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STRYCHNINE SULFATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Strychnine sulfate is an alkaloid produced from seeds of Strynchos species and some other plants.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C21-H22-N2-O2.1/2H2-O4-S.5/2H2-0

Available Forms Sources

    A) FORMS
    1) Strychnine poisoning may result from the ingestion of strychnine rodenticides or the intranasal insufflation ("snorting") or intravenous injection of street drugs such as cocaine, heroin, or amphetamine which have been adulterated or contaminated with strychnine.
    2) Strychnine is rapidly absorbed from the gastrointestinal and respiratory tracts, and can result in generalized convulsions within 15 to 60 minutes after ingestion (Morgan, 1989). It is also well absorbed intranasally, resulting in toxicity within 30 minutes (O'Callaghan et al, 1982). It may also be absorbed after parenteral administration (Sax & Lewis, 1989; Davis & Yeh, 1969). No information was found on whether or not strychnine can be absorbed through the skin at the time of this review.
    3) Strychnine releases toxic and irritating fumes of oxides of nitrogen and sulfur when heated to decomposition (Sax & Lewis, 1989) AAR, 1987).
    B) SOURCES
    1) Strychnine sulfate is a bitter tasting alkaloid extracted from the seeds of an Indian tree, Nux vomica (Morgan, 1989). It is usually found as the pentahydrate, and is a colorless to white, odorless, bitter tasting, water soluble crystalline solid which will burn, but is difficult to ignite (Budavari, 1989) AAR, 1987; (EPA, 1985).
    C) USES
    1) Strychnine sulfate was formerly used as a tonic and stimulant veterinary medication and a rodenticide (Budavari, 1989; EPA, 1985). More recently, strychnine has been used in the treatment of impotence (Savion et al, 1987), sleep apnea (Remmers et al, 1980), and nonketotic hyperglycemia (Sankaran et al, 1982). Its efficacy for these conditions has not been established.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Strychnine is a CNS stimulant which can cause tonic convulsions. It causes violent epileptiform seizures, and which can result in death from interference with respiration.
    B) Strychnine is rapidly absorbed from the gastrointestinal and respiratory tracts, and can cause generalized convulsions within 15 to 60 minutes following ingestion. It is also well absorbed intranasally, resulting in toxicity within 30 minutes. It is absorbed following parenteral administration. At the time of this review, no information was found on whether or not strychnine can be absorbed through intact skin.
    C) A prodromal syndrome includes muscular cramps, and stiffness, and agitation is commonly reported prior to the onset of convulsions; generalized convulsions may be the initial event. Severe lactic acidemia is associated with prolonged seizures. Rhabdomyolysis and associated myoglobinuria resulting in renal failure may ensue.
    D) Prognosis is good if the patient can be supported over the first 6 to 12 hours. Convulsions generally subside within 12 to 24 hours after ingestion.
    E) Strychnine releases toxic and irritating fumes of oxides of nitrogen and sulfur when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with chemical pneumonitis, bronchospasm, or noncardiogenic pulmonary edema.
    0.2.3) VITAL SIGNS
    A) Death in acute strychnine poisoning is usually due to interference with pulmonary function. Hypothermia and hypertension were seen in one case of acute strychnine poisoning. Hypotension may also occur.
    0.2.4) HEENT
    A) Nystagmus has been reported following strychnine intoxication. Mydriasis, proptosis, and conjugate or dissociated deviations of the eyes have been described in acute strychnine poisoning.
    0.2.5) CARDIOVASCULAR
    A) Bradycardia and prolongation of the PR, QRS, and QT intervals, hypertensio, and hypotension have all been reported in acute strychnine poisoning.
    0.2.6) RESPIRATORY
    A) Involvement of the respiratory muscles leads to respiratory compromise with hypoxia. Death is usually due to hypoxia.
    B) Strychnine releases toxic and irritating fumes of oxides of nitrogen and sulfur when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with chemical pneumonitis, bronchospasm, or noncardiogenic pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Strychnine produces characteristic tonic extensor convulsions.
    B) Hypertonicity of muscles, opisthotonus, convulsions, and painful muscle spasms may occur. The patient may be alert.
    C) Severe headache and numbness of the extremities were noted in one case of acute strychnine poisoning.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and profuse diarrhea were noted in one case of acute strychnine poisoning.
    0.2.10) GENITOURINARY
    A) Crystalluria, myoglobinuria, and acute renal failure secondary to rhabdomyolysis have been reported.
