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Isopropyl alcohol

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main brand names/main trade names
   1.6 Manufacturers, importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/form
      3.3.3 Description
   3.4 Hazardous characteristics
4. USES/HIGH RISK CIRCUMSTANCES OF POISONING
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstances of poisoning
   4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
6. KINETICS
   6.1 Absorption by route of exposure
      6.1.1 Oral
      6.1.2 Inhalation
      6.1.3 Dermal contact
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination and excretion by route of exposure
7. TOXICOLOGY
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Animal data
      7.2.3 In-vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI)
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL AND OTHER ANALYSES
   8.1 Sample
      8.1.1 Collection
      8.1.2 Storage
      8.1.3 Transport
   8.2 Toxicological analytical methods
      8.2.1 Test for active ingredient
      8.2.2 Test for biological sample
   8.3 Other laboratory analyses
      8.3.1 Haematological investigations
         8.3.1.1 Blood
         8.3.1.2 Urine
      8.3.2 Biochemical investigations
         8.3.2.1 Blood
         8.3.2.2 Urine
         8.3.2.3 Other
      8.3.3 Arterial blood gas analysis
      8.3.4 Other relevant biochemical analyses
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
   8.6 References
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Description of clinical effects by system
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurologic
         9.4.3.1 Central Nervous system (CNS)
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Others
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatologic
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunologic
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbances
         9.4.12.2 Fluid and electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks: pregnancy, breast feeding, enzyme deficiencies.
   9.5 Others
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic treatment
   10.3 Decontamination
   10.4 Enhanced Elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from the literature
12.ADDITIONAL INFORMATION
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)
    ISOPROPYL ALCOHOL

    International Programme on Chemical Safety
    Poisons Information Monograph 290
    Chemical

    1.  NAME

        1.1  Substance

             Isopropyl alcohol

        1.2  Group

             Aliphatic alcohol hydrocarbon

        1.3  Synonyms

             Pseudo propyl alcohol; 2-propanol;
             dimethyl carbinol; isopropanol;
             sec-propyl alcohol; persprit;
             secondary propyl alcohol; IPA;
             propan-2-ol; alcohol isopropylicus;
             petrohol

         1.4 Identification numbers

             1.4.1  CAS number

                    67-63-0

             1.4.2  Other numbers

                    UN/NA (PIN): 1219
                    EC Number: 603-003-00-0
                    RTECS: NT 8050000
                    (Budavari, 1996)

        1.5  Main brand names/main trade names

             Avantine (UK)
             IPS.1 and IPS/C (Shell)
             Sterets (Schering-Prebbles UK)
             Sterile Pack Fluid (Ethicon)

        1.6  Manufacturers, importers

             Manufactured by: Shell Chemicals
                              British Petroleum
                              Mobil Oil

    2.  SUMMARY

        2.1  Main risks and target organs

             Coma, central bnervous system (CNS) depression, liver,
             kidney, cardiovascular depression and brain damage.

        2.2  Summary of clinical effects

             Drowsiness, ataxia and stupor.
    
             Coma and respiratory depression.
    
             Irritation of mucous membranes and eyes.
    
             Gastritis, gastric haemorrhage, vomiting and pancreatitis.
    
             Cold and clammy skin, hypothermia, miosis pupils,
             tachycardia, respiration slow and noisy.
    
             Hypotension
    
             Cardiodepression
    
             Brain, liver and kidney damage at a later stage.

        2.3  Diagnosis

             Blood and urine for biomedical analysis should be collected.
    
             Fluid balance.
    
             Electrolytes and blood gases.
    
             Blood glucose.
    
             Urinalysis
    
             Hepatic and renal function tests.
    
             Blood pressure, temperature and vital signs.
    
             Blood levels of isopropyl alcohol and acetone are clinically
             useful.

        2.4  First-aid measures and management principles

             Seek medical attention immediately and transfer patient
             to hospital.
    

             Inhalation: Remove source of contamination or move patient
             into fresh air.  Begin artificial respiration immediately if
             victim is not breathing and administer supplemental oxygen if
             available.  Obtain medical attention.
    
             Eye contact: Flood affected eye(s) with copious amounts of
             lukewarm, gently running water for at least 15 minutes. 
             During this time the upper and lower eyelids should be held
             apart.
    
             Skin contact:  Rinse the affected area(s) with copious
             amounts of lukewarm, gently running water for at least 15
             minutes.  Remove contaminated clothing and shoes. 
             Wash/thoroughly clean all clothing before re-using or
             discard.  If skin irritation exists, seek medical
             attention.
    
             Ingestion: Induce emesis at an early stage if not
             contraindicated.  Empty stomach by gastric aspiration and
             lavage, care being taken not to induce pulmonary aspiration
             of the return flow.  Keep the patient warm.  If respiration
             is depressed or absent, endotracheal intubation and assisted
             respiration may be required.  Obtain medical assistance
             immediately.
    
             In severe poisonings:
    
             maintain respiration;
             maintain fluid balance;
             initiate haemodialysis or peritoneal dialysis;
             treat convulsions with intravenous (IV) benzodiazepines.
    
             First aid summary:
    
             Provide the patient with general supportive measures (warmth,
             comfort and rest).  Obtain medical advice and/or assistance
             for all cases of ingestion or eye contact, and all but
             trivial cases of inhalation or skin contact.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Synthetic:  Prepared from propylene, which is obtained
             in the cracking of petroleum or by the reduction of acetone
             (Budavari, 1996).

        3.2  Chemical structure

             Chemical name: Isopropyl alcohol
    
             Molecular weight: 60.09
    

             Structural formula: CH3-CH(OH)-CH3

        3.3  Physical properties

             3.3.1  Colour

                    Colourless

             3.3.2  State/form

                    Liquid-other

             3.3.3  Description

                    Boiling point: 82.5C
    
                    Melting point: 89.5C
    
                    Flash point: 11.7C (closed cup)
                                 17C (open cup)
    
                    Autoignition temperature: 455.6C
    
                    Relative density: 0.785 (Water = 1)
    
                    Vapour pressure: 4399.62 Pa at 20C
                                     7879.33 Pa at 30C
    
                    Solubility: In water in all proportions at 20C
                                In alcohol in all proportions at 20C
                                In ether in all proportions at 20C
    
                    Also soluble in acetone, benzene and chloroform,
                    insoluble in salt solutions.
    
