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Sodium metasilicate

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 Brand names, 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/CIRCUMSTANCES OF POISONING
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance 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
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination 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 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI) and other guideline levels.
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood gas analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple Qualitative Test(s)
         8.2.1.2 Advanced Qualitative Confirmation Test(s)
         8.2.1.3 Simple Quantitative Method(s)
         8.2.1.4 Advanced Quantitative Method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple Qualitative Test(s)
         8.2.2.2 Advanced Qualitative Confirmation Test(s)
         8.2.2.3 Simple Quantitative Method(s)
         8.2.2.4 Advanced Quantitative Method(s)
         8.2.2.5 Other Dedicated Method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
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 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         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 & reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbances
         9.4.12.2 Fluid & electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures
   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 literature
12. ADDITIONAL INFORMATION
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S),ETC.
    SODIUM METASILICATE

    International Programme on Chemical Safety
    Poisons Information Monograph 500
    Chemical

    1.  NAME

        1.1  Substance

             Sodium Metasilicate

        1.2  Group

             Silicon oxide, sodium compound

        1.3  Synonyms

             Disodium Metasilicate; Sodium Silicate;
             Sodium Metasilicate, 9-hydrate;
             Sodium Metasilicate, anhydrous Soluble Glass;
             Waterglass

        1.4  Identification numbers

             1.4.1  CAS number

                    6834-92-0 (anhydrous)

             1.4.2  Other numbers

                    10213-79-3 (pentahydrate)
                    13517-24-3 (nonahydrate)

                    RTECS Number VV9275000  (sodium metasilicate)
                    (IPCS/CEC,1993).

        1.5  Brand names, Trade names

             To be completed by each Centre using the monograph.

        1.6  Manufacturers, Importers

             To be completed by each Centre using the monograph.

    2.  SUMMARY

        2.1  Main risks and target organs

             Sodium metasilicate is strongly irritating to the skin,
             eyes and respiratory tract. Acute exposures involving the
             inhalation of dusts may  result in irritation of the
             respiratory tract and corrosive damage may result from

             contact with mucous membranes. Prolonged exposures can lead
             to inflammatory changes and ulcerative problems in the mouth.
             Possible bronchial and gastrointestinal problems can occur,
             depending upon concentration and duration of exposure.

        2.2  Summary of clinical effects

             Initial clinical manifestations of acute ingestion can
             include dysphagia, drooling, pain and haematemesis. Oral,
             oesophageal, and gastric burns may be present. Extensive
             mucosal damage leads to fever, tachypnoea, tachycardia,
             hypertension, and shock. Acute complications include
             aspiration pneumonia, burns of the epiglottis and vocal
             cords, and laryngeal obstruction. Acute perforation of the
             oesophagus or stomach with mediastinal or peritoneal abscess,
             sepsis, and death may occur. Possible longterm sequelae of 
             acute exposure include oesophageal stricture, squamous cell
             oesophageal cancer, vocal cord paralysis, and pyloric
             stenosis.

        2.3  Diagnosis

             Diagnosis is based on a history of exposure to this
             corrosive agent and characteristic findings of skin, eye, or
             mucosal irritation or redness and the presence of injury to
             the gastrointestinal tract. Victims with oral or oesophageal
             injury nearly always have drooling or pain on swallowing.

        2.4  First-aid measures and management principles

             Inhalation: Remove from exposure; give supplemental
             oxygen if required. Skin and eyes: Remove all affected
             clothing and wash skin and irrigate eyes with copious water
             or saline.
    
             Ingestion: Immediately give water or milk to drink if the
             patient is able to swallow. The volume administered should
             not be so excessive as to cause gastric distension and induce
             vomiting. Do not induce emesis or give pH-neutralising
             solutions such as dilute vinegar or bicarbonate.  If
             oesophageal or gastric perforation is suspected, obtain
             immediate surgical or endoscopic consultation.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Fusing silica (sand) with sodium carbonate at 1400C
             produces sodium metasilicate. The various hydrates of sodium
             metasilicate, range from the anhydrous to the nonahydrate,
             with the anhydrous and the penta- and nonahydrates being the
             most common forms (Clayton & Clayton, 1993).