    0.2.11) ACID-BASE
    A) Lactic acidosis has been reported.
    0.2.12) FLUID-ELECTROLYTE
    A) Hypocalcemia with typical electrocardiographic changes has been reported.
    0.2.15) MUSCULOSKELETAL
    A) Rhabdomyolysis may occur.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Strychnine can be detected in the urine, blood, gastric aspirate, and other organs by colorimetry or ultraviolet spectrophotometry, but gas-liquid chromatography with a flame ionization detector (FID) is more specific.
    1) A gas chromatography-mass spectrometry method has been used to determine strychnine in biological samples.
    B) Strychnine can be measured in pharmaceutical preparations with a gas-liquid chromatography technique.
    C) Blood levels do not correlate with the need for therapy. Toxicity has been reported with a blood level of 0.1 mg/100 mL.
    D) Increased serum levels of SGOT (AST), LDH, and CPK have been reported. Leukocytosis may also occur.
    1) 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.
    E) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS/GASTRIC LAVAGE NOT RECOMMENDED -
    1) Emesis and gastric lavage NOT RECOMMENDED as these procedures may precipitate convulsions. Activated charcoal should be administered.
    B) 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.
    C) Avoid sensory stimulation; this may precipitate seizure activity.
    D) Monitor arterial blood gases in patients with seizure activity. Seizures are frequently associated with lactic acidemia.
    E) Severe acidosis should be corrected with intravenous sodium bicarbonate. Monitor blood gases to guide frequency of bicarbonate administration.
    F) SEIZURES - Administer a benzodiazepine IV; DIAZEPAM (ADULT: 5 to 10 mg, repeat every 10 to 15 minutes as needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 minutes as needed) or LORAZEPAM (ADULT: 4 to 8 mg; CHILD: 0.05 to 0.1 mg/kg).
    1) Consider phenobarbital if seizures are uncontrollable or recur after diazepam 30 mg (adults) or 10 mg (children > 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression and the need for endotracheal intubation.
    3) Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    G) REFRACTORY SEIZURES - For seizures refractory to combinations of benzodiazepines and phenobarbital consider continuous infusions of midazolam, propofol or pentobarbital.
    1) Hyperthermia, lactic acidosis and muscle destruction may necessitate use of nondepolarizing neuromuscular blocking agents with continuous EEG monitoring.
    H) Death is usually due to interference with pulmonary function. Monitor and maintain adequate respirations and oxygenation. Endotracheal intubation and artificial ventilation with supplemental oxygenation may be necessary.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) INHALATION ABSORPTION - Strychnine sulfate may be absorbed by inhalation.
    C) 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.
    D) Avoid sensory stimulation; this may precipitate seizure activity.
    E) Monitor arterial blood gases in patients with seizure activity. Seizures are frequently associated with lactic acidemia.
    F) Severe acidosis should be corrected with intravenous sodium bicarbonate. Monitor blood gases to guide frequency of bicarbonate administration.
    G) SEIZURES - Administer a benzodiazepine IV; DIAZEPAM (ADULT: 5 to 10 mg, repeat every 10 to 15 minutes as needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 minutes as needed) or LORAZEPAM (ADULT: 4 to 8 mg; CHILD: 0.05 to 0.1 mg/kg).
    1) Consider phenobarbital if seizures are uncontrollable or recur after diazepam 30 mg (adults) or 10 mg (children > 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression and the need for endotracheal intubation.
    3) Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    H) REFRACTORY SEIZURES - For seizures refractory to combinations of benzodiazepines and phenobarbital consider continuous infusions of midazolam, propofol or pentobarbital.
    1) Hyperthermia, lactic acidosis and muscle destruction may necessitate use of nondepolarizing neuromuscular blocking agents with continuous EEG monitoring.
    I) Death is usually due to interference with pulmonary function. Monitor and maintain adequate respirations and oxygenation. Endotracheal intubation and artificial ventilation with supplemental oxygenation may be necessary.
    J) The efficacy of hemodialysis and hemoperfusion have not been investigated in acute strychnine poisoning.
    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) It is unclear whether or not dermal exposure to strychnine sulfate can result in systemic absorption and toxicity, although one reported case is suggestive. If systemic poisoning is suspected from dermal exposure, the treatment recommendations listed under INHALATION EXPOSURE above should be followed.