                    Relative molecular mass: 60.09
                    (C: 59.96%; H: 13.42%; O: 26.62%)
    
                    pH: N/A
    
                    Viscosity: 0.00243 Poises (2.43 cP) at 20C
    
                    Odour: Slight odour resembling a mixture of ethanol
                    and acetone.
                    Taste: Slightly bitter taste

        3.4  Hazardous characteristics

             Explosive limits:
             Lower explosive limit: 2.5% (in air)
             Upper explosive limit: 12% (in air)
    
             Dangers associated with the vapour:

    
             Dispersion: inflammable mixture with air.
             Possible ignition: flammable liquid; may autoignite. Vapour
             is heavier than air and will travel along the ground, into
             work pits, etc.
    
             Possible chemical reaction in air: none.
    
             Possible chemical reactions with other chemicals:
    
             Strong oxidizing agents (nitrates, perchlorates, peroxides).
             Phosgene - forms isopropyl chloroformate and
             hydrogenchloride.
             Iron salts - explosive thermal decomposition may occur.
             Hydrogen-palladium-mixture can ignite in air.
             Potassium t-Butoxide
             Trinitromethane (Nitroform) (Cheminfo, 1989).
    
             Electrical and thermal conductivity with possible
             consequences: no data available.
    
             Products of combustion: carbon dioxide and carbon monoxide.
    
             Environmental risks:
    
             Safe disposal - dispose in a designated landfill site, or
             burn in an approved solvent burner.  If small amounts are
             disposed of into a sink or sewer, rinse with copious amounts
             of water to prevent accumulation of flammable vapours. 
             Notify environmental agencies (local health and wildlife
             officials) in the event of any significant release of this
             material into the environment.
    
             Isopropanol is dangerous to aquatic life in high
             concentrations, so prevent entry into water intakes and
             waterways.
    
             Clean up spills - stop the flow if it can be done safely. 
             Contain the spill.  Recover liquid for recycling or disposal
             if feasible.  Otherwise absorb the liquid on clay, sand,
             sawdust or other absorbent material.
    
             Food chain concentration potential: None.
    
             (EPS Canada, 1984).

    4.  USES/HIGH RISK CIRCUMSTANCES OF POISONING

        4.1  Uses

             4.1.1  Uses

                    Antifreeze; 
                    vehicle; 
                    industrial Solvent; 
                    industrial
                    Miscellaneous industrial function

             4.1.2  Description

                    In antifreeze products; solvent for gums,
                    shellac, essential oils, in quick drying oils,
                    creosote and resins: extraction of alkaloids; in quick
                    drying inks; in denaturing ethyl alcohol; in body
                    rubs, hand lotions, after-shave lotions, cosmetics and
                    pharmaceuticals; in manufacture of acetone, glycerol,
                    isopropyl acetate; antiseptic; rubefacient
                    pharmaceutic aid (solvent) (in concentrations up to
                    70%) (Ellenhorn, 1988).

        4.2  High risk circumstances of poisoning

             Accidental ingestion of rubbing alcohols/toiletries by
             children.
    
             Dermal/inhalation exposure in children during isopropyl
             alcohol sponging for control of fever.
    
             Intentional ingestion for alcoholic effect, or in suicide
             attempts.
    
             Occupational or accidental exposure to liquid or its vapour.

        4.3  Occupationally exposed populations

             Process workers in the pharmaceutical industry.
             Process workers in the cosmetic industry.
             Process workers in the chemical industry.
             Process workers in the petroleum industry.
             Analytical and other laboratory workers.
             Printers.
             Painters.
             Carpenters and cabinet makers.

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             Oral ingestion of rubbing alcohols and toilet
             preparations, constitute the most common route of
             exposure.
             Doses of above 20 mL may produce toxic effects.

        5.2  Inhalation

             Inhalation of vapour from preparations.
    
             Inhalation may occur in children being sponged with isopropyl
             alcohol to control fever.
    
             Short-term exposure limit is 500 ppm.  At levels above this,
             respirator or self-contained breathing apparatus is
             necessary.  A level of 12,000 ppm is immediately dangerous to
             health and life.

        5.3  Dermal

             Dermal exposure to the liquid and vapour.
    
             There is little absorption through intact skin, but
             significant delayed absorption over 4 hours postulated
             (Martinez, 1986).
    
             Note risk of inhalation after prolonged skin exposure
             (sponging, etc.).

        5.4  Eye

             Eye exposure to liquid and vapour.
    
             Both the liquid and solvent are severely irritant.

        5.5  Parenteral

             No data available.

        5.6  Others

             No data available.

    6.  KINETICS

        6.1  Absorption by route of exposure

             6.1.1  Oral

                    80% of an oral dose is absorbed within 30
                    minutes. Absorption is complete within 2 hours
                    although this may be delayed in a large overdose
                    (Ellenhorn, 1988).

             6.1.2  Inhalation

                    Alveolar concentration is correlated to the
                    environmental concentration at any given time, and the
                    mean alveolar clearance has been calculated at 8 L/min
                    (Ellenhorn, 1988).

             6.1.3  Dermal contact

                    Absorbed through intact skin on prolonged
                    exposure (Martinez, 1986).

        6.2  Distribution by route of exposure

             Isopropyl alcohol distributes in body water with an
             apparent volume of distribution of 0.6 to 0.7 L/kg. Two hours
             are required for complete tissue distribution (Ellenhorn,
             1986).

        6.3  Biological half-life by route of exposure

             Isopropyl alcohol most closely follows first order
             kinetics, with a half-life of 2.5 to 3.2 hours (Daniel,
             1981).  The elimination half-life of the active metabolite,
             acetone, is significantly prolonged  to about 5 hours in rats
             (Teramoto, 1987) and 22.4 hours in man (Natowicz et al.,
             1985).

        6.4  Metabolism

             20 to 50% of an absorbed dose is excreted unchanged.
             Most isopropyl alcohol is oxidized in the liver by alcohol
             dehydrogenase to acetone, which is probably further
             metabolized to acetate, formate, and finally carbon dioxide. 
             Acetone may contribute to the CNS depression seen in
             isopropanol poisoning.

        6.5  Elimination and excretion by route of exposure

             20 to 50% of an absorbed dose is excreted unchanged (2%
             of dose excreted in exhaled air).
    

             Acetone is slowly eliminated by the lung (40%) or kidney. 
             Clinically insignificant excretion occurs into the stomach
             and saliva (Teramoto, 1987).
    
