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PENTABORANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Pentaborane is a boron hydride.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) B5-H9

Available Forms Sources

    A) FORMS
    1) Pentaborane is a colorless liquid with a strong, foul odor similar to that of sour milk (HSDB , 1993). It is corrosive to natural and some synthetic rubbers (HSDB , 1993). It can SPONTANEOUSLY IGNITE at ambient temperatures in the presence of impurities and moist air (AAR, 1987; (Budavari, 1989).
    2) Pentaborane has a median odor threshold of approximately 1.3 ppm; therefore, ODOR IS NOT AN ADEQUATE WARNING TO PREVENT OVEREXPOSURE (Clayton & Clayton, 1981).
    3) Pentaborane is the most toxic of the boron hydrides (Clayton & Clayton, 1981). It reacts with water, less rapidly than DIBORANE, to form BORIC ACID (ACGIH, 1986; Lowe & Freeman, 1957). The following review is based on the properties of boron hydrides in general. Effects attributed specifically to pentaborane are indicated. The toxicology of borane compounds has been reviewed (Roush, 1959).
    B) USES
    1) Pentaborane has been used as a gasoline additive and rocket propellant (Sittig, 1985). It is no longer produced commercially in the USA (Clayton & Clayton, 1981).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Pentaborane causes primarily neurologic effects, including CNS depression and excitability, spasms, seizures, coma, and permanent neuropsychological deficits. Symptoms may appear immediately, or may be delayed by at least 24 hours. It is the most toxic of the boron hydrides.
    0.2.3) VITAL SIGNS
    A) Cough, wheezing, tachypnea, mild hypertension, or fever may be noted after exposure to the boron hydrides, but pentaborane is generally less active than diborane for effects on respiration.
    0.2.4) HEENT
    A) Headaches have been reported following exposure to pentaborane or decaborane. Borohydrides have also caused irreversible eye damage.
    0.2.5) CARDIOVASCULAR
    A) Dysrhythmias and cardiac arrest have been seen in human poisonings with pentaborane. Hypertension and bradycardia have been produced in dogs.
    0.2.6) RESPIRATORY
    A) Tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after exposure to boron hydrides. Diborane is the most active boron hydride for respiratory effects; pentaborane and decaborane have fewer respiratory symptoms.
    0.2.7) NEUROLOGIC
    A) Dizziness, weakness, CNS depression and excitation, hallucinations, and incoordination have been seen. Mental deficits have been produced by acute exposures. Tremors leading to seizures and severe brain injury have been seen in high dose pentaborane intoxication.
    0.2.8) GASTROINTESTINAL
    A) Nausea is one of the first symptoms seen. Hypersalivation and anorexia may occur.
    0.2.9) HEPATIC
    A) Fatty degeneration of the liver may occur. Liver function tests may be abnormal.
    0.2.10) GENITOURINARY
    A) Kidney damage may rarely occur. One case of fatal human intoxication showed complete lack of spermatozoa at autopsy.
    0.2.11) ACID-BASE
    A) Profound metabolic acidosis without respiratory compensation may occur secondary to seizures.
    0.2.13) HEMATOLOGIC
    A) Persistent leukocytosis may appear after 24 to 48 hours.
    0.2.14) DERMATOLOGIC
    A) Pentaborane can be rapidly fatal by the dermal route. Pentaborane is an irritant of the skin and mucous membranes. Reddened skin may occur from exposure to the vapor. The liquid can cause blisters.
    0.2.15) MUSCULOSKELETAL
    A) Weakness, fatigue, and muscle pain may follow exposure to the boron hydrides. Tremors, diffuse fasciculations and muscle spasms have all been reported with severe decaborane or pentaborane intoxication. CPK values over 3000 have been reported.
    0.2.18) PSYCHIATRIC
    A) Mild brain dysfunction has been reported in persons exposed to pentaborane.
    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.
    B) In one fatal case of pentaborane poisoning, no mature spermatozoa were seen on day eight after exposure.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    0.2.22) OTHER
    A) Pentaborane has caused toxicity by the inhalation, oral, and dermal routes.

