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ETHYL ETHER

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Diethyl ether is an anesthetic and industrial solvent for fats, oils, gums, alkaloids, resins, and waxes (Budavari, 1996).

Specific Substances

    1) Diethyl ether
    2) Diethyl oxide
    3) Ethoxyethane
    4) Ether
    5) Ethyl oxide
    6) Sulfuric ether
    7) Sweet vitral
    8) Anesthesia ether
    9) 1,1'-oxybisethane
    10) CAS 60-29-7
    11) 3-OXYPENTANE
    1.2.1) MOLECULAR FORMULA
    1) C4-H10-O

Available Forms Sources

    A) FORMS
    1) Ethyl ether is a colorless, very volatile, mobile, hygroscopic liquid (below 34 degrees C (94 degrees F)) with a pungent, aromatic odor and a burning and sweet taste. It is available in ACS Reagent, ACS Absolute, CP, concentrated, USP 1880, USP (anesthesia), washed, motor, and electronic grades (AAR, 1998; (ACGIH, 1991; Ashford, 1994; Budavari, 1996; Harbison, 1998; ILO, 1998; Lewis, 1996; Lewis, 1997; Lewis, 1998) NFPA, 1994; (Verschueren, 1983).
    2) The USP formulation contains 3% ethanol and is marketed in sealed containers with copper liners to retard oxidation.
    B) SOURCES
    1) Ethyl ether is produced by dehydration of ethanol and catalytic hydration of ethylene (Ashford, 1994; Budavari, 1996; Lewis, 1997).
    C) USES
    1) Ethyl ether is used as a diesel fuel ignition primer, a smokeless powder, an extractant, and as an industrial solvent for waxes, fats, oils, perfumes, alkaloids, and gums. It is an important reagent in organic syntheses and analytic chemistry, especially in Grignard/Wurtz reactions. It was formerly used as an anesthetic gas (ACGIH, 1991; Ashford, 1994; Harbison, 1998; Hathaway et al, 1996; Lewis, 1997; Lewis, 1998).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Ingestion poisonings are similar to ethanol overdoses except for a more rapid onset and shorter duration of symptoms. Inhalation may result in dizziness, giddiness, euphoria, and CNS depression. Deliberate abuse has been reported with repeated exposures producing ether jags. Deaths from acute industrial exposure are rare. Death due to respiratory depression may result from severe and continued exposure.
    B) Ethyl ether is a severe eye and moderate skin irritant.
    0.2.3) VITAL SIGNS
    A) Irregular breathing, hypothermia, and bradycardia have been noted as early effects in industrial exposures.
    0.2.4) HEENT
    A) Excessive salivation has been reported. Prolonged exposure to high vapor concentrations may cause eye injury.
    0.2.5) CARDIOVASCULAR
    A) Bradycardia has been reported in industrial exposures.
    0.2.6) RESPIRATORY
    A) Ether is irritating to mucous membranes. Cough and laryngeal spasm have been reported.
    B) Death has been reported due to respiratory depression.
    0.2.7) NEUROLOGIC
    A) Exhaustion, dizziness, excitation, headache, CNS depression, and seizures have occurred.
    0.2.8) GASTROINTESTINAL
    A) Ether is irritating to mucous membranes and vomiting might be expected after ingestion. Anorexia has been reported in patients with deliberate ether abuse.
    0.2.9) HEPATIC
    A) When used in anesthesia, liver changes are generally mild and of short duration. When ether is given to patients with preexisting hepatic injury, hepatotoxicity is more likely.
    0.2.10) GENITOURINARY
    A) Albuminuria and nephritis have been reported as transient complications in ether intoxication.
    B) Severe cystitis has resulted from instillation of ether into the urinary bladder.
    C) Animal experiments demonstrated degenerative changes in the epithelium of the convoluted tubules of the kidneys.
    0.2.13) HEMATOLOGIC
    A) Polycythemia has been reported after ether exposure and thrombophlebitis has developed in patients treated intravenously with a 15 percent solution.
    0.2.14) DERMATOLOGIC
    A) Ether will defat the skin with multiple exposures.
    B) Ulcers have been reported following intramuscular injections of ether.
    C) Intra-arterial injection has caused severe tissue edema, pain, cyanosis, ecchymosis, skin necrosis, gangrene, and amputation.
    0.2.15) MUSCULOSKELETAL
    A) The same level of relaxation is not produced by other anesthetic agents.
    0.2.16) ENDOCRINE
    A) Hyperglycemia is common following anesthesia with blood glucose level increases ranging from 27 to 62 milligrams/deciliter.
    0.2.20) REPRODUCTIVE
    A) Ether readily passes the placental barrier. Concentrations in the fetus are expected to be the same as in the maternal blood.
    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) Deliberate abuse has been reported with repeated exposures producing ether jags. Death from acute industrial exposure is rare.
    B) Ethyl ether is moderately toxic to humans by ingestion. It is poisonous experimentally by the subcutaneous route. It is moderately toxic by intraperitoneal and intravenous routes and mildly toxic by inhalation. Olfactory changes resulted from human inhalation.
    C) Ethyl ether is not dangerously reactive, but is HIGHLY FLAMMABLE.

