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SODIUM THIOSULFATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sodium thiosulfate is an inorganic reducing agent used as a fixative, chrome tanning and dying agent, dechlorinating agent, in silver extraction from ores, and in bleaching of bone, straw and ivory. It is found in a variety of pharmaceutical and veterinary preparations and is a part of the Cyanide Antidote kit.
    B) Thiosulfate is also a normally-occurring constituent of the body and may be an intermediate metabolite of sulfur-containing amino acids.

Specific Substances

    1) Ametox
    2) Antichlor
    3) Chlorine control
    4) Declor-It
    5) Disodium thiosulfate
    6) "Hypo"
    7) Molecular Formula: O3-S2.2Na (Anhydrous form)
    8) Molecular Formula: H10-O8-S-Na (Pentahydrate form)
    9) NIOSH/RTECS XN 6476000
    10) S-Hydril
    11) Sodium Hyposulfite
    12) Sodium oxide sulfide
    13) Sodium thiosulfate anhydrous
    14) Sodium thiosulphate
    15) Sodothiol
    16) Sulfothiorine
    17) CAS 7772-98-7 (Anhydrous form)
    18) CAS 10102-17-7 (Pentahydrate form)
    19) References: RTECS, 1988
    20) HYDRO THIOSULFATE
    21) SODOTHIOL (CAS 7772-98-7)
    22) THIOSULFURIC ACID, DISODIUM SALT
    1.2.1) MOLECULAR FORMULA
    1) Na2O.3S2 Na2S2O3 O3-S2.2Na (Anhydrous form) H10-O8-S-Na (Pentahydrate form)

Available Forms Sources

    A) FORMS
    1) Sodium thiosulfate occurs in both anhydrous and the pentahydrate forms, with the pentahydrate predominating under ambient conditions (Budavari, 1996).
    2) Thiosulfate is a normally-occurring constituent of the body and may be an intermediate metabolite of sulfur-containing amino acids. It is generally the rate-limiting substrate for the endogenous enzyme, rhodanase, in the detoxification of cyanide (Ivankovich et al, 1983).
    B) SOURCES
    1) Sodium thiosulfate occurs as white, transparent, almost odorless crystals or powder with a salty taste (ITI, 1985; Persson & Walter, 1987; HSDB , 2000).
    C) USES
    1) Sodium thiosulfate is an inorganic reducing agent used as a fixative, chrome tanning agent, dechlorinating agent, in silver extraction from ores, and in bleaching of bone, straw and ivory.
    2) It is also used as a reducing agent for chrome dying, in manufacture of leather, a mordant in dyeing and printing textiles, and in a variety of pharmaceutical and veterinary preparations (ITI, 1985; Budavari, 1996; HSDB , 2000)
    3) For decontaminating fish bowls, the concentration of sodium thiosulfate is less than 1% and non-toxic.
    4) MEDICAL USES
    a) It is part of the Cyanide Antidote kit (used in combination with amyl nitrite and sodium nitrite for the treatment of cyanide poisoning).
    b) It has been recommended for use as a 10 percent ointment or solution for SELENIUM DIOXIDE burns (Finkel, 1983).
    c) It is used in veterinary medicine to treat bloat, as a "general detoxifier," and topically to treat ringworm (Budavari, 1996; HSDB , 2000).
    d) It has been used to prevent undesirable side effects from a variety of drugs.
    e) Other uses have included topical treatment of tinea versicolor, tinea cruris, and other dermatophytoses. It has been used in the past as an antitubercular agent and antioxidant (HSDB , 2000).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) ANIMAL STUDIES
    1) Rapid intravenous infusion of large amounts has caused transient hypotension and ECG changes in dogs.
    2) Metabolic acidosis and hypernatremia occurred in dogs given large doses.
    B) WITH POISONING/EXPOSURE
    1) Sodium thiosulfate is an agent with a low order of toxicity. It may be a mild irritant in the solid form. Ingestion can cause gastrointestinal disturbances. It can cause allergic dermatitis.
    2) Ingestion of a large quantity may cause diarrhea.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Ingestion of large doses may result in gastroenteritis and a cathartic action.
    0.2.20) REPRODUCTIVE
    A) Sodium thiosulfate is classified as FDA pregnancy category C. There are no adequate and well-controlled studies of sodium thiosulfate use in pregnant women. Animal studies indicated no teratogenic effects occurred when hamsters were given IV sodium thiosulfate in doses similar to those used for cyanide poisoning in humans, and no embryotoxicity or teratogenicity was reported for mice, rats, or rabbits . It is unknown whether systemic sodium thiosulfate is excreted in breast milk, although the WHO states that the topical form is compatible with breastfeeding. Studies to evaluate the potential effects of sodium thiosulfate use on human fertility are not available.

