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CHLORDIMEFORM

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chlordimeform is an organochlorine pesticide and acaricide used to control several types of ticks, mites, and Lepidopteran larva.

Specific Substances

    1) CDM
    2) N'-(4-chloro-o-tolyl)-N,N-dimethylformamide
    3) CAS 6164-98-3
    4) CAS 19750-95-9 (hydrochloride)
    5) N'-(4-chloro-2-methylphenyl)-N,
    6) N-dimethylmethanimidamide
    7) Chlorophenamidine
    8) Chlorophenamidin
    9) Ciba 8514
    10) Shering 36, 268
    11) Chlordimeforme
    12) Methanimidamide, N'-(4-chloro-2-methylphenyl)
    13) N,N-dimethyl-
    14) ENT-27335
    15) ENT-27567
    16) EP-333
    17) Molecular Formula: C10-H13-Cl-N2
    18) CAS 6164-98-3
    19) CHLORPHENAMIDIN
    20) CHLORPHENAMIDINE
    21) SCHERING 36,268

Available Forms Sources

    A) FORMS
    1) The emulsifiable concentrate contains 500 grams of chlordimeform per liter (Knowles, 1991).
    2) The soluble powder formulation contains 800 grams of chlordimeform (as hydrochloride) per kilogram (Knowles, 1991).
    B) SOURCES
    1) Trade names include Galecron, Fundal, Bermat C8514, Ovatoxin, Carzol, Chlorfenamidine, Ciba 8514, Ciba C8514, Fundal 500, Fundex, RS 141, Schering 36268, SN 36268, Spanon, and Spandone (IARC, 1983).
    C) USES
    1) Chlordimeform is used to control several types of ticks, mites, and Lepidopteran larva (Lund et al, 1978).

Overview

Laboratory Monitoring

    A) Exposure to chlordimeform may be monitored by testing for the metabolite, 2-methyl-4-chloroaniline.
    B) Patients exposed should have serial urinalysis to monitor bladder function.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and 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) 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.
    F) METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    G) METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg.
    H) Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome.
    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).

Range Of Toxicity

    A) 214 mg/kg was fatal to an adult human.
    B) LD50 (ORAL) MOUSE - 195 to 310 mg/kg

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Vomiting, lethargy, muscular weakness, cyanosis, methemoglobinemia, and coma have been reported following large oral ingestions in humans. Animals poisoned have experienced CNS excitation, seizures, respiratory arrest, hypotension, and liver injury.
    0.2.5) CARDIOVASCULAR
    A) Hypotension, peripheral vasodilation, and heat abnormalities have been reported in animals. Cardiac arrest was seen in one human case.
    0.2.6) RESPIRATORY
    A) Respiratory arrest may occur.
    0.2.7) NEUROLOGIC
    A) Lethargy, generalized muscular weakness, and coma have occurred in humans. Animals have experienced seizures, an anesthetic effect, and excitation followed by death.
    0.2.8) GASTROINTESTINAL
    A) Anorexia and a sweetish taste in the mouth were noted in workers who repackaged this chemical. Vomiting was reported following a large ingestion of chlordimeform.
    0.2.9) HEPATIC
    A) Liver damage has been reported in cats.
    0.2.10) GENITOURINARY
    A) Acute hemorrhagic cystitis, increased urgency and frequency of urination, nocturia, urethral discharge, and abdominal pain have been noted following occupational exposure.
    0.2.13) HEMATOLOGIC
    A) Methemoglobinemia has been reported.
    0.2.14) DERMATOLOGIC
    A) Exposed workers have developed a pruritic rash.
    0.2.17) METABOLISM
    A) Animals poisoned developed increased glucose levels and decreased insulin and insulin release.
    0.2.20) REPRODUCTIVE
    A) Progeny of rats, given approximately 100 mcg/kg from the fifth day of pregnancy on, showed no abnormalities except an impaired swimming ability. Chlordimeform delayed luteinizing hormone by one day in female rats.
    0.2.21) CARCINOGENICITY
    A) Mutagenicity testing has been negative.
    B) Some case studies in mice would indicate an increase in hemangiosarcomas.

Clinical Effects

Summary Of Exposure

    A) Vomiting, lethargy, muscular weakness, cyanosis, methemoglobinemia, and coma have been reported following large oral ingestions in humans. Animals poisoned have experienced CNS excitation, seizures, respiratory arrest, hypotension, and liver injury.

