a) There is little evidence that fluoroacetate can be absorbed systemically in toxic amounts through intact skin. Remove contaminated clothing and wash skin with soap and water.

a) INCIDENCE: In a series of 38 adults with fluoroacetate ingestion, 34% developed hypotension (Chi et al, 1996). Hypotension was more common (100%) in patients with fatal overdose.

a) Initially, tachycardia occurs with an increase in amplitude of T waves followed by ST elevation and irregular rhythm with premature ventricular contractions; this may progress to a bigeminal pattern (Reigart et al, 1975).

a) Ventricular fibrillation is commonly noted. QTc prolongation may occur in the presence of hypocalcemia (Roy et al, 1980). Hypocalcemia and hypomagnesemia with associated QTc prolongation and ventricular dysrhythmias including bigeminy, ventricular tachycardia, refractory ventricular fibrillation, and cardiac arrest may occur following severe intoxications (Chi et al, 1996). Positive inotropic effects are most likely due to facilitation of sodium influx by sodium fluoroacetate and are not generally improved by treatment with alpha or beta receptor antagonists (Robinson et al, 2002).
b) PVCS have been reported following fluoroacetate overdose.
c) VENTRICULAR TACHYCARDIA has been reported following fluoroacetate ingestions.

a) INCIDENCE: In a retrospective study of 25 patients with fluoroacetate ingestion in whom ECGs were obtained, 4 (16%) developed atrial fibrillation with a rapid ventricular response (Chi et al, 1996).

a) Asystole may occur suddenly (McTaggart, 1970). In children, the final stage of acute fluoroacetate poisoning is usually heart failure and arrest (Reigart et al, 1975).

a) Hypotension may develop after acute exposure (Grant & Schuman, 1993). Chi et al (1996) identified hypotension and the early onset of metabolic acidosis to be associated with poor short-term survival (Chi et al, 1996).
b) INCIDENCE: In a series of 38 adults with fluoroacetate ingestion, 34% developed hypotension (Chi et al, 1996). Hypotension was more common (100%) in patients with fatal overdose.
c) CASE REPORT: A 26-year-old woman was taken to the emergency department 24 hours after intentionally ingesting 32 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented with nausea and vomiting, tachypnea, tachycardia (120 beats/minute), and hypotension (80/40 mmHg). Arterial blood gas analysis indicated metabolic acidosis. She was treated aggressively with vasopressors, hydration, and electrolyte correction. However, she suffered irreversible vascular collapse (mean arterial pressure 75 mmHg; mean pulmonary arterial pressure 14 mmHg; cardiac output 13 L/minute) and died 48 hours after ingestion (Chi et al, 1999).

a) ST-T WAVE CHANGES are common following exposures.
b) QTc PROLONGATION may occur following exposures.

a) In CATS treated with sodium fluoroacetate, blood ionized calcium dropped by 27.2% accompanied by a prolongation of the QTc interval (Shapira et al, 1980).
b) CATS exposed to sodium 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% for cats receiving treatment (Collicchio-Zuanaze et al, 2006).

a) Respiratory depression and cyanosis may occur (HSDB , 1996a; Ellenhorn & Barceloux, 1988a). Death may be due to respiratory depression and hypoxia (HSDB , 1996a).

a) Intoxications have resulted in pulmonary edema, as seen on chest radiograph (Robinson et al, 2002). Pulmonary edema is usually secondary to bronchopneumonia. Hemorrhagic pulmonary edema was found at autopsy in a fatal case of sodium fluoroacetate ingestion (Proctor et al, 1988).

a) Hyperactivity may be noted initially, gradually leading to seizures, coma, cyanosis and death. Severe effects such as seizures may be delayed as long as 20 hours. Severe neurologic sequelae have been noted (Robinson et al, 2002; McTaggart, 1970; Trabes et al, 1983).

a) CASE REPORT: Cerebellar dysfunction was described in a 15-year-old patient (Trabes et al, 1983).
b) CASE SERIES: Ten suicide attempts involving ethyl fluoroacetate (FEA), a derivative of sodium fluoroacetate, resulted in residual cerebellar dysfunction. The mean amount of FEA ingested was 1200 mg (range 600 to 1800 mg), and all cases displayed a decreased level of consciousness or coma for more than 7 days (range 7 to 20 days, mean 12 days). After awakening, patients were extremely tremulous and had severe ataxia and dysarthria; neurological deficits improved over months to years, but recovery plateaued for all patients.
c) Kim et al (2009) detailed two cases of ethyl fluoroacetate (FEA) ingestion that resulted in residual and persistent cerebellar dysfunction (Kim & Jeon, 2009).

