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ISODRIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Isodrin is a chlorinated hydrocarbon insecticide in the cyclodiene family; it is an isomer of aldrin.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C12-H8-Cl6

Available Forms Sources

    A) FORMS
    1) Isodrin is a chlorinated hydrocarbon insecticide in the cyclodiene family; it is an isomer of aldrin (Sax & Lewis, 1987). It occurs as a crystalline solid which is soluble in ether, acetone, alcohol, and benzene (HSDB, 1993).
    B) USES
    1) It was formerly used as an insecticide, but is no longer marketed in the USA (EPA, 1985).

Overview

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Isodrin is a chlorinated hydrocarbon insecticide in the chlorinated ethane/cyclodiene/hexachlorocyclohexane family. This review is based on the properties of chlorinated hydrocarbon insecticides in general, with effects specific to isodrin identified. The primary target of action is the central nervous system. CNS excitation and seizures may occur. Respiratory depression may occur concurrently with coma and is a common cause of death.
    0.2.3) VITAL SIGNS
    A) Respiratory depression can occur from aldrin, dieldrin, endrin, and presumably isodrin. Hyperthermia, hypertension, or hypotension may occur.
    0.2.4) HEENT
    A) Hypersalivation, headache, and foaming from the mouth or nose may occur.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dysrhythmias can occur from cardiac sensitization. Tachycardia may be caused by isodrin.
    0.2.6) RESPIRATORY
    A) Irritation, reduced gas exchange, and chemical pneumonitis may occur.
    0.2.7) NEUROLOGIC
    A) Excitation with myoclonic jerking and convulsions may occur. In extreme overdose CNS depression and coma may occur. Permanent damage may occur from acute exposure.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and diarrhea may occur following ingestion.
    0.2.9) HEPATIC
    A) Liver injury may occur from isodrin poisoning.
    0.2.10) GENITOURINARY
    A) Renal insufficiency occurred in a case of endrin ingestion. Hematuria and albuminuria have occurred with aldrin poisoning.
    0.2.11) ACID-BASE
    A) Severe metabolic acidosis may be a consequence of convulsions and an immediate cause of death.
    0.2.13) HEMATOLOGIC
    A) Aplastic and megaloblastic anemia have occurred in rare cases. Thromobocytopenia may occur in severe poisonings.
    0.2.14) DERMATOLOGIC
    A) Extensive contact results in dermal irritation. Isodrin may cause acne and skin rashes.
    0.2.18) PSYCHIATRIC
    A) Alterations in mental function occur as a result of the neurotoxicity of chlorinated hydrocarbon insecticides.
    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.
    0.2.22) OTHER
    A) Isodrin can be absorbed by inhalation, ingestion, and contact with the skin.

Laboratory Monitoring

    A) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds they reflect cumulative exposure over a period of months or years rather than recent exposure.
    B) Urinary metabolites may be detected, but the procedures are complex and may not be useful for monitoring low exposures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Emesis is not recommended due to potential CNS depression or seizures.
    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) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) 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.
    E) Do not give oils by mouth.
    F) Do not administer adrenergic amines, which may further increase myocardial irritability and produce refractory ventricular arrhythmias.
    G) CHOLESTYRAMINE - Oral administration may enhance the excretion of kepone and chlordane which are trapped in the enterohepatic circulation.
    H) HEMODIALYSIS - Probably ineffective.
    I) EXCHANGE TRANSFUSION - Probably ineffective.
    J) HEMOPERFUSION - Effectiveness unknown.
    K) See treatment of oral exposure in the main body of this document for complete information.
    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) See treatment of inhalation exposure in the main body of this document for complete information.
    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) If clothing is contaminated remove, and wash skin and hair three times; do an initial soap washing followed by an alcohol washing followed by a soap washing. Leather absorbs pesticides. Hence, leather should not be worn in the presence of pesticides and all contaminated leather should be discarded.
    2) See treatment of dermal exposure in the main body of this document for complete information.