Vital Signs

    3.3.2) RESPIRATIONS
    A) Respiratory arrest may occur after significant exposures (was seen with 214 mg/kg) (FAO/WHO, 1972).
    3.3.4) BLOOD PRESSURE
    A) Overdose may result in hypotension (Lund et al, 1978).

Heent

    3.4.3) EYES
    A) In the standard Draize test, 100 mg chlordimeform was applied to rabbit eyes which subsequently developed severe irritation (RTECS , 2000).

Cardiovascular

    3.5.1) SUMMARY
    A) Hypotension, peripheral vasodilation, and heat abnormalities have been reported in animals. Cardiac arrest was seen in one human case.
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOTENSION
    a) Due to peripheral vasodilation and direct myocardial depression was seen in dogs given this agent (Lund et al, 1978). The effect was dose-dependent, with 50 to 75 mg/kg producing irreversible hypotension. Hypotensive effects were also seen in rabbits given 200 mg/kg IP (Beeman & Matsumura, 1974) and in weanling rats (Watkinson, 1986).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory arrest may occur.
    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) Respiratory arrest was reported in one human case (FAO/WHO, 1972).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) Respiratory arrest was reported in dogs given 50 to 75 mg/kg (Lund et al, 1978), and in one human case (FAO/WHO, 1972).

Neurologic

    3.7.1) SUMMARY
    A) Lethargy, generalized muscular weakness, and coma have occurred in humans. Animals have experienced seizures, an anesthetic effect, and excitation followed by death.
    3.7.2) CLINICAL EFFECTS
    A) DROWSY
    1) Generalized muscular weakness and lethargy progressing to coma were reported in a 76-year-old male following an ingestion of 100 grams of chlordimeform (Arima et al, 1976).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) Seizures have been seen in dogs given overdoses of 3 to 30 mg/kg (Lund et al, 1978).
    2) ANESTHESIA LOCAL
    a) In animal studies, chlordimeform has shown a local anesthetic effect on nerves (Chinn et al, 1976).
    3) CNS STIMULATION
    a) Hyperexcitability followed by death was seen in rats poisoned with 200 mg/kg (Gosselin et al, 1984; Matsumura & Beeman, 1976).

Gastrointestinal

    3.8.1) SUMMARY
    A) Anorexia and a sweetish taste in the mouth were noted in workers who repackaged this chemical. Vomiting was reported following a large ingestion of chlordimeform.
    3.8.2) CLINICAL EFFECTS
    A) LOSS OF APPETITE
    1) Anorexia was noted in workers exposed to chlordimeform while repackaging the chemical (Folland et al, 1978).
    B) TASTE SENSE ALTERED
    1) These same workers had a sweet taste in their mouths (Folland et al, 1978).
    C) VOMITING
    1) Vomiting was reported following an ingestion of 100 grams of chlordimeform in a 76-year-old male (Arima et al, 1976).

Hepatic

    3.9.1) SUMMARY
    A) Liver damage has been reported in cats.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Liver injury developed in two of three cats given 50 mg/kg subcutaneously daily for up to 5 days (Kimbrough, 1980; Folland et al, 1978).

Genitourinary

    3.10.1) SUMMARY
    A) Acute hemorrhagic cystitis, increased urgency and frequency of urination, nocturia, urethral discharge, and abdominal pain have been noted following occupational exposure.
    3.10.2) CLINICAL EFFECTS
    A) HEMORRHAGIC CYSTITIS
    1) Acute hemorrhagic cystitis was seen in 41% of 22 workers who packaged chlordimeform. Frequently reported symptoms included urinary frequency, increase urgency, dysuria, nocturia, urethral discharge, and abdominal pain. When chlordimeform was further investigated in cats, it was found that subcutaneously injected chlordimeform produced similar, but less severe effects (Folland et al, 1978).
    2) Similar effects were not seen in similar workers in two other studies (Lemesch et al, 1987; Kurtz et al, 1987; Jurincic et al, 1991).
    3) It is unknown if chlordimeform is the specific bladder irritant. Its metabolite, para-chloro-ortho toluidine, is a known human bladder irritant (Currie, 1933; HSDB , 2000).

Hematologic

    3.13.1) SUMMARY
    A) Methemoglobinemia has been reported.
    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) CASE REPORT - A 76-year-old male presented with lip, nail, and skin cyanosis. At 5 hours after ingestion of 100 gram of chlordimeform his methemoglobin concentration in the blood was 17% of the total hemoglobin. Moderate neutrophilic leukocytosis was also noted (Arima et al, 1976).