Range Of Toxicity

    A) When ingested by a small child, 15 milligrams may produce a lethal effect; adult lethal doses are variable, but have been said to be from 5 to 8 mg/kg. Fatal oral doses reported in the literature range from 30 to 120 milligrams.
    B) An ingested dose of 3.75 grams was not fatal in one case. In humans injected intramuscularly with 4 mg of strychnine nitrate, no effects on visual acuity were observed.

Clinical Effects

Summary Of Exposure

    A) Strychnine is a CNS stimulant which can cause tonic convulsions. It causes violent epileptiform seizures, and which can result in death from interference with respiration.
    B) Strychnine is rapidly absorbed from the gastrointestinal and respiratory tracts, and can cause generalized convulsions within 15 to 60 minutes following ingestion. It is also well absorbed intranasally, resulting in toxicity within 30 minutes. It is absorbed following parenteral administration. At the time of this review, no information was found on whether or not strychnine can be absorbed through intact skin.
    C) A prodromal syndrome includes muscular cramps, and stiffness, and agitation is commonly reported prior to the onset of convulsions; generalized convulsions may be the initial event. Severe lactic acidemia is associated with prolonged seizures. Rhabdomyolysis and associated myoglobinuria resulting in renal failure may ensue.
    D) Prognosis is good if the patient can be supported over the first 6 to 12 hours. Convulsions generally subside within 12 to 24 hours after ingestion.
    E) Strychnine releases toxic and irritating fumes of oxides of nitrogen and sulfur when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with chemical pneumonitis, bronchospasm, or noncardiogenic pulmonary edema.

Vital Signs

    3.3.1) SUMMARY
    A) Death in acute strychnine poisoning is usually due to interference with pulmonary function. Hypothermia and hypertension were seen in one case of acute strychnine poisoning. Hypotension may also occur.
    3.3.2) RESPIRATIONS
    A) PULMONARY FUNCTION - Death from acute strychnine poisoning is usually due to interference with pulmonary function (Morgan, 1989).
    3.3.3) TEMPERATURE
    A) HYPOTHERMIA was noted in one case of acute strychnine poisoning (Ennis, 1959).
    3.3.4) BLOOD PRESSURE
    A) HYPERTENSION was seen in one case of acute strychnine poisoning (Ennis, 1959).
    B) HYPOTENSION and prolongation of the PR, QRS, and QT intervals have been seen in acute poisoning (Heiser et al, 1989).

Heent

    3.4.1) SUMMARY
    A) Nystagmus has been reported following strychnine intoxication. Mydriasis, proptosis, and conjugate or dissociated deviations of the eyes have been described in acute strychnine poisoning.
    3.4.3) EYES
    A) NYSTAGMUS - Bilateral horizontal pendular nystagmus, unresponsive to diazepam has been reported in strychnine intoxication has been reported (Blain et al, 1982).
    B) MYDRIASIS, proptosis, and conjugate or dissociated deviations of the eyes have been described in acute strychnine poisoning (Grant, 1993).
    C) BLINDNESS - One case of persistent blindness has been reported; no such cases have been reported since 1913 (Grant, 1993).

Cardiovascular

    3.5.1) SUMMARY
    A) Bradycardia and prolongation of the PR, QRS, and QT intervals, hypertensio, and hypotension have all been reported in acute strychnine poisoning.
    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) Bradycardia, hypotension, and prolongation of the PR, QRS, and QT intervals were reported in a 51-year-old male who ingested 4.8 grams of strychnine (Heiser et al, 1989).

Respiratory

    3.6.1) SUMMARY
    A) Involvement of the respiratory muscles leads to respiratory compromise with hypoxia. Death is usually due to hypoxia.
    B) Strychnine releases toxic and irritating fumes of oxides of nitrogen and sulfur when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with chemical pneumonitis, bronchospasm, or noncardiogenic pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) HYPOXEMIA
    1) Involvement of respiratory muscles leads to respiratory compromise with hypoxia (Morgan, 1989). Death is usually due to hypoxia.
    B) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS
    1) DECOMPOSITION PRODUCTS - Strychnine releases toxic and irritating fumes of oxides of nitrogen and sulfur when heated to decomposition (Lewis, 1996; AAR, 1994). Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with chemical pneumonitis, bronchospasm, or noncardiogenic pulmonary edema.

