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BARIUM NITRATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Barium nitrate is a soluble barium salt used in the manufacture of pyrotechnics (fireworks) and barium peroxide, for green signal lights and neon lights, and in the vacuum-tube industry (Budavari, 1996; ITI, 1995).

Specific Substances

    1) Barium dinitrate
    2) Barium(II) nitrate (1:2)
    3) Nitric acid, barium salt
    4) Nitrobarite
    5) Nitrato barico (Spanish)
    6) Nitrate de baryum (French)
    7) CAS 10022-31-8
    8) References: RTECS, 1998; HSDB, 1998
    9) BARIUM (II) NITRATE
    10) DUSICNAN BARNATY (CZECH)

Available Forms Sources

    A) USES
    1) Barium nitrate is a soluble barium salt used in the manufacture of pyrotechnics (fireworks) and barium peroxide, for green signal lights and neon lights, and in the vacuum-tube industry (Budavari, 1996; ITI, 1995).
    2) Barium nitrate is also used in ceramic glazes, incendiaries, electronics, tracer bullets, primers and detonators; it was formerly used in some rodenticides (HSDB , 1998).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Barium nitrate is a soluble barium salt used in the manufacture of pyrotechnics (fireworks) and barium peroxide, for green signal lights and neon lights, and in the vacuum-tube industry. It is also used in ceramic glazes, incendiaries, electronics, tracer bullets, primers and detonators; it was formerly used in some rodenticides.
    B) TOXICOLOGY: Rapid onset, severe hypokalemia is caused by sequestration of potassium in skeletal muscle cells, secondary to barium blocking potassium efflux via the sodium-potassium pump in those cells.
    C) EPIDEMIOLOGY: Poisoning is rare, and most often occurs after deliberate ingestion.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE POISONING: Nausea, vomiting, colicky abdominal pain, and diarrhea.
    2) SEVERE POISONING: Profound hypokalemia, severe muscle weakness/paralysis including diaphragmatic muscles leading to hypoventilation, hypertension, and ventricular dysrhythmias/fibrillation.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Ventricular dysrhythmias and hypertension may occur.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Hypoventilation may develop with severe poisoning.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) CNS excitation followed by depression may occur.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and diarrhea may occur.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH POISONING/EXPOSURE
    1) Hypokalemia may occur with soluble barium salts.
    0.2.15) MUSCULOSKELETAL
    A) WITH POISONING/EXPOSURE
    1) Muscle stimulation, weakness, or flaccid paralysis may be seen.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    B) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    C) Determine potassium levels frequently (every 1 to 2 hours until stabilized).
    D) Serum barium concentrations are not readily available or useful in guiding therapy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Monitor serum potassium and correct as necessary. Administer intravenous fluids to maintain urine.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Profound hypokalemia may develop rapidly, causing profound weakness, respiratory insufficiency, and dysrhythmias. Monitor for weakness and respiratory insufficiency, manage airway early. Monitor serial serum potassium and correct aggressively. Dysrhythmias are usually secondary to hypokalemia and generally respond to potassium administration. Administer intravenous fluids to maintain adequate urine output. Hemodialysis should be performed in patients with severe hypokalemia, severe weakness, or ventricular dysrhythmias that are not responding to potassium supplementation.
    C) DECONTAMINATION
    1) Administer oral magnesium sulfate to convert barium to insoluble barium sulfate. Dose: 250 mg/kg for children and 30 g for adults. Sodium sulfate is an alternative. ADULT: 30 g in 250 mL water orally.
    2) Activated charcoal likely ineffective in adsorbing barium. Consider insertion of a nasogastric tube to aspirate gastric contents, or gastric lavage, in patients with recent ingestion who can protect their airway or who are intubated.
    3) Wash exposed skin with soap and water. Remove contaminated clothing.
    D) AIRWAY MANAGEMENT
    1) Severe hypokalemia may result in respiratory muscle weakness and respiratory failure. Monitor adequacy of respirations, and manage airway early if necessary.
    E) MAGNESIUM SULFATE
    1) Magnesium sulfate when given orally results in the formation of nonabsorbable barium sulfate within the gastrointestinal tract. Dose: 250 mg/kg for children and 30 g for adults. Sodium sulfate is an alternative. ADULT: 30 g in 250 mL water orally.
    F) HYPOKALEMIA
    1) Profound hypokalemia can develop rapidly. Aggressive supplementation, both orally and intravenously, is the mainstay of therapy.
    G) DYSRHYTHMIAS
    1) Dysrhythmias are usually secondary to hypokalemia. Aggressive intravenous and oral potassium supplementation is the mainstay of treatment. Antidysrhythmics such as lidocaine or amiodarone may be used, but efficacy may be limited in patients with persistent hypokalemia.
    H) HEMODIALYSIS
    1) Hemodialysis is effective (corrects hypokalemia, and associated weakness and dysrhythmias, enhances barium elimination) in patients with severe poisoning. It should be considered early in patients with hypokalemia, severe weakness or dysrhythmias that are not responding to potassium supplementation.
    I) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: All patients who have ingested barium nitrate should be sent to a healthcare facility for evaluation and treatment. Patients should be observed for 6 to 8 hours with ECG monitoring, serial serum potassium concentrations, and evaluation for weakness. Patients who are asymptomatic with normal serum potassium during 6 to 8 hours of observation may be discharged.
    2) ADMISSION CRITERIA: Patients with hypokalemia, weakness or dysrhythmias should be admitted to an intensive care setting for cardiac, respiratory and neurologic monitoring and aggressive potassium replacement.
    3) CONSULT CRITERIA: Consult a medical toxicologist and/or poison center for any patient with significant barium poisoning or in whom the diagnosis is unclear. Consult a nephrologist for emergent dialysis in any patients with severe poisoning.
    J) PITFALLS
    1) Inadequate monitoring for weakness, respiratory insufficiency, hypokalemia, dysrhythmias.
    2) Since barium does not decrease total body potassium, but rather shifts it intracellularly; hyperkalemia may develop once barium toxicity has resolved.
    K) DIFFERENTIAL DIAGNOSIS
    1) Toluene toxicity, renal tubular acidosis, hypokalemic periodic paralysis.

