a) CASE REPORT: A 25-year-old man presented to the emergency department with palpitations, and difficulty in opening his eyes, swallowing, talking, and breathing approximately 4 hours after intentionally inhaling the fumes of a dry chemical fire extinguisher containing monoammonium phosphate. At presentation he was irritable with facial flushing, diaphoresis, stridor, and drooling. His blood pressure, pulse, and respiratory rate were 90/60 mmHg, 110, and 28, respectively. Examination of his oropharynx revealed a swollen, erythematous vocal cord, requiring intubation and mechanical ventilation secondary to airway obstruction. Arterial blood gas analysis revealed metabolic acidosis and laboratory data values indicated hyperphosphatemia, hypocalcemia, and hypomagnesemia. His QTc interval was prolonged at 498 msec. The patient received supportive therapy, including calcium gluconate and magnesium sulfate infusions; however, 2 hours post-presentation, he developed a generalized seizure refractory to IV lorazepam, but responsive to a 100-mg IV bolus of calcium gluconate. Subsequently 4 episodes of pulseless ventricular tachycardia occurred that were successfully cardioverted. Following several days of aggressive supportive management and 2 cycles of hemodialysis, the patient gradually recovered with normalization of laboratory values and no evidence of pulmonary or renal sequelae at follow-up (Senthilkumaran et al, 2012).

a) CASE REPORT: A 25-year-old man presented to the emergency department after intentionally ingesting a large amount of dry fire extinguisher powder containing ammonium dihydrogen phosphate. Laboratory data revealed hyperphosphatemia (peak level 30.6 mg/dL, normal range 2.7 to 4.5 mg/dL), hypokalemia (3.1 mEq/L, normal range 3.5 to 5.1 mEq/L), hypocalcemia (4.3 mg/dL, normal range 8.9 to 10.3 mg/dL), and metabolic acidosis (pH 7.24, HCO3 16.4 mmol/L). Four hours post-presentation, the patient developed cardiac arrest and underwent cardioversion and cardiopulmonary resuscitation. An ECG revealed ventricular tachycardia. He received calcium gluconate and sodium bicarbonate infusions; however, despite aggressive supportive therapy, he subsequently died (Lin et al, 2009).

a) Irritation of the respiratory tract (coughing, shortness of breath) may occur with inhalation exposure (Prod Info, 1996) (RMPDC, 1984).
b) If ammonium phosphate, monobasic is heated to decomposition and evolves fumes of oxides of phosphorus, oxides of nitrogen, and ammonia (Sax, 1984), more severe respiratory tract irritation could be expected to occur with inhalation.

a) CASE REPORT: A 25-year-old man presented to the emergency department with palpitations, and difficulty in opening his eyes, swallowing, talking, and breathing approximately 4 hours after intentionally inhaling the fumes of a dry chemical fire extinguisher containing monoammonium phosphate. At presentation he was irritable with facial flushing, diaphoresis, stridor, and drooling. His blood pressure, pulse, and respiratory rate were 90/60 mmHg, 110, and 28, respectively. Examination of his oropharynx revealed a swollen, erythematous vocal cord, requiring intubation and mechanical ventilation secondary to airway obstruction. Arterial blood gas analysis revealed metabolic acidosis and laboratory data values indicated hyperphosphatemia, hypocalcemia, and hypomagnesemia. His QTc interval was prolonged at 498 msec. The patient received supportive therapy, including calcium gluconate and magnesium sulfate infusions; however, 2 hours post-presentation, he developed a generalized seizure refractory to IV lorazepam, but responsive to a 100-mg IV bolus of calcium gluconate. Subsequently 4 episodes of pulseless ventricular tachycardia occurred that were successfully cardioverted. Following several days of aggressive supportive management and 2 cycles of hemodialysis, the patient gradually recovered with normalization of laboratory values and no evidence of pulmonary or renal sequelae at follow-up (Senthilkumaran et al, 2012).
b) CASE REPORT: A 62-year-old man presented to the emergency department, complaining of respiratory distress, approximately 30 minutes after intentionally ingesting/inhaling a dry chemical fire extinguisher powder containing ammonium dihydrogen phosphate. His oxygen saturation was 95% on room air. Laboratory data, obtained 6 hours post presentation, revealed a phosphorus level of 18 mg/dL and a calcium level of 7.6 mg/dL. With supportive therapy, including hemodialysis, the patient's laboratory values improved, and he was discharged 72 hours post-exposure (Loschiavo et al, 2015).

a) CASE REPORT: A generalized seizure occurred in a 25-year-old man who intentionally inhaled fumes of a dry chemical fire extinguisher containing monoammonium phosphate. The seizure was refractory to lorazepam administration, but was responsive to 100 mg of IV calcium gluconate (Senthilkumaran et al, 2012).

a) Nausea and vomiting may occur with inhalation or ingestion (Lin et al, 2009) (Prod Info, 1996) (RMPDC, 1984).

a) Diarrhea and abdominal cramps may develop following ingestion (Gosselin et al, 1984) (Prod Info, 1996).

a) Nephropathy and acute renal failure may occur with phosphate toxicity (Loschiavo et al, 2015; Lin et al, 2009).

a) Metabolic acidosis has been reported in several patients following ingestion or inhalation of dry fire extinguisher powder consisting of ammonium dihydrogen phosphate (Loschiavo et al, 2015; Senthilkumaran et al, 2012; Lin et al, 2009).

a) Mild dermal irritation may occur with direct exposure to concentrated solutions (Prod Info, 1996).

a) Obtain an ECG and institute continuous cardiac monitoring.

a) Monitor vital signs and mental status.

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.

a) Administer intravenous fluids to restore electrolyte balance. Replace calcium and magnesium intravenously, but overaggressive repletion can theoretically cause precipitation of calcium phosphate in tissue. Institute continuous cardiac monitoring and monitor ECG for evidence of QT prolongation or dysrhythmias. Symptomatic patients with severe electrolyte abnormalities should be treated with hemodialysis. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate 1 to 2 mEq/kg.

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) 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.