Range Of Toxicity

    A) From its acute oral toxicity in animals, isodrin would be considered in the EXTREMELY TOXIC group of chlorohydrocarbon insecticides. The probable oral lethal dose for humans is in the range of 5 to 50 mg/kg (between 7 drops and 1 teaspoon for a 150-pound person).

Life Support

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

Clinical Effects

Summary Of Exposure

    A) Isodrin is a chlorinated hydrocarbon insecticide in the chlorinated ethane/cyclodiene/hexachlorocyclohexane family. This review is based on the properties of chlorinated hydrocarbon insecticides in general, with effects specific to isodrin identified. The primary target of action is the central nervous system. CNS excitation and seizures may occur. Respiratory depression may occur concurrently with coma and is a common cause of death.

Vital Signs

    3.3.1) SUMMARY
    A) Respiratory depression can occur from aldrin, dieldrin, endrin, and presumably isodrin. Hyperthermia, hypertension, or hypotension may occur.
    3.3.2) RESPIRATIONS
    A) Aldrin, dieldrin, endrin, chlordane, camphechlor, and DDT are respiratory depressants, and isodrin may be similar.
    3.3.3) TEMPERATURE
    A) Hyperthermia occurred in a fatal case of endrin ingestion (Runhaar et al, 1985). Fever may occur with isodrin poisoning (EPA, 1985; HSDB , 1998).
    3.3.4) BLOOD PRESSURE
    A) Hypertension may occur with isodrin poisoning (EPA, 1985). Recurrent hypotension occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Heent

    3.4.1) SUMMARY
    A) Hypersalivation, headache, and foaming from the mouth or nose may occur.
    3.4.2) HEAD
    A) Headache is a symptom of isodrin poisoning (HSDB , 1998).
    3.4.5) NOSE
    A) A white, foamy exudate from the nose occurred with acute endrin poisoning (Reddy et al, 1966). A similar effect may be seen with isodrin.
    3.4.6) THROAT
    A) Foaming at the mouth was observed in a 20-year-old male one hour after ingestion of 200 mL of 30% endosulfan (Shemesh et al, 1988). Hypersalivation occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dysrhythmias can occur from cardiac sensitization. Tachycardia may be caused by isodrin.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) High concentrations of organochlorine insecticides can cause cardiac dysrhythmias by increasing myocardial irritability (Morgan, 1989).
    B) TACHYARRHYTHMIA
    1) Tachycardia may occur with isodrin poisoning (EPA, 1985; HSDB , 1998).

Respiratory

    3.6.1) SUMMARY
    A) Irritation, reduced gas exchange, and chemical pneumonitis may occur.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Irritation may occur from the organochlorine substance itself or from the hydrocarbon solvent in commercial formulations.
    B) RESPIRATORY FAILURE
    1) Severe convulsions can limit pulmonary gas exchange, and this may be an immediate cause of death (Morgan, 1989).
    C) PNEUMONITIS
    1) Aspiration of petroleum distillate solvent is likely to cause a hydrocarbon pneumonitis, which is potentially fatal.

Neurologic

    3.7.1) SUMMARY
    A) Excitation with myoclonic jerking and convulsions may occur. In extreme overdose CNS depression and coma may occur. Permanent damage may occur from acute exposure.
    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) Early signs of organochlorine poisoning involve hyperesthesia and paresthesia of the face and extremities, headache, dizziness, and incoordination (Morgan, 1989).
    B) MYOCLONUS
    1) As the severity of the poisoning increases, myoclonic jerking movements appear (Morgan, 1989).
    C) SEIZURE
    1) Generalized tonic-clonic convulsions occur in severe poisonings. Coma and respiratory depression may ensue (Morgan, 1989). Aldrin, dieldrin, and endrin are CNS excitants and convulsants (Clinical Note, 1984).
    2) Convulsions may appear as an early sign, in the absence of the above symptoms, with the cyclodienes such as isodrin (Morgan, 1989).
    3) Convulsions lasting for four days occurred in a fatal case of endrin ingestion (Runhaar et al, 1985). Seizures may recur over several days after an acute exposure (Morgan, 1989). They may alternate with periods of severe CNS depression (HSDB , 1998).
    D) COMA
    1) Coma may persist for longer than the convulsive phase with isodrin poisoning (HSDB , 1998).
    E) TOXIC ENCEPHALOPATHY
    1) Severe mental impairment was evident one year after ingestion of endosulfan in one case. It is not clear if the brain damage was due to a direct effect of endosulfan, or to the hypoxemia accompanying convulsions and respiratory insufficiency (Shemesh et al, 1988).
    F) SECONDARY PERIPHERAL NEUROPATHY
    1) Occasional reports have associated peripheral neuropathy with exposure to organochlorines.

