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FLUOROACETIC ACID

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Fluoroacetic acid is used as a rodenticide.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C2-H3-F-O2

Available Forms Sources

    A) FORMS
    1) Fluoroacetic acid is a strong acid (pKa = 2.66) (HSDB , 1993). It occurs as colorless, odorless crystals, needles, or powder and is soluble in water (Lewis, 1993) and alcohol (HSDB , 1993).
    2) Fluoroacetic acid is a HIGHLY TOXIC SUBSTANCE.
    3) Little toxicologic data were available specifically for fluoroacetic acid; its toxicity is thought to be similar to that of FLUOROACETATE (Budavari, 1989; Sax & Lewis, 1989; EPA, 1985). This review is based on the properties of fluoroacetate (as SODIUM FLUOROACETATE). Effects attributed specifically to fluoroacetic acid are identified.
    B) USES
    1) Fluoroacetic acid is used as a rodenticide (Budavari, 1989; EPA, 1985). It is also a metabolite of the series of fluoro ester compounds.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Fluoroacetic acid is the major metabolite of the series of fluoro ester compounds. It is used as a rodenticide. Little specific data were available specifically about the toxicity of fluoroacetic acid; its toxicity is expected to be similar to that of FLUOROACETATE.
    1) The following review discusses the toxicity and treatment of poisoning with FLUOROACETATE.
    2) Fluoroacetic acid is a colorless crystalline solid which burns with a green flame and which is soluble in water and alcohol. It can be irritating. It may be absorbed following ingestion, inhalation, and dermal contact.
    B) Clinical effects are usually seen within 1/2 hour of exposure. Symptoms of nausea, vomiting, excessive salivation, abdominal pain, numbness, a tingling sensation, and apprehension are seen initially, and may last for up to 6 hours. Muscular twitching, blurred vision, and hypotension may develop.
    1) Severe effects such as coma, convulsions, and cardiac arrhythmias may be delayed in onset as long as 20 hours. One death due to subacute fluoroacetate poisoning has been reported.
    2) The cardiac effects noted include tachycardia, ventricular fibrillation, and sudden onset of asystole.
    3) Death may occur from respiratory depression and hypoxia during convulsions or cardiac arrest.
    4) Neurologic sequelae and acute renal failure have been described after acute poisoning.
    5) Metabolic acidosis, hyperglycemia, hyperuricemia, elevated levels of hepatic transaminases, and elevated serum creatinine may occur in fluoroacetate poisoning.
    C) At least one case of severe poisoning with numbness and tingling of the face, excessive salivation, blurred vision, peripheral paresthesias, convulsions, and coma has occurred from inhalation and dermal contact with fluoroacetate. In general, fluoroacetate is absorbed following ingestion and inhalation, but not through intact skin.
    D) Fluoroacetate mimics acetic acid and reacts with coenzyme A and oxaloacetic acid, forming fluorocitric acid which enters and blocks the Kreb's cycle, allowing accumulation of citric acid.
    E) Fluoroacetamide releases toxic and irritating fumes of sodium oxide and fluoride when heated to decomposition. Inhalation exposure to such fumes would be expected to result in respiratory irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression, hypothermia, tachycardia, and hypotension may occur.
    0.2.4) HEENT
    A) Blurred vision, facial paresthesias, and hypersalivation may be noted.
    0.2.5) CARDIOVASCULAR
    A) Tachycardia, ventricular fibrillation, and sudden onset of asystole may occur.
    0.2.6) RESPIRATORY
    A) Respiratory depression and cyanosis may develop. Death may be due to hypoxia and respiratory depression during seizures.
    B) Fluoroacetamide releases toxic and irritating fumes of sodium oxide and fluoride when heated to decomposition. Inhalation exposure to such fumes would be expected to result in respiratory irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Apprehension, diaphoresis, disorientation, agitation, paresthesias, muscle twitching, hyperactive behavior, tingling, coma, and convulsions may develop. Status epilepticus has been described.
    B) Neurologic sequelae have been noted following acute poisoning, such as hypertonicity with arm and leg spasms, severe mental deficits, and moderate residual paresis.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, hypersalivation, abdominal or epigastric pain, and diarrhea may be seen.
    0.2.9) HEPATIC
    A) Elevations of hepatic transaminases may be noted.
    0.2.10) GENITOURINARY
    A) Acute renal failure may be a sequelae of acute poisoning. Elevated levels of serum creatinine and uric acid may be noted.
    0.2.11) ACID-BASE