        3.2  Chemical structure

             Chemical formula: Na2SiO3.nH2O
    
             Relative molecular mass 122.07 anhydrous
                                     212.15 pentahydrate
                                     284.21 nonahydrate
             (Clayton & Clayton, 1993).

        3.3  Physical properties

             3.3.1  Colour

                    Colourless to white or grayish white

             3.3.2  State/Form

                    Solid-crystals

             3.3.3  Description

                    The anhydrous and the pentahydrate are produced
                    as amorphous beads, whereas the nonahydrate appears as
                    efflorescent sticky crystals.
    
                    Melting point 1089C anhydrous
                                  72C   pentahydrate
                                  47.8C nonahydrate (Clayton & Clayton,
                                  1993).
    
                    pH of a 1% aqueous solution is about 13  (Clayton &
                    Clayton, 1993).
    
                    Solubility: The metasilicates are highly water soluble 
                    (Clayton & Clayton, 1993).
                    Insoluble in alcohol, acid and salt solutions 
                    (Budavari, 1989).
    
                    Flammability: Not combustible  (IPCS/CEC, 1993).
    
                    Stability: Solutions of sodium metasilicate, when
                    heated or acidified, are hydrolysed to free sodium
                    ions and silicic acid (Clayton & Clayton, 1993).

        3.4  Hazardous characteristics

             Corrosiveness:  In moist air it is corrosive to metals
             like zinc, aluminium, tin and lead, forming hydrogen gas
             (IPCS/CEC, 1993).
    
             Reactivity: The substance is a strong base, it reacts
             violently with acid (IPCS/CEC, 1993).

    4.  USES/CIRCUMSTANCES OF POISONING

        4.1  Uses

             4.1.1  Uses

                    Soap; detergent; bath/washing product

             4.1.2  Description

                    A major use is as a builder (a material that
                    enhances or maintains the cleaning efficiency of the
                    surfactant, principally by inactivating water
                    hardness) in soaps and detergents. It is also used
                    extensively as an anti-corrosion agent in boiler-water
                    feed  (Clayton & Clayton, 1993).

        4.2  High risk circumstance of poisoning

             Unintentional ingestion by children of a dishwashing
             detergent directly from the container or of the residue from
             an automatic dishwasher soap compartment. Intentional
             ingestion.

        4.3  Occupationally exposed populations

             Factory workers involved in formulation and packaging of
             sodium metasilicate or metasilicate containing products.

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             Ingestion of this chemical is the most common route of
             entry with subsequent corrosive injury of the
             gastrointestinal tract being the major concern rather than
             systemic absorption as for other toxins.

        5.2  Inhalation

             Inhalation of dusts of sodium metasilicate may result in
             irritation of the respiratory tract and corrosive damage may
             result from contact with mucous membranes.

        5.3  Dermal

             Skin exposure to corrosive agents usually results in
             immediate pain and redness. Serious full thickness burns can
             occur.

        5.4  Eye

             Eye exposure to corrosive agents commonly results in
             conjunctivitis and lachrymation. Blindness can occur.

        5.5  Parenteral

             No data available.

        5.6  Others

             No data available.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Radio-labelled 31Si sodium metasilicate, partially
             neutralized, was given orally to dogs. It was rapidly
             absorbed and excreted in the urine but a significant amount
             was retained in the tissues (Clayton & Clayton, 1993).

        6.2  Distribution by route of exposure

             Radio-labeled 31Si sodium metasilicate, partially
             neutralized, was given orally to dogs. It was rapidly
             absorbed. A significant amount was retained in the tissues.
             These findings are consistent with the recognition that
             silicon is an essential trace element for bone formation in
             animals (Clayton & Clayton, 1993).

        6.3  Biological half-life by route of exposure

             No data available

        6.4  Metabolism

             No data available

        6.5  Elimination by route of exposure

             Radio-labelled 31Si sodium metasilicate, partially
             neutralized, was given orally to dogs. It was rapidly
             excreted in the urine (Clayton & Clayton, 1993).