Laboratory Monitoring

    A) Monitor renal and liver function following ether exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    B) Activated charcoal is of questionable value because of rapid absorption.
    C) RESPIRATORY SUPPORT - Patients should be monitored carefully for respiratory depression and apnea. Respiratory support should be available.
    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) Monitor the patient for hyperglycemia, hepatic dysfunction, or renal dysfunction.
    F) EUPHORIA - Patients intoxicated with ether may be euphoric and can experience hallucinations. To minimize sensory input, provide a darkened, low stimulus room.
    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.
    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) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) One to two ounces may be fatal if swallowed. Dizziness may develop from continued inhalation of an airborne concentration of 2000 ppm, but 7000 ppm has been tolerated for short periods of time without untoward effects. Industrial exposure to airborne levels of 500 to 1000 ppm did not result in demonstrable injury to health.

Clinical Effects

Summary Of Exposure

    A) Ingestion poisonings are similar to ethanol overdoses except for a more rapid onset and shorter duration of symptoms. Inhalation may result in dizziness, giddiness, euphoria, and CNS depression. Deliberate abuse has been reported with repeated exposures producing ether jags. Deaths from acute industrial exposure are rare. Death due to respiratory depression may result from severe and continued exposure.
    B) Ethyl ether is a severe eye and moderate skin irritant.

Vital Signs

    3.3.1) SUMMARY
    A) Irregular breathing, hypothermia, and bradycardia have been noted as early effects in industrial exposures.
    3.3.2) RESPIRATIONS
    A) Irregular breathing has been noted as an early effect in industrial exposures (Kirwin & Sandmeyer, 1981).
    3.3.3) TEMPERATURE
    A) Hypothermia has been reported as an early effect in industrial exposures (Kirwin & Sandmeyer, 1981).
    3.3.4) BLOOD PRESSURE
    A) Bradycardia has been reported as an early effect in industrial exposures (Kirwin & Sandmeyer, 1981).

Heent

    3.4.1) SUMMARY
    A) Excessive salivation has been reported. Prolonged exposure to high vapor concentrations may cause eye injury.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Eyes may be irritated by splash contact with the liquid or high concentrations of the vapor (HSDB , 2002) Grant & Schuman, 1993; (Anon, 1981; ACGIH, 1991).
    1) Prolonged exposure to high vapor concentrations may cause superficial epithelial injury, but recovery is rapid (Grant & Schuman, 1993).
    B) PAIN - Exposure may cause painful red eyes (HSDB , 2002; ILO, 1998).
    C) EXPERIMENTAL ANIMALS - Ether tested in rabbits caused a grade 2 reaction (mild reversible injury) on a scale of 1 to 10 (Grant & Schuman, 1993).
    3.4.6) THROAT
    A) SALIVATION - Excessive salivation has been noted in patients undergoing ethyl ether anesthesia and in industrial exposures (Bingham et al, 2001; Knape, 1980; Kirwin & Sandmeyer, 1981).

Cardiovascular

    3.5.1) SUMMARY
    A) Bradycardia has been reported in industrial exposures.
    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) Bradycardia has been reported as an early effect in industrial exposures (Kirwin & Sandmeyer, 1981).
    B) TACHYARRHYTHMIA
    1) Tachycardia may occur (HSDB , 2002).
    C) CONDUCTION DISORDER OF THE HEART
    1) Supraventricular cardiac dysrhythmias may occur (HSDB , 2002).