    A) Metabolic acidosis may be seen.
    0.2.12) FLUID-ELECTROLYTE
    A) Hypocalcemia may occur.
    0.2.15) MUSCULOSKELETAL
    A) Muscle twitching may be an early effect.
    0.2.16) ENDOCRINE
    A) Elevated blood glucose levels may be seen in fluoroacetate poisoning.
    0.2.17) METABOLISM
    A) Fluoroacetate mimics acetic acid and reacts with coenzyme A and oxaloacetic acid, forming fluorocitric acid which enters and blocks the Kreb's cycle, allowing accumulation of citric acid.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) ANIMAL STUDIES - In mice, oral administration of fluoroacetamide resulted in a prolonged pregnancy and the young suffered from cyanosis, respiratory distress, reduced growth, and decreased survival. It has also caused testicular degeneration in rats.
    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) Fluoroacetate levels are not clinically useful.
    B) Monitor serum calcium, magnesium, and potassium concentrations.
    C) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    D) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    E) BLOOD GASES
    1) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    F) Monitor EKG and vital signs frequently.
    G) If respiratory tract irritation is present, monitor chest x-ray.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) 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.
    C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    D) THERE IS NO KNOWN EFFECTIVE ANTIDOTE for fluoroacetate intoxication. Symptomatic and supportive care should be provided. Animal experiments suggest that calcium gluconate administration may be helpful, but there is no data on human intoxication.
    E) 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.
    F) REFRACTORY SEIZURES: Consider continuous infusion of midazolam, propofol, and/or pentobarbital. Hyperthermia, lactic acidosis and muscle destruction may necessitate use of neuromuscular blocking agents with continuous EEG monitoring.
    G) MONITOR ECG AND VITAL SIGNS frequently.
    H) CALCIUM - Calcium gluconate or calcium chloride should be administered parenterally in patients with documented hypocalcemia.
    I) HYPOTENSION
    1) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    J) MONITORING PARAMETERS
    1) Monitor ECG and VITAL SIGNS frequently; ventricular arrhythmias may occur suddenly. Monitor serum electrolytes, including calcium, magnesium, and potassium. Monitor blood sugar, liver and renal function tests, and urinalysis.
    K) PATIENT DISPOSITION
    1) As DELAYED ONSET of SERIOUS or LIFE-THREATENING TOXICITY may occur, all patients with possible significant exposure should be observed for up to 20 hours in a controlled setting.
    L) 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) SYSTEMIC ABSORPTION
    1) Systemic poisoning has occurred following inhalation exposure to fluoroacetate (Ellenhorn & Barceloux, 1988).
    C) THERE IS NO KNOWN EFFECTIVE ANTIDOTE for fluoroacetate intoxication. Symptomatic and supportive care should be provided.
    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) REFRACTORY SEIZURES: Consider continuous infusion of midazolam, propofol, and/or pentobarbital. Hyperthermia, lactic acidosis and muscle destruction may necessitate use of neuromuscular blocking agents with continuous EEG monitoring.
    F) MONITOR ECG AND VITAL SIGNS frequently.
    G) CALCIUM - Calcium gluconate or calcium chloride should be administered parenterally in patients with documented hypocalcemia.
    H) HYPOTENSION
    1) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    I) MONITORING PARAMETERS
    1) Monitor ECG and VITAL SIGNS frequently; ventricular arrhythmias may occur suddenly. Monitor serum electrolytes, including calcium, magnesium, and potassium. Monitor blood sugar, liver and renal function tests, and urinalysis.
    J) PATIENT DISPOSITION
    1) As DELAYED ONSET of SERIOUS or LIFE-THREATENING TOXICITY may occur, all patients with possible significant exposure should be observed for up to 20 hours in a controlled setting.
    K) 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.
    B) SYSTEMIC TOXICITY
    1) There is no evidence that fluoroacetate can be absorbed in toxic quantities following ocular exposure. Should systemic symptoms develop following exposure by this route -
    2) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    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) SYSTEMIC ABSORPTION
    a) There is little evidence that fluoroacetate can be absorbed systemically in toxic amounts through intact skin (Ellenhorn & Barceloux, 1988). Should systemic symptoms develop following dermal contact with this material -
    b) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Range Of Toxicity