a) Loss of speech has been reported after inhalation exposure (Grant & Schuman, 1993).

a) Paresthesias of the arms and legs occurred following inhalation of sodium fluoroacetate (Grant & Schuman, 1993).
b) Facial and peripheral paresthesias, a tingling sensation, numbness, and mental apprehension may be early symptoms (HSDB , 1990; Ellenhorn & Barceloux, 1988a; Grant, 1986).

a) Seizures may commonly occur following sodium fluoroacetate poisoning (Robinson et al, 2002; Grant & Schuman, 1993; McTaggart, 1970; Lewis, 1996; RTECS , 1996). Seizures may be delayed in onset as long as 20 hours after exposure.
b) CASE REPORT: An 8-year-old boy was admitted to the hospital in status epilepticus following ingestion of sodium fluoroacetate (McTaggart, 1970).
c) CASE REPORTS: In two human poisoning cases serious cardiac dysrhythmias and repeated grand mal seizures occurred (Taitelman et al, 1983).
d) CASE REPORT: A 32-year-old woman treated with olanzapine for schizophrenia presented to the emergency department with nausea and vomiting 1 hour after intentionally ingesting 48 mg (1 bottle) of sodium monofluoroacetate (SMFA). Upon examination, vital signs and laboratory analyses were normal. However, 3 hours after arrival her mental status deteriorated and she experienced a seizure. She was admitted to the intensive care unit (ICU), intubated, and treated with supportive therapy. She was discharged home 12 days after admission and remained stable at a follow-up examination 3 months later (Im & Yi, 2009).

a) Coma has been reported following inhalation and ingestion of sodium fluoroacetate (Robinson et al, 2002; Grant & Schuman, 1993; McTaggart, 1970). In one case, mild diffuse slowing was seen on EEG with no evidence of brain atrophy noted on computed tomography (Robinson et al, 2002).

a) CASE REPORT: After successful resuscitation from cardiac arrest, a child was left with severe neurological impairment (McTaggart, 1970).

a) CASE REPORT: A 32-year-old woman treated with olanzapine for schizophrenia presented to the emergency department with nausea and vomiting 1 hour after intentionally ingesting 48 mg (1 bottle) of sodium monofluoroacetate (SMFA). Upon examination, vital signs and laboratory analyses were normal. However, 3 hours after arrival her mental status deteriorated and she experienced a seizure. She was admitted to the intensive care unit (ICU), intubated, and treated with supportive therapy. Head CT scans indicated no abnormal findings. She was extubated 3 days after ICU admission. Brain DW MR imaging revealed increased bilateral signal intensity. Neurologic exam showed that she was alert and oriented but exhibited right-sided spastic motor weakness and ataxia. These neurologic symptoms resolved spontaneously within 5 days. Ten days after admission, repeat brain DW MR imaging showed no high signal lesions. However, she complained of continuing headaches, dizziness while standing, and vague paresthesias involving all extremities. On the 12th day after admission, no indication of perfusion defects were shown on brain perfusion SPECT imaging. Additional testing showed no evidence of demyelination. She was discharged home and remained stable at a follow-up examination 3 months later (Im & Yi, 2009).
b) Severe mental deficits, memory disturbance, and depression have been noted after sodium fluoroacetate ingestion (McTaggart, 1970).

a) Auditory hallucinations may occur (Proctor et al, 1988).

a) MICE poisoned with sodium fluoroacetate, single IP doses of 7.9 mg/kg to 23.1 mg/kg, developed severe prostration and intermittent seizures following a latent period of 15 to 25 minutes. Some of the mice that recovered demonstrated abnormal behavior ranging from circling and resting with their heads tucked under the abdomen or brisket (Omara & Sisodia, 1990).
b) CATS exposed to 0.45 mg/kg sodium 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).