Respiratory

    3.6.1) SUMMARY
    A) Ether is irritating to mucous membranes. Cough and laryngeal spasm have been reported.
    B) Death has been reported due to respiratory depression.
    3.6.2) CLINICAL EFFECTS
    A) COUGH
    1) Ether is irritating to mucous membranes. Cough and laryngeal spasm have been reported during ethyl ether anesthesia (Bingham et al, 2001; Knape, 1980).
    B) ACUTE RESPIRATORY INSUFFICIENCY
    1) Respiratory depression was the cause of death in fatal cases (Kringsholm, 1980; Lewis, 1998).

Neurologic

    3.7.1) SUMMARY
    A) Exhaustion, dizziness, excitation, headache, CNS depression, and seizures have occurred.
    3.7.2) CLINICAL EFFECTS
    A) FATIGUE
    1) Exhaustion has been reported as a symptom of ether intoxication (Anon, 1981).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Sleepiness and drowsiness leading to anesthesia and coma are the primary physiologic responses to ether (Wilford, 1981; Gosselin et al, 1984; Lewis, 1996; Sittig, 1991; Harbison, 1998).
    2) CASE REPORT - A 46-year-old female died during diethyl ether anesthesia for amputation of a leg. The anesthetic effects of the ether, significant trauma, and a lack of knowledge of resuscitation contributed to the patient's death (Cooper, 1991).
    C) DIZZINESS
    1) Dizziness, ataxia, and slurred speech are common effects reported after ether intoxication (Anon, 1981; Wilford, 1981; Gosselin et al, 1984; Sittig, 1991).
    D) EUPHORIA
    1) Ether has often been deliberately abused. Users describe excitement, euphoria, delusions, unusual strength, visual and auditory hallucinations, a sense of reckless abandon and omnipotence, perceptual difficulties, and a "floating" feeling (Wilford, 1981).
    E) SEIZURE
    1) Ether use has been associated with seizures and increased intracranial pressure (Knape, 1980).
    F) HEADACHE
    1) Headache has been reported during ether intoxication (Bingham et al, 2001; Baselt, 2000; Anon, 1981; Sittig, 1991).
    G) PARAPLEGIA
    1) CASE REPORT - Paraparesis has been reported after accidental injection of 5 mL of diethyl ether into the epidural space. An immediate hot and burning pain was felt in the patient's legs followed by paraparesis. Recovery occurred within 4 hours (Mappes & Schauer, 1991).

Gastrointestinal

    3.8.1) SUMMARY
    A) Ether is irritating to mucous membranes and vomiting might be expected after ingestion. Anorexia has been reported in patients with deliberate ether abuse.
    3.8.2) CLINICAL EFFECTS
    A) SWOLLEN ABDOMEN
    1) Ether is a volatile compound which may distend the stomach (Gosselin et al, 1984).
    B) LOSS OF APPETITE
    1) Anorexia has been reported in patients with deliberate ether abuse (Anon, 1981).
    C) VOMITING
    1) Ether is irritating to the mucous membranes. Vomiting might be expected after ingestion. Vomiting is common (85 percent) in patients following ether anesthesia (Bingham et al, 2001; Knape, 1980).

Hepatic

    3.9.1) SUMMARY
    A) When used in anesthesia, liver changes are generally mild and of short duration. When ether is given to patients with preexisting hepatic injury, hepatotoxicity is more likely.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) When used in anesthesia, liver changes are generally characterized by an elevated SGOT (AST) and an increase in alkaline phosphatase, which are of short duration and return to normal (Bingham et al, 2001; Kirwin & Sandmeyer, 1981). When ether is given to patients with pre-existing hepatic injury, hepatotoxicity is more likely to occur (Price & Dripps, 1975).
    2) Various types of hepatic injury have been reported in both humans and experimental animals (Sewall, 1947). These include diffuse necrosis of the liver (Cantarow & Gehret, 1931), reduced capacity to synthesize and detoxify (Boyce, 1941), fatty changes in the centrilobular region (Stander, 1926), and parenchymatous degeneration of the liver (Sewall, 1947).