Dermatologic

    3.14.1) SUMMARY
    A) Exposed workers have developed a pruritic rash.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) DERMATITIS - 6 of 22 workers who packaged this insecticide developed a fine papular rash which then desquamated and became pruritic in 2 to 3 days (Anon, 1975).

Immunologic

    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNE SYSTEM DISORDER
    a) LACK OF TOXICITY - Using an animal test model, Shoppe et al (1985) concluded that relatively high doses of chlordimeform do NOT result in consistent immunotoxicity.

Reproductive

    3.20.1) SUMMARY
    A) Progeny of rats, given approximately 100 mcg/kg from the fifth day of pregnancy on, showed no abnormalities except an impaired swimming ability. Chlordimeform delayed luteinizing hormone by one day in female rats.
    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) CONGENITAL ANOMALY
    1) Progeny of rats, given approximately 100 mcg/kg from the fifth day of pregnancy on, showed no abnormalities except an impaired swimming ability from days 7 to 17 (Olson et al, 1978).
    3.20.5) FERTILITY
    A) FERTILITY DECREASED FEMALE
    1) Chlordimeform delayed luteinizing hormone by one day in female rats; the number of pregnant females, live pups and implantation sites were reduced (Cooper et al, 1994).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS6164-98-3 (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) IARC Classification
    a) Listed as: Chlordimeform
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) Mutagenicity testing has been negative.
    B) Some case studies in mice would indicate an increase in hemangiosarcomas.
    3.21.3) HUMAN STUDIES
    A) NEOPLASM
    1) Hemangiosarcomas were found in the spleen and other tissues of mice exposed to the chlordimeform metabolite 4-chloro-2-toluidine (Weisburger et al, 1978; IARC, 1983).
    B) BLADDER CARCINOMA
    1) CASE REPORT - One case of bladder cancer was noted by Currie (1933) in workers exposed to chlordimeform's metabolite para-chloro-ortho-toluidine.
    2) Exposure to the metabolite, 4-chloro-o-toluidine, is associated with an increase in risk of bladder cancer (HSDB , 2000).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Exposure to chlordimeform may be monitored by testing for the metabolite, 2-methyl-4-chloroaniline.
    B) Patients exposed should have serial urinalysis to monitor bladder function.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Although not seen in humans, cats have developed liver damage. Until more human case data are available, monitoring liver function tests is suggested.
    4.1.3) URINE
    A) URINALYSIS
    1) Because of the potential for cystitis, exposed patients should have serial urinalysis to check for hematuria and other abnormalities.

Methods

    A) CHROMATOGRAPHY
    1) Exposure to chlordimeform may be monitored by examining the urine for 2-methyl-4-chloroaniline by gas chromatography (Coye et al, 1986).
    2) Analysis of 4-chloro-o-toluidine may also be done by reverse phase high performance liquid chromatography (Geyer & Fattal, 1987).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