a) Nausea, vomiting, abdominal or epigastric pain, hypersalivation, and diarrhea may occur (McTaggart, 1970; Trabes et al, 1983; Grant, 1986; Ellenhorn & Barceloux, 1988a; RTECS , 1996). Generally following a latent period of 30 to 150 minutes, nausea, vomiting and abdominal pain occur (Robinson et al, 2002).
b) INCIDENCE: In a retrospective study of 38 patients with fluoroacetate ingestion, 28 (74%) developed nausea or vomiting (Chi et al, 1996).
c) CASE REPORT: A 26-year-old woman presented to the emergency department 24 hours after intentionally ingesting 32 mL of 1% sodium monofluoroacetate (SMFA) solution. Examination revealed nausea and vomiting in addition to tachypnea, tachycardia, and hypotension. Arterial blood gas analysis indicated metabolic acidosis. She was treated aggressively with vasopressors, hydration, and electrolyte correction. However, she suffered irreversible vascular collapse and died 48 hours after ingestion (Chi et al, 1999).
d) CASE REPORT: Nausea and vomiting was reported in a 62-year-old woman with a history of COPD after she intentionally ingested 16 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented to the emergency department 1 hour after ingestion with nausea and vomiting, systolic hypertension, and tachycardia. Arterial blood gas analysis indicated metabolic acidosis. She was admitted to the intensive care unit and treated aggressively with hydration, electrolyte correction, and vasopressors. She was ventilated and hospitalized for 21 days and discharged with no additional complications (Chi et al, 1999).

a) Excessive salivation may occur (Grant & Schuman, 1993; HSDB , 1991).

a) Elevated serum levels of hepatic transaminases may be observed (Ellenhorn & Barceloux, 1988a).
b) INCIDENCE: In a retrospective study of 38 patients with fluoroacetate ingestion, 4 (10%) developed hyperbilirubinemia and 8 (21%) developed increased ALT levels. Hyperbilirubinemia was more common in the 7 patients who died than in those who survived (57% vs 0 respectively). Increased ALT was more common in the patients who died than in those who survived (83% vs 16% respectively) (Chi et al, 1996).
c) CASE REPORT: An elevated ALT concentration of 124 units/L and total bilirubin of 1.5 mg/dL were detected in a 26-year-old woman 24 hours after she intentionally ingested 32 mL of 1% sodium monofluoroacetate (SMFA) solution. Despite aggressive treatment, she died 48 hours after ingestion as a result of irreversible vascular collapse (Chi et al, 1999).
d) CASE REPORT: Laboratory analysis revealed an ALT of 65 units/L in a 62-year-old woman with a history of COPD after she intentionally ingested 16 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented to the emergency department 1 hour after ingestion with nausea and vomiting, systolic hypertension, and tachycardia. She was treated aggressively, admitted to the intensive care unit, and ventilated. After 21 days of hospitalization, she was discharged with no additional complications (Chi et al, 1999).
e) CASE REPORT: Mild hepatic dysfunction was reported in an exterminator who was repeatedly exposed to sodium fluoroacetate over a 10-year period and in a rabbiter who was repeatedly exposed to monofluoroacetate (Parkin et al, 1977; Proctor et al, 1988).

a) CASE REPORT: Degeneration of renal tubules was found at autopsy in a fatal case of sodium fluoroacetate ingestion (Proctor et al, 1988).
b) CASE REPORT: An exterminator who was repeatedly exposed over a period of 10 years presented with severe and progressive lesions of the renal tubular epithelium (Proctor et al, 1988).

a) CASE REPORT: Renal failure occurred in a rabbiter who was repeatedly exposed to sodium monofluoroacetate (Parkin et al, 1977).
b) Acute renal failure may follow serious acute fluoroacetate poisoning (Baselt & Cravey, 1989; Ellenhorn & Barceloux, 1988a; Chung, 1984). Elevated serum creatinine and uric acid levels may occur (Ellenhorn & Barceloux, 1988a). Chi et al (1996) identified hypotension, early onset of metabolic acidosis and increased serum creatinine to be associated with poor short-term survival following acute ingestions.
c) INCIDENCE: In a retrospective study of 38 patients with fluoroacetate ingestion, 10 (26%) developed increased serum creatinine. Increased serum creatinine was more common in the 7 patients who died than in those who survived (86% vs 13%, respectively) (Chi et al, 1996).
d) CASE REPORT: A 26-year-old woman was taken to the emergency department 24 hours after intentionally ingesting 32 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented with nausea and vomiting, tachypnea, tachycardia, and hypotension. Laboratory analysis revealed a creatinine level of 1.8 mg/dL and BUN of 26 mg/dL. She was treated aggressively with vasopressors, hydration, and electrolyte correction. However, she suffered irreversible vascular collapse and died 48 hours after ingestion (Chi et al, 1999).
e) CASE REPORT: Laboratory analysis revealed a BUN of 50 mg/dL in a 62-year-old woman with a history of COPD after she intentionally ingested 16 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented to the emergency department 1 hour after ingestion with nausea and vomiting, systolic hypertension, and tachycardia. Arterial blood gas analysis indicated metabolic acidosis. She was admitted to the intensive care unit and treated aggressively with hydration, electrolyte correction, and vasopressors. She was ventilated and hospitalized for 21 days and discharged with no additional complications (Chi et al, 1999).
f) CASE REPORT: Following the ingestion of an unknown quantity of sodium fluoroacetate, a 47-year-old man developed declining renal function (BUN 53 mg/dL; serum creatinine 4.3 mg/dL) over a 3 day period. Anion gap metabolic acidosis was also evident. The patient recovered following aggressive supportive management (Robinson et al, 2002).