    7.  TOXICOLOGY

        7.1  Mode of Action

             Sodium metasilicate is markedly corrosive and
             penetrating. Solubilizing reactions occur with protein and
             collagen, saponifying effects on lipids and dehydration of
             tissues and cells. (Houck et al., 1962). Sodium metasilicate
             is highly corrosive due to its buffer capacity, which means
             that the high pH is well sustained in the presence of tissue
             components that quickly neutralize other alkalis such as
             sodium hydroxide (Gosselin et al., 1984).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             There is no specific toxic oral
                             dose, because the concentration of corrosive
                             solutions and the potency of caustic effect
                             vary widely. The concentration or the pH of
                             the solution may indicate the potential for
                             serious injury. The titratable alkalinity is
                             a better predictor of corrosive effect than
                             the pH (Olson, 1994). Application to human
                             skin (250mg sodium metasilicate for 24 hours)
                             caused a severe reaction (RTECS, 1996).

                    7.2.1.2  Children

                             No data available

             7.2.2  Relevant animal data

                    Acute oral toxicity LD50 to rats is 1280 mg/kg
                    as a 10% aqueous solution.  (Clayton & Clayton, 1993).
                    Acute oral toxicity LD50 to mice is 2400 mg/kg as a
                    10% aqueous solution. (Clayton & Clayton, 1993). Skin
                    Irritation (rabbit): Application of  0.5 mL of 10%
                    sodium metasilicate for 4 hours caused mild irritation
                    (primary irritation score: erythema 1.11/4; oedema
                    0.11/4)  (ECETOC, 1995). Dogs were fed sodium silicate
                    in their diet at a dose of 2.4 g/kg per day for 4
                    weeks. Polydipsia and polyuria were observed in some
                    animals. Damage to renal tubules was observed in 15/16
                    dogs. (Clayton & Clayton, 1993). A study of detergent
                    emesis in 11 dogs by gastric intubation, found that 8
                    mg/kg as a 10.5% aqueous solution of a sodium silicate
                    (SiO2:Na2O, 3.2:1) produced emesis in 6 minutes which
                    continued for up to 33 minutes. (Clayton & Clayton,
                    1993).

             7.2.3  Relevant in vitro data

                    No data available.

             7.2.4  Workplace standards

                    Not established

             7.2.5  Acceptable daily intake (ADI) and other guideline
                    levels.

                    Not established

        7.3  Carcinogenicity

             An increased risk of squamous cell oesophageal cancer is
             considered possible following ingestion of corrosive agents
             such as sodium metasilicate (Gorman et al., 1992).

        7.4  Teratogenicity

             No data available.

        7.5  Mutagenicity

             No data available.

        7.6  Interactions

             No data available.

    8.  TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    8.1.1.1  Toxicological analyses

                    8.1.1.2  Biomedical analyses

                    8.1.1.3  Arterial blood gas analysis

                    8.1.1.4  Haematological analyses

                    8.1.1.5  Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

                    8.1.2.1  Toxicological analyses

                    8.1.2.2  Biomedical analyses

                    8.1.2.3  Arterial blood gas analysis

                    8.1.2.4  Haematological analyses

                    8.1.2.5  Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

                    8.1.3.1  Toxicological analyses

                    8.1.3.2  Biomedical analyses

                    8.1.3.3  Arterial blood gas analysis

                    8.1.3.4  Haematological analyses

                    8.1.3.5  Other (unspecified) analyses

        8.2  Toxicological Analyses and Their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

                    8.2.1.1  Simple Qualitative Test(s)

                    8.2.1.2  Advanced Qualitative Confirmation Test(s)

                    8.2.1.3  Simple Quantitative Method(s)

                    8.2.1.4  Advanced Quantitative Method(s)

             8.2.2  Tests for biological specimens

                    8.2.2.1  Simple Qualitative Test(s)

                    8.2.2.2  Advanced Qualitative Confirmation Test(s)

                    8.2.2.3  Simple Quantitative Method(s)

                    8.2.2.4  Advanced Quantitative Method(s)

                    8.2.2.5  Other Dedicated Method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

                    8.3.1.1  Blood, plasma or serum

                             Ancilliary tests that may be useful
                             include a complete blood count, electrolytes,
                             creatinine, type and cross for several units
                             of blood,  and a haemocult test for blood in
                             stool.

                    8.3.1.2  Urine

                             "Basic analyses"
                             "Dedicated analyses"
                             "Optional analyses"

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

                    "Basic analyses"
                    "Dedicated analyses"
                    "Optional analyses"

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their
             interpretation

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             Sample collection
    
             Not relevant
    
             Biomedical analysis
    
             Ancilliary tests that may be useful include a complete blood
             count, electrolytes, creatinine, type and cross for several
             units of blood, and a haemocult test for blood in stool.
    