Neurologic

    3.7.1) SUMMARY
    A) Strychnine produces characteristic tonic extensor convulsions.
    B) Hypertonicity of muscles, opisthotonus, convulsions, and painful muscle spasms may occur. The patient may be alert.
    C) Severe headache and numbness of the extremities were noted in one case of acute strychnine poisoning.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) Strychnine produces excitation of all portions of the CNS by selectively blocking inhibition, resulting in a characteristic tonic extensor convulsion pattern (Morgan, 1989).
    2) Reduction of reciprocal inhibition of antagonistic muscles occurs; therefore the pattern of convulsions is determined by the most powerful muscle(s) acting at a particular joint.
    3) Hypertonicity of muscles, opisthotonus, convulsions, and painful muscle spasms may occur. The patient may be alert.
    4) There is no effect directly on skeletal muscles. Onset of signs and symptoms occurs within 15 to 20 minutes following ingestion. Any secondary stimulus can produce a violent motor response.
    B) HEADACHE
    1) Severe headache was noted in one case of acute strychnine poisoning (Ennis, 1959).
    C) PARESTHESIA
    1) Numbness of the extremities was noted in one case of acute strychnine poisoning (Ennis, 1959).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and profuse diarrhea were noted in one case of acute strychnine poisoning.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Nausea, vomiting, and profuse diarrhea were noted in one case of acute strychnine poisoning (Ennis, 1959).

Genitourinary

    3.10.1) SUMMARY
    A) Crystalluria, myoglobinuria, and acute renal failure secondary to rhabdomyolysis have been reported.
    3.10.2) CLINICAL EFFECTS
    A) MYOGLOBINURIA
    1) Myoglobinuria may occur, secondary to rhabdomyolysis due to intense muscular contractions.
    B) CASE REPORT
    1) CRYSTALLURIA - Microscopic crystals were found in the urine of a 32-year-old farmer poisoned with strychnine (Burn et al, 1989).
    2) ACUTE RENAL FAILURE was reported in a 32-year-old farmer with strychnine poisoning (Burn et al, 1989). RHABDOMYOLYSIS secondary to strychnine poisoning was the suggested cause.

Acid-Base

    3.11.1) SUMMARY
    A) Lactic acidosis has been reported.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Muscle spasms and seizures may lead to hyperthermia and lactic acidosis (Boyd et al, 1983).

Musculoskeletal

    3.15.1) SUMMARY
    A) Rhabdomyolysis may occur.
    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) Rhabdomyolysis may occur as a complication of strychnine poisoning secondary to intense muscular contractions (Burn et al, 1989).