    A) A milligram of pure compound is probably enough to cause severe toxicity, and less may be toxic. Extrapolation of experimental animal toxicity data to humans indicates that a dose of 2 to 10 mg/kg may be fatal.

Clinical Effects

Summary Of Exposure

    A) Fluoroacetic acid is the major metabolite of the series of fluoro ester compounds. It is used as a rodenticide. Little specific data were available specifically about the toxicity of fluoroacetic acid; its toxicity is expected to be similar to that of FLUOROACETATE.
    1) The following review discusses the toxicity and treatment of poisoning with FLUOROACETATE.
    2) Fluoroacetic acid is a colorless crystalline solid which burns with a green flame and which is soluble in water and alcohol. It can be irritating. It may be absorbed following ingestion, inhalation, and dermal contact.
    B) Clinical effects are usually seen within 1/2 hour of exposure. Symptoms of nausea, vomiting, excessive salivation, abdominal pain, numbness, a tingling sensation, and apprehension are seen initially, and may last for up to 6 hours. Muscular twitching, blurred vision, and hypotension may develop.
    1) Severe effects such as coma, convulsions, and cardiac arrhythmias may be delayed in onset as long as 20 hours. One death due to subacute fluoroacetate poisoning has been reported.
    2) The cardiac effects noted include tachycardia, ventricular fibrillation, and sudden onset of asystole.
    3) Death may occur from respiratory depression and hypoxia during convulsions or cardiac arrest.
    4) Neurologic sequelae and acute renal failure have been described after acute poisoning.
    5) Metabolic acidosis, hyperglycemia, hyperuricemia, elevated levels of hepatic transaminases, and elevated serum creatinine may occur in fluoroacetate poisoning.
    C) At least one case of severe poisoning with numbness and tingling of the face, excessive salivation, blurred vision, peripheral paresthesias, convulsions, and coma has occurred from inhalation and dermal contact with fluoroacetate. In general, fluoroacetate is absorbed following ingestion and inhalation, but not through intact skin.
    D) Fluoroacetate mimics acetic acid and reacts with coenzyme A and oxaloacetic acid, forming fluorocitric acid which enters and blocks the Kreb's cycle, allowing accumulation of citric acid.
    E) Fluoroacetamide releases toxic and irritating fumes of sodium oxide and fluoride when heated to decomposition. Inhalation exposure to such fumes would be expected to result in respiratory irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression, hypothermia, tachycardia, and hypotension may occur.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression and cyanosis may be seen (Ellenhorn & Barceloux, 1988).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Fluoroacetate poisoning causes hypothermia in experimental animals (HSDB , 1998).
    2) Hypothermia (< 35 degrees Celsius) developed in CATS approximately 6 hours after exposure to fluoroacetate 0.45 mg/kg, regardless of treatment measures (Collicchio-Zuanaze et al, 2006).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypotension may be seen in fluoroacetate poisoning (HSDB , 1998).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) Tachycardia leading to serious cardiac arrhythmias may be noted (Ellenhorn & Barceloux, 1988).

Heent

    3.4.1) SUMMARY
    A) Blurred vision, facial paresthesias, and hypersalivation may be noted.
    3.4.3) EYES
    A) Blurred vision may be seen in acute fluoroacetate poisoning (HSDB , 1998).