Laboratory Monitoring

    A) Tissue pentaborane levels have not yet been established as useful. Liver and renal function tests may be indicated. Boron levels are elevated in blood and document exposures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Ingestion of pentaborane is unusual. Most exposures occur either by inhalation or dermal contact.
    B) Do NOT induce emesis.
    C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    D) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    E) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    F) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.3) INHALATION EXPOSURE
    A) Plastic gloves should also be worn by rescuers.
    B) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    C) Patients should be evaluated for liver and kidney damage.
    D) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    F) Prophylactic antibiotic therapy may reduce the chances of respiratory infection.
    G) Anyone who has breathed vapor must be seen in an emergency department acutely and followed for several months. Long term follow-up should include observations for neuropsychiatric abnormalities.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Remove all contaminated clothing. Dilute the area copiously with cool water. These substances may hydrolyze exothermically, so small amounts of water may result in thermal burns. A physician may need to examine the area if irritation or pain persists.
    2) Anyone who has had significant dermal exposure must be seen in an emergency department acutely and followed for several months. Long term follow-up should include observations for neuropsychiatric abnormalities.

Range Of Toxicity

    A) Pentaborane can be detected by smell in the range of 0.2 to 6 mg/m(3) without causing symptoms. Inhalation of concentrations as low as 25 ppm may cause symtoms.

Clinical Effects

Summary Of Exposure

    A) Pentaborane causes primarily neurologic effects, including CNS depression and excitability, spasms, seizures, coma, and permanent neuropsychological deficits. Symptoms may appear immediately, or may be delayed by at least 24 hours. It is the most toxic of the boron hydrides.

Vital Signs

    3.3.1) SUMMARY
    A) Cough, wheezing, tachypnea, mild hypertension, or fever may be noted after exposure to the boron hydrides, but pentaborane is generally less active than diborane for effects on respiration.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) Dyspnea, cough, wheezing, and breathing difficulty lasting several days have occurred with acute exposure to diborane (Cordasco et al, 1962) and to a lesser extent with pentaborane and decaborane (Lowe & Freeman, 1957).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Fever has been reported in some cases of pentaborane intoxication (Yarbrough et al, 1986).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Mild hypertension was observed in dogs poisoned by diborane (Kunkel et al, 1956), and in a few human cases (Lowe & Freeman, 1957).

Heent

    3.4.1) SUMMARY
    A) Headaches have been reported following exposure to pentaborane or decaborane. Borohydrides have also caused irreversible eye damage.
    3.4.2) HEAD
    A) WITH POISONING/EXPOSURE
    1) Headache has been noted after accidental spills, and low level exposures to pentaborane or decaborane (Lowe & Freeman, 1957; Finkel, 1983).
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CONJUNCTIVITIS - Keratoconjunctivitis with ulceration may be seen (Plunkett, 1976; Sittig, 1985). One mg of borohydride (sodium) instilled in rabbit eyes caused irreversible damage (Clayton & Clayton, 1981).
    2) MIOSIS - Constriction of the pupils was an early sign in dogs exposed to sublethal concentrations of pentaborane vapor. Visual disturbances and difficulty in focusing have been reported anecdotally in humans (Grant, 1993; Weir & Meyers, 1966).
    3) OPACIFICATION - Corneal opacification has been seen in experimental animals (Hathaway et al, 1996).
    4) NYSTAGMUS - Transient nystagmus and drooping of the eyelids may occur with moderate intoxication (Hathaway et al, 1996).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Pentaborane is an irritant (Sittig, 1991).

Cardiovascular

    3.5.1) SUMMARY
    A) Dysrhythmias and cardiac arrest have been seen in human poisonings with pentaborane. Hypertension and bradycardia have been produced in dogs.
    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Mild hypertension was observed in dogs poisoned by pentaborane (Weir & Meyers, 1966).
    B) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Bradycardia has been noted in dogs (Weir & Meyers, 1966).
    C) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Atrial fibrillation, asystole, ventricular tachycardia, sinus tachycardia, and cardiac arrest were seen in two cases of human exposures to pentaborane (Yarbrough et al, 1986).
    D) LACK OF EFFECT
    1) Of 137 human cases of exposure to diborane, pentaborane, and decaborane reviewed by Lowe & Freeman (1957), no cardiac toxicity was noted (Lowe & Freeman, 1957).

Respiratory

    3.6.1) SUMMARY
    A) Tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after exposure to boron hydrides. Diborane is the most active boron hydride for respiratory effects; pentaborane and decaborane have fewer respiratory symptoms.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) These substances are respiratory irritants (Plunkett, 1976). One may see tightness in the chest, dyspnea, nonproductive cough and wheezing for 3 to 5 days after an exposure (Cordasco et al, 1962; Proctor et al, 1988). Pneumonia may also develop. Diborane has the most activity on the lungs; pentaborane and decaborane have fewer respiratory tract symptoms (Lowe & Freeman, 1957; Finkel, 1983).