Genitourinary

    3.10.1) SUMMARY
    A) Albuminuria and nephritis have been reported as transient complications in ether intoxication.
    B) Severe cystitis has resulted from instillation of ether into the urinary bladder.
    C) Animal experiments demonstrated degenerative changes in the epithelium of the convoluted tubules of the kidneys.
    3.10.2) CLINICAL EFFECTS
    A) ALBUMINURIA
    1) Albuminuria is a transient side effect seen with ether and may be seen in overdose (Anon, 1981).
    B) NEPHRITIS
    1) Nephritis may develop in rare cases (Bingham et al, 2001; Kirwin & Sandmeyer, 1981). Parenchymatous degeneration of the kidney was seen in a patient treated with 1.5 percent intravenous ether (Sewall, 1947).
    C) ABNORMAL RENAL FUNCTION
    1) Effects during anesthesia may include renal vasoconstriction, decreased glomerular filtration, decreased effective renal plasma flow, an increase in filtration fraction, and an increase in tubular resorption of water (Price & Dripps, 1975).
    D) CYSTITIS
    1) Instillation of ether into obstructed Foley catheter balloons has been associated with severe hemorrhagic cystitis (Nellans et al, 1985). Urinary bladder damage can be permanent and necessitate surgical correction (Gattegno et al, 1988; Lebowitz & Effmann, 1978).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL TUBULAR DISORDER
    a) Animal experiments done by Stander (1926) demonstrated degenerative changes in the epithelium of the convoluted tubules of the kidneys.

Hematologic

    3.13.1) SUMMARY
    A) Polycythemia has been reported after ether exposure and thrombophlebitis has developed in patients treated intravenously with a 15 percent solution.
    3.13.2) CLINICAL EFFECTS
    A) ERYTHROCYTOSIS
    1) Polycythemia has been reported after ether exposure, especially in women (Bingham et al, 2001; Anon, 1981; ACGIH, 1991).
    B) THROMBOPHLEBITIS
    1) Thrombophlebitis developed in patients treated with a 15 percent solution injected intravenously for treatment of peripheral vascular disease. As much as a 20 percent decrease in coagulation time has also been reported (Sewall, 1947).

Dermatologic

    3.14.1) SUMMARY
    A) Ether will defat the skin with multiple exposures.
    B) Ulcers have been reported following intramuscular injections of ether.
    C) Intra-arterial injection has caused severe tissue edema, pain, cyanosis, ecchymosis, skin necrosis, gangrene, and amputation.
    3.14.2) CLINICAL EFFECTS
    A) DRY SKIN
    1) Single ether exposures produce little effect, but continued exposures produce cracking and drying due to extraction of fats and oils (Bingham et al, 2001; Anon, 1981; ACGIH, 1991).
    B) INJECTION SITE NECROSIS
    1) When ether was used intramuscularly (for the treatment of peripheral vascular disease), 6 of 34 patients developed ulcers at the injection site (Sewall, 1947).
    C) SKIN NECROSIS
    1) Intra-arterial injection has caused severe tissue edema, pain, cyanosis, ecchymosis, skin necrosis, gangrene, and amputation (King & Hawtof, 1963).

Musculoskeletal

    3.15.1) SUMMARY
    A) The same level of relaxation is not produced by other anesthetic agents.
    3.15.2) CLINICAL EFFECTS
    A) DECREASED MUSCLE TONE
    1) Other anesthetic agents do not result in the same degree of muscle relaxation (Price & Dripps, 1975).

Endocrine

    3.16.1) SUMMARY
    A) Hyperglycemia is common following anesthesia with blood glucose level increases ranging from 27 to 62 milligrams/deciliter.
    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) Hyperglycemia is common following anesthesia (HSDB , 2002; Knape, 1980). Blood glucose level increases may range from 27 to 62 milligrams/deciliter for periods of up to an hour. The average increase in blood glucose during anesthesia was 2.9 milligrams/deciliter per ounce of ether administered (Cantarow & Gehret, 1931).