Range Of Toxicity

    A) TOXICITY: The minimum lethal exposure of barium nitrate has not been determined. The minimum lethal exposure to other soluble barium salts is from 1 to 15 grams. With supportive care, a 16-year-old girl survived after intentionally ingesting 20 g of barium nitrate.

Clinical Effects

Summary Of Exposure

    A) USES: Barium nitrate is a soluble barium salt used in the manufacture of pyrotechnics (fireworks) and barium peroxide, for green signal lights and neon lights, and in the vacuum-tube industry. It is also used in ceramic glazes, incendiaries, electronics, tracer bullets, primers and detonators; it was formerly used in some rodenticides.
    B) TOXICOLOGY: Rapid onset, severe hypokalemia is caused by sequestration of potassium in skeletal muscle cells, secondary to barium blocking potassium efflux via the sodium-potassium pump in those cells.
    C) EPIDEMIOLOGY: Poisoning is rare, and most often occurs after deliberate ingestion.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE POISONING: Nausea, vomiting, colicky abdominal pain, and diarrhea.
    2) SEVERE POISONING: Profound hypokalemia, severe muscle weakness/paralysis including diaphragmatic muscles leading to hypoventilation, hypertension, and ventricular dysrhythmias/fibrillation.

Vital Signs

    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPERTENSION may develop (Clayton & Clayton, 1994).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) An IRREGULAR PULSE may be noted, as ventricular tachydysrhythmias including ventricular fibrillation could occur (Gosselin et al, 1984).