             Related ketoacids are not produced in sufficient quantities
             to cause a severe metabolic acidosis.

    7.  TOXICOLOGY

        7.1  Mode of action

             Isopropyl alcohol is an irritant to mucous membranes and
             eyes.
    
             Isopropyl alcohol is a potent central nervous system (CNS)
             depressant, and in large doses causes cardiovascular
             depression.  Acetone, its main metabolite, can potentiate and
             lengthen the duration of the CNS symptoms.  Mild acidosis may
             develop from the conversion of acetone to acetic acid and
             formic acid.  The alcohol dehydrogenase-induced shift in
             NAD/NADH may cause decreased gluconeogenesis and
             hypoglycaemia (Addison, 1962).
    
             Inebriation, peripheral vasodilation and hypothermia may also
             occur.
    
             In children, hypoglycaemia is particularly severe when
             poisoning follows fasting, exercise or chronic
             malnutrition.
    
             Lactic acidosis may occur in patients with severe liver
             disease, pancreatitis or receiving biguanide therapy, or as a
             result of the hypovolaemia which frequently accompanies
             severe intoxication.
    
             In rat hepatocytes (Hormann et al., 1989), the following
             sequence has been observed:

             marked depletion of glutathione
             increased malondialdehyde production
             decreased protein sulphydryls content
             leakage of lactic dehydrogenase with loss of membrane
             integrity.

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             Adults:  1 mL/kg of a 70% solution,
                             but as little as 0.5 mL/kg may cause
                             symptoms.
    

                             The lethal dose may be as low as 240 mL (2 to
                             4 mL/kg).  Death has been reported at a blood
                             level of 150 mg/dL (25 mmol/L); however,
                             survival after dialysis has been reported at
                             levels as high as 560 mg/dL.
    
                             Maximal air concentration allowable to
                             prevent irritation of eyes, nose and throat
                             is:
    
                                     440 ppm (USA)
                                     400 ppm long-term (UK)
                                     500 ppm short-term (UK)
                                     200 ppm (Japan).

                    7.2.1.2  Children

                             6 mL/kg (9 mL/kg of 70%) has
                             produced coma with a blood level of 380
                             mg/dL.  The lethal dose is approximately 100
                             mL
    
                             Pediatric patients have survived serum levels
                             from 128 to 520 mg/dL with supportive
                             care.
    
                             (Ellenhorn, 1988; Martinez, 1986).

             7.2.2  Animal data

                    LD50 (rat, oral): 4.42 to 5.84 g/kg
                    LD50 (mouse, oral): 4.8 g/kg
                    LD50 (rabbit, oral): 7.9 g/kg
                    (Lehman, 1944: 6.4 mL/kg)
                    LD50 (rabbit, dermal): 13 g/kg
    
                    Irritant dose (rabbit, skin): 500 mg/24 h (mild)
                    Irritant dose (rabbit, eye): 0.1 mL 70% solution
                    (severe eye irritant)
    
                    Common signs of acute isopropyl alcohol intoxication
                    of animals are hind leg paralysis, unsteadiness, lack
                    of muscular coordination, respiratory depression and
                    stupor (Cheminfo, 1989).

             7.2.3  In-vitro data

                    No data available.

             7.2.4  Workplace standards

                    Threshold Limit Values (TLVs)/American
                    Conference of Governmental Industrial Hygienists 1987
                    to 1988 are:
    

                    Time weighted average:
    
                    TLV-TWA  400 ppm (980 mg/m3)
    
                    Short-term exposure limit:
    
                    TLV-STEL  500 ppm (1225 mg/m3)
                    IDLH Value  20,000 ppm
                    (NIOSH, 1985; ACGIH, 1988)
    
                    OSHA PEL Final Rule Limits (OSHA, 1989):
    
                    PEL-TWA Final Rule Limit:400 ppm (>>980 mg/m3)
                    PEL/STEL Final Rule Limit:500 ppm (>>1225 mg/m3)
                    no ceiling limit
    
                    Odour threshold: 90 mg/m3 (Chris, 1985).
    
                    NIOSH REL: 400 ppm (TWA)
                               800 ppm (ceiling for 15 min) (CDC, 1988).

             7.2.5  Acceptable daily intake (ADI)

                    400 ppm (TWA OSHA).
    
                    Other guideline levels:
    
                    Respiratory Protection Guidelines (NIOSH):
    
                    up to 1,000 ppm: Use a powered air purifying
                    respirator with organic vapour cartridge, or full
                    facepiece chemical cartridge.
    
                    up to 10,000 ppm: (CCROVF) respirator with organic
                    vapour cartridge; use a supplied air respirator
                    operating in continuous flow mode (GMOVc).
    
                    up to 12 000 ppm: use a gas mask with organic vapour
                    canister; or full facepiece self-contained breathing
                    apparatus; or, full facepiece supplied air respirator,
                    (GMOVfb/SAF/SCBAF).
    
                    Escape Respirator: GMOV/SCBA.

        7.3  Carcinogenicity

             Not carcinogenic by animal controls (Cheminfo, 1989).
    
             A waste product, isopropyl oil, has been suspected to cause
             respiratory tract neoplasms after occupational exposure (Weil
             et al., 1952).

        7.4  Teratogenicity

             Decreased fetal weights and increased skeletal
             malformations were noted when pregnant rats were exposed by
             inhalation to concentrations that also caused maternal
             toxicity (Nelson et al., 1988).

        7.5  Mutagenicity

             Not mutagenic in animal models (RTECS, 1989).

        7.6  Interactions

             Isopropyl alcohol potentiates the hepatic and renal
             toxicity produced by halokenes (e.g., carbon tetrachloride)
             (Ellenhorn, 1981).

    8.  TOXICOLOGICAL AND OTHER ANALYSES

        8.1  Sample

             8.1.1  Collection

                    Whole blood, urine, stomach contents.  Collect
                    and store in tightly closed containers and store in a
                    cool place.  Samples should be processed quickly to be
                    of use clinically.  Sample size at least 5 mL.  Glass
                    containers are preferable to plastic.
    
                    Urine samples should be collected hourly.  If the air
                    is to be sampled for vapour concentrations, at least
                    50 mL is required, and this needs to be stored in a
                    tightly closed container.
    
                    For active material, use a sampling pump with
                    appropriate collecting medium: NIOSH Method S 65
                    (NIOSH, 1985).

