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
C) Pulse oximetry may be useful in monitoring patients for hypoxia.
D) Monitoring selenium blood levels may be useful to follow the course of the poisoning.
E) Monitoring urine selenium excretion may be useful to follow the course of acute poisoning or for biological monitoring of exposed workers.
F) 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.

4.1.2)

A) BLOOD/SERUM CHEMISTRY

1) Monitoring selenium blood levels may be useful to follow the course of the poisoning.
2) 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).

a) 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

3) 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 concentrations found normally (Schellmann et al, 1986).
4) 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 percent selenious acid were 2,435 and 2,765 nanograms/milliliter respectively (normals: 86 to 125 nanograms/milliliter) (Pentel et al, 1985).

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)

A) URINARY LEVELS

1) Monitoring urine selenium excretion may be useful to follow the course of acute poisoning or for biological monitoring of exposed workers (Baselt & Cravey, 1989; Baselt, 1988).
2) Urinary Concentrations (Baselt, 1988)

Normal Persons:   undetectable to 150 mcg/L
(average:  34 mcg/L)
Persons drinking
  high selenium
  content water:  22 to 203 mcg/L (average:  79 mcg/L)
Asymptomatic
  exposed
  selenium
  workers:        120 to 350 mcg/L

B) URINALYSIS

1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.

4.1.4)

A) OTHER

1) PULMONARY FUNCTION TESTS

a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

2) 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) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
c) Pulse oximetry may be useful in monitoring patients for hypoxia.

Radiographic Studies

1) If respiratory tract irritation is present, monitor chest x-ray.

Treatment

Life Support

Monitoring

Oral Exposure

6.5.2)

A) EMESIS/NOT RECOMMENDED

1) Because of the potential for rapid development of seizures, coma, and shock with cardiorespiratory arrest following ingestion of selenious acid, EMESIS SHOULD NOT BE INDUCED.

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) 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.
2) 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)

A) SUPPORT

1) CARDIAC LIFE SUPPORT - 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).

B) MONITORING OF PATIENT

1) Monitor EKG, vital signs, and urine output carefully.
2) 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.

C) AIRWAY MANAGEMENT

1) 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.

D) 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, 2010; 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).

E) 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).

F) 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).

G) IRRITATION SYMPTOM

1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
2) If esophageal or GI tract burns are suspected or present, surgical consultation is advisable.

H) CHELATION THERAPY

1) 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) 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 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) 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.

I) ENDOSCOPIC PROCEDURE

1) There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of concentrated selenium oxychloride 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.

J) 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).

K) 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.

L) OBSERVATION REGIMES

1) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Inhalation Exposure

6.7.1)

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)

A) IRRITATION SYMPTOM

1) Initial respiratory tract irritation may appear to improve, but can then worsen between 2 and 12 hours after exposure. 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. They 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) ACUTE LUNG INJURY

D) OBSERVATION REGIMES

1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
2) CARDIAC LIFE SUPPORT - 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).

E) MONITORING OF PATIENT

F) AIRWAY MANAGEMENT

G) SEIZURE

1) SUMMARY

2) DIAZEPAM

3) NO INTRAVENOUS ACCESS

4) LORAZEPAM

5) PHENOBARBITAL

6) OTHER AGENTS

H) HYPOTENSIVE EPISODE

1) SUMMARY

2) DOPAMINE

3) NOREPINEPHRINE

I) CHELATION THERAPY

1) In general, chelation or antagonist therapy with available agents HAS NOT BEEN RECOMMENDED in cases of poisoning with selenious acid.
2) Calcium Disodium EDTA -

3) BAL - (Dimercaprol) -

a) In 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 -

5) Others -

J) OBSERVATION REGIMES

1) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
2) 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.

K) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

6.8.1)

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)

A) OPHTHALMIC EXAMINATION AND EVALUATION

1) CONSULTATION - 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)

A) DERMAL DECONTAMINATION

1) 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)

A) IRRITATION SYMPTOM

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 percent aqueous solution of sodium thiosulfate followed by topical application of a 10 percent 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) BURN

1) APPLICATION

a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.

2) DEBRIDEMENT

a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).

3) TREATMENT

a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
c) WOUND DRESSING:

1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.

d) DRESSING CHANGES:

1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.

e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.

4) TETANUS PROPHYLAXIS

a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.

D) 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.

E) GENERAL TREATMENT

1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

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, 1987). This procedure has not been utilized in human poisoning cases and cannot be recommended at this time.

1) No mention of early exchange transfusion for the treatment of selenious acid poisoning has been made in the literature.

Abstracts

Range Of Toxicity

Summary

Minimum Lethal Exposure

1) For an average-sized human, the calculated fatal dose applied to the skin would be 0.2 mL (Clayton & Clayton, 1993).

1) Selenium oxychloride was fatal to rabbits in 24 hours when less than 0.1 milliliter was applied to the skin; systemic absorption was demonstrated (Clayton & Clayton, 1993)

1) INFANT

a) A 22-month-old child died after ingestion of 20 milliliters of a selenious acid gun blueing solution (Normann et al, 1984).

2) PEDIATRIC

a) A three-year-old child who ingested a 1.8 percent selenious acid containing gun blueing solution died approximately one and one-half hours after the ingestion (Carter, 1966). In a similar case, a 22-month-old child died one and one-half hours after ingestion of 20 mL of a gun-blueing compound containing selenious acid (Normann et al, 1984).
b) Ingestion of 15 milliliters of a 2 percent selenious acid-containing gun blueing compound by a 2-year-old child was fatal, and a 30 to 60 mL ingestion of a similar agent caused death in an adult (Ellenhorn & Barceloux, 1988).

3) ADULT

a) A 17-year-old male died approximately two 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).
b) A 17-year-old died after ingestion of approximately 10 grams of selenium dioxide (Koppel et al, 1986).
c) A 40-year-old woman died after ingestion of nearly 90 milliliters of a 4 percent selenious acid gun blueing solution (Matoba et al, 1986).

4) OCCUPATIONAL

a) An adult industrial worker suffered fatal selenious acid poisoning during an explosion (Schellmann et al, 1986). Approximately 450 liters 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.

1) 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 percent of the total body surface area.

Maximum Tolerated Exposure

1) ADULT

a) Application of 0.005 milliliter of selenious oxychloride to the skin in a man resulted in a painful, swollen burn which required one month to heal (Clayton & Clayton, 1981).

2) PEDIATRIC

a) Ingestion of as much as 2.9 grams of selenium (11 milliliters of a selenious acid gun blueing compound) caused moderately severe symptoms in a 2-year-old child (Lombeck et al, 1987). 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).

Workplace Standards

1) Not Listed

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
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

1) Not Listed

Toxicity Information

7.7.1)

A) Published Values RTECS, 1999

Pharmacology Toxicology

Physicochemical

Physical Characteristics

Molecular Weight

Animal Toxicology

References

General Bibliography

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FeedBack

SELENIUM OXYCHLORIDE

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Vital Signs

Heent

Cardiovascular

Respiratory

Neurologic

Gastrointestinal

Hepatic

Genitourinary

Acid-Base

Hematologic

Dermatologic

Carcinogenicity

Genotoxicity

Musculoskeletal

Reproductive

Monitoring Parameters Levels

Radiographic Studies

Life Support

Monitoring

Oral Exposure

Inhalation Exposure

Eye Exposure

Dermal Exposure

Enhanced Elimination

Summary

Minimum Lethal Exposure

Maximum Tolerated Exposure

Workplace Standards

Toxicity Information

Physical Characteristics

Molecular Weight

General Bibliography