Heent

    3.4.2) HEAD
    A) WITH POISONING/EXPOSURE
    1) MUSCULAR WEAKNESS may result in disorders of speech and deglutition (Gosselin et al, 1984).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Ventricular dysrhythmias and hypertension may occur.
    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Ventricular tachydysrhythmias including ventricular fibrillation may occur (Gosselin et al, 1984).
    b) Electrocardiographic changes consistent with hypokalemia may be noted (Gosselin et al, 1984).
    c) CASE REPORT: A 22-year-old man developed diarrhea, vomiting, cardiac dysrhythmias, severe hypokalemia (serum potassium level 1.5 mmol/L), and muscular weakness after ingesting an unknown amount of barium nitrate. ECG revealed atrial fibrillation and torsade de pointes. Although he was treated with potassium supplementation, his serum potassium remained low for several hours. Veno-venous hemodialysis was started approximately 15 hours postingestion and after 4 hours of hemodialysis, his serum levels of potassium and barium normalized. He was discharged the next day (Bahlmann et al, 2005).
    d) CASE REPORT: A 75-year-old woman developed severe hypokalemia (2.1 mmol/L) after intentionally ingesting a burrow mole fumigant containing 12.375 g barium nitrate and 6.255 g sublimed sulphur powder. An ECG indicated the presence of polymorphic premature ventricular complexes. With administration of oral and IV magnesium sulfate and IV potassium replacement, the patient recovered and was discharged following 3 days of uneventful observation (Payen et al, 2011).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Elevated blood pressure may develop (Clayton & Clayton, 1994).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hypoventilation may develop with severe poisoning.
    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) Muscle weakness or paralysis may involve the diaphragm and necessitate mechanical ventilation (Phelan et al, 1984).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) CNS excitation followed by depression may occur.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Central nervous system stimulation followed by depression may be observed (Gosselin et al, 1984).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and diarrhea may occur.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and crampy abdominal pain may be observed (Payen et al, 2011; Bahlmann et al, 2005; Plunkett, 1976; Phelan et al, 1984).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea may occur (Bahlmann et al, 2005; Plunkett, 1976).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) INCONTINENCE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 17-year-old experienced fecal and urinary incontinence due to paralyzed sphincters after intentionally ingesting 7 g of barium nitrate (Szajewski, 2004a).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Mixed respiratory and metabolic acidosis (pH 7.28, PaCO2 6.5 kPa, HCO3 20 mmol/L, Base Excess -4 mmol/L) was reported in a 22-year-old man who intentionally ingested an unknown amount of barium nitrate (Bahlmann et al, 2005a).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Leukocytosis with a shift to the left was seen in one case after oral ingestion of about 20 g of barium nitrate (HSDB , 1998).

Musculoskeletal

    3.15.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Muscle stimulation, weakness, or flaccid paralysis may be seen.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Motor disorders including stiffness, cramps, and weakness of smooth and skeletal muscles may be seen (Bahlmann et al, 2005; Gosselin et al, 1984). Weakness may progress to flaccid paralysis in the presence of normal motor nerve conduction (Phelan et al, 1984).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) No data are available to assess the potential of barium nitrate for teratogenicity or maternal toxicity.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS10022-31-8 (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
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) No data are available to assess the potential of barium nitrate for carcinogenicity.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    B) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    C) Determine potassium levels frequently (every 1 to 2 hours until stabilized).
    D) Serum barium concentrations are not readily available or useful in guiding therapy.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Baseline serum potassium should be obtained in all significant exposures. The occurrence of any muscular, central nervous system, or cardiovascular signs should prompt further, frequent monitoring of serum potassium.
    2) Follow serial serum electrolytes in serious exposures.
    3) When plasma barium concentrations can be determined in symptomatic patients, they may correlate better than the serum potassium with the intensity of muscular blockade (Phelan et al, 1984). Plasma barium concentrations are not readily available in most institutions.
    B) ACID/BASE
    1) Arterial blood gas measurements aid in the treatment of respiratory acidosis caused by the paralysis of the muscles involved in respiration.
    4.1.4) OTHER
    A) OTHER
    1) ECG
    a) Institute continuous cardiac monitoring and obtain an ECG after significant exposure.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with hypokalemia, weakness or dysrhythmias should be admitted to an intensive care setting for cardiac, respiratory and neurologic monitoring and aggressive potassium replacement.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist and/or poison center for any patient with significant barium poisoning or in whom the diagnosis is unclear. Consult a nephrologist for emergent dialysis in any patients with severe poisoning.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) All patients who have ingested barium nitrate should be sent to a healthcare facility for evaluation and treatment. Patients should be observed for 6 to 8 hours with ECG monitoring, serial serum potassium concentrations, and evaluation for weakness. Patients who are asymptomatic with normal serum potassium during 6 to 8 hours of observation may be discharged.