             8.1.2  Storage

                    Store in a cool place, sample could be
                    inflammable.

             8.1.3  Transport

                    Transport to nearest laboratory as quickly as
                    possible in cool containers.  Material may be
                    inflammable.

        8.2  Toxicological analytical methods

             8.2.1  Test for active ingredient

                    Simple qualitative:
    
                    Acetest tablets can be used in the presumptive
                    diagnosis of isopropyl alcohol ingestion.  These will
                    detect the presence of acetone in the urine, which
                    appears approximately 3 hours after ingestion.  As the
                    level of isopropyl alcohol drops, the level of acetone
                    will initially rise and then decline.
    
                    Recommended quantitative:
    
                    Gas-liquid chromatography or other specific methods
                    (Parker et al., 1962) similar to those used for
                    ethanol detection constitute the methods of
                    choice.
    
                    The GLC should be equipped with flame ionization
                    detection.  Ideally the apparatus should have a
                    capsule sampler and recorder and the results should be
                    processed with calculating integrator.
    
                    Acetone can be assayed using the same apparatus.  The
                    blood sample, 9.5 mL, is placed in an aluminium
                    capsule (3 mm diam. x 6 mm length), and cold welded
                    using a crimping tool. The sealed capsule is inserted
                    into the injection port of the gas chromatograph.  The
                    injector is flushed with carrier gas (e.g., helium 30
                    mL/min), to remove any atmosphere introduced with the
                    probe.  The capsule is held in the heated zone for 60
                    seconds to allow for vapourization of the solvents
                    within the capsule.  The capsule is then pierced and
                    carrier gas takes the volatiles into the hollow needle
                    and then on to the chromatographic columns.  A
                    suitable column is 6' x 1/8" S.S., with 20% Carbowax
                    20 M on Chromosrob W, AW-DCMS, 60/80 mesh.
    
                    The retention times are: isopropanol 2.17 minutes, and
                    acetone: 1.22 minutes.
    
                    Suitable temperatures are: injector: 200C; column:
                    70C; and detector: 200C.
    
                    Typical flow rates are:  carrier gas He = 30 mL/min;
                    hydrogen = 35 mL/min; air = 450 mL/min.
    
                    Calibration curves may be determined using
                    concentrations of 0.005 to 1.5 mg/mL of isopropanol
                    injected into fresh blood samples.
    

                    The concentration of each standard solution can be
                    calculated on a mg/mL basis, using the specific
                    gravity of blood and isopropyl alcohol and acetone.  A
                    calibration graph is plotted by plotting peak height
                    (cm) against isopropyl alcohol and acetone
                    concentrations (mg/mL).  The limit detection is 0.001
                    mg/mL for both solvents (Laham et al., 1979, 1980).

             8.2.2  Test for biological sample

                    No data available.

        8.3  Other laboratory analyses

             8.3.1  Haematological investigations

                    8.3.1.1  Blood

                             Full blood count
                             Blood film.
                             Haematocrit.

                    8.3.1.2  Urine

                             Myoglobinuria (secondary to coma-induced
                             rhabdomyolysis)
                             Red and white blood cells

             8.3.2  Biochemical investigations

                    8.3.2.1  Blood

                             Osmolal Gap:
    
                             Used to estimate blood isopropanol
                             concentration using the following
                             equation:
    
                             Osmolal gap x 6 = predicted isopropyl alcohol
                             level mg/dL
    
                             Osmolal gap = measured osmolality -
                             calculated osmolality
    
                             Anion gap
                             Serum electrolytes
                             Blood urea nitrogen
                             Creatinine
                             Glucose
                             Serum acetone
                             Hepatic transferases

                    8.3.2.2  Urine

                             Glucose
                             Ketone bodies (acetone)

                    8.3.2.3  Other

                             No data available.

             8.3.3  Arterial blood gas analysis

                    Arterial pO2 and pCO2 concentrations.
                    Acid-base balance.

             8.3.4  Other relevant biochemical analyses

                    No data available.

        8.4  Other biomedical (diagnostic) investigations and their
             interpretation

             Isopropyl alcohol values do not correlate with severity
             of poisoning as the metabolite acetone also interferes with
             symptomatology.
    
             High serum ketones with minimal acidosis are common in
             isopropyl alcohol ingestion.
    
             Osmolal Gap: A rise in blood isopropyl alcohol of 2 mg/dL
             produces a change of 0.17 mosm/kg H2O in the osmolal gap. 
             A 50 mg/dL toxic blood level produces an 8 to 9 mosm increase
             in the osmolal gap, and seriously toxic levels of 200 mg/dL
             produce a 34 mosm change in osmolal gap. Acetone levels must
             also be considered as they produce similar changes.

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             Sample collection
    
             Isopropanol serum levels are clinically useful and
             significant.  Collect in glass where possible, keep cool and
             tightly closed, until analysed.  During treatment,
             measurement of isoprpyl alcohol in hourly urine samples is
             clinically useful.
    
             Retention of samples of gastric lavage if performed, and
             obtaining samples of product ingested, may be useful if
             diagnostic confirmation is desired.
    
             Biomedical analysis
             Routine blood and urine analysis should be performed, with
             special emphasis on:
    
             Blood glucose (for hypoglycaemia).
    
             Osmolal gap by freezing point depression (for predicted
             isopropanol levels).
    
             Arterial blood gas analysis (for assessment metabolic
             acidosis).
    
             Serum acetone (serum ketone bodies).
    
             Urinary acetone (for presumptive diagnosis with Acetest
             tablets).
    
             Monitoring of fluids and electrolytes.  (Acid-base balance
             for normoglycaemic ketoacidosis).
    
             Hepatic function tests (for hepatic aminotransferases).
    
             Toxicological analysis
             Plasma levels of isopropanol are indicative of the level of
             poisoning.  The time of ingestion is critical in determining
             treatment options.
    
             Other investigations
             Respiratory function tests to gauge the degree of respiratory
             depression may be useful in selected, severe poisonings.
    
             Blood pressure (for hypotension).
    
             Temperature (for hypothermia).

        8.6  References

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    This is the common route of poisoning. 
                    Absorption (80%) occurs within 30 minutes, and is
                    complete within 2 hours.  Symptoms are drowsiness,
                    gastrointestinal pain, cramps, nausea, vomiting and
                    diarrhoea, with unconsciousness and death following
                    massive exposure.  In children, more than three
                    swallows of 70% isopropyl alcohol results in symptoms
                    requiring medical observation.
    