Neurologic

    3.7.1) SUMMARY
    A) Dizziness, weakness, CNS depression and excitation, hallucinations, and incoordination have been seen. Mental deficits have been produced by acute exposures. Tremors leading to seizures and severe brain injury have been seen in high dose pentaborane intoxication.
    3.7.2) CLINICAL EFFECTS
    A) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness, often accompanied by weakness, is seen with industrial spill exposures. Even low levels may produce this effect (Finkel, 1983; Rozendaal, 1951).
    B) EUPHORIA
    1) WITH POISONING/EXPOSURE
    a) Moderate exposures may produce various signs of hyperexcitability, including hiccups and spasms in the extremities and face, and hallucinations (Lowe & Freeman, 1957; Yarbrough et al, 1986; Sittig, 1985).
    C) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Muscle fasciculations; opisthotonic spasm; spasms of the face; neck, extremities, and abdomen; and tremors leading to seizures have been seen with high exposure to pentaborane (Finkel, 1983; Yarbrough et al, 1986; Clayton & Clayton, 1994; Hathaway et al, 1996).
    D) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Drowsiness is often seen in those patients exposed accidentally. Coma may also be seen (Lowe & Freeman, 1957) Clayton & Clatyon, 1994).
    E) IMPAIRED COGNITION
    1) WITH POISONING/EXPOSURE
    a) Workers generally show performance deficits in the first 50 hours (Clayton & Clayton, 1981). Performance decrements were noted on 5 of 11 neuropsychological tests administered to workers and rescue squad members with a mild exposure to pentaborane 2 months previously (Hart et al, 1984). Confusion and inability to concentrate occur with low exposure to pentaborane (Hathaway et al, 1996).
    F) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) Higher exposures to pentaborane can produce incoordination and slurred speech (Hathaway et al, 1996; Proctor et al, 1988).
    G) DELAYED REACTION TIME - FINDING
    1) WITH POISONING/EXPOSURE
    a) Effects may be delayed up to 48 hours following exposure (Zenz, 1994).
    H) SEQUELA
    1) WITH POISONING/EXPOSURE
    a) PERMANENT EFFECTS - Severe neurologic damage requiring institutionalization occurred in a person who was acutely exposed to pentaborane. The effects involved weakness, ataxia, spasticity, and visual defects. Cognitive defects which were still apparent two months after exposure occurred in persons exposed to a lesser extent in the same incident (Hart et al, 1984).
    b) Widespread degeneration of the brain was seen at autopsy in one fatal case of pentaborane poisoning (Yarbrough et al, 1986).
    I) CENTRAL STIMULANT ADVERSE REACTION
    1) WITH POISONING/EXPOSURE
    a) DOGS injected with 0.6 to 3.6 mg/kg liquid pentaborane showed alternating periods of CNS excitation and depression (Weir & Meyers, 1966).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea is one of the first symptoms seen. Hypersalivation and anorexia may occur.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) WITH POISONING/EXPOSURE
    a) Nausea is often one of the first symptoms seen after boron hydride intoxications (Lowe & Freeman, 1957; Plunkett, 1976).
    B) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) Anorexia was seen in animals exposed to 0.2 ppm for 6 months (Levinskas, 1958).
    C) EXCESSIVE SALIVATION
    1) WITH POISONING/EXPOSURE
    a) Ten percent of patients seen by Cordasco et al (1962) reported hypersalivation, nausea and anorexia (Cordasco et al, 1962).

Hepatic

    3.9.1) SUMMARY
    A) Fatty degeneration of the liver may occur. Liver function tests may be abnormal.
    3.9.2) CLINICAL EFFECTS
    A) STEATOSIS OF LIVER
    1) WITH POISONING/EXPOSURE
    a) Boron hydrides may cause fatty degeneration of the liver (Krackow, 1953; Lowe & Freeman, 1957). Abnormalities of liver function tests have been seen (Finkel, 1983; HSDB , 1999).

Genitourinary

    3.10.1) SUMMARY
    A) Kidney damage may rarely occur. One case of fatal human intoxication showed complete lack of spermatozoa at autopsy.
    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) WITH POISONING/EXPOSURE
    a) These substances may rarely cause kidney damage (Lowe & Freeman, 1957; Rozendaal, 1951). Abnormalities of renal function tests have been seen (Finkel, 1983).
    B) DISORDER OF TESTIS
    1) WITH POISONING/EXPOSURE
    a) In one fatal case of pentaborane poisoning, no mature spermatozoa were seen on day eight after exposure (Yarbrough et al, 1986).