             Toxicological analysis
    
             There are no relevant toxicological analyses for this
             chemical. However, the concentration or the pH of the
             solution may indicate the potential for serious injury. The
             titratable alkalinity is a better predictor of corrosive
             effect than the pH (Olson, 1994).
    
             Other investigations
    
             Radiographic studies may demonstrate air in the mediastinum
             from oesophageal perforation or free abdominal air from
             gastric perforation (Olson, 1994).

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    Ingestion of corrosives can cause oral pain,
                    dysphagia, drooling, and pain in the throat, chest, or
                    abdomen. Oesophageal or gastric  perforation may
                    occur, manifested by severe chest or abdominal pain,
                    signs of peritoneal irritation, or pancreatitis.
                    Haematemesis and shock may occur. Scarring of the
                    oeosophagus or stomach may result in permanent
                    stricture formation and chronic dysphagia. (Olson,
                    1994).

             9.1.2  Inhalation

                    Acute exposures involving the inhalation of
                    dusts of sodium metasilicate may result in irritation
                    of the respiratory tract and corrosive damage may
                    result from contact with mucous membranes. (Clayton &
                    Clayton, 1993).

             9.1.3  Skin exposure

                    Skin exposure to corrosive agents usually
                    results in immediate pain and redness. Serious full
                    thickness burns can occur (Olson, 1994).

             9.1.4  Eye contact

                    Eye exposure to corrosive agents commonly
                    results in conjunctivitis and lachrymation. Blindness
                    can occur. Sodium metasilicate is used with sodium
                    carbonate in heavy duty alkaline laundry detergents.
                    In rabbits, this type of detergent causes damage to
                    the cornea, with opacification, proportional to the
                    alkalinity of the preparation  (Scharpf et al., 1972).

             9.1.5  Parenteral exposure

                    No data available

             9.1.6  Other

                    No data available

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Prolonged exposures can lead to inflammatory
                    changes and ulcerative problems in the mouth.
                    Bronchial and gastrointestinal problems may occur,
                    depending upon concentration, duration and frequency
                    of exposure (Clayton & Clayton, 1993).

             9.2.2  Inhalation

                    Prolonged and repeated inhalation may lead to
                    ulceration of respiratory membranes  (Clayton &
                    Clayton, 1993).

             9.2.3  Skin exposure

                    Prolonged and repeated skin exposure with
                    dilute solutions may lead to dermatitis.  (Clayton &
                    Clayton, 1993).

             9.2.4  Eye contact

                    Irritation and other effects described
                    following acute exposure are likely to be
                    seen.

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             Initial clinical manifestations can include dysphagia,
             drooling, pain and haematemesis. Oral, oesophageal, and
             gastric burns may be present. Extensive mucosal damage leads
             to fever, tachypnoea, tachycardia, hypertension, and shock.
             Acute complications include aspiration pneumonia, burns of
             the epiglottis and vocal cords, and laryngeal obstruction.
             Acute perforation of the oesophagus or stomach with
             mediastinitis or peritonitis, sepsis, and death may occur. 
             Longterm sequelae of acute exposure may include oesophageal
             stricture, squamous cell oesophageal cancer, vocal cord
             paralysis, and pyloric stenosis (Gorman et al., 1992).

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Tachycardia, hypertension, and shock may occur
                    (Gorman et al., 1992).

             9.4.2  Respiratory

                    Irritation of the respiratory tract,
                    tachypnoea, mucosal damage, aspiration pneumonia.
                    (Clayton & Clayton, 1993; Gorman et al.,
                    1992).

             9.4.3  Neurological

                    9.4.3.1  Central Nervous System (CNS)

                             No data available

                    9.4.3.2  Peripheral nervous system

                             No data available

                    9.4.3.3  Autonomic nervous system

                             No data available

                    9.4.3.4  Skeletal and smooth muscle

                             No data available

             9.4.4  Gastrointestinal

                    Oesophageal and gastric burns may be present.
                    Acute perforation of the oesophagus or stomach with
                    mediastinitis or peritonitis and sepsis, may occur.
                    Longterm sequelae of acute exposure may include
                    oesophageal stricture, squamous cell oesophageal
                    cancer, vocal cord paralysis, and pyloric stenosis
                    (Gorman et al., 1992).