                    Isopropyl alcohol intoxication has a rapid onset of
                    action (30 to 60 minutess) with peak effects occurring
                    within several hours.  Severe poisoning presents early
                    with stupor leading to deep coma, respiratory
                    depression and hypotension.  Other symptoms are
                    dizziness, poor coordination, headache, confusion,
                    gastric irritation, abdominal pain, vomiting,
                    haematemesis, hypotension, tachycardia, (and
                    cardiodepression) and loss of deep tendon
                    reflexes.

             9.1.2  Inhalation

                    Common route of poisoning. Mild irritation of
                    the respiratory tract occurs at 400 ppm.  High
                    concentrations can cause nausea, headache,
                    lightheadedness, drowsiness, ataxia and deep
                    narcosis.

             9.1.3  Skin exposure

                    Brief exposures are not irritating, but
                    prolonged contact (4 hours) has led to toxicity with
                    central nervous system (CNS) effects (Martinez, 1986). 
                    Sponging children with isopropyl alcohol for fever
                    control may result in significant absorption.

             9.1.4  Eye contact

                    Vapour is mildly irritating at 400 ppm.  Direct
                    eye contact with the liquid can cause severe
                    irritation (Cheminfo, 1989) and even corneal abrasion
                    (Osborn and Rosales, 1981).

             9.1.5  Parenteral exposure

                    No data available.

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    No significant changes were found in the
                    chemical or cellular composition of the blood or urine
                    after humans ingestion of 6.4 mg/kg of isopropyl alcohol
                    on a daily basis for 6 weeks (Cheminfo, 1989).

                    No long-term health effects have been reported in
                    humans.  Rapid metabolism in the body precludes
                    accumulation.

             9.2.2  Inhalation

                    An excess of sinus cancers and laryngeal
                    cancers has been found among workers producing
                    isopropyl alcohol.  This could be due to the by
                    product, isopropyl oil.

             9.2.3  Skin exposure

                    Chronic toxic exposure may lead to coma and
                    death (Broughton, 1944).
    
                    Drying, cracking and eczema may result from repeated
                    or prolonged skin contact.

             9.2.4  Eye contact

                    Oxygen uptake of corneal epithelium is reduced
                    in the rabbit (Roseman, 1987).

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             Central nervous system depression often lasts for 24
             hours.  The development of hypotension is a poor prognostic
             feature.  Haemodialysis should be used in severely poisoned
             patients to remove the isopropyl alcohol, and to shorten the
             duration of coma, together with other supportive
             measures.
    
             Death results from central nervous system (CNS) and
             respiratory depression during coma.

        9.4  Description of clinical effects by system

             9.4.1  Cardiovascular

                    Hypotension from peripheral dilatation
                    Tachycardia
                    Serious arrhythmias have not been reported.
                    (Ellenhorn, 1988).

             9.4.2  Respiratory

                    Respiratory depression and death.
                    Acetone can be detected on the breath.
                    (Teramoto, 1987; Buckley, 1986).

             9.4.3  Neurologic

                    9.4.3.1  Central Nervous system (CNS)

                             Dizziness, poor coordination,
                             headache, confusion, progressing to stupor,
                             coma and loss of deep tendon reflexes. 
                             Serious nervous system depression often lasts
                             for 24 hours.  Elation does not
                             occur.

                    9.4.3.2  Peripheral nervous system

                             No data available.

                    9.4.3.3  Autonomic nervous system

                             Pupils are often miotic, and
                             nystagmus is normally present.

                    9.4.3.4  Skeletal and smooth muscle

                             Deep tendon reflexes are not present
                             during coma.

             9.4.4  Gastrointestinal

                    Gastric irritation appears early, abdominal
                    pain and vomiting are prominent, and haematemesis may
                    occur (Buckley, 1986).

             9.4.5  Hepatic

                    Hepatic dysfunction has been reported (Kulig,
                    1984).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             Acute tubular necrosis and
                             myoglobinuria have been reported (Buckley,
                             1986).

                    9.4.6.2  Others

                             No data available.

             9.4.7  Endocrine and reproductive systems

                    No data available.

             9.4.8  Dermatologic

                    Dryness, irritation, allergic eczema, with
                    repeated or chronic direct contact.

             9.4.9  Eye, ear, nose, throat: local effects

                    Eye: vapour causes irritation, liquid may cause
                    intense irritation including corneal abrasion.

             9.4.10 Haematological

                    Myoglobinuria and haemolytic anaemia have been
                    reported.

             9.4.11 Immunologic

                    No data available.

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             Mild metabolic acidosis may develop
                             from the conversion of acetone to acetic and
                             formic acid.

                    9.4.12.2 Fluid and electrolyte disturbances

                             Abnormalities of serum in
                             electrolytes, blood urea nitrogen,
                             creatinine, may be noted.

                    9.4.12.3 Others

                             Hypoglycaemia, and hypothermia from
                             peripheral vasodilation.
    
                             Osmolal gap may be clinically significant in
                             suspecting the diagnosis.
    
                             Elevations of hepatic aminotransferases may
                             occur.

             9.4.13 Allergic reactions

                    Allergic eczema has been reported.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risks: pregnancy, breast feeding, enzyme
                    deficiencies.

                    No data available.

        9.5  Others

             No data available.

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             If a small quantity of isopropyl alcohol has been
             recently ingested, i.e., within 30 minutes, then emesis with
             syrup of ipecac may be used.  It should not be used with
             ingestion of large quantities, or in the presence of central
             nervous system (CNS) depression.
    
             Gastric lavage is the treatment of choice for the removal of
             large volumes of isopropyl alcohol from the stomach.  In the
             case of skin contamination, wash the skin thoroughly with
             soap and water.  If irritation and pain persist seek medical
             advice.
    
             Exposed eyes should be irrigated with copious amounts of room
             temperature water for at least 15 minutes.  If irritation,
             pain, swelling, lachrymation persist after 15 minutes of
             irrigation, seek ophthalmological advice.

        10.2 Life supportive procedures and symptomatic treatment

             Support respiratory function.
    
             Support cardiovascular function.
    
             Treat hypotension with intravenous (IV) fluids and place in
             the Trendelburg position.  If the patient is unresponsive,
             correct dehydration and acidosis with fluids and electrolytes
             and administer dopamine.
    