Reproductive

    3.20.1) SUMMARY
    A) Ether readily passes the placental barrier. Concentrations in the fetus are expected to be the same as in the maternal blood.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) Ether was one of many solvents linked with CNS birth defects in a Scandinavian study (Barlow & Sullivan, 1982; (Holmberg, 1979; Holmberg & Nurminen, 1980). Other epidemiological studies found increased risks of miscarriages and birth defects in operating room attendants (Infante & Tsongas, 1981; Purdham, 1981). However, multiple substances were involved, and it cannot be determined if ether alone was the causative agent.
    B) ANIMAL STUDIES
    1) Ether was teratogenic in rats, mice and chickens, causing increased fetal resorptions and skeletal anomalies, but no increase in soft tissue defects (Schwetz & Becker, 1970; H Shepard , 1995; Smith, 1968). It was readily transferred to the fetus in rats, mice, and guinea pigs (Dybing & Stormorken, 1952). It altered development of fruit flies (Bownes & Seiler, 1977). When given during the critical period for formation of cleft palate in rats, it was not active (Jacobs, 1971).
    3.20.3) EFFECTS IN PREGNANCY
    A) PLACENTAL BARRIER
    1) Ether readily passes the placental barrier. Concentrations in the fetus are expected to be the same as in the maternal blood (Price & Dripps, 1975). Although there is little human or experimental animal data, the AMA Council on Scientific Affairs concluded that the risk is negligible with permissible occupational exposure (AMA, 1985).
    B) ABORTION
    1) Other epidemiological studies found increased risks of miscarriages and birth defects in operating room attendants (Infante & Tsongas, 1981; Purdham, 1981). However, multiple substances were involved, and it cannot be determined if ether alone was the causative agent.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS60-29-7 (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.

Genotoxicity

    A) Ethyl ether induced DNA repair in E. coli, DNA inhibition in mouse embryos, and was positive in other mutation test systems in hamster fibroblasts.
    B) One occupational cytogenetics study reported elevated levels of sister chromatid exchanges and chromosome aberrations in laboratory technicians exposed to ether and other chemicals, although ethyl ether did not induce sister chromatid exchanges in cultured Chinese hamster ovary cells or mice.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor renal and liver function following ether exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor the patient for hyperglycemia, hepatic dysfunction, or renal dysfunction.
    B) HEMATOLOGIC
    1) Monitor for polycythemia.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Gas chromatography is used most frequently for biological specimen assays, but mass spectrophotometry and infrared spectrophotometry have also been investigated (Baselt, 2000).

Treatment

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) Extracorporeal methods of elimination are seldom necessary, since ether has a short half-life.

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor renal and liver function following ether exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) Activated charcoal is of questionable value because of rapid absorption.
    6.5.2) PREVENTION OF ABSORPTION
    A) DILUTION
    1) Concentrated ether causes mucosal necrosis (Gattegno et al, 1988). If performed soon after ingestion, dilution may decrease the potential for gastrointestinal irritation.
    2) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is of questionable value because of rapid absorption.
    6.5.3) TREATMENT
    A) AIRWAY MANAGEMENT
    1) Monitor carefully for respiratory depression and apnea. Respiratory support should be available at all times.
    B) SEIZURE
    1) Correct hypoxia and manage the patients airway as clinically indicated.
    2) 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).
    3) 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 .
    4) 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).
    5) 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).
    6) 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).
    7) 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) MONITORING OF PATIENT
    1) Monitor the patient for hyperglycemia, hepatic dysfunction, or renal dysfunction.
    D) HALLUCINATIONS
    1) Patients intoxicated with ether may be euphoric and can experience hallucinations. To minimize sensory input, provide a darkened, low stimulus room. Pharmacologic intervention for the hallucinations is seldom necessary.