Cardiovascular

    3.5.1) SUMMARY
    A) Tachycardia, ventricular fibrillation, and sudden onset of asystole may occur.
    3.5.2) CLINICAL EFFECTS
    A) VENTRICULAR FIBRILLATION
    1) WITH POISONING/EXPOSURE
    a) Ventricular fibrillation is commonly noted. QTc prolongation may occur in the presence of hypocalcemia (Roy et al, 1980; HSDB , 1998).
    B) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) Asystole may occur suddenly and can be delayed for several hours after exposure (McTaggart, 1970).
    C) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Sinus tachycardia may be seen initially (McTaggart, 1970; Trabes et al, 1983).
    D) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension may be seen in acute fluoroacetate poisoning (HSDB , 1998; Ellenhorn & Barceloux, 1988).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CARDIOTOXICITY
    a) CATS exposed to fluoroacetate 0.45 mg/kg developed cardiotoxicity including sinus tachycardia and prolongation of the QTc interval, regardless of receiving treatment with calcium gluconate and sodium succinate or not. Overall survival was 37.5% in cats receiving no treatment and 75% in cats receiving treatment (Collicchio-Zuanaze et al, 2006).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory depression and cyanosis may develop. Death may be due to hypoxia and respiratory depression during seizures.
    B) Fluoroacetamide releases toxic and irritating fumes of sodium oxide and fluoride when heated to decomposition. Inhalation exposure to such fumes would be expected to result in respiratory irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) Respiratory depression and cyanosis may occur (Ellenhorn & Barceloux, 1988). Death may be due to respiratory paralysis and hypoxia occurring during seizures (HSDB , 1998).
    B) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS
    1) WITH POISONING/EXPOSURE
    a) Fluoroacetamide releases toxic and irritating fumes of sodium oxide and fluoride when heated to decomposition (Lewis, 1996). Inhalation exposure to such fumes would be expected to result in respiratory irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

Neurologic

    3.7.1) SUMMARY
    A) Apprehension, diaphoresis, disorientation, agitation, paresthesias, muscle twitching, hyperactive behavior, tingling, coma, and convulsions may develop. Status epilepticus has been described.
    B) Neurologic sequelae have been noted following acute poisoning, such as hypertonicity with arm and leg spasms, severe mental deficits, and moderate residual paresis.
    3.7.2) CLINICAL EFFECTS
    A) HYPERACTIVE BEHAVIOR
    1) WITH POISONING/EXPOSURE
    a) Hyperactive behavior may be rapidly noted, gradually leading to convulsions, coma, cyanosis and death. Diaphoresis, disorientation, and agitation may be early effects (Trabes et al, 1983).
    B) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Facial and peripheral paresthesias, a tingling sensation, numbness, and mental apprehension may be early symptoms (Ellenhorn & Barceloux, 1988; Sittig, 1991).
    C) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Coma and convulsions may occur. Status epilepticus has been described (McTaggart, 1970; HSDB , 1998; Lewis, 1996). Severe effects such as convulsions may be delayed in onset as long as 20 hours after exposure.
    D) SEQUELA
    1) WITH POISONING/EXPOSURE
    a) Neurologic sequelae have been noted following acute poisoning, such as hypertonicity with arm and leg spasms, severe mental deficits, and moderate residual paresis (McTaggart, 1970). Severe cerebellar dysfunction, ataxia, and depression were described in a 15-year-old patient who survived acute fluoroacetate poisoning (Trabes et al, 1983).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CONVULSIONS
    a) CATS exposed to 0.45 mg/kg fluoroacetate received either no treatment or treatment with calcium gluconate and sodium succinate. Onset of convulsions following exposure was 12 hours (+/- 1 hour, 11 minutes) in cats that survived and 10 hours (+/- 4 hours, 26 minutes) in cats that expired. Convulsions presented as hyperexcitability, tremors, limb and neck spasticity, nystagmus and transient apnea. Survival was 37.5% in cats receiving no treatment and 75% for cats receiving treatment (Collicchio-Zuanaze et al, 2006).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, hypersalivation, abdominal or epigastric pain, and diarrhea may be seen.
    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) The initial response is nausea, vomiting, abdominal or epigastric pain, hypersalivation, and diarrhea (McTaggart, 1970; Trabes et al, 1983; HSDB , 1998; Ellenhorn & Barceloux, 1988).