             Add 200 to 400 mg dopamine to 250 mL sodium chloride 0.9%
             (normal saline, NS) or glucose 5% injection, (Dextrose, D5W),
             to produce 800 or 1600 mg/mL. Alternatively, add 400 mg to
             500 mL of NS or D5W to produce 800 mg/mL.  Begin infusion at

             2 to 5 mg/kg/min, progressing in 5 to 10 mg/kg/min increments
             as needed.  If ventricular arrhythmias occur decrease the
             rate of administration.
    
             Support neurological function.

        10.3 Decontamination

             Measures to eliminate isopropanol from the
             gastrointestinal tract must usually be initiated within 2
             hours of ingestion and, preferably within 30 min, due to its
             rapid absorption.
    
             Due to the onset of CNS depression (which usually occurs
             within 30 minutes of ingestion), ipecac-induced emesis is not
             recommended.
    
             Gastric lavage may be indicated if performed soon after
             ingestion.  If coma or convulsions occur, protect the airway
             by cuffed endotracheal intubation. Use a large bore
             orogastric tube:
    
             Adult: 36 to 42 French
             Child: 24 to 28 French.
    
             Repeat as necessary. Lavage should return approximately the
             same volume of fluid as has been given.
    
             Lukewarm tap water or normal saline is recommended, at a rate
             of 150 to 200 mL per wash (in children over 5 and adults) and
             50 to 100 mL per wash in young children.
    
             Continue until the lavage return is clear.
    
             Activated charcoal
    
             Administer charcoal as a slurry in water at a dilution of
             30 g charcoal to 240 mL aqueous diluent. The diluent may also
             be a saline cathartic or sorbitol.  Usual doses are 30 to
             100 g of charcoal in adults (15 to 30 g in children, and 1 to
             2 g/kg in infants).
    
             Note:  Activated charcoal has limited absorptive properties
             for isopropanol (1 g absorbs approximately 500 mg of
             isopropanol), and the optimum dose of charcoal has not been
             established.
    
             Cathartics
    
             Administer one dose of a saline cathartic or sorbitol mixed
             with the charcoal or preferably administered separately.
    

             Note:  The safety of more than one dose of a cathartic has
             not been established.
    
             Hypermagnesaemia has been reported after repeated
             administration of magnesium-containing cathartics in patients
             with normal renal function.  Repeated cathartic dosing should
             be done with extreme caution if at all; admiistration of
             cathartics should be stopped when a charcoal-coloured stool
             appears.
    
             Cathartics should not be used in patients with ileus and
             saline cathartics should not be used in patients with
             impaired renal function.  Magnesium sulphate or sodium
             sulphate are suitable cathartics and the usual dose is 20 to
             30 g in adults and 250 mg/kg in children over 2 years. 
             Magnesium citrate oral solution  USP may also be used in a
             dose for both adults and children of 4 mL/kg/dose up to 200
             to 300 mL/dose.
    
             Catharsis may be effective 12 to 24 h after ingestion.
    
             Sorbitol:
    
             Adult: The usual dose for sorbitol will vary but is in the
             order of 1 to 2 g/kg/dose to a maximum of 150 g.
    
             Children: Over 1 year old, 1 to 1.5 g/kg/dose to a maximum of
             150 g/dose.  It is administered under direct medical
             supervision monitoring fluid and electrolyte status.  It
             should be given as a 35% aqueous solution.
    
             Skin decontamination: Wash the skin thoroughly with soap and
             water.  Seek medical advice if pain or irritation
             persist.
    
             Eyes: Irrigate with copious amounts of tepid water
             (preferably isotone saline solution) for at least 15 minutes. 
             Seek specialist medical advice if pain, irritation, swelling,
             lachrymation or photophobia persist.

        10.4 Enhanced Elimination

             Forced diuresis is not effective and should not be
             used.
    
             Haemodialysis:
    
             Haemodialysis is useful in patients with severe life-
             threatening symptoms unresponsive to standard treatment
             therapy.
    
             Note:  Using haemodialysis, the metabolism of isopropanol to
             acetone is rapid and should be monitored carefully.
    

             Peritoneal dialysis:
    
             This appears to be only minimally effective, and should only
             be used in selected severe cases of poisoning where
             haemodialysis is not possible.

        10.5 Antidote treatment

             10.5.1 Adults

                    There is no specific antidote.

             10.5.2 Children

                    There is no specific antidote.

        10.6 Management discussion

             Haemodialysis is used on the basis that it removes
             isopropanol and shortens the duration of coma.  Removal of
             isopropanol alcohol is 52 times, and of acetone 40 times,
             more efficient through haemodialysis than through urinary
             excretion (Rosansky, 1982).
    
             Peritoneal dialysis is considerably less effective. No
             advantage is to be gained by infusing ethanol to block
             alcohol dehydrogenase, as the toxicity of isopropanol is
             principally due to the parent compound.
    
             Isopropanol is oxidized in the liver to acetone and treatment
             options are limited to the symptomatic and supportive
             measures.

    11. ILLUSTRATIVE CASES

        11.1 Case reports from the literature

             A 2-year-old boy weighing 21 kg reportedly ingested a
             small amount of 70% isopropyl alcohol rubbing alcohol.  There
             were no symptoms and emesis with dilute dishwashing liquid
             was tried.  The child refused this and was referred to the
             nearest hospital.  On arrival, 30 minutes after ingestion,
             the child was in an unresponsive condition with laboured
             respiration.  No emesis had occurred.  The child was started
             on intravenous (IV) fluids, intubated, lavaged, and then
             transferred to a children's hospital.  It was found that the
             child had been sponged with isopropanol for several hours in
             an attempt to reduce fever.  Three-and-a-half hours after
             ingestion, the child was still unconscious and was
             transferred to the intensive care unit (ICU) with artificial
             ventilation and haemodialysis.  Approximately 16 hours after

             ingestion and following treatment the child was alert and
             responsive.  Intravenous (IV) fluids were discontinued and
             the child made an uneventful recovery (Martinez, 1986).
    
