MONOGRAPH FOR UKPID
LYE
Nicky Bates
National Poisons Information Service (London Centre)
Medical Toxicology Unit
Guy's & St Thomas' Hospital Trust
Avonley Road
London
SE14 5ER
UK
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
1 SUBSTANCE/PRODUCT NAME
1.1 Origin of substance
Made by reacting calcium hydroxide with sodium carbonate, from sodium
chloride electrolysis and from sodium metal and water vapour at low
temperature.
1.2 Name
1.2.1 Brand/trade name
1.2.2 Generic name
1.2.3 Synonyms
Sodium hydroxide, lye (sodium hydroxide solution, but may also refer
to potassium hydroxide solution), caustic soda, sodium hydrate, white
caustic, caustic flake, natriumhydroxide (German), natriumhydroxyde
(Dutch).
1.2.4 Common names/street names
Not applicable.
1.3 Chemical group/family
Alkali.
1.4 Substance identifier and/or classification by use
1.5 Reference numbers
CAS 1310-73-2
RTECS WB 4900000
EINECS 2151855
UN 1823 (dry solid)
1.6 Manufacturer
No data.
1.7 Supplier/importer/agent/ licence holder
Bayer Diagnostics, Bayer plc, Evans House, Hamilton Close,
Basingstoke, Hants, RG21 2YE Tel: 01256 29181
Diversey Ltd, Weston Favell Centre, Northampton, NN3 8PD Tel: 01604
405311 Fax: 01604 406809
Evans Vanodine International plc, Brierley Rd, Walton Summit Centre,
Preston, PR5 8AH Tel: 01772 322200 Fax: 01772 626000
Lever Brother s Ltd, 3 St James; Rd, Kingston-upon-Thames, Surrey
KT1 2 BA Tel: 0181 542 8200
SC Johnson, Frimley Green, Camberley, Surrey, GU16 5AU Tel: 01276
852377 Fax: 01276 852688
SC Johnson Professional, Frimley Green, Camberley, Surrey, GU16 5AU
Tel: 01276 852706 Fax: 01276 852800
1.8 Presentation
1.8.1 Form
Clinitest(R): white pale blue mottled tablets.
Auto Dishwash: thin yellow liquid.
Auto Dishwash Extra: thin yellow liquid.
Auto Glass Wash: thin yellow liquid.
Beerline: thin colourless liquid.
Chlorinated Dishwash: thin pale yellow liquid.
Crystal: white powder.
D9 Oven Cleaner: thin brown liquid.
Diverforce L3: thin yellow/green liquid.
Diverforce L4: thin straw coloured liquid.
Diverforce L6: thin straw coloured liquid.
Divocare MSD: thin red liquid.
Divocare MSD Super: thin red liquid.
Divocare OC: brown gel.
Filter Cleaner: thin yellow liquid.
Green Top Bottle Washing Detergent: pale yellow powder.
HMD Plus: thin straw coloured liquid.
M1: thin red liquid.
Mr Muscle Drain Opener, sachet: granules.
Mr Muscle Oven Cleaner: aerosol.
Mr Muscle Professional Oven Cleaner: aerosol.
Mr Muscle Sink and Plughole Opener: hazy, straw coloured liquid.
Oven Cleaner: viscous colourless liquid.
Pastueriser Cleaner Liquid: thin yellow liquid.
Pastueriser Powder: white powder.
SPA Plus: thin straw coloured liquid.
Sun Liquid: white viscous liquid.
Sun Lemon Fresh Liquid: white viscous liquid.
TC Plus: thin yellow/green liquid.
Unipak G1: white powder.
Unipak G3: white powder.
Unipak G5: white powder.
Pastueriser Cleaner Liquid: thin yellow liquid.
Vanosan: thin pale yellow liquid.
1.8.2 Formulation details
Clinitest(R) tablets (Bayer Diagnostics): sodium hydroxide 232.5mg.
