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DIBORANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Diborane is a boron hydride.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) B2-H6

Available Forms Sources

    A) FORMS
    1) Diborane is a colorless, flammable gas with an offensive, sickly-sweet odor (EPA, 1985; AAR, 1998; ACGIH, 1991; Lewis, 1997; Budavari, 1996). It can SPONTANEOUSLY IGNITE at ambient temperatures in the presence of impurities (Budavari, 1996). Diborane reacts rapidly with water, as may occur in the body, to form BORIC ACID (AAR, 1998).
    2) The odor threshold for diborane is approximately 3.3 ppm (Hathaway et al, 1996). ODOR IS NOT A SUFFICIENT WARNING TO PREVENT OVEREXPOSURE. In any event, odor alone should never be used to determine if an environment is safe.
    3) The following review is based on the toxicologic properties of BORON HYDRIDES in general, with effects attributed specifically to diborane noted.
    B) USES
    1) It is used in rocket propellants, as a dopant for p-type semiconductors, as a reducing agent, rubber vulcanizer, flame-speed accelerator, and catalyst for olefin polymerization (Lewis, 1997; Budavari, 1996; ACGIH, 1991). It is also used extensively in the microelectronics industry (LaDou, 1983).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Diborane is a strong irritant to the respiratory system, skin, eyes, and mucous membranes. It may also cause neurological effects, liver, and kidney damage, but its primary effects are on the respiratory system. It is the least systemically toxic of the boron hydrides.
    0.2.3) VITAL SIGNS
    A) Cough, wheezing, tachypnea, mild hypertension, or fever may be noted after exposure to diborane.
    0.2.4) HEENT
    A) Diborane is an eye and mucous membrane irritant. Headache has been noted after spills and low level exposures to pentaborane or decaborane. Borohydrides have caused irreversible eye damage.
    0.2.5) CARDIOVASCULAR
    A) Mild hypertension was noted in a few human cases. No cardiac toxicity was noted in 137 human cases. Hypertension, bradycardia, and ventricular fibrillation have been produced in animals.
    0.2.6) RESPIRATORY
    A) Diborane is a respiratory irritant and has caused pulmonary edema in humans and animals. One may see tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after an exposure. 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 incoordination have been seen, but diborane is less active for neurological effects than pentaborane or decaborane. Coma and seizure generally do not occur with diborane.
    0.2.8) GASTROINTESTINAL
    A) Nausea is one of the first symptoms seen. Anorexia and hypersalivation have been reported with diborane exposure.
    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. Effects on spermatogenesis have been seen in animals exposed to boron compounds.
    0.2.11) ACID-BASE
    A) Metabolic acidosis secondary to seizures may occur.
    0.2.14) DERMATOLOGIC
    A) Diborane 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 and fatigue may follow exposure to diborane. Tremors, diffuse fasciculations and muscle spasms have all been reported with severe decaborane or pentaborane intoxication, and could presumably occur with diborane at sufficient doses. Rhabdomyolysis may occur.
    0.2.18) PSYCHIATRIC
    A) Post-traumatic stress disorder has been reported in persons exposed to pentaborane. Diborane is thought to be less potent for neuropsychiatric effects.
    0.2.20) REPRODUCTIVE
    A) No data were found for diborane for possible effects on teratogenesis, pregnancy, or lactation.

Laboratory Monitoring

    A) 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 diborane is extremely unlikely as it is a gas at ambient temperatures.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) Patients should be evaluated for liver and kidney damage.
    C) 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.
    D) 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.
    E) Prophylactic antibiotic therapy may reduce the chances of respiratory infection.
    F) Anyone who has breathed vapor must be seen in an emergency department acutely and followed for several months. Long term follow-up should seek neuropsychiatric abnormality.
    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.

Range Of Toxicity

    A) The minimum lethal and maximum tolerated doses for diborane have not been determined for humans.