Laboratory Monitoring

    A) Measuring thiosulfate levels is unlikely to be of use in assessing overexposures.
    B) Monitoring serum electrolytes and arterial blood gases may be advisable if a serious overexposure has occurred. Obtain a baseline level in any patient with a history of kidney disease being treated with sodium thiosulfate; repeat as needed.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) 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.
    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.
    0.4.4) EYE EXPOSURE
    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.
    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).
    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.
    0.4.6) PARENTERAL EXPOSURE
    A) Monitor vital signs, ECG, acid-base and fluid and electrolyte status carefully.
    B) Hypotension from large intravenous infusions is predicted to be transient and self-limited, but fluid administration or vasopressors could be required.
    1) 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.

Range Of Toxicity

    A) Ingestion of 12 g of sodium thiosulfate was virtually non-toxic except for producing violent catharsis.
    B) The lowest toxic intravenous doses for humans were 0.2 to 1.5 g/kg. As much as 9.9 g/m(2) has been given IV with no apparent ill effects.
    C) Rapid IV administration of 500 mg/kg to dogs caused self-limited transient hypotension.

Clinical Effects

Summary Of Exposure

    A) ANIMAL STUDIES
    1) Rapid intravenous infusion of large amounts has caused transient hypotension and ECG changes in dogs.
    2) Metabolic acidosis and hypernatremia occurred in dogs given large doses.
    B) WITH POISONING/EXPOSURE
    1) Sodium thiosulfate is an agent with a low order of toxicity. It may be a mild irritant in the solid form. Ingestion can cause gastrointestinal disturbances. It can cause allergic dermatitis.
    2) Ingestion of a large quantity may cause diarrhea.

Vital Signs

    3.3.4) BLOOD PRESSURE
    A) HYPOTENSION
    1) ANIMAL STUDIES - Rapid intravenous infusion of 500 mg/kg caused self-limited, transient hypotension in dogs (Mizoule, 1965).

Heent

    3.4.3) EYES
    A) IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Dust and concentrated solutions can irritate the eyes and mucous membranes.
    B) LACK OF TOXICITY
    1) WITH THERAPEUTIC USE
    a) When given intravenously to humans as an antidote for various poisonings, no disturbances of the eyes or vision have been reported (Grant & Schuman, 1993).
    b) TOPICAL ocular application of sodium thiosulfate and potassium ferricyanide had no apparent injurious effect to humans (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Dust and concentrated solutions can irritate the eyes and mucous membranes.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH THERAPEUTIC USE
    a) No cases of symptomatic hypotension have been reported in humans treated with the recommended dose of sodium thiosulfate for cyanide poisoning. Hypotension is predicted to only follow rapid intravenous infusion of very large doses and should be self-limited and transient.
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ECG ABNORMAL
    a) ECG changes occurred in dogs given a high intravenous dose of 3000 mg/kg (Dennis & Fletcher, 1966).
    2) HYPOTENSION
    a) Rapid intravenous infusion of 500 mg/kg caused self-limited transient hypotension in dogs (Mizoule, 1965).
    1) In contrast, the dose recommended for a 70 kg adult for the treatment of cyanide poisoning is about 179 mg/kg.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Inhalation may cause irritation of the upper respiratory tract.

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Ingestion of large doses may result in gastroenteritis and a cathartic action.
    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Ingestion of large amounts may cause gastrointestinal irritation, nausea, vomiting, abdominal cramping, and diarrhea. Large oral doses have a cathartic action (Reynolds, 2000).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 71-year-old woman with nondialysis chronic kidney disease, obesity, diabetes and cardiovascular disease was admitted due to a loss of consciousness and required cardiopulmonary resuscitation. She had a previous 8 day admission (30 hours prior to her current admission) for a gastrointestinal bleed and was started on sodium thiosulfate (25 g daily) for calciphylaxis (calcification of tissue) as an off-label indication. During this admission, she was transferred to a higher level of care and she had another episode of cardiac arrest. An ABG following the second resuscitation effort showed a pH of less than 6.80, PCO2 53 mm Hg, HCO3 6 mmol/L, and anion gap 45. Hemodialysis was initiated. No laboratory study or diagnostic study was able to identify the source of the severe anion gap acidosis. Sodium thiosulfate was discontinued. By the following day, repeat levels showed a HCO3 of 23 mmol/L and an anion gap of 12. Her cardiopulmonary status continued to stabilize but she had ongoing pain secondary to calciphylaxis and was discharged to hospice. Due to a lack of potential other causes, severe anion gap acidosis was associated with sodium thiosulfate therapy in this patient (Mao et al, 2013).
    3.11.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ACIDOSIS
    a) Metabolic acidosis occurred in dogs given a high intravenous dose of 3000 mg/kg, and was probably due to hyperosmolality and high sodium levels (Dennis & Fletcher, 1966).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Dust and concentrated solutions can irritate the skin.
    B) CONTACT DERMATITIS
    1) WITH THERAPEUTIC USE
    a) Sodium thiosulfate has caused allergic contact dermatitis (Rudzki, 1980).