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and diarrhea may occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) When ingested, these agents cause nausea and vomiting (HSDB , 1998).
    B) DIARRHEA
    1) Diarrhea may occur.

Hepatic

    3.9.1) SUMMARY
    A) Liver injury may occur from isodrin poisoning.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) Liver injury may occur from isodrin poisoning (Lewis, 1996).

Genitourinary

    3.10.1) SUMMARY
    A) Renal insufficiency occurred in a case of endrin ingestion. Hematuria and albuminuria have occurred with aldrin poisoning.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) Renal insufficiency occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).
    B) BLOOD IN URINE
    1) Transient hematuria and albuminuria have occurred with aldrin poisoning (HSDB , 1998).

Acid-Base

    3.11.1) SUMMARY
    A) Severe metabolic acidosis may be a consequence of convulsions and an immediate cause of death.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Severe metabolic acidosis may be a consequence of severe convulsions, and the acidosis may be an immediate cause of death (Morgan, 1989).

Hematologic

    3.13.1) SUMMARY
    A) Aplastic and megaloblastic anemia have occurred in rare cases. Thromobocytopenia may occur in severe poisonings.
    3.13.2) CLINICAL EFFECTS
    A) APLASTIC ANEMIA
    1) Rare cases of aplastic and megaloblastic anemia have been attributed to exposure to organochlorine insecticides (Morgan, 1989; Infante et al, 1978; Sharp et al, 1986).
    B) THROMBOCYTOPENIC DISORDER
    1) Thrombocytopenia occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) Extensive contact results in dermal irritation. Isodrin may cause acne and skin rashes.
    3.14.2) CLINICAL EFFECTS
    A) ACNE
    1) Isodrin can cause acne and skin rashes (Lewis, 1996).

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) HUMANS
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) ANIMAL STUDIES
    1) Isodrin was more toxic to chick embryos than most of the organochlorines (HSDB , 1998). Implications of this finding to the human situation are unknown.
    2) Aldrin, a closely related compound, has affected fertility and has been fetotoxic and teratogenic in several species of experimental animals.
    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) BREAST MILK
    1) Highly lipophilic compounds which are stored in body fat such as dieldrin are likely to be transferred to breast milk (Morgan, 1989). Those chlorinated hydrocarbon insecticides which are more rapidly metabolized are less likely to be detected in breast milk (Morgan, 1989). No data were available on isodrin in breast milk at the time of this review.
    2) The daily intake of total organochlorine pesticides residues calculated for the suckling infant was significantly higher when compared with the acceptable daily intake (ADI) as recommended by FAO/WHO (FAO/WHO, 1970).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS465-73-6 (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.
    B) DELAYED RESPONSE
    1) With few exceptions, the delayed effects of pesticides on human health have been difficult to detect. Perhaps the health risks are sufficiently small that they are below the power of epidemiologic studies to detect (Sharp et al, 1986).
    3.21.4) ANIMAL STUDIES
    A) RELATED COMPOUNDS
    1) Endrin, lindane, dieldrin, aldrin, kepone, camphechlor and chlordane induced neoplasms of the liver, as well as carcinomas and sarcomas in other organs, in rats, and induced high incidences of carcinoma of the liver in mice (Reuber, 1987).