Reproductive

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

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS60-41-3 (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) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Strychnine can be detected in the urine, blood, gastric aspirate, and other organs by colorimetry or ultraviolet spectrophotometry, but gas-liquid chromatography with a flame ionization detector (FID) is more specific.
    1) A gas chromatography-mass spectrometry method has been used to determine strychnine in biological samples.
    B) Strychnine can be measured in pharmaceutical preparations with a gas-liquid chromatography technique.
    C) Blood levels do not correlate with the need for therapy. Toxicity has been reported with a blood level of 0.1 mg/100 mL.
    D) Increased serum levels of SGOT (AST), LDH, and CPK have been reported. Leukocytosis may also occur.
    1) 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.
    E) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Blood levels do not correlate with the need for therapy. Toxicity has been reported with a blood level of 0.1 mg/100 mL.
    2) Elevation of SGOT, LDH, and CPK have been reported. Leukocytosis may also occur.
    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.
    3) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) POSTMORTEM
    a) In a 56 year old male who died following a deliberate suicide attempt, strychnine levels were highest in the stomach contents (175 mg/L), stomach wall (14.9 mg/L), bile (9.2 mg/L), and liver (6.2 mg/L) (Perper, 1985; Winek et al, 1986).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Strychnine can be detected in the urine, blood, gastric aspirate, and other organs by colorimetry or ultraviolet spectrophotometry, but gas-liquid chromatography with a flame ionization detector (FID) is more specific.
    1) A gas chromatography-mass spectrometry method has been used to determine strychnine in biological samples.
    B) Strychnine can be measured in pharmaceutical preparations with a gas-liquid chromatography technique.
    C) Blood levels do not correlate with the need for therapy. Toxicity has been reported with a blood level of 0.1 mg/100 mL.
    D) Increased serum levels of SGOT (AST), LDH, and CPK have been reported. Leukocytosis may also occur.
    1) 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.
    E) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) EMESIS/GASTRIC LAVAGE NOT RECOMMENDED -
    a) Emesis or lavage is NOT RECOMMENDED since these procedures may precipitate convulsions. Spontaneous vomiting and tonic convulsions have been reported (Burn et al, 1989). Activated charcoal should be administered immediately to minimize gastrointestinal absorption.
    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).
    6.5.3) TREATMENT
    A) SEIZURE
    1) 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 .
    2) 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).
    3) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    4) 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).
    5) 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).
    6) RECURRING SEIZURES
    a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
    1) MIDAZOLAM: ADULT DOSE: An initial dose of 0.2 mg/kg slow bolus, at an infusion rate of 2 mg/minute; maintenance doses of 0.05 to 2 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: 0.1 to 0.3 mg/kg followed by a continuous infusion starting at 1 mcg/kg/minute, titrated upwards every 5 minutes as needed (Loddenkemper & Goodkin, 2011).
    2) PROPOFOL: ADULT DOSE: Start at 20 mcg/kg/min with 1 to 2 mg/kg loading dose; maintenance doses of 30 to 200 mcg/kg/minute continuous infusion dosing, titrated to EEG; caution with high doses greater than 80 mcg/kg/minute in adults for extended periods of time (ie, longer than 48 hours) (Brophy et al, 2012); PEDIATRIC DOSE: IV loading dose of up to 2 mg/kg; maintenance doses of 2 to 5 mg/kg/hour may be used in older adolescents; avoid doses of 5 mg/kg/hour over prolonged periods because of propofol infusion syndrome (Loddenkemper & Goodkin, 2011); caution with high doses greater than 65 mcg/kg/min in children for extended periods of time; contraindicated in small children (Brophy et al, 2012).
    3) PENTOBARBITAL: ADULT DOSE: A loading dose of 5 to 15 mg/kg at an infusion rate of 50 mg/minute or lower; may administer additional 5 to 10 mg/kg. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: A loading dose of 3 to 15 mg/kg followed by a maintenance dose of 1 to 5 mg/kg/hour (Loddenkemper & Goodkin, 2011).
    4) THIOPENTAL: ADULT DOSE: 2 to 7 mg/kg, at an infusion rate of 50 mg/minute or lower. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusing dosing, titrated to EEG (Brophy et al, 2012)
    b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
    c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).
    B) SUPPORT
    1) Avoid sensory stimulation; this may precipitate seizure activity.
    C) MONITORING OF PATIENT
    1) Monitor arterial blood gases in patients with seizure activity. Seizures are frequently associated with development of lactic acidemia.
    D) ACIDOSIS
    1) Severe acidosis should be corrected with intravenous sodium bicarbonate. Monitor blood gases to guide frequency of bicarbonate administration.
    E) AIRWAY MANAGEMENT
    1) Death is usually due to interference with pulmonary function (Morgan, 1989).
    2) Monitor and maintain adequate respirations and oxygenation. Endotracheal intubation and artificial ventilation with supplemental oxygenation may be necessary.
    F) 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).