Hepatic

    3.9.1) SUMMARY
    A) Elevations of hepatic transaminases may be noted.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Elevated serum levels of hepatic transaminases may be observed (Ellenhorn & Barceloux, 1988).

Genitourinary

    3.10.1) SUMMARY
    A) Acute renal failure may be a sequelae of acute poisoning. Elevated levels of serum creatinine and uric acid may be noted.
    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Acute renal failure may follow serious acute fluoroacetate poisoning (Baselt & Cravey, 1989; Ellenhorn & Barceloux, 1988; Chung, 1984). Elevated serum creatinine and uric acid levels may occur (Ellenhorn & Barceloux, 1988).

Acid-Base

    3.11.1) SUMMARY
    A) Metabolic acidosis may be seen.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Metabolic acidosis may be seen in fluoroacetate poisoning (Ellenhorn & Barceloux, 1988).

Musculoskeletal

    3.15.1) SUMMARY
    A) Muscle twitching may be an early effect.
    3.15.2) CLINICAL EFFECTS
    A) SPASMODIC MOVEMENT
    1) WITH POISONING/EXPOSURE
    a) Muscle twitching may be an early symptom of fluoroacetate poisoning (Ellenhorn & Barceloux, 1988; HSDB , 1998).

Endocrine

    3.16.1) SUMMARY
    A) Elevated blood glucose levels may be seen in fluoroacetate poisoning.
    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) Elevated blood glucose levels may be seen in fluoroacetate poisoning (Ellenhorn & Barceloux, 1988).

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) ANIMAL STUDIES - In mice, oral administration of fluoroacetamide resulted in a prolonged pregnancy and the young suffered from cyanosis, respiratory distress, reduced growth, and decreased survival. It has also caused testicular degeneration in 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) ANIMAL STUDIES
    1) In mice, oral administration of fluoroacetamide resulted in a prolonged pregnancy and the young suffered from cyanosis, respiratory distress, reduced growth, and decreased survival (HSDB , 1998).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS144-49-0 (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) Fluoroacetate levels are not clinically useful.
    B) Monitor serum calcium, magnesium, and potassium concentrations.
    C) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    D) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    E) BLOOD GASES
    1) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    F) Monitor EKG and vital signs frequently.
    G) If respiratory tract irritation is present, monitor chest x-ray.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Fluoroacetate levels are not clinically useful.
    2) Monitor serum calcium, magnesium, and potassium concentrations.
    3) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    4) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    B) ACID/BASE
    1) BLOOD GASES
    a) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor EKG and vital signs frequently.