             A 38-year-old woman with Type I diabetes mellitus complained
             of discomfort after applanation tonometry of the right eye. 
             The tonometer tip had been swabbed with a 70% isopropyl
             alcohol wipe immediately before use.  On examination of the
             right eye, a circular area of corneal epithelial
             opacification corresponding to the size of the tonometer tip
             was noted.  This area stained faintly with fluorescein but
             stained strongly with Rose Bengal.  A patch was placed on the
             eye for 2 h and then removed, the patient seemed comfortable. 
             But 2 to 3 h later she noted significant discomfort that
             persisted for 16 hours.  The discomfort resolved by the next
             day.  A second patient showed lesser symptoms that resolved
             after 24 hours (Soukiasian, 1988).
    
             An 18-month-old child was wrapped in towels soaked with
             rubbing alcohol, by her mother, in an attempt to control a
             40C fever due to otitis media.  The towels were wrapped
             about the child's waist for periods up to 4 hours.  The child
             became progressively lethargic and unresponsive to verbal and
             tactile stimulation.  She was admitted to the ICU unit
             unconscious and unresponsive to pain, with midline fixed
             miotic pupils, a temperature of 35.8C, a pulse of 153
             beats/min, and blood pressure of 100/50 mm Hg.  Nasogastric
             aspiration yielded strongly haem-positive "coffee-ground"
             material.  Laboratory studies were performed, including
             arterial blood gases, electrolytes, CSF and urinalysis.  Her
             osmolal gap was calculated at 70 mOsm/kg (70 mmol/kg).  She
             was diagnosed as having mild metabolic acidosis and this
             coupled with an anion gap of 20 mmol/L (20 mEq/L) and a
             significant elevation in the osmolality gap, suggested the
             possibility of acute intoxication with an osmotically active
             substance of low molecular weight.
    
             Toxicological studies performed 8 to 10 hours after ingestion
             showed a serum level of isopropanol of 162 mg/dl (27 mmol/L),
             (measured by gas chromatography). The serum acetone level was
             180 mg/dL (31 mmol/L).  The child received supportive care,
             including airway management and intravenous hydration.  She
             improved over the next 12 to 24 h and was extubated and
             discharged to a paediatric ward 36 hours after admission to
             the ICU.  She was discharged home on the 7th day with no
             evidence of neurologic or other sequelae.  The child
             continued to do well 3 months after the event (Arditi,
             1987).
    
             A similar case was reported by Webster et al. (1985) of a
             9-month-old girl. Osmolality and anion gap was seen as being
             diagnostic of isopropanol poisoning.  Treatment consisted of

             mechanical ventilation and parenteral fluids.  She was
             discharged from hospital 3 days after admission, with no
             evidence of neurologic or other sequelae.
    
             A 55-year-old woman was found unconscious and unresponsive in
             her home.  There was no palpable pulse, HR 140 beats/min, RR
             6 breaths/min.  She was intubated, ventilated, but no venous
             access could be obtained.  The patient had been bathed with
             approximately 1 litre of 70% isopropanol by her daughter. 
             Four hours after admission, an isopropanol level of 98 mg/dL
             (165 mmol/L) and an acetone level of 43 mg/dL (7 mmol/L) were
             obtained. The patient had massive skin lesions and it was
             believed that absorption through the skin had occurred
             (McGrath, 1989).
    
             A 61-year-old patient was found unconscious and unresponsive
             after ingesting 1480 mL of 70% isopropyl alcohol.  He was
             admitted to ICU 4 hours later and was immediately intubated
             and started on fluid replacement with a dopamine drip for
             hypotension.  On examination, the patient was completely
             unresponsive; pulse was 60;  BP was 80/60, and pinpoint
             pupils, acetone odour on breath, bradycardia and no response
             to painful stimuli were noted.  The following laboratory
             tests were performed: blood gases; electrolytes; BUN; serum
             creatinine; ketone bodies and glucose. Haemodialysis with
             minimal ultrafiltration was instituted 9 hours after
             ingestion, and within 1 hour the patient had spontaneous
             movements and started assisting ventilation.  By 2 hours, the
             patient responded to verbal commands.  The paper concludes
             that haemodialysis is a life-saving procedure in this case,
             removing approximately 27 g/hour of alcohol (50 times greater
             than the amount eliminated by urinary excretion) (Rosansky,
             1982).
    
             A 4-year-old mentally retarded girl was found unconscious in
             her bed by her mother, 27 hours after she had been
             intentionally scalded.  The mother subsequently applied gauze
             soaked with isopropanol to the scald burns.  The child was
             then left alone in her room without food or water until she
             was discovered dead.  The paper suggests that a contributory
             cause of death was isopropanol intoxication, resulting from
             application of this chemical to burns (Russo, 1986).
    
             A review of acute isopropyl alcohol poisoning (Lacouture et
             al., 1983), provides an overview of acute poisoning with
             special emphasis on clinical management.  Two case reports
             were presented.
    
             A 42-year-old woman was admitted to hospital in an
             unresponsive and unconscious condition.  Initial treatment
             consisted of endotracheal intubation, respiratory support,
             administration of intravenous (IV) fluids, and gastric
             lavage.  There was no response to naloxone or glucose.  She

             was given 4 litres of lactated Ringers solution prior to her
             transfer to ICU.  Her depth of coma decreased and 12 hours
             after admission she was alert and awake and able to breathe
             on her own.
    
             A 32-year-old man was admitted to hospital unconscious (Grade
             III to IV coma).  He was areflexic and unresponsive to deep
             pain.  There was no response to naloxone, thiamine or
             glucose.  Laboratory tests included isopropyl alcohol levels,
             serum electrolytes, BUN, and blood gases.  During intubation,
             the patient suffered a cardiac arrest.  He was resuscitated. 
             However, an arryhthmia refractory to standard therapy
             necessitated insertion of a transvenous pacemaker.  He was
             also started on a dopamine drip and was prepared for
             haemodialysis.  Twenty-four hours after admission he awoke
             and was orientated and co-operative.
    
             The authors suggest that haemodialysis should be considered
             in patients with hypotension and those with serum isopropyl
             alcohol concentrations exceeding 400 to 500 mg/dL (66 to 83
             mmol/L).  They also conclude that the management of acute
             isopropanol intoxication may involve supportive care only, or
             may include haemodialysis.
    
             A 23-month-old boy was admitted to hospital comatose and
             unresponsive to deep stimuli.  He was intubated. His pulse
             became unperceptible, and cardiac compression was initiated,
             together with controlled ventilation with 100% oxygen and 20
             mmol of sodium bicarbonate by slow intravenous (IV) infusion
             through a scalp vein.  Nonadrenaline was required to correct
             and maintain the BP within normal limits.  It was
             subsequently discovered that he had ingested approximately
             200 mL of isopropanol.  He was comatose for 2 days and then
             slowly recovered (Light, 1969).
    