Monitoring

    A) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    B) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    C) Determine potassium levels frequently (every 1 to 2 hours until stabilized).
    D) Serum barium concentrations are not readily available or useful in guiding therapy.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) MAGNESIUM
    1) Magnesium sulfate when given orally results in the formation of nonabsorbable barium sulfate within the gastrointestinal tract. Dose: 250 mg/kg for children and 30 g for adults. Sodium sulfate is an alternative. ADULT: 30 g in 250 mL water orally.
    B) ACTIVATED CHARCOAL/ NOT RECOMMENDED
    1) Charcoal administration is not advised since ionic barium would likely not be adsorbed by charcoal. Spontaneous vomiting and risk of loss of airway protection both due to the barium puts the patient at risk for charcoal aspiration.
    C) DERMAL EXPOSURE
    1) Wash exposed skin with soap and water. Remove contaminated clothing.
    6.5.2) PREVENTION OF ABSORPTION
    A) MAGNESIUM SULFATE
    1) Magnesium sulfate when given orally results in the formation of nonabsorbable barium sulfate within the gastrointestinal tract. Dose: 250 mg/kg for children and 30 grams for adults.
    B) GASTRIC LAVAGE
    1) Gastric lavage or insertion of a nasogastric tube to aspirate gastric contents may be considered in patients with a recent ingestion who can protect their airway or in whom airway is protected.
    C) ACTIVATED CHARCOAL
    1) Charcoal administration is not advised since ionic barium would likely not be adsorbed by charcoal. The spontaneous vomiting and risk of loss of airway protection due to the barium puts the patient at risk for charcoal aspiration.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Institute continuous cardiac monitoring and obtain an ECG (evaluate for evidence of hypokalemia including T wave flattening and prominent U waves).
    2) Monitor vital signs, with particular attention to evidence of respiratory insufficiency. Perform serial neurologic exams to evaluate for muscle weakness.
    3) Determine potassium levels frequently (every 1 to 2 hours until stabilized).
    4) Serum barium concentrations are not readily available or useful in guiding therapy.
    B) DIURESIS
    1) Administer sufficient intravenous fluids to maintain brisk urine output. Routine administration of diuretics has not been shown to be beneficial.
    C) HYPOKALEMIA
    1) Treat hypokalemia by infusing potassium (KCl) intravenously (up to 250 milliequivalents administered over 24 hours has been used) (Jourdan et al, 2001; Agarwal et al, 1986; Berning, 1975; Diengott et al, 1964; Gould et al, 1973; Wetherill et al, 1981). Oral supplementation may also be used in patients who are alert or in whom airway is protected.
    2) PLASMA POTASSIUM CONCENTRATIONS should be monitored frequently for hypokalemia.
    3) SKELETAL MUSCLE PARALYSIS, cardiac dysrhythmias, and diarrhea appear to respond to potassium therapy, but no effect is seen on barium-induced hypertension (Roza & Berman, 1971; Smith & Gosselin, 1976).
    4) Administration of potassium should be effective in the treatment of paralysis (Diengott et al, 1964; Gould et al, 1973; Roza & Berman, 1971).
    D) VENTRICULAR ARRHYTHMIA
    1) POTASSIUM
    a) Cardiac dysrhythmias appear to respond to potassium therapy (Roza & Berman, 1971; Smith & Gosselin, 1976). Correction of hypokalemia is the preferred treatment of ventricular tachycardia associated with barium poisoning.