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

Monitoring

    A) Exposure to chlordimeform may be monitored by testing for the metabolite, 2-methyl-4-chloroaniline.
    B) Patients exposed should have serial urinalysis to monitor bladder function.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/ NOT RECOMMENDED -
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and 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) 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).
    B) 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).
    C) MONITORING OF PATIENT
    1) Serial urinalysis may be required to assess whether their has been damage to the bladder and urinary tract (Morgan, 1989).
    D) DRUG INTERACTION
    1) Chlordimeform has MAOI activity. Although this is not its main mechanism of toxicity, persons exposed should avoid excessive amounts of sympathomimetic drugs or foods with high concentrations of tryptophan (e.g. broad beans) or tyramine (e.g. cheese, beers, wines, pickled herring, yeast extract, or chicken livers) (Prod Info, 1972).
    E) METHEMOGLOBINEMIA
    1) Oxygen should be administered to all cyanotic patients. Cyanosis secondary to methemoglobinemia or sulfhemoglobinemia will not respond to oxygen therapy.
    2) Profound cyanosis may occur in individuals with methemoglobinemia or sulfhemoglobinemia who appear to be in no respiratory distress. The blood should be examined and compared to normal blood to identify chocolate-brown color, signifying a methemoglobin level of at least 15%.
    3) SUMMARY
    a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    4) METHYLENE BLUE
    a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
    b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
    c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
    d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).
    5) TOLUIDINE BLUE OR TOLONIUM CHLORIDE (GERMANY)
    a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
    b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
    c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.
    6) ADVERSE EFFECTS
    a) METHEMOGLOBINEMIA - Although methylene blue has been reported to itself cause methemoglobin formation up to about 7% of total hemoglobin (Whitwam et al, 1979; Goluboff & Wheaton, 1961; Nadler et al, 1934), this hypothesis has been disputed (Stossel & Jennings, 1966; Rentsch & Wittekind, 1967) and the amounts said to be induced are clinically insignificant (Hall et al, 1986).
    b) HEMOLYSIS - Repeated large doses (up to 15 milligrams/kilogram) may cause hemolysis (Jaffe, 1979; Harvey & Keitt, 1983) particularly in the presence of G-6-PD deficiency. The dangers of repeated appropriate doses of methylene blue (1 to 2 milligrams/kilogram) are uncertain, but it is recommended that with rare exceptions the total dosage should not exceed 7 milligrams/kilogram (Wintrobe, 1974; Harvey & Keitt, 1983). Methylene blue may be ineffective in patients with G-6-PD deficiency (Rosen et al, 1971).
    c) Other reported adverse effects from high doses of methylene blue include chest pain, dyspnea, anxiety, and tremors (Nadler et al, 1934).
    7) FALSE POSITIVE CO-OXIMETER RESULTS - Methylene blue may cause a false positive methemoglobin level when measuring arterial blood gases using a co-oximeter (Kirlangitis et al, 1990).

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) Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

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

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) ORAL: A patient who ingested 30 mL of a 50% formulation of chlordimeform (214 mg/kg) was admitted to the hospital with no detectable respiration or heart beat, and although maintained on respiratory support equipment, died within 24 hours (FAO/WHO, 1972).

Range Of Toxicity

Summary

    A) 214 mg/kg was fatal to an adult human.
    B) LD50 (ORAL) MOUSE - 195 to 310 mg/kg

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) One fatality has been reported at a dose of 214 mg/kg (FAO/WHO, 1972).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Minimum lethal human exposure is unknown.

Workplace Standards

    A) ACGIH TLV Values for CAS6164-98-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS6164-98-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS6164-98-3 :
    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): 3 ; Listed as: Chlordimeform
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    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 CAS6164-98-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)MOUSE:
    1) 195-310 mg/kg (Hollingworth, 1976)
    2) 160 mg/kg (RTECS, 2000)
    B) LD50- (SKIN)MOUSE:
    1) 225 mg/kg (RTECS, 2000)
    C) LD50- (ORAL)RAT:
    1) 160 mg/kg (RTECS, 2000)
    D) LD50- (SKIN)RAT:
    1) 263-337 mg/kg (Gaines & Linder, 1986; RTECS, 2000)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) CDM and similar compounds are known to inhibit monoamine oxidase in both the mouse and rat liver, but this is not thought to be the mechanism behind its toxicity (Beeman & Matsumura, 1973; Aziz & Knowles, 1973; Robinson & Smith, 1977).
    B) Although Wang et al (1975) reported decreased sensitivity to acetylcholine, other experimenters have shown neither cholinergic or anticholinergic properties in animal models (Beeman & Matsumura, 1974; Dittrich, 1966).
    C) In invertebrates, CDM is toxic by activating an octopamine-dependent adenylate cyclase (Nathanson, 1985).
    D) Formamidine pesticides (like CDM) have been shown to inhibit prostaglandin biosynthesis (Yim et al, 1978), block neuromuscular transmission (Wang et al, 1975), and interfere with amine-mediated control of nervous endocrine systems (Matsumura & Beeman, 1976).

Toxicologic Mechanism

    A) CDM is also known to uncouple oxidative phosphorylation and electrotransport (approximately as potent as 2,4-dinitrophenol). This may account for some of the toxic effects, but not all (Abo-Khatwa & Hollingworth, 1974).
    B) Work by Costa et al (1988) would indicate the site of toxicity as being alpha-2-adrenoceptors.

Physicochemical

Physical Characteristics

    A) This compound exists as a colorless crystalline solid (Budavari, 1996).

Molecular Weight

    A) 196.67 (Budavari, 1996)
    B) Hydrochloride salt: 233.2 (Budavari, 1996)

References

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