Acid-Base

    3.11.1) SUMMARY
    A) Profound metabolic acidosis without respiratory compensation may occur secondary to seizures.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Accumulation of lactic acid may be secondary to convulsive activity. In three cases of pentaborane poisoning, profound metabolic acidosis without respiratory compensation occurred; pH ranged from 6.41 to 7.026 (Yarbrough et al, 1986).

Hematologic

    3.13.1) SUMMARY
    A) Persistent leukocytosis may appear after 24 to 48 hours.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Persistent leukocytosis may appear after 24 to 48 hours (Sittig, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) Pentaborane can be rapidly fatal by the dermal route. Pentaborane is an irritant of the skin and mucous membranes. Reddened skin may occur from exposure to the vapor. The liquid can cause blisters.
    3.14.2) CLINICAL EFFECTS
    A) SKIN ABSORPTION
    1) WITH POISONING/EXPOSURE
    a) RAPID EFFECTS - There is one case of a fatality involving dermal exposure to pentaborane. Severe neuromuscular effects appeared within four minutes after exposure (Yarbrough et al, 1986).
    B) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Exposure to vapor may lead to reddening of the skin. Direct contact with the liquid can cause redness, swelling, blisters, and local inflammation (Sax & Lewis, 1989; Hathaway et al, 1996).
    C) FLUSHING
    1) WITH POISONING/EXPOSURE
    a) Flushing and marked sweating may begin on the second day following exposure and persist 2 to 3 days (HSDB , 1999).

Musculoskeletal

    3.15.1) SUMMARY
    A) Weakness, fatigue, and muscle pain may follow exposure to the boron hydrides. Tremors, diffuse fasciculations and muscle spasms have all been reported with severe decaborane or pentaborane intoxication. CPK values over 3000 have been reported.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Muscle pain or cramps have been common in human cases of pentaborane poisoning (Lowe & Freeman, 1957; HSDB , 1999).
    B) MUSCLE FASCICULATION
    1) WITH POISONING/EXPOSURE
    a) Tremors, diffuse fasciculations and muscle spasms have all been reported with severe decaborane or pentaborane intoxication (Cordasco et al, 1962; Rozendaal, 1951). CPK values over 3000 have been reported (Yarborough et al, 1985).