Clinical Effects

Summary Of Exposure

    A) Diborane is a strong irritant to the respiratory system, skin, eyes, and mucous membranes. It may also cause neurological effects, liver, and kidney damage, but its primary effects are on the respiratory system. It is the least systemically 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 diborane.
    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).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER, with symptoms similar to those of metal fume fever, has occurred with exposure to diborane. Symptoms may appear after approximately 24 hours, and may persist for 1 to 3 days or longer (Sittig, 1991).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPERTENSION - 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) Diborane is an eye and mucous membrane irritant. Headache has been noted after spills and low level exposures to pentaborane or decaborane. Borohydrides have 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; Harbison, 1998). Diborane could presumably cause headache if the dose is sufficient.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CONJUNCTIVITIS - Keratoconjunctivitis may be seen (Plunkett, 1976). One mg of borohydride (sodium) instilled in rabbit eyes caused irreversible damage (Clayton & Clayton, 1981).
    a) Diborane is as potent as phosgene, chlorine, fluorine, or arsine in its irritant activity (Lewis, 1996).
    2) OPACIFICATION - Corneal opacification has been seen in experiments on mice with boron hydrides (Clayton & Clayton, 1981).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Diborane is a mucous membrane irritant (Lewis, 1996).

Cardiovascular

    3.5.1) SUMMARY
    A) Mild hypertension was noted in a few human cases. No cardiac toxicity was noted in 137 human cases. Hypertension, bradycardia, and ventricular fibrillation have been produced in animals.
    3.5.2) CLINICAL EFFECTS
    A) CARDIOVASCULAR FINDING
    1) WITH POISONING/EXPOSURE
    a) LACK OF ADVERSE EFFECT
    1) Of 137 human cases reviewed by Lowe & Freeman (1957), no cardiac toxicity was noted (Lowe & Freeman, 1957).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CARDIOVASCULAR FINDING
    a) DOGS: Ventricular fibrillation or disappearance of ventricular activity, mild hypertension, and bradycardia, was seen in dogs as a terminal effect of diborane poisoning (Kunkel et al, 1956; Lowe & Freeman, 1957).

Respiratory

    3.6.1) SUMMARY
    A) Diborane is a respiratory irritant and has caused pulmonary edema in humans and animals. One may see tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after an exposure. 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; Hathaway et al, 1996). Pneumonia is also possible. Diborane has the most activity on the lungs; pentaborane and decaborane have fewer respiratory tract symptoms (Finkel, 1983).
    b) High exposures can produce symptoms similar to metal fume fever (Budavari, 1989). Refer Metal Fume Fever for more information.
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Animal tests have demonstrated that diborane creates exothermic hydrolysis which leads to pulmonary irritation and edema (Schechter, 1958; Lowe & Freeman, 1957; Kunkel et al, 1956).
    1) Diborane may be absorbed by the inhalation, oral, or dermal route. The inhalation route is considered to be the most significant, because diborane is a gas under ambient conditions.

Neurologic

    3.7.1) SUMMARY
    A) Dizziness, weakness, CNS depression, and incoordination have been seen, but diborane is less active for neurological effects than pentaborane or decaborane. Coma and seizure generally do not occur with diborane.
    3.7.2) CLINICAL EFFECTS
    A) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness, often accompanied by weakness, has been seen with industrial spill exposures to boranes (Rozendaal, 1951). Even low levels may produce this effect (Finkel, 1983).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Muscle fasciculations and tremors leading to seizures have been seen with high dose severe pentaborane (Harbison, 1998) and boron hydride intoxication (Rozendaal, 1951). Seizures could presumably occur with exposure to diborane at sufficient doses, but one source has stated that convulsions typically do not occur with diborane poisoning (Sittig, 1991).
    C) 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).
    D) COORDINATION PROBLEM
    1) WITH POISONING/EXPOSURE
    a) Studies indicate marked decreases in performance in monkeys injected with 2 to 4 mg of decaborane. 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). Workers exposed are often confused, have difficulty concentrating and have memory loss (Rozendaal, 1951).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea is one of the first symptoms seen. Anorexia and hypersalivation have been reported with diborane exposure.
    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).

Genitourinary

    3.10.1) SUMMARY
    A) Kidney damage may rarely occur. Effects on spermatogenesis have been seen in animals exposed to boron compounds.
    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) Toxic effects of boron compounds have been seen in experiments on animal spermatogenesis, but similar effects have NOT been shown in humans exposed in industry (Lee et al, 1978; Finkel, 1983).