    b) Traditional antidysrhythmics (lidocaine, amiodarone) may be used but efficacy may be limited in patients with persistent hypokalemia.
    c) Sustained ventricular tachycardia refractory to intravenous lidocaine boluses of 100 and 50 milligrams was reported in a 48-year-old male secondary to barium intoxication (Johnson & VanTassell, 1991). Resolution of ventricular dysrhythmias in this patient was associated with correction of hypokalemia.
    2) VENTRICULAR DYSRHYTHMIAS SUMMARY
    a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.
    3) LIDOCAINE
    a) LIDOCAINE/INDICATIONS
    1) Ventricular tachycardia or ventricular fibrillation (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010; Vanden Hoek et al, 2010).
    b) LIDOCAINE/DOSE
    1) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest.
    a) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
    2) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015).
    c) LIDOCAINE/MAJOR ADVERSE REACTIONS
    1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
    d) LIDOCAINE/MONITORING PARAMETERS
    1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    4) AMIODARONE
    a) AMIODARONE/INDICATIONS
    1) Effective for the control of hemodynamically stable monomorphic ventricular tachycardia. Also recommended for pulseless ventricular tachycardia or ventricular fibrillation in cardiac arrest unresponsive to CPR, defibrillation and vasopressor therapy (Link et al, 2015; Neumar et al, 2010). It should be used with caution when the ingestion involves agents known to cause QTc prolongation, such as fluoroquinolones, macrolide antibiotics or azoles, and when ECG reveals QT prolongation suspected to be secondary to overdose (Prod Info Cordarone(R) oral tablets, 2015).
    b) AMIODARONE/ADULT DOSE
    1) For ventricular fibrillation or pulseless VT unresponsive to CPR, defibrillation, and a vasopressor therapy give an initial dose of 300 mg IV followed by 1 dose of 150 mg IV. For stable ventricular tachycardias: Infuse 150 milligrams over 10 minutes, and repeat if necessary. Follow by a 1 milligram/minute infusion for 6 hours, then a 0.5 milligram/minute. Maximum total dose over 24 hours is 2.2 grams (Neumar et al, 2010).
    c) AMIODARONE/PEDIATRIC DOSE
    1) Infuse 5 milligrams/kilogram as a bolus for pulseless ventricular tachycardia or ventricular fibrillation; may repeat twice up to 15 mg/kg. Infuse 5 milligrams/kilogram over 20 to 60 minutes for perfusing tachycardias. Maximum single dose is 300 mg. Routine use with other drugs that prolong the QT interval is NOT recommended (Kleinman et al, 2010).
    d) ADVERSE EFFECTS
    1) Hypotension and bradycardia are the most common adverse effects (Neumar et al, 2010).
    5) PROCAINAMIDE
    a) PROCAINAMIDE/INDICATIONS
    1) An alternative drug in the treatment of PVCs or recurrent ventricular tachycardia when lidocaine is contraindicated or not effective. It should be avoided when the ingestion involves agents with quinidine-like effects (e.g. tricyclic antidepressants, phenothiazines, chloroquine, antidysrhythmics) and when the ECG reveals QRS widening or QT prolongation suspected to be secondary to overdose(Neumar et al, 2010; Vanden Hoek,TL,et al).
    b) PROCAINAMIDE/ADULT LOADING DOSE