Reproductive

    3.20.1) SUMMARY
    A) Sodium thiosulfate is classified as FDA pregnancy category C. There are no adequate and well-controlled studies of sodium thiosulfate use in pregnant women. Animal studies indicated no teratogenic effects occurred when hamsters were given IV sodium thiosulfate in doses similar to those used for cyanide poisoning in humans, and no embryotoxicity or teratogenicity was reported for mice, rats, or rabbits . It is unknown whether systemic sodium thiosulfate is excreted in breast milk, although the WHO states that the topical form is compatible with breastfeeding. Studies to evaluate the potential effects of sodium thiosulfate use on human fertility are not available.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) No epidemiologic studies are available to assess the risk for congenital anomalies in infants born to women treated with sodium thiosulfate during pregnancy (Prod Info NITHIODOTE intravenous injection solution, 2011).
    B) ANIMAL STUDIES
    1) Animal studies indicated no teratogenic effects occurred when hamsters were given IV sodium thiosulfate in doses similar to those used for cyanide poisoning in humans (Prod Info NITHIODOTE intravenous injection solution, 2011). Additional data suggest that treatment with sodium thiosulfate ameliorates the teratogenic effects of maternal cyanide poisoning in hamsters (Prod Info NITHIODOTE intravenous injection solution, 2011).
    2) Sodium thiosulfate was not teratogenic in mice, rats, hamsters, or rabbits at maternal doses of up to 550, 400, 400, and 580 mg/kg/day, respectively (Prod Info NITHIODOTE intravenous injection solution, 2011).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) There are no adequate and well-controlled studies of sodium thiosulfate use in pregnant women (Prod Info NITHIODOTE intravenous injection solution, 2011).
    B) PREGNANCY CATEGORY
    1) Sodium thiosulfate is classified as FDA pregnancy category C (Prod Info NITHIODOTE intravenous injection solution, 2011).
    C) ANIMAL STUDIES
    1) Sodium thiosulfate was not embryotoxic in mice, rats, hamsters, or rabbits at maternal doses of up to 550, 400, 400, and 580 mg/kg/day, respectively (Prod Info NITHIODOTE intravenous injection solution, 2011).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) It is not known whether sodium thiosulfate is excreted in human breast milk and the effects on the nursing infant from exposure to the drug are unknown (Prod Info NITHIODOTE intravenous injection solution, 2011).
    2) The WHO states that there is no data available on the use of systemic sodium thiosulfate in breastfeeding, but the topical form is compatible with breastfeeding (Anon, 2002).
    B) LACK OF EFFECT
    1) The WHO states that there is no data available on the use of systemic sodium thiosulfate in breastfeeding, but the topical form is compatible with breastfeeding (Anon, 2002).
    3.20.5) FERTILITY
    A) LACK OF INFORMATION
    1) Studies to evaluate the potential effects of sodium thiosulfate use on human fertility are not available (Prod Info NITHIODOTE intravenous injection solution, 2011).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7772-98-7 (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
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Measuring thiosulfate levels is unlikely to be of use in assessing overexposures.
    B) Monitoring serum electrolytes and arterial blood gases may be advisable if a serious overexposure has occurred. Obtain a baseline level in any patient with a history of kidney disease being treated with sodium thiosulfate; repeat as needed.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Normal serum levels of thiosulfate were 1.13 +/- 0.11 mg/dL in plasma for nonfasting adults. Measuring thiosulfate levels is unlikely to be of use in assessing overexposures.
    2) Monitoring serum electrolytes may be advisable if a serious overexposure has occurred.
    B) ACID/BASE
    1) Monitoring arterial blood gases may be advisable if a serious overexposure has occurred. Obtain a baseline level in any patient with a history of kidney disease being treated with sodium thiosulfate; repeat as needed.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Normal urinary levels of thiosulfate were 0.28 +/- 0.02 mg/dL in nonfasting adults. Measuring thiosulfate levels is unlikely to be of use in assessing overexposures.

Radiographic Studies

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

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Thiosulfate can be detected in the body fluids by reduction by iodine, but this assay is nonspecific for thiosulfate (Persson & Walter, 1987).
    2) Thiosulfate can be detected by reduction of methylene blue (Ivankovich et al, 1983).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    6.3.2) DISPOSITION/PARENTERAL EXPOSURE
    6.3.2.5) OBSERVATION CRITERIA/PARENTERAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) Measuring thiosulfate levels is unlikely to be of use in assessing overexposures.
    B) Monitoring serum electrolytes and arterial blood gases may be advisable if a serious overexposure has occurred. Obtain a baseline level in any patient with a history of kidney disease being treated with sodium thiosulfate; repeat as needed.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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) 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).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs and ECG carefully.
    2) Monitor acid-base and fluid and electrolyte status carefully and correct any disturbances noted as required.
    B) HYPOTENSIVE EPISODE
    1) Hypotension is predicted to only follow rapid intravenous infusion of very large doses and should be self-limited and transient.
    2) 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.
    3) 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).
    4) 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).