Acid-Base

    3.11.1) SUMMARY
    A) Metabolic acidosis secondary to seizures may occur.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Acidosis caused by an accumulation of lactic acid may be secondary to convulsive activity.

Dermatologic

    3.14.1) SUMMARY
    A) Diborane 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) 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; Lewis, 1996).
    b) Diborane can irritate the skin and mucous membranes; it is as potent as phosgene, chlorine, fluorine, or arsine in its irritant activity (Lewis, 1996).

Musculoskeletal

    3.15.1) SUMMARY
    A) Weakness and fatigue may follow exposure to diborane. Tremors, diffuse fasciculations and muscle spasms have all been reported with severe decaborane or pentaborane intoxication, and could presumably occur with diborane at sufficient doses. Rhabdomyolysis may occur.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Muscle weakness and fatigue have occurred with diborane exposure (Rozendaal, 1951; Sittig, 1991).
    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). While diborane is less active for neuromuscular effects, these could presumably occur with sufficient exposures in susceptible individuals.

Reproductive

    3.20.1) SUMMARY
    A) No data were found for diborane for possible effects on teratogenesis, pregnancy, or lactation.
    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 CAS19287-45-7 (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
    3.21.3) 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) No genetic data were available for diborane.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) 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) 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) 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) SUMMARY
    1) Ingestion of diborane is extremely unlikely as it is a gas at ambient temperatures.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Ingestion of diborane is extremely unlikely as it is a gas at ambient temperatures.

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) 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 percent oxygen therapy by intermittent inspiratory positive pressure breathing (IPPD-I-O2) produced 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) OBSERVATION REGIMES
    1) Patients with known mild inhalation 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 to prolong life (Merritt, 1965). Human trials are lacking.
    G) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) 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 i.e., 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 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 (Merritt, 1965). Human trials are lacking.
    G) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) The minimum lethal and maximum tolerated doses for diborane have not been determined for humans.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) Six of ten animals died after dermal application of 400 mg of diborane. Results were not consistent and absorption may have depended on moisture being on the skin (Clayton & Clayton, 1981).
    2) A concentration of 5 ppm was fatal to 17 of 18 rats and 2 of 2 dogs, while exposures of 1 to 2 ppm were fatal to 10 of 20 rats, 1 of 2 dogs and none of 10 guinea pigs; deaths appeared to be primarily from respiratory infections (ACGIH, 1986).
    3) Male mice were exposed to 1 or 5 ppm diborane for 1, 2, 4, or 8 hours. Panbronchiolitis was noted in the animals exposed to 5 ppm for 2 hours or more. No effect was noted at 1 ppm. In an extension of the same study, mice were exposed to 0.2 or 0.7 ppm for 6 hours per day, 5 days per week, for 2 or 4 weeks. Slight pathological lung changes were noted even with the 0.2 ppm concentration at 2 and 4 weeks (Nomiyama, 1995). Pathological lung changes were reported in mice after 15 ppm exposures for 1 to 8 hours and after 5 ppm for 2 or 4 weeks, with a 4 hour LC50 of 31.5 ppm (Uemura et al, 1995).
    4) Using bronchoalveolar lavage, evidence of alveolar capillary and alveolar lining cell damage was documented in rats following inhalation of 1, 10, or 20 ppm diborane for 4 hours (Nomiyama, 1995).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.

Workplace Standards

    A) ACGIH TLV Values for CAS19287-45-7 (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) Diborane
    a) TLV:
    1) TLV-TWA: 0.1 ppm
    2) TLV-STEL:
    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): URT irr; headache
    d) Molecular Weight: 27.69
    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 CAS19287-45-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Diborane
    2) REL:
    a) TWA: 0.1 ppm (0.1 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 15 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS19287-45-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Diborane
    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: Diborane
    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 CAS19287-45-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Diborane
    2) Table Z-1 for Diborane:
    a) 8-hour TWA:
    1) ppm: 0.1
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.1
    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, 2000

Physicochemical

Physical Characteristics

    A) Diborane is a colorless flammable gas with a repulsive, sickly-sweet odor (Budavari, 1996).

Molecular Weight

    A) 27.69

References

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