Radiographic Studies

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

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Fluoroacetate levels are not clinically useful.
    B) Monitor serum calcium, magnesium, and potassium concentrations.
    C) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    D) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    E) BLOOD GASES
    1) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    F) Monitor EKG and vital signs frequently.
    G) If respiratory tract irritation is present, monitor chest x-ray.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Because of the risk of seizures, DO NOT INDUCE EMESIS.
    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) SUPPORT
    1) There is no known effective specific treatment for fluoroacetate exposure; symptomatic and supportive treatment should be provided.
    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).
    7) 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) 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).
    D) MONITORING OF PATIENT
    1) Monitor ECG and VITAL SIGNS frequently; ventricular arrhythmias may occur suddenly.
    2) Monitor serum electrolytes, including calcium, magnesium, and potassium.
    3) Monitor blood sugar, liver and renal function tests, and urinalysis.
    E) CALCIUM
    1) Correction of decreased serum ionized calcium to normal prolonged survival in cats poisoned with fluoroacetate (Taitelman et al, 1983) and may normalize ECG changes in patients with prolonged QTc (Roy et al, 1980).
    2) Treatment with a combination of calcium gluconate and sodium succinate improved survival rates in cats poisoned with fluoroacetate. Survival rates were 75% in cats receiving treatment v. 37.5% survival rate in cats receiving no treatment (Collicchio-Zuanaze et al, 2006).
    3) Administer intravenous calcium chloride (10 to 20 mL of 10% in adults or 10 to 20 mg/kg in children) or calcium gluconate (0.1 to 0.2 mL/kg of 10% solution, up to 10 mL per dose) to patients with ECG changes (QTc prolongation), neuromuscular changes (carpopedal spasm), or laboratory evidence of hypocalcemia. Repeat doses as necessary to correct hypocalcemia.
    4) PRECAUTIONS - Administer under continuous ECG monitoring, and measure serial calcium, potassium, and magnesium levels. The calcium chloride salt is irritating and may produce acidosis. Calcium gluconate is preferred in patients with acidosis. Rapid IV injection may cause vasodilation. Administer slowly through a small needle into a large vein, taking care to avoid extravasation.
    F) EXPERIMENTAL THERAPY
    1) Administration of ETHANOL (approximately 800 mg/kg given within 30 minutes of exposure) has been reported to be helpful in the treatment of mice, guinea pigs and rabbits poisoned with fluoroacetate (Proudfoot et al, 2006). This is EXPERIMENTAL. In an anecdotal report of simultaneous sodium fluoroacetate and ethanol ingestion in a 29-year-old man, restlessness, a single seizure, aggressiveness, and confusion were the only signs noted (Ramirez, 1986).
    a) DOSE - Ethanol is administered as in a methanol poisoning. First dose should be 1 to 1.5 mL/kg of a 50% solution followed 4 hours later by the same dose. The goal is to have blood alcohol at 100 mg/dL; the dose may have to be increased or given as a continuous drip. Constant monitoring of the blood ethanol and blood glucose is crucial. Glucose must be included in the IV fluid to prevent hypoglycemia.
    G) OBSERVATION REGIMES
    1) As DELAYED ONSET of SERIOUS or LIFE-THREATENING TOXICITY may occur, all patients with possible significant exposure should be observed for up to 20 hours in a controlled setting.