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) PROCEDURE EDUCATION
    1) Strychnine sulfate may be absorbed following inhalation exposure (Morgan, 1989; Ennis, 1959). Avoid sensory stimulation; this may precipitate seizure activity.
    B) SEIZURE
    1) 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 .
    2) 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).
    3) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    4) 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).
    5) 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).
    6) RECURRING SEIZURES
    a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
    1) MIDAZOLAM: ADULT DOSE: An initial dose of 0.2 mg/kg slow bolus, at an infusion rate of 2 mg/minute; maintenance doses of 0.05 to 2 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: 0.1 to 0.3 mg/kg followed by a continuous infusion starting at 1 mcg/kg/minute, titrated upwards every 5 minutes as needed (Loddenkemper & Goodkin, 2011).
    2) PROPOFOL: ADULT DOSE: Start at 20 mcg/kg/min with 1 to 2 mg/kg loading dose; maintenance doses of 30 to 200 mcg/kg/minute continuous infusion dosing, titrated to EEG; caution with high doses greater than 80 mcg/kg/minute in adults for extended periods of time (ie, longer than 48 hours) (Brophy et al, 2012); PEDIATRIC DOSE: IV loading dose of up to 2 mg/kg; maintenance doses of 2 to 5 mg/kg/hour may be used in older adolescents; avoid doses of 5 mg/kg/hour over prolonged periods because of propofol infusion syndrome (Loddenkemper & Goodkin, 2011); caution with high doses greater than 65 mcg/kg/min in children for extended periods of time; contraindicated in small children (Brophy et al, 2012).
    3) PENTOBARBITAL: ADULT DOSE: A loading dose of 5 to 15 mg/kg at an infusion rate of 50 mg/minute or lower; may administer additional 5 to 10 mg/kg. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: A loading dose of 3 to 15 mg/kg followed by a maintenance dose of 1 to 5 mg/kg/hour (Loddenkemper & Goodkin, 2011).
    4) THIOPENTAL: ADULT DOSE: 2 to 7 mg/kg, at an infusion rate of 50 mg/minute or lower. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusing dosing, titrated to EEG (Brophy et al, 2012)
    b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
    c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).
    C) MONITORING OF PATIENT
    1) Monitor arterial blood gases in patients with seizure activity. Seizures are frequently associated with development of lactic acidemia.
    D) ACIDOSIS
    1) Severe acidosis should be corrected with intravenous sodium bicarbonate. Monitor blood gases to guide frequency of bicarbonate administration.
    E) AIRWAY MANAGEMENT
    1) Death is usually due to interference with pulmonary function (Morgan, 1989).
    2) Monitor and maintain adequate respirations and oxygenation. Endotracheal intubation and artificial ventilation with supplemental oxygenation may be necessary.
    F) 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).
    G) 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) SKIN ABSORPTION
    1) It is unclear whether or not dermal exposure to strychnine sulfate can result in systemic absorption and toxicity, although one reported case is suggestive (Ennis, 1959). If systemic poisoning is suspected from dermal exposure, the treatment recommendations listed above under INHALATION EXPOSURE should be followed.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) The efficacy of hemodialysis and hemoperfusion have not been investigated in acute strychnine poisoning (Morgan, 1989).

Range Of Toxicity

Summary

    A) When ingested by a small child, 15 milligrams may produce a lethal effect; adult lethal doses are variable, but have been said to be from 5 to 8 mg/kg. Fatal oral doses reported in the literature range from 30 to 120 milligrams.
    B) An ingested dose of 3.75 grams was not fatal in one case. In humans injected intramuscularly with 4 mg of strychnine nitrate, no effects on visual acuity were observed.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) When ingested by a small child, 15 milligrams of strychnine may produce a lethal effect; adult lethal doses are variable, but have been said to be from 5 to 8 mg/kg (Morgan, 1989). Fatal oral doses reported in the literature range from 30 to 120 milligrams.

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) An ingested dose of 3.75 grams was not fatal in one case. In humans injected intramuscularly with 4 mg of strychnine nitrate, no effects on visual acuity were observed (Grant, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS60-41-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS60-41-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS60-41-3 :
    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 CAS60-41-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (RTECS, 1996)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 900 mcg/kg
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) 1250 mcg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 1 mg/kg
    4) LD50- (ORAL)RAT:
    a) 2600 mcg/kg
    5) LD50- (SUBCUTANEOUS)RAT:
    a) 1700 mcg/kg

Physicochemical

Physical Characteristics

    A) Strychnine sulfate is a colorless to white, odorless, bitter tasting, water soluble crystalline solid or powder. It effloresces in dry air (Budavari, 1996; (EPA, 1985).

Ph

    A) 5.5 (for a 1:100 solution) (Budavari, 1996)

Molecular Weight

    A) 766.92 (Budavari, 1996)

References

General Bibliography

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    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
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    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
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    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
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