a) Metabolic acidosis has been reported, associated with elevated serum creatinine and transaminase levels (Ellenhorn & Barceloux, 1988). Chi et al (1996) identified hypotension and the early onset of metabolic acidosis to be associated with poor short-term survival (Chi et al, 1996).
b) INCIDENCE: In a retrospective study of 38 patients with fluoroacetate ingestion, 8 (21%) developed metabolic acidosis (Chi et al, 1996). Metabolic acidosis was more common in the 7 patients who died than in those who survived (100% vs 4%, respectively).
c) CASE REPORT: A 26-year-old woman was taken to the emergency department 24 hours after intentionally ingesting 32 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented with nausea and vomiting, tachypnea (32 breaths/minute), tachycardia, and hypotension. Arterial blood gas analysis showed metabolic acidosis (pH 7.34; PCO(2) 32.1; PO2 74.4, HCO(3) 17.4; O2 saturation with 40% oxygenation 94.4%). She was treated aggressively with vasopressors, hydration, and electrolyte correction. However, she died 48 hours after ingestion as a result of irreversible vascular collapse (Chi et al, 1999).
d) CASE REPORT: A 62-year-old woman with a history of COPD presented to the emergency department 1 hour after intentionally ingesting 16 mL of 1% sodium monofluoroacetate (SMFA) solution. Physical examination showed nausea and vomiting, systolic hypertension, and tachycardia. Arterial blood gas analysis indicated metabolic acidosis (pH 7.3; PCO(2) 39.5; PO(2) 123; HCO(3) 19.4; O2 saturation with 28% oxygenation 98.3%). She was admitted to the intensive care unit and treated aggressively with hydration, electrolyte correction, and vasopressors. She was ventilated and hospitalized for 21 days and discharged with no additional complications (Chi et al, 1999).
e) CASE REPORT: Anion gap metabolic acidosis (pH 7.3, pCO2 29 mmHg, HCO3 14 mEq/L, anion gap 24 mEq/L) resulted following the intentional ingestion of an unknown quantity of fluoroacetate-1080 in a 47-year-old man about 4 hours post-ingestion. The patient also experienced tonic-clonic seizures, agitation and subsequent coma, and pulmonary edema. The patient recovered following aggressive supportive management (Robinson et al, 2002).

a) Muscle twitching may be an early symptom of fluoroacetate poisoning (Ellenhorn & Barceloux, 1988a; HSDB , 1990).

a) CASE REPORT: Mild thyroid dysfunction was reported in an exterminator repeatedly exposed to sodium fluoroacetate for a 10-year period and in a rabbiter who was repeatedly exposed to sodium monofluoroacetate (Parkin et al, 1977; Proctor et al, 1988).

a) Hyperglycemia has been reported (Ellenhorn & Barceloux, 1988).
b) CASE REPORT: A 26-year-old woman developed hyperglycemia (248 mg/dL) after intentionally ingesting 32 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented to the emergency department 24 hours after ingestion with nausea and vomiting, tachypnea, tachycardia, and hypotension. Arterial blood gas analysis indicated metabolic acidosis. She was treated aggressively with vasopressors, hydration, and electrolyte correction. However, she suffered irreversible vascular collapse and died 48 hours after ingestion (Chi et al, 1999).
c) CASE REPORT: A 62-year-old woman with a history of COPD developed hyperglycemia (478 mg/dL) after intentionally ingesting 16 mL of 1% sodium monofluoroacetate (SMFA) solution. She presented to the emergency department 1 hour after ingestion with nausea and vomiting, systolic hypertension, and tachycardia. Arterial blood gas analysis indicated metabolic acidosis. She was admitted to the intensive care unit and treated aggressively with hydration, electrolyte correction, and vasopressors. She was ventilated and hospitalized for 21 days and discharged with no additional complications (Chi et al, 1999).