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) SUPPORT
    1) Systemic poisoning has occurred following inhalation exposure to fluoroacetate (Grant. 1986; (Ellenhorn & Barceloux, 1988).
    B) SUPPORT
    1) There is no known effective specific treatment for fluoroacetate exposure; symptomatic and supportive treatment should be provided.
    C) 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).
    7) 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).
    D) 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).
    E) MONITORING OF PATIENT
    1) Monitor ECG and VITAL SIGNS frequently; ventricular arrhythmias may occur suddenly.
    2) Monitor serum electrolytes, including calcium, magnesium, and potassium.
    3) Monitor blood sugar, liver and renal function tests, and urinalysis.
    F) CALCIUM
    1) Correction of decreased serum ionized calcium to normal prolonged survival in cats poisoned with fluoroacetate (Taitelman et al, 1983) and may normalize ECG changes in patients with prolonged QTc (Roy et al, 1980).
    2) Treatment with a combination of calcium gluconate and sodium succinate improved survival rates in cats poisoned with fluoroacetate. Survival rates were 75% in cats receiving treatment v. 37.5% survival rate in cats receiving no treatment (Collicchio-Zuanaze et al, 2006).
    3) Administer intravenous calcium chloride (10 to 20 mL of 10% in adults or 10 to 20 mg/kg in children) or calcium gluconate (0.1 to 0.2 mL/kg of 10% solution, up to 10 mL per dose) to patients with EKG changes (QTc prolongation), neuromuscular changes (carpopedal spasm), or laboratory evidence of hypocalcemia. Repeat doses as necessary to correct hypocalcemia.
    4) PRECAUTIONS - Administer under continuous ECG monitoring, and measure serial calcium, potassium, and magnesium levels. The calcium chloride salt is irritating and may produce acidosis. Calcium gluconate is preferred in patients with acidosis. Rapid IV injection may cause vasodilation. Administer slowly through a small needle into a large vein, taking care to avoid extravasation.
    G) EXPERIMENTAL THERAPY
    1) Administration of ETHANOL (approximately 800 mg/kg given within 30 minutes of exposure) has been reported to be helpful in the treatment of mice, guinea pigs and rabbits poisoned with fluoroacetate (Proudfoot et al, 2006). This is EXPERIMENTAL. In an anecdotal report of simultaneous sodium fluoroacetate and ethanol ingestion in a 29-year-old man, restlessness, a single seizure, aggressiveness, and confusion were the only signs noted (Ramirez, 1986).
    a) DOSE - Ethanol is administered as in a methanol poisoning. First dose should be 1 to 1.5 mL/kg of a 50% solution followed 4 hours later by the same dose. The goal is to have blood alcohol at 100 mg/dL; the dose may have to be increased or given as a continuous drip. Constant monitoring of the blood ethanol and blood glucose is crucial. Glucose must be included in the IV fluid to prevent hypoglycemia.
    2) Administration of CALCIUM GLUCONATE to reverse hypocalcemia in combination with SODIUM SUCCINATE (but not with sodium alphaketoglutarate) to reconstitute the citric acid cycle was effect in the treatment of sodium fluoroacetate poisoning in mice. The agents must be injected in separate sites or mixed immediately prior to use, or effectiveness is lost (Omara & Sisodia, 1990)
    a) Dose: 130 mg/kg of calcium gluconate in combination with 240 mg/kg of sodium succinate was effective in mice. Further increases in sodium succinate dosage did not increase effectiveness. The proper dosage and the efficacy, if any, in humans is not known.
    b) Treatment with a combination of calcium gluconate (130 mg/kg) and sodium succinate (240 mg/kg) improved survival rates in cats poisoned with fluoroacetate. Survival rates were 75% in cats receiving treatment v. 37.5% survival rate in cats receiving no treatment (Collicchio-Zuanaze et al, 2006).
    H) OBSERVATION REGIMES
    1) As DELAYED ONSET of SERIOUS or LIFE-THREATENING TOXICITY may occur, all patients with possible significant exposure should be observed for up to 20 hours in a controlled setting.
    I) 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).
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) SYSTEMIC TOXICITY - There is no evidence that fluoroacetate can be absorbed in toxic quantities following ocular exposure. Should systemic symptoms develop following exposure by this route -
    2) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.9.2) TREATMENT
    A) GENERAL TREATMENT
    1) SYSTEMIC ABSORPTION - There is little evidence that fluoroacetate can be absorbed systemically in toxic amounts through intact skin (Ellenhorn & Barceloux, 1988). Should systemic symptoms develop following dermal contact with this material -
    2) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) A milligram of pure compound is probably enough to cause severe toxicity, and less may be toxic. Extrapolation of experimental animal toxicity data to humans indicates that a dose of 2 to 10 mg/kg may be fatal.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) A milligram of pure compound is probably enough to cause severe toxicity, and less may be toxic. Extrapolation of experimental animal toxicity data to humans indicates that a dose of 2 to 10 mg/kg (140 to 700 mg for a 70-kg adult) may be fatal (Egekeze & Oehme, 1979; Baselt & Cravey, 1989).
    B) CASE REPORTS
    1) A death was reported after ingestion of 465 mg or more in an adult (Harrisson et al, 1952).
    2) Prior to 1955, there were 23 cases of poisoning in humans, 17 with fatal outcomes (Brockmann et al, 1955).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) A milligram of pure compound is probably enough to cause severe toxicity, and less may be toxic.

Workplace Standards

    A) ACGIH TLV Values for CAS144-49-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS144-49-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS144-49-0 :
    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 CAS144-49-0 (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- (INTRAPERITONEAL)MOUSE:
    a) 6600 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 7 mg/kg
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 281 mg/kg
    4) LD50- (ORAL)RAT:
    a) 4680 mcg/kg
    5) LD50- (SUBCUTANEOUS)RAT:
    a) 5 mg/kg

Physicochemical

Physical Characteristics

    A) Colorless crystals (Lewis, 1993)

Molecular Weight

    A) 78.04 (Budavari, 1996)

References

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