             9.4.5  Hepatic

                    No data available.

             9.4.6  Urinary

                    9.4.6.1  Renal

                             No human data available. Polydipsia
                             and polyuria were observed in some dogs fed
                             sodium silicate in their diet at a dose of
                             2.4 g/kg per day for 4 weeks. Damage to renal
                             tubules was observed in 15/16 dogs (Clayton &
                             Clayton, 1993).

                    9.4.6.2  Others

                             No data available.

             9.4.7  Endocrine & reproductive systems

                    Pancreatitis may occur (Olson, 1994).

             9.4.8  Dermatological

                    Skin exposure to corrosive agents usually
                    results in immediate pain and redness. Serious full
                    thickness burns can occur (Olson, 1994).

             9.4.9  Eye, ears, nose, throat: local effects

                    Dysphagia, drooling, pain. Burns of the
                    epiglottis and vocal cords, and laryngeal obstruction.
                    Possible longterm sequelae of acute exposure include
                    oesophageal stricture and vocal cord paralysis.
                    (Gorman et al., 1992). Eye exposure to corrosive

                    agents commonly results in conjunctivitis and
                    lachrymation. Blindness can occur. Sodium metasilicate
                    is used with sodium carbonate in heavy duty alkaline
                    laundry detergents. In rabbits this type of detergent
                    causes damage to the cornea, with opacification,
                    proportional to the alkalinity of the preparation 
                    (Scharpf et al., 1972).

             9.4.10 Haematological

                    No data available

             9.4.11 Immunological

                    No data available.

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             No data available.

                    9.4.12.2 Fluid & electrolyte disturbances

                             Dehydration may occur if vomiting
                             is excesssive.

                    9.4.12.3 Others

                             No data available.

             9.4.13 Allergic reactions

                    No data available.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risks

                    No data available.

        9.5  Others

             No data available.

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             Management is essentially symptomatic and supportive.

        10.2 Life supportive procedures

             Administer oxygen if required. Endotracheal intubation,
             tracheostomy for life threatening pharyngeal/ tracheal
             oedema.  If shock is present administer intravenous fluids.

        10.3 Decontamination

             Skin: Remove all jewellery and affected clothing and
             wash skin  with copious water or saline.
    
             Irrigation of the eye with water must be done within 60
             seconds to reduce the severity of injury (Scharpf et al.,
             1972) measurements of the the aqueous humor in alkali burned
             and saline irrigated rabbit eyes it has been reported that
             more than 2 hours of irrigation might be needed before the
             aqueous humor pH comes down to a desirable level. Testing of
             the conjunctival sac with wide range pH paper, every five to
             ten minutes in the course of irrigation can be used to obtain
             a measure of the rate at which the pH is returning to a
             tolerable value, such as pH 8 or 8.5. It may take from 48 to
             72 hours before an ocular burn can be properly assessed. The
             amount of corneal opacification and perilimbal whitening are
             used as the basis to assess the seriousness of the burn.
             (Grant & Schuman, 1993). Ingestion: Immediately give water or
             milk to drink if the patient is able to swallow. The volume
             administered should not be so excessive as to cause gastric
             distension and induce vomiting. Do not induce emesis.  Do not
             give pH-neutralizing solutions such as dilute vinegar or
             bicarbonate.  If oesophageal or gastric perforation is
             suspected, obtain immediate surgical or endoscopic
             consultation.   See section 10.7 for discussion of
             decontamination controversies.

        10.4 Enhanced Elimination

             These procedures are not relevant for corrosive agents.

        10.5 Antidote treatment

             10.5.1 Adults

                    There is no specific antidote. Do not use
                    neutralizing agents.

             10.5.2 Children

                    There is no specific antidote. Do not use
                    neutralizing agents.