a) The effects of sodium fluoroacetate on respiratory metabolism were studied in rat embryos. No embryonic abnormalities were noted and it was concluded that rat embryos during the time of organogenesis are able to overcome inhibition of energy metabolism that is not too severe (Spielmann et al, 1973).

a) Institute continuous cardiac monitoring and obtain an ECG.
b) Monitor vital signs.
c) Monitor pulse oximetry and/or blood gases in patients with pulmonary symptoms.

1) A woman developed nausea and vomiting, tachypnea, tachycardia, hypotension (80/40 mmHg), and metabolic acidosis after intentionally ingesting 32 mL of 1% sodium monofluoroacetate (SMFA) solution. Despite aggressive therapy with vasopressors, hydration, and electrolyte correction, she suffered irreversible vascular collapse and died 48 hours after ingestion (Chi et al, 1999).

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.

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).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) Treatment is symptomatic and supportive. Manage mild hypotension with IV fluids. Manage nausea with antiemetics.

a) Treatment is symptomatic and supportive. Administer oxygen and assist ventilation for respiratory depression. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Electrolyte abnormalities are frequent and should be rapidly corrected. Treat agitation with benzodiazepines. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Treat ventricular dysrhythmias using ACLS protocols.

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.

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).

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

a) Withdraw the causative agent. Hemodynamically unstable patients with Torsades de pointes (TdP) require electrical cardioversion. Emergent treatment with magnesium (first-line agent) or atrial overdrive pacing is indicated. Detect and correct underlying electrolyte abnormalities (ie, hypomagnesemia, hypokalemia, hypocalcemia). Correct hypoxia, if present (Drew et al, 2010; Neumar et al, 2010; Keren et al, 1981; Smith & Gallagher, 1980).
b) Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. Overdrive pacing or isoproterenol may be successful in terminating TdP, particularly when accompanied by bradycardia or if TdP appears to be precipitated by pauses in rhythm (Neumar et al, 2010). In patients with polymorphic VT with a normal QT interval, magnesium is unlikely to be effective (Link et al, 2015).

a) Magnesium is recommended (first-line agent) for the prevention and treatment of drug-induced torsades de pointes (TdP) even if the serum magnesium concentration is normal. QTc intervals greater than 500 milliseconds after a potential drug overdose may correlate with the development of TdP (Charlton et al, 2010; Drew et al, 2010). ADULT DOSE: No clearly established guidelines exist; an optimal dosing regimen has not been established. Administer 1 to 2 grams diluted in 10 milliliters D5W IV/IO over 15 minutes (Neumar et al, 2010). Followed if needed by a second 2 gram bolus and an infusion of 0.5 to 1 gram (4 to 8 mEq) per hour in patients not responding to the initial bolus or with recurrence of dysrhythmias (American Heart Association, 2005; Perticone et al, 1997). Rate of infusion may be increased if dysrhythmias recur. For persistent refractory dysrhythmias, a continuous infusion of up to 3 to 10 milligrams/minute in adults may be given (Charlton et al, 2010).
b) PEDIATRIC DOSE: 25 to 50 milligrams/kilogram diluted to 10 milligrams/milliliter for intravenous infusion over 5 to 15 minutes up to 2 g (Charlton et al, 2010).
c) PRECAUTIONS: Use with caution in patients with renal insufficiency.
d) MAJOR ADVERSE EFFECTS: High doses may cause hypotension, respiratory depression, and CNS toxicity (Neumar et al, 2010). Toxicity may be observed at magnesium levels of 3.5 to 4.0 mEq/L or greater (Charlton et al, 2010).
e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respiratory rate, motor strength, deep tendon reflexes, serum magnesium, phosphorus, and calcium concentrations (Prod Info magnesium sulfate heptahydrate IV, IM injection, solution, 2009).