    1) 20 to 50 milligrams/minute IV until dysrhythmia is suppressed or toxicity develops from procainamide (hypotension develops or the QRS is widened by 50%), or a total dose of 17 milligrams/kilogram is given (1.2 grams for a 70 kilogram person) (Neumar et al, 2010).
    2) ALTERNATIVE DOSING: 100 mg every 5 minutes until dysrhythmia is controlled, or toxicity develops from procainamide (hypotension develops or the QRS is widened by 50%) or 17 mg/kg have been given (Neumar et al, 2010).
    3) MAXIMUM DOSE: 17 milligrams/kilogram (Neumar et al, 2010).
    c) PROCAINAMIDE/CONTROLLED INFUSION
    1) In conscious patients, procainamide should be administered as a controlled infusion (20 milligrams/minute) because of the risk of QT prolongation and its hypotensive effects (Link et al, 2015)
    d) PROCAINAMIDE/ADULT MAINTENANCE DOSE
    1) 1 to 4 milligrams/minute via an intravenous infusion (Neumar et al, 2010).
    e) PROCAINAMIDE/PEDIATRIC LOADING DOSE
    1) 15 milligrams/kilogram IV/Intraosseously over 30 to 60 minutes; discontinue if hypotension develops or the QRS widens by 50% (Kleinman et al, 2010).
    f) PROCAINAMIDE/PEDIATRIC MAINTENANCE DOSE
    1) Initiate at 20 mcg/kg/minute and increase in 10 mcg/kg/minute increments every 15 to 30 minutes until desired effect is achieved; up to 80 mcg/kg/minute (Bouhouch et al, 2008; Ratnasamy et al, 2008; Mandapati et al, 2000; Luedtke et al, 1997; Walsh et al, 1997).
    g) PROCAINAMIDE/PEDIATRIC MAXIMUM DOSE
    1) 2 grams/day (Bouhouch et al, 2008; Ratnasamy et al, 2008; Mandapati et al, 2000; Luedtke et al, 1997; Walsh et al, 1997).
    h) MONITORING PARAMETERS
    1) ECG, blood pressure, and blood concentrations (Prod Info procainamide HCl IV, IM injection solution, 2011). Procainamide can produce hypotension and QT prolongation (Link et al, 2015).
    i) AVOID
    1) Avoid in patients with QT prolongation and CHF (Neumar et al, 2010).
    E) AIRWAY MANAGEMENT
    1) Monitor respiratory status carefully. Diaphragmatic weakness may produce severe hypoventilation requiring prolonged mechanical ventilation.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis is effective (corrects hypokalemia, and associated weakness and dysrhythmias, enhances barium elimination) in patients with severe poisoning. In one case report, the dialysate used contained greater than normal quantities of potassium (7 mMol/L). Emergent hemodialysis should be considered early in patients with hypokalemia, severe weakness, or dysrhythmias that are not responding to potassium supplementation.
    2) CASE REPORT: Hypokalemia (serum potassium level 1.3 to 1.7 mM/L) developed in a 17-year-old boy who intentionally ingested 7 grams of barium nitrate (urine barium level 5.7 mg/mL). He was treated with high-potassium (7 mMol/L; approximately double the usual level) hemodialysis and his plasma potassium level increased to 3.7 mM/L after 45 minutes. He recovered without further sequelae (Szajewski, 2004).
    3) CASE REPORT: A 22-year-old man developed diarrhea, vomiting, cardiac dysrhythmias, severe hypokalemia (serum potassium level 1.5 mmol/L), and muscular weakness after ingesting an unknown amount of barium nitrate. Although he was treated with potassium supplementation, his serum potassium remained low for several hours. Veno-venous hemodialysis was started approximately 15 hours postingestion and after 4 hours of hemodialysis, his serum potassium concentration normalized and serum barium concentration declined from 0.06 mmol/L to 0.02 mmol/L. He was discharged the next day (Bahlmann et al, 2005).