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) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds they reflect cumulative exposure over a period of months or years rather than recent exposure.
    B) Urinary metabolites may be detected, but the procedures are complex and may not be useful for monitoring low exposures.
    4.1.2) SERUM/BLOOD
    A) OTHER
    1) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds they reflect cumulative exposure over a period of months or years rather than recent exposure (Coye et al, 1986).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds they reflect cumulative exposure over a period of months or years rather than recent exposure.
    B) Urinary metabolites may be detected, but the procedures are complex and may not be useful for monitoring low exposures.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Emesis is not recommended due to potential CNS depression or seizures.
    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) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) DECONTAMINATION
    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. Rescue personnel and bystanders should avoid direct contact with contaminated skin, clothing, or other objects (Burgess et al, 1999). Since contaminated leather items cannot be decontaminated, they should be discarded (Simpson & Schuman, 2002).
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) CONTRAINDICATED TREATMENT
    1) Do NOT give oils by mouth. They tend to increase intestinal absorption of these lipophilic toxicants.
    2) Do NOT administer adrenergic amines, which further increase myocardial irritability and produce refractory ventricular arrhythmias (Dreisbach, 1983; Bryson, 1986).
    D) CHOLESTYRAMINE
    1) Cholestyramine (4 grams every eight hours) accelerated excretion of kepone and chlordane in excessively exposed workers, and probably would have a similar effect on other slowly excreted organochlorines which are trapped in the enterohepatic circulation (Cohn et al, 1978) Garrettson et al, 1984, 1985; (Boylan et al, 1978).
    E) PULMONARY ASPIRATION
    1) Evaluate the patient for pulmonary complications, especially if the ingested product contained a petroleum solvent.
    F) EXPERIMENTAL THERAPY
    1) Peters et al (1982) report that symptoms of chronic exposure to hexachlorobenzene improved following treatment with intravenous and oral edetic acid therapy.

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.

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 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. Rescue personnel and bystanders should avoid direct contact with contaminated skin, clothing, or other objects (Burgess et al, 1999). Since contaminated leather items cannot be decontaminated, they should be discarded (Simpson & Schuman, 2002).
    2) Do an alcohol washing followed by a soap washing after the initial soap washing.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) HEMODIALYSIS: Has not proven effective.
    2) HEMOPERFUSION: Effectiveness not known due to limited experience.
    3) Exchange transfusion, extracorporeal, and peritoneal dialysis have not proven effective in management of these poisonings. There has been little or no experience with charcoal hemoperfusion in organochlorine poisonings.

Range Of Toxicity

Summary

    A) From its acute oral toxicity in animals, isodrin would be considered in the EXTREMELY TOXIC group of chlorohydrocarbon insecticides. The probable oral lethal dose for humans is in the range of 5 to 50 mg/kg (between 7 drops and 1 teaspoon for a 150-pound person).

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) LDLo (IP) MOUSE - 6400 mcg/kg (RTECS , 1998)
    B) ACUTE
    1) From its acute oral toxicity in animals, isodrin would be considered in the EXTREMELY TOXIC group of organochlorine insecticides (EPA, 1985). The probable oral lethal dose for humans is in the range of 5 to 50 mg/kg (between 7 drops and 1 teaspoon for a 150-pound person)(EPA, 1985).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Toxic doses of these compounds vary enormously with route and rate of absorption. Based on reports of poisonings and laboratory studies, isodrin would be considered in the group of highest toxicity.

Workplace Standards

    A) ACGIH TLV Values for CAS465-73-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS465-73-6 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS465-73-6 :
    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 CAS465-73-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1998
    1) LD50- (ORAL)MOUSE:
    a) 8800 mcg/kg
    2) LD50- (ORAL)RAT:
    a) 7 mg/kg
    3) LD50- (SKIN)RAT:
    a) 23 mg/kg

Physicochemical

Physical Characteristics

    A) Crystals (Lewis, 1993)

Molecular Weight

    A) 364.90 (Lewis, 1996)

References

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