             A further case reported by Visudhiphan (1971), concerned a
             2-year-old boy suffering from isopropanol intoxication.,  His
             blood pressure was maintained with metaraminol tartrate and
             levaterenol bitartrate.  His respiration was assisted with a
             positive pressure respirator.  He gradually improved over 2
             days and made an uneventful recovery.
    
             A comatose 46-year-old woman was admitted to hospital with
             isopropanol and acetone levels of 2,000 mg/L and 120 mg/L
             respectively.  Pharmacokinetic analysis showed that both
             isopropanol and acetone obeyed apparent first order kinetics
             with half-lives of 6.4 and 22.4 hours respectively, with
             similar values in cerebrospinal fluid. Two days after
             admission the patient was alert and responsive.  She was
             subsequently discharged.
    

             A 59-year-old man was admitted in a coma to hospital after
             ingesting 1 litre of isopropyl alcohol. Laboratory data were
             normal except for proteinuria and ketonuria.  His condition
             deteriorated rapidly, with development of hypotension and
             respiratory depression.  Pupils were miotic and all deep
             reflexes were absent.  Extra corporeal haemodialysis was
             instituted;  within 1 hour he was responding weakly to
             painful stimuli.  After 3 hour of dialysis the patient was
             very active, and so the procedure was terminated (Freireich,
             1967).
    
             An 850 g girl of 25 weeks gestation was intubated at birth
             and placed in a ventilator.  During surgical preparation for
             umbilical artery catheterization, isopropyl alcohol was
             poured over the umbilical stump.  After the procedure was
             completed it was noted that there were two areas of erythema
             bilaterally on the flank, each approximately 2 x 5 cm.  These
             progressed to areas of second- and third-degree burns.  The
             burns were treated with an antibiotic ointment and a steroid
             cream, and continued to heal over a period of 3 months
             (Schick, 1981; Martindale, 1989).
    
             Similar cases were reported by Weintraub (1982), giving
             details of skin burns in premature infants.  The isopropyl
             alcohol had been used either for conduction on ECG or for
             arterial catheterization.  The 4 premature infants reported
             were all less than 26 weeks gestational age and their birth
             weight was less than 750 g;  they had suffered severe
             perinatal asphyxia, hypothermia and acidosis, and they all
             developed severe respiratory distress insufficiency and died
             within 48 hours despite mechanical ventilation and other
             supportive measures.  It is recommended that the skin be
             dried after application of isopropyl alcohol.
    
             A 45-year-old white man was comatose on admission to hospital
             after apparently falling from a stepladder.  He was intubated
             and placed on a respirator.  He was found to have an osmolal
             gap of 304 mOsm/kg.  Serum ethanol concentration was
             determined by enzymatic alcohol dehydrogenase giving a
             concentration of 1.86 g/L.  The osmolal gap indicated that
             there was another alcohol present, and that the enzymatic
             alcohol determination was in error because of its lack of
             specificity.  A gas chromatographic analysis showed the
             presence of ethanol, acetone and isopropanol.  The authors
             warn of the danger of using an enzymatic procedure for
             ethanol, because the method is not specific for ethanol.  The
             patient recovered and was discharged 2 days later.
    
             A 28-year-old man ingested 1 litre of rubbing alcohol over a
             10 minute period, and was admitted to hospital 45 minutes
             later.  He was comatose and unresponsive.  A tracheostomy was
             performed and therapy with intravenous fluids was initiated. 
             He made little progress and so, 16 hours after admission,

             haemodialysis was started.  After 2 hours he was agitated,
             alert and responsible, and haemodialysis was discontinued
             (King, 1970).
    
             Junco (1969), reported a case of a 35-year-old man who had
             ingested 1 pint of rubbing alcohol.  The patient was
             inebriated confused and tremulous.  His right arm was
             swollen, erythematous, tender and painful on motion. This
             swelling progressed, and by the 3rd day the entire limb was
             swollen.  A phlebogram demonstrated blockage of the axillary
             vein.  He received therapy over the next 25 days, being
             treated for renal failure and thrombosis.  The patient was
             given phenytoin, supportive fluids, electrolytes, vitamins
             and whole blood.  The outcome is unknown.

    12.ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             Respiratory protection:
    
             Use self-contained breathing apparatus (in fire).
             Respirator selection: see 7.2.5.1
             Gloves: rubber or plastic.
             Protective clothing: suitable to prevent repeated or
             prolonged skin contact, e.g., coveralls, etc.
             Eyes: wear suitable eye protection.
             Boots: rubber.
    
             Note:  remove clothing immediately if wet or contaminated to
             avoid flammability hazard.

        12.2 Other

             No data available.

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        Alexander CB, McBay AJ, Hudson RP (1982).  Isopropanol and
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        Antonova VI, Salmina ZA (1978).  The maximum permissable
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        Arditi M et al (1987).  Coma following the use of rubbing alcohol
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        Cahaplin MA (1949).  Isopropyl alcohol poisoning with acute renal
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        Chris (1985).  Hazardous chemical data  US Department of
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    14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)

        Authors:  Dr Peter Hayes
        Lecturer in Pharmaceutical
        Technology/Manager Production Services
        Department of Pharmacy
        Faculty of Medicine
        University of Otago
        PO Box 913
        Dunedin
        New Zealand
    
        Tel: 64-3-797272/740999 Ext 8347
        Fax: 64-3-797618
    
        Trudi P Martin, MPS
        Senior Pharmacist
        Pharmacy Production Unit
        Dunedin Hospital
        Private Bag
        201 Gt King Street
        Dunedin
        New Zealand
    
        Tel: 64-3-740999 Ext 8347
        Fax: 64-3-797618
    

        Date: February 1990
    
        Reviewer: Dr Per Kulling
        Swedish Poison Information Centre
        Karolinska Hospital
        Box 60500
        10401 Stockholm
        Sweden
    
        Tel: 46-8-338765
        Fax: 46-8-327584
    
        Date: March 1990
    
        Peer Review: Strasbourg, France, April 1990
    
        Editor: Dr M. Ruse (October, 1997)
    


    See Also:
       Toxicological Abbreviations
       Isopropyl alcohol (ICSC)
       ISOPROPYL ALCOHOL (JECFA Evaluation)