a) Institute electrical overdrive pacing at a rate of 130 to 150 beats per minute, and decrease as tolerated. Rates of 100 to 120 beats per minute may terminate torsades (American Heart Association, 2005). Pacing can be used to suppress self-limited runs of TdP that may progress to unstable or refractory TdP, or for override refractory, persistent TdP before the potential development of ventricular fibrillation (Charlton et al, 2010). In a case series overdrive pacing was successful in terminating TdP associated with bradycardia and drug-induced QT prolongation (Neumar et al, 2010).

a) Potassium supplementation, even if serum potassium is normal, has been recommended by many experts (Charlton et al, 2010; American Heart Association, 2005). Supplementation to supratherapeutic potassium concentrations of 4.5 to 5 mmol/L has been suggested, although there is little evidence to determine the optimal range in dysrhythmia (Drew et al, 2010; Charlton et al, 2010).

a) Isoproterenol has been successful in aborting torsades de pointes that was resistant to magnesium therapy in a patient in whom transvenous overdrive pacing was not an option (Charlton et al, 2010) and has been successfully used to treat torsades de pointes associated with bradycardia and drug induced QT prolongation (Keren et al, 1981; Neumar et al, 2010). Isoproterenol may have a limited role in pharmacologic overdrive pacing in select patients with drug-induced torsades de pointes and acquired long QT syndrome (Charlton et al, 2010; Neumar et al, 2010). Isoproterenol should be avoided in patients with polymorphic VT associated with familial long QT syndrome (Neumar et al, 2010).
b) DOSE: ADULT: 2 to 10 micrograms/minute via a continuous monitored intravenous infusion; titrate to heart rate and rhythm response (Neumar et al, 2010).
c) PRECAUTIONS: Correct hypovolemia before using; contraindicated in patients with acute cardiac ischemia (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
d) MAJOR ADVERSE EFFECTS: Tachycardia, cardiac dysrhythmias, palpitations, hypotension or hypertension, nervousness, headache, dizziness, and dyspnea (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respirations and central venous pressure to guide volume replacement (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).

a) Mexiletine, verapamil, propranolol, and labetalol have also been used to treat TdP, but results have been inconsistent (Khan & Gowda, 2004).

a) Avoid class Ia antidysrhythmics (eg, quinidine, disopyramide, procainamide, aprindine), class Ic (eg, flecainide, encainide, propafenone) and most class III antidysrhythmics (eg, N-acetylprocainamide, sotalol) since they may further prolong the QT interval and have been associated with TdP.

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).

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 .

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).

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).

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).

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):

a) 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 toxic effects noted (Ramirez, 1986).
b) ETHANOL THERAPY: Ethanol (ETOH) partially inhibits the formation of toxic metabolites. LOADING DOSE: Administer 10 mL/kg of 10% ETOH in D5W over 60 minutes. MAINTENANCE DOSE: Administer 1.5 mL/kg/hr of 10% ETOH in D5W by intravenous infusion. Aim at achieving and maintaining 100 to 130 mg/dL blood ethanol concentration. PRECAUTION: Monitor hourly blood glucose and ETOH concentrations during ethanol administration.

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) Treatment is symptomatic and supportive. Manage mild hypotension with IV fluids. Manage nausea with antiemetics.

a) Treatment is symptomatic and supportive. Administer oxygen and assist ventilation for respiratory depression. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Electrolyte abnormalities are frequent and should be rapidly corrected. Treat agitation with benzodiazepines. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Treat ventricular dysrhythmias using ACLS protocols.

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

1) Sodium fluoroacetate

a) TWA: 0.05 mg/m(3)
b) STEL: 0.15 mg/m(3)
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: [skin]
f) Note(s):

a) IDLH: 2.5 mg/m3
b) Note(s): Not Listed

a) 8-hour TWA:

a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.

a) DERMAL - No reports exist of toxicity due to dermal exposure to this compound; however, decontamination is advised on dermal exposure. Bathe in mild detergent (animal shampoo or Ivory liquid). Wear gloves to avoid human exposure. Clip hair as necessary to facilitate removal.
b) CAUTION - Carefully examine animals with chemical exposure before inducing emesis. If signs of oral, pharyngeal, or esophageal irritation, a depressed gag reflex, or central nervous system excitation or depression are present, EMESIS SHOULD NOT BE INDUCED. Emesis is only indicated prior to onset of clinical signs (may be as little as 30 minutes). The animal should be monitored for seizures after giving an emetic (Beasley et al, 1990).