        10.6 Management discussion

             Gastric lavage to remove the corrosive material is
             controversial but is probably beneficial in acute liquid
             corrosive ingestion. Use a  soft flexible tube and lavage
             with repeated aliquots of water or saline, frequently
             checking the pH of the washings. In general, do not give
             activated charcoal as it may interfere with visibility at
             endoscopy and is of limited value in adsorbing alkalis
             (Olson, 1994). Early positive oesophagoscopies identify those
             patients requiring hospital treatment as well as patients
             without burns who require no therapy. Oesophagoscopy is
             invasive and not without discomfort, cost, and risk. Perform
             endoscopy within the first 24 hours in patients with a
             history of definite ingestion, or when stridor, dysphagia, or
             drooling are present. Do not pass endoscope beyond the first
             circumferential burn. If burns are found, follow 10 to 20
             days with barium swallow (Gorman et al., 1992; Previtera et
             al., 1990; Gaudreault et al., 1983; Crain et al., 1984).
             Corticosteroids are not indicated. In the past they were used
             in the hope of reducing the incidence of  oesophageal
             scarring but have since proved ineffective. Moreover,
             steroids may be harmful in the patient with perforation by
             masking early signs of inflammation and inhibiting resistance
             to infection (Olson, 1994). Laparotomy and resection of
             necrotic gastrointestinal tract in the event of gastric
             necrosis should be considered. (Wu M-H & Lai W-W, 1993). In
             cases of ocular exposure, topical mydriatic-cycloplegics
             twice daily may be used to guard against the development of
             posterior synechiae and ciliary spasm. An ophthalmologist
             should be consulted in cases of ocular burns  (Grant &
             Schuman, 1993).

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             A 16-month-old girl swallowed an unknown amount of
             automatic-dishwasher detergent. Immediate symptoms were
             coughing and vomiting. She was given milk as a first aid
             measure and vomited subsequently. On arrival at a primary
             healthcare facility, she appeared to have oral burns only.
             However during transfer to a children's hospital for
             endoscopic evaluation, she developed severe inspiratory
             stridor and marked respiratory distress. Examination under
             anaesthesia revealed third-degree burns to the oropharynx,
             false vocal cords and upper third of the oesophagus. She
             required nasotracheal intubation for three days and was given

             hydrocortisone and antibiotics for 10 days. Nine days post
             ingestion, she was tolerating a normal diet and was
             discharged home on day 11. Forty-four days post ingestion,
             she was again admitted to hospital with severe respiratory
             distress. A barium-swallow examination showed a marked 
             stricture of the upper oesophagus and evidence of aspiration.
             Further examination revealed supraglottic and pharyngeal
             stenosis and a narrow but patent oesophagus. She underwent
             the construction of a tracheostomy, a gastrostomy and the
             insertion of laryngeal and oesophageal stents. She required
             feeding by the gastrostomy for 16 months and experienced 18
             admissions to hospital over a period of 2 years for multiple
             endoscopic dilatations and bronchoscopies, a supraglottic
             laryngectomy, the excision of scar-tissue and, finally, the
             construction of a jejunal conduit from the cervical
             oesophagus to the pharynx, decannulation of the tracheostomy
             and the closure of the gastrostomy. (Kynaston, 1989).
    
             An 11-month-old boy was admitted to hospital following the
             ingestion of a small quantity of automatic-dishwashing
             detergent. He vomited immediately, his mother washed out his
             mouth and gave him water to drink. On examination, he was
             crying and was drooling saliva. Extensive burns to the tongue
             and buccal cavity were noted, as well as a swollen uvula.
             Oesophagoscopy revealed an oedematous epiglottis and non-
             circumferential burns to the oesophagus. In view of his
             significant pharyngeal burns and the potential for airway
             obstruction, he remained intubated for 48 hours. The
             oesophagus was stented with a nasogastric tube which was used
             for feeding. Steroid and antibiotic therapy was undertaken
             for 48 hours. In order to exclude gastric burns, endoscopy
             was repeated with a flexible endoscope, and the mucosa was
             found to be normal. He was discharged home after 7 days,
             taking a normal diet (Kynaston, 1989).

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             Containers of dishwashing powders and similar
             preparations containing sodium metasilicate should be
             appropriately labelled and fitted with child resistant
             closures. Standard industrial hygiene procedures should be
             employed to keep workplace exposure levels to an acceptable
             amount. Respiratory protection should be available.
             Protective clothing and gloves should be worn to prevent skin
             contact. Eye protection, goggles and face shield should be
             used. Emergency wash facilities, particularly for eyes,
             should be available.