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.
    B) In one fatal case of pentaborane poisoning, no mature spermatozoa were seen on day eight after exposure.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS19624-22-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Tissue pentaborane levels have not yet been established as useful. Liver and renal function tests may be indicated. Boron levels are elevated in blood and document exposures.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    2) In one fatal case of pentaborane poisoning, serum boron was 300 ppb the night of admission; levels in 10 unexposed controls averaged 25 ppb (Yarbrough et al, 1985-86).
    3) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Tissue pentaborane levels have not yet been established as useful. Liver and renal function tests may be indicated. Boron levels are elevated in blood and document exposures.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Care is symptomatic and supportive ie, oxygen, chlorpromazine, meperidine (Clayton & Clayton, 1981). Patients with significant inhalation exposure should be treated in the intensive care unit, with frequent cardiac, respiratory, and central venous pressure monitoring; arterial gas studies should be performed as necessary in cases of suspected or confirmed pulmonary edema (Cordasco & Stone, 1973).
    a) Use of 95% to 100% oxygen therapy by intermittent inspiratory positive pressure breathing (IPPD-I-O2) produced a striking response in one victim of diborane inhalation. Clearing occurred within 48 hours (Cordasco et al, 1968).
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    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)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) MONITORING OF PATIENT
    1) Monitor kidney and liver functions. Monitor cardiac, respiratory, and central venous pressure frequently. Monitor arterial gases.
    E) ANTIBIOTIC
    1) PROPHYLACTIC ANTIBIOTIC THERAPY: Penicillin 200,000 units 4 times a day for 3 days, has been used in addition to oxygen therapy, to prevent respiratory infections in victims of diborane inhalation (Cordasco & Stone, 1973; Cordasco et al, 1968).
    F) OBSERVATION REGIMES
    1) Patients with known exposure should be followed to detect psychiatric abnormalities (Silverman et al, 1985).
    G) EXPERIMENTAL THERAPY
    1) Borane hydrides have a marked reducing potential, so methylene blue, a readily available oxidizing agent, was injected into rabbits for 2 days after a lethal dose of decaborane was administered. Methylene blue appeared to prevent brain and heart norepinephrine depletion and prolonged life (Merritt, 1965). Human trials are lacking.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Rescuers must be protected from inhalation by self-contained breathing and from contact by plastic gloves.
    B) 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.
    C) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Care is symptomatic and supportive ie, oxygen, chlorpromazine, meperidine (Clayton & Clayton, 1981). Patients with significant inhalation exposure should be treated in the intensive care unit, with frequent cardiac, respiratory, and central venous pressure monitoring; arterial gas studies should be performed as necessary in cases of suspected or confirmed pulmonary edema (Cordasco & Stone, 1973).
    a) Use of 95% to 100% oxygen therapy by intermittent inspiratory positive pressure breathing (IPPD-I-O2) produced a striking response in one victim of diborane inhalation. Clearing occurred within 48 hours (Cordasco et al, 1968).
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    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)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) MONITORING OF PATIENT
    1) Monitor kidney and liver functions. Monitor cardiac, respiratory, and central venous pressure frequently. Monitor arterial gases.
    E) ANTIBIOTIC
    1) Prophylactic antibiotic therapy, such as penicillin 200,000 units 4 times a day for 3 days, has been used in addition to oxygen therapy, to prevent respiratory infections in victims of diborane inhalation (Cordasco & Stone, 1973; Cordasco et al, 1968).
    F) OBSERVATION REGIMES
    1) Patients with known mild inhalation exposure should be followed to detect psychiatric abnormalities (Silverman et al, 1985).
    G) EXPERIMENTAL THERAPY
    1) Borane hydrides have a marked reducing potential, so methylene blue, a readily available oxidizing agent, was injected into rabbits for 2 days after a lethal dose of decaborane was administered. Methylene blue appeared to prevent brain and heart norepinephrine depletion and prolonged life (Merritt, 1965). Human trials are lacking.
    H) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) SUPPORT
    1) Persons with significant eye exposure should be observed for systemic effects under controlled conditions, and treatment recommendations under the DERMAL EXPOSURE section should be followed where appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) PERSONNEL PROTECTION
    1) Rescuers must be protected from inhalation by self-contained breathing and from contact by plastic gloves.
    B) DERMAL DECONTAMINATION
    1) These substances may be absorbed through the skin. Patients exposed dermally should dilute the area copiously with cool water. These substances may hydrolyze exothermically, so using small amounts of water may result in thermal burns.
    6.9.2) TREATMENT
    A) SUPPORT
    1) Care is symptomatic/supportive ie, oxygen, chlorpromazine, meperidine (Clayton & Clayton, 1981).
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    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)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) MONITORING OF PATIENT
    1) Monitor kidney and liver functions. For high exposures, monitor cardiac, respiratory, and central venous pressure frequently. Monitor arterial gases.
    E) OBSERVATION REGIMES
    1) Patients with known dermal exposure should be followed to detect psychiatric abnormalities (Silverman et al, 1985).
    F) EXPERIMENTAL THERAPY
    1) Borane hydrides have a marked reducing potential, so methylene blue, a readily available oxidizing agent, was injected into rabbits for 2 days after a lethal dose of decaborane was administered. Methylene blue appeared to prevent brain and heart norepinephrine depletion and prolonged life (Merritt, 1965). Human trials are lacking.
    G) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Pentaborane can be detected by smell in the range of 0.2 to 6 mg/m(3) without causing symptoms. Inhalation of concentrations as low as 25 ppm may cause symtoms.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Pentaborane can be detected by smell in the range of 0.2 to 6 mg/m(3) without causing symptoms (Comstock & Oberst, 1953). Inhalation of concentrations as low as 25 ppm may cause symtoms (Lewis, 1998).

Workplace Standards

    A) ACGIH TLV Values for CAS19624-22-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Pentaborane
    a) TLV:
    1) TLV-TWA: 0.005 ppm
    2) TLV-STEL: 0.015 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): CNS convul; CNS impair
    d) Molecular Weight: 63.17
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS19624-22-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Pentaborane
    2) REL:
    a) TWA: 0.005 ppm (0.01 mg/m(3))
    b) STEL: 0.015 ppm (0.03 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS19624-22-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Pentaborane
    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: Pentaborane
    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 CAS19624-22-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Pentaborane
    2) Table Z-1 for Pentaborane:
    a) 8-hour TWA:
    1) ppm: 0.005
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.01
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1999
    1) LD50- (INTRAPERITONEAL)RAT:
    a) 11,100 mcg/kg

Physicochemical

Physical Characteristics

    A) Colorless liquid with strong, pungent, foul odor of sour milk (EPA, 1985; NFPA, 1991)

Molecular Weight

    A) 63.13 (Budavari, 1996)

References

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