a) DERMAL - No reports exist of toxicity due to dermal exposure to this compound; however, decontamination is advised on dermal exposure. Wash exposed animals with soap and water. If possible, shave or clip long hair to facilitate thorough cleaning. All handlers should wear gloves and protect themselves from exposure.
b) EMESIS - Do not attempt to induce emesis in ruminants (cattle) or equids (horses).
c) ACTIVATED CHARCOAL
d) CATHARTICS

a) Seizures are best controlled by barbiturates. One regimen recommended beginning treatment with a dose of pentobarbital followed by a prophylactic dose of phenobarbital and additional pentobarbital as needed (Tourtellotte & Coon, 1950).
b) PHENOBARBITAL may be used at 5 to 30 mg/kg over 5 to 10 minutes intravenously.
c) PENTOBARBITAL is administered to DOGS and CATS at a dose of 3 to 15 mg/kg intravenously slowly to effect. May need to repeat in 4 to 8 hours. Be sure to protect the airway.

a) EKG must be monitored.

a) Glyceryl monoacetate 0.1 to 0.5 mg/kg intramuscularly every hour for several hours (up to a total of 2 to 4 mg/kg). This regimen may not be feasible because of short shelf life and difficulty in getting glyceryl monoacetate; it also may not work if the dose of fluoroacetate is over the LD50 (Beasley et al, 1990).
b) Calcium gluconate may aid in controlling seizures and hypocalcemia (Buck et al, 1976). Dose is 0.2 to 0.5 mL/kg of 5% solution slowly intravenously (Beasley et al, 1990).
c) Intravenous ethanol has been reported to be helpful in the treatment of dogs poisoned with fluoroacetate. First dose should be 1 to 1.5 mg/kg of a 50% solution followed 4 hours later by the same dose. The goal is to maintain blood alcohol level at 100 milligram percent and the dose may have to be increased or dripped continuously. Blood ethanol and glucose concentration should be monitored hourly during ethanol administration. Supplemental glucose should be included in the intravenous solution to minimize the chance of hypoglycemia. This regimen is unproven; barbiturates remain the treatment of choice (Buck et al, 1976).
d) Solutions containing 50% alcohol and 5% acetic acid have been given orally at 8.8 mg/kg; this therapy has been ineffective in almost all cases and has been associated with prolonged anesthesia and pneumonia when combined with barbiturates (Beasley et al, 1990). This regimen is undesirable and cannot be recommended; barbiturates are the treatment of choice (Buck et al, 1976).

a) Secure airway, supply oxygen and begin supportive fluid therapy if necessary.

a) Seizures may be controlled with diazepam or barbiturates.

a) EKG must be monitored.

a) Glyceryl monoacetate 0.1 to 0.5 mg/kg intramuscularly every hour for several hours (up to a total of 2 to 4 mg/kg). This regimen may not be feasible because of short shelf life and difficulty in getting glyceryl monoacetate; and it also may not work if the dose of fluoroacetate is over the LD50 (Beasley et al, 1990) or if given after clinical signs develop (Robinson, 1987).
b) Calcium gluconate may aid in controlling seizures and hypocalcemia (Buck et al, 1976). Dose is 0.2 to 0.5 mL/kg of 5% solution slowly intravenously (Beasley et al, 1990).
c) Solutions containing 50% alcohol and 5% acetic acid have been given orally at 8.8 mg/kg; this therapy has been ineffective in almost all cases and has been associated with prolonged anesthesia and pneumonia when combined with barbiturates (Beasley et al, 1990). This regimen is undesirable and cannot be recommended; barbiturates are the treatment of choice (Beasley et al, 1990).

1) Begin treatment immediately.
2) Keep animal warm and do not handle unnecessarily.
3) Sample vomitus, blood, urine, and feces for analysis.
4) Remove the patient and other animals from the source of contamination.
5) Treatment should always be done on the advice and with the consultation of a veterinarian. Additional information regarding treatment of poisoned animals may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
6) ANIMAL POISON CONTROL CENTERS
7) Despite proper treatment, this toxicity is often fatal.

1) DOGS/CATS
2) RUMINANTS/HORSES/SWINE

1) Treatment is symptomatic and supportive.

1) GENERAL

1) Plasma: 0.098 mcg/gram
2) Kidney: 0.057 mcg/gram
3) Heart: 0.052 mcg/gram
4) Muscle: 0.042 mcg/gram
5) Spleen: 0.026 mcg/gram
6) Liver: 0.021 mcg/gram
7) Reference: (Eason et al, 1994)