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) Observe for potential respiratory tract irritation.
    2) Administration of humidified supplemental oxygen could be required if irritation is severe.
    B) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) 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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    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) TREATMENT
    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) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) Ingestion of 12 g of sodium thiosulfate was virtually non-toxic except for producing violent catharsis.
    B) The lowest toxic intravenous doses for humans were 0.2 to 1.5 g/kg. As much as 9.9 g/m(2) has been given IV with no apparent ill effects.
    C) Rapid IV administration of 500 mg/kg to dogs caused self-limited transient hypotension.

Therapeutic Dose

    7.2.1) ADULT
    A) CYANIDE ANTIDOTE
    1) The recommended dose is 12.5 g (50 mL solution) immediately following administration of sodium nitrate. Repeat dose should be one-half the original dose (Prod Info sodium thiosulfate intravenous injection, 2012; Prod Info NITHIODOTE intravenous injection solution, 2011).
    7.2.2) PEDIATRIC
    A) CYANIDE ANTIDOTE
    1) The recommended dose is 1 mL/kg of body weight (250 mg/kg or approximately 30 to 40 mL/m(2) of body surface area) immediately following administration of sodium nitrate. MAX dose: 50 mL. Repeat dose should be one-half the original dose (Prod Info sodium thiosulfate intravenous injection, 2012; Prod Info NITHIODOTE intravenous injection solution, 2011).

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) The lowest published lethal subcutaneous dose for a rabbit is 4 grams/kilogram (RTECS , 2000).
    2) The lowest published lethal subcutaneous dose for a frog is 6 grams/kilogram (RTECS , 2000).

Maximum Tolerated Exposure

    A) ACUTE
    1) Ingestion of 12 grams of sodium thiosulfate was virtually non-toxic except for producing violent catharsis. Large doses are expected to have a cathartic action (Reynolds, 2000).
    2) The lowest toxic intravenous doses in humans were 0.2 to 1.5 grams/kilogram (ITI, 1985).
    3) 9.9 grams/square meter given intravenously to counteract the nephrotoxicity of cisplatin had no apparent ill effects (Pfeifle et al, 1985).

Workplace Standards

    A) ACGIH TLV Values for CAS7772-98-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7772-98-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7772-98-7 :
    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

    D) OSHA PEL Values for CAS7772-98-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 5200 mg/kg (RTECS, 2000)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) CYANIDE ANTIDOTE - The metabolic basis for thiosulfate therapy in cyanide overdose is its reaction with cyanide catalyzed by the RHODANASE enzyme to form THIOCYANATE, which is much less toxic and is excreted by the kidney (Naughton, 1974).
    1) The detoxification reaction is intracellular and most of the endogenous thiosulfate is extracellular, and high extracellular concentrations of thiosulfate need to be achieved in cyanide therapy (Ivankovich et al, 1983).
    2) The reaction with thiosulfate and cyanide is largely irreversible and can compete with cyanide already bound to cytochrome oxidase.
    B) The protection against nephrotoxicity by thiosulfate and its failure to prevent other undesirable side effects from cisplatin may be due to the selective concentration of thiosulfate in the urine (Ozols & Young, 1985), where it forms a thiosulfate-cisplatin complex (de Broe & Weeden, 1986).
    C) The ability of sodium thiosulfate to counteract such a wide variety of drugs may be due to its activity as a strong NUCLEOPHILE.
    1) Many mutagens and anti-cancer drugs are strong electrophiles, and one could predict that sodium thiosulfate may have protective value against any strongly electrophilic substance which is free in solution in the extracellular fluid.
    D) Sodium thiosulfate and other nucleophiles may also have activity in preventing cancer by endogenous or environmental electrophiles (Wattenberg et al, 1987).

Toxicologic Mechanism

    A) Toxic effects of extremely high doses of sodium thiosulfate in animals have been mainly due to nonspecific alterations of osmolality and sodium concentration.

Physicochemical

Physical Characteristics

    A) Sodium thiosulfate occurs as white, transparent, almost odorless crystals or powder with a salty taste (ITI, 1985; Persson & Walter, 1987; HSDB , 2000) Reynolds, 2000).

Ph

    A) 6.5-8.0

Molecular Weight

    A) ANHYDROUS: 158.13 (Budavari, 1996)
    B) PENTAHYDRATE: 248.2 (Budavari, 1996)

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