Inhalation Exposure

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

Range Of Toxicity

Summary

    A) One to two ounces may be fatal if swallowed. Dizziness may develop from continued inhalation of an airborne concentration of 2000 ppm, but 7000 ppm has been tolerated for short periods of time without untoward effects. Industrial exposure to airborne levels of 500 to 1000 ppm did not result in demonstrable injury to health.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) There is little data on deaths resulting from exposure to ethyl ether. Humans generally refrain from ingesting ethyl ether due to its irritating effect on mucous membranes; however, deaths have been reported following the intentional ingestion of as little as 30 mL of liquid ethyl ether. (Bingham et al, 2001; Baselt, 2000; Baselt & Cravey, 1995).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Ethyl ether is quickly absorbed through the lungs and the primary result is CNS depression and anesthesia. However, there is a wide range of concentrations between nasal irritation (200 ppm) and more serious health hazards (100,000- 150,000 ppm) which may include respiratory arrest. Exposure to liquid or high concentrations of vapor ethyl ether causes eye and mucous membrane irritation. Brief skin exposure to ethyl ether has no effect; repeated skin exposures causes drying and cracking (Bingham et al, 2001; Baselt, 2000; ACGIH, 1991; Baselt & Cravey, 1995; Hathaway et al, 1996; Zenz, 1994).
    2) Industrial exposures of 500-1000 ppm did not result in demonstrable injury to health and concentrations of up to 7000 ppm have been tolerated, but a 500 ppm limit seems appropriate to avoid irritation (ACGIH, 1991; Hathaway et al, 1996; Zenz, 1994).
    3) Early symptoms of acute inhalation overexposure include excitement or drowsiness, vomiting, paleness, lowered pulse and body temperature, irregular respiration, muscular relaxations, and excessive salivation. Temporary aftereffects of acute exposure include vomiting, salivation, respiratory passage irritation, headaches, and depression or excitation (Bingham et al, 2001; Baselt, 2000; Baselt & Cravey, 1995; Harbison, 1998; Hathaway et al, 1996; Lewis, 1998; Zenz, 1994).
    4) A degree of tolerance may be acquired from repeated exposures to ethyl ether. Symptoms resulting from chronic inhalation exposure include loss of appetite, exhaustion, headache, sleepiness, dizziness, excitation, and psychic disturbances; albuminuria and polycythemia may result (Baselt, 2000; ACGIH, 1991; Baselt & Cravey, 1995; Harbison, 1998; Hathaway et al, 1996; Zenz, 1994).

Serum Plasma Blood Concentrations

    7.5.1) THERAPEUTIC CONCENTRATIONS
    A) THERAPEUTIC CONCENTRATION LEVELS
    1) GENERAL
    a) ANALGESIA DOSE - Results in arterial blood concentrations of 100 to 500 milligrams/liter (Falconer Jr, 1952).
    b) ANESTHESIA DOSE - Arterial blood concentrations of 500 to 1500 milligrams/liter with the average surgical anesthesia being 1200 milligrams/liter (Faulconer Jr, 1952).
    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ADULT
    a) Henderson & Haggart (1943) estimated that inhalation of 400 parts per million in the average man could result in 1.25 grams being absorbed and a blood level of 0.018 grams/liter (sub-toxic). If 2000 parts per million were inhaled to equilibrium, absorption would be 6.25 grams (0.09 grams/liter) and would cause dizziness.

Workplace Standards

    A) ACGIH TLV Values for CAS60-29-7 (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) Ethyl ether
    a) TLV:
    1) TLV-TWA: 400 ppm
    2) TLV-STEL: 500 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 impair; URT irr
    d) Molecular Weight: 74.12
    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 CAS60-29-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Ethyl ether
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix D
    3) IDLH:
    a) IDLH: 1900 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    C) Carcinogenicity Ratings for CAS60-29-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Ethyl ether
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Ethyl ether
    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: Ethyl ether
    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 CAS60-29-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Ethyl ether
    2) Table Z-1 for Ethyl ether:
    a) 8-hour TWA:
    1) ppm: 400
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1200
    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: Lewis, 1996 RTECS, 2002
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 2420 mg/kg
    2) LD50- (ORAL)RAT:
    a) 1215 mg/kg
    3) TCLo- (INHALATION)HUMAN:
    a) 200 ppm

Pharmacology Toxicology

Pharmacologic Mechanism

    A) During ether anesthesia, amplitude and frequency of brain waves are decreased. The neural basis of the anesthetic state consists of several factors including reduction or blockage of impulses conducted corticopetally through the multisynaptic medial brain stem system, depressed local cortical events, and elimination of the normal influences of the central cephalic brain stem activity system on the cortex and diencephalon. At the spinal cord, ether depresses both 2-neuron arc reflexes and multineuron arc reflexes (Price & Dripps, 1975).

Physicochemical

Physical Characteristics

    A) Ethyl ether is a colorless, very volatile, mobile, hygroscopic liquid (below 34 degrees C (94 degrees F)) with a pungent, aromatic odor and a burning and sweet taste (AAR, 1998; (ACGIH, 1991; Ashford, 1994; Budavari, 1996; Harbison, 1998; ILO, 1998; Lewis, 1996; Lewis, 1997; Lewis, 1998; NFPA, 1997; Verschueren, 1983).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 74.12

Other

    A) ODOR THRESHOLD
    1) 8.9 ppm (ACGIH, 1991)

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