        12.2 Other

             Not relevant

    13. REFERENCES

        Budavari S (1989) The Merck Index, An encyclopedia of chemicals,
        drugs and biologicals, eleventh edition Merck & Co., Inc.
    
        Clayton GD & Clayton FE (1993) Patty's Industrial Hygiene and
        Toxicology, 4th ed. New York, John Wiley & Sons Inc., Volume II,
        Part A Toxicology 776-778.
    
        Crain EF, Gershel JC & Mezey AP (1984) Caustic Ingestions. Am J
        Dis Child, 138:863-865.
    
        Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W, Oderda GM, Benson
        B, Litovitz T, McCormick M, McElwee N, Spiller H & Krenzelok E
        (1992) Initial symptoms as predictors of esophageal injury in
        alkaline corrosive ingestions Am J Emerg Med, 10:189-194.
    
        ECETOC (1995) Technical Report no. 66. Skin irritation and
        corrosion. Reference Chemicals Data Bank.
    
        Gaudreault P, Parent M, McGuigan MA (1983) Predictability of
        esophageal injury from signs and symptoms: a study of caustic
        ingestion in 378 children. Pediatrics 71:767-770.
    
        Gosselin RE, Smith RP & Hodge HC (1984) Clinical Toxicology of
        Commercial Products, Fifth edition, Williams & Wilkins,
    
        Grant WM & Schuman (1993) Toxicology of the eye: effects on the
        eyes and visual system from chemicals and drugs, metals and
        minerals, plants, toxins, and venoms: also systemic side effects
        from eye medications Fourth edition Charles C Thomas Publisher,
        Springfield Illinois USA.
    
        Houck JC, DeAngelo L & Jacob RA (1962) The dermal chemical
        response to alkali injury. Surgery, 51:503-507.
    
        IPCS/CEC (1993) ICSC # 0359  Sodium Metasilicate, anhydrous.
    
        Kynaston JA, Patrick MK, Shepherd RW, Raivadera PV & Cleghorn GJ
        (1989) The hazards of automatic-dishwasher detergent. Med  J Aust,
        151(1):5-7.
    
        Olson KR (1994) Poisoning and Drug overdose, 2nd edition, Appleton
        & Lange, Norfolk, Connecticut.
    
        Previtera C, Giusti F & Guglielmi M (1990) Predictive value of
        visible lesions (cheeks, lips, oropharynx) in suspected caustic 
        ingestion: may endoscopy reasonably be ommitted in completely
        negative pediatric patients? Pediatr Emerg Care 6:176-178.
    
        RTECS (1996) National Institute for Occupational Safety and
        Health, Canadian Centre for Occupational Health and Safety Issue
        96-2.
    

        Scharpf Jr LG, Hill ID & Kelby RE (1972) Relative eye injury
        potential of heavy duty phosphate and non-phoshate laundry
        detergents  Food Cosmet Toxicol, 10:829-837.
    
        Winter M & Ellis M (1986) Automatic dishwashing detergents: their
        pH, ingredients and a retrospective look, Vet Hum Toxicol,
        28(6):536-5.
    
        Wu M-H & Lai W-W (1993) Surgical management of extensive corrosive
        injuries of the alimentary tract. Surg Gynecol Obstet  177:12-16.

    14. AUTHOR(S),ETC.

        Authors: Dr Wayne A Temple
        National Toxicology Group
        Dunedin School of Medicine
        University of Otago
        Box 913
        Dunedin
        New Zealand
    
        Phone:  64-3-4797244
        Fax:  64-3-4770509
        E-mail: wtemple@gandalf.otago.ac.nz
    
        Nerida A Smith
        School of Pharmacy
        University of Otago
        Box 913
        Dunedin
        New Zealand
    
        Phone:  64-3-4797239
        Fax:  64-3-4770509
    
        E-mail: nerida.smith@stonebow.otago.ac.nz

        Reviewer: Dr Lindsay Murray,
        Prince of Wales Hospital,
        Randwick,
        NSW,
        Australia
    
        Peer Review:  Intox-9, Cardiff, September 1996 (A Borges, A Brown,
        R Ferner, M Hanafy, L Murray, MO Rambourg, W Temple).
    
        Editor: Dr M. Ruse (October, 1997)
    



    See Also:
       Toxicological Abbreviations