Abstracts

Case Reports

    A) ADULT
    1) A 35-year-old man ingested approximately 4 ounces of a soft drink from a bottle that was found to contain a partially burned sparkler (barium nitrate content, probably 44%). The patient immediately noted a foul taste, and shortly thereafter developed nausea and mild abdominal cramping. Diarrhea and continued abdominal cramps were noted after treatment with activated charcoal and a cathartic, although it was not certain whether these symptoms were due to the cathartic or to the ingested material. The patient also developed transient headache and a burning sensation in the mouth, throat, and chest. No dysrhythmias, hypertension, or neurological or musculoskeletal complaints were noted. Serum electrolytes (especially serum potassium) and liver and renal function tests were normal. Analysis of the material remaining in the soda bottle showed barium present at 52 ppm, although the specific salt involved was not identified. The patient's symptoms resolved over about 8 to 10 hours, and he recovered fully (RMPDC, 1986).
    B) PEDIATRIC
    1) A 16-year-old girl ingested approximately 20 g of barium nitrate in a suicide attempt. She did not develop paralysis, but did exhibit incoordinated muscle contractions and tachyarrhythmias. A leukocytosis with a shift to the left also developed (HSDB , 1998).

Range Of Toxicity

Summary

    A) TOXICITY: The minimum lethal exposure of barium nitrate has not been determined. The minimum lethal exposure to other soluble barium salts is from 1 to 15 grams. With supportive care, a 16-year-old girl survived after intentionally ingesting 20 g of barium nitrate.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum human lethal exposure has not been determined for barium nitrate. The minimum lethal exposure for other soluble barium salts has been reported to be from 1 to 15 grams (Gosselin et al, 1984).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) CASE REPORT: Hypokalemia (serum potassium level 1.3 to 1.7 mM/L) developed in a 17-year-old boy who intentionally ingested 7 grams of barium nitrate (urine barium level 5.7 mg/mL). He was treated with high-potassium (7 mM/L; approximately double the usual level) hemodialysis and his plasma potassium level increased to 3.7 mM/L after 45 minutes. He recovered without further sequelae (Szajewski, 2004).
    2) CASE REPORT: A 16-year-old girl ingested approximately 20 grams of barium nitrate in a suicide attempt. She did not develop paralysis, but did exhibit incoordinated muscle contractions and tachyarrhythmias. A leukocytosis with a shift to the left also developed (HSDB , 1998).
    3) CASE REPORT: A 75-year-old woman developed severe hypokalemia (2.1 mmol/L) after intentionally ingesting a burrow mole fumigant containing 12.375 g barium nitrate and 6.255 g sublimed sulphur powder. An ECG indicated the presence of polymorphic premature ventricular complexes. With administration of oral and IV magnesium sulfate and IV potassium replacement, the patient recovered and was discharged following 3 days of uneventful observation (Payen et al, 2011).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) Plasma barium concentrations greater than 140 micromoles/liter were noted in a case of severe poisoning from barium carbonate (Phelan et al, 1984).
    b) The blood barium concentration of a 75-year-old woman, who intentionally ingested a burrow mole fumigant containing 12.375 g barium nitrate, was 17.2 mg/L (125.5 mcmol/L). The patient's blood sample was obtained approximately 1 hour post-ingestion (Payen et al, 2011).

Workplace Standards

    A) ACGIH TLV Values for CAS10022-31-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS10022-31-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Barium nitrate (as Ba)
    2) REL:
    a) TWA: 0.5 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): [*Note: The REL also applies to other soluble barium compounds (as Ba) except Barium sulfate.]
    3) IDLH:
    a) IDLH: 50 mg Ba/m3 (as Ba)
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS10022-31-8 :
    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 ; Listed as: Barium nitrate (as Ba)
    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 CAS10022-31-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) 355 mg/kg (RTECS, 1998)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Absorbed barium ion stimulates smooth, striated, and cardiac muscles and produces vasoconstriction by a direct effect on vascular musculature (Clayton & Clayton, 1994).
    B) Barium ion first stimulates and then depresses the central nervous system (Clayton & Clayton, 1982). The observed hypokalemia is probably due to an intracellular migration of potassium (Gosselin et al, 1984).
    C) Oxides of nitrogen evolved from burning barium nitrate are direct irritants of the respiratory tract.

Physicochemical

Physical Characteristics

    A) Barium nitrate is a white crystalline solid (Student, 1981).

Molecular Weight

    A) 261.37

Other

    A) ODOR THRESHOLD
    1) Odorless (CHRIS , 2002)

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