Auto Dishwash (Evans Vanodine): sodium hydroxide 8.33% (pH 13.6 as
supplied), 11.3 (working solution), TAR 8.71g NaOH/100g)
Auto Dishwash Extra (Evans Vanodine): sodium hydroxide 8.83% (pH 13.7
as supplied), 11.6 (working solution), TAR 10g NaOH/100g)
Auto Glass Wash (Evans Vanodine): sodium hydroxide 4.75% (pH 13.6 as
supplied), 11.7 (working solution), TAR 5.58g NaOH/100g)
Beerline (Evans Vanodine): sodium hydroxide 14.8% (pH 13.7 as
supplied), 12.6 (working solution), TAR 14.8g NaOH/100g)
Chlorinated Dishwash (Evans Vanodine): sodium hydroxide 10-20% (pH
13.65 as supplied), 11.8 (working solution), TAR 10.22g NaOH/100g)
Crystal (Evans Vanodine): sodium hydroxide 45% (pH 13, TAR 44.1%
NaOH/100g)
D9 Oven Cleaner (Diversey): sodium hydroxide 10% (pH 13.9)
Diverforce L3 (Diversey): sodium hydroxide 10% (pH 13 (as supplied),
11 (working solution))
Diverforce L4 (Diversey): sodium hydroxide 14% (pH 13.9 (as supplied),
11(working solution))
Diverforce L6 (Diversey): sodium hydroxide 10% (pH 13.9 (as supplied),
11(working solution))
Divocare MSD (Diversey): sodium hydroxide 14% (pH 13.9 (as supplied),
11(working solution))
Divocare MSD Super (Diversey): sodium hydroxide 14% (pH 13.9 (as
supplied), 11(working solution))
Divocare OC (Diversey): sodium hydroxide 6% (pH 13.9)
Filter Cleaner (Evans Vanodine): sodium hydroxide 8.33% (pH 13.6 as
supplied), 11.3 (working solution), TAR 8.71g NaOH/100g)
Green Top Bottle Washing Powder: (Evans Vanodine): sodium hydroxide
76%, (pH 12.5, TAR 67.85g NaOH/ 100g)
HMD Plus (Diversey): sodium hydroxide 14% (pH 13 (as supplied),
11(working solution))
M1 (Diversey): sodium hydroxide 5.5% (pH 13.9 (as supplied),
11.5(working solution))
Mr Muscle Drain Opener, sachet (SC Johnson): sodium hydroxide 52% (pH
13.5)
Mr Muscle Oven Cleaner (SC Johnson): sodium hydroxide 1-5% (pH 13.2)
Mr Muscle Professional Oven Cleaner (SC Johnson Professional): sodium
hydroxide 1-5% (pH 13.5-14)
Mr Muscle Sink and Plughole Opener (SC Johnson): sodium hydroxide 1-5%
(pH 13)
Oven Cleaner (Evans Vanodine): sodium hydroxide 5-10% (pH 13.8, TAR
9.67g NaOH/100g)
Pastueriser Cleaner Liquid (Evans Vanodine): sodium hydroxide 8.83%
(pH 13.7 (as supplied), 11.6 (working solution), TAR 10g NaOH/100g)
Pastueriser Powder (Evans Vanodine): sodium hydroxide 40% (pH 12.5,
TAR 40.65g NaOH/100g)
SPA Plus (Diversey): sodium hydroxide 10% (pH 13 (as supplied),
11(working solution))
Sun liquid (Lever): sodium hydroxide 1-5% (pH 13.6)
Sun Lemon Fresh Liquid (Lever): sodium hydroxide 1-5% (pH 13.6)
TC Plus (Diversey): sodium hydroxide 10% (pH 13 (as supplied), 11
(working solution))
Unipak G1 (Diversey): sodium hydroxide 57% (pH 12)
Unipak G3 (Diversey): sodium hydroxide 35% (pH 12)
Unipak G5 (Diversey): sodium hydroxide 20% (pH 12)
Vanosan (Evans Vanodine): sodium hydroxide 10-20% (pH 13.65 (as
supplied), 11.5 (working solution), TAR 10.91 NaOH/100g)
1.8.3 Pack sizes available
Clinitest(R) tablets: 36 tablet pack.
Auto Dishwash: 5 L and 25 L bottles.
Auto Dishwash Extra: 5 L and 25 L bottles.
Auto Glass Wash: 5 L and 25 L bottles.
Beerline: 5 L and 25 L bottles.
Chlorinated Dishwash: 25 L bottles.
Crystal: 15 kg buckets.
D9 Oven Cleaner: 2 L bottle.
Diverforce L3: 20 L drum.
Diverforce L4: 5 L, 25 L and 200 L drums.
Diverforce L6: 5 L and 20 L drums.
Divocare MSD: 20 L and 5L drums.
Divocare MSD Super: 20 L and 5L drums.
Divocare OC: 5 L drums.
Green Top Washing Powder: 25 kg bucket.
HMD Plus: 20 L drum.
M1: 2L bottle.
Mr Muscle Drain Opener, sachet: 60g.
Mr Muscle Oven Cleaner: 250ml, 300ml, 450ml, 500ml.
Mr Muscle Professional Oven Cleaner: 500ml.
Mr Muscle Sink and Plughole Opener: 500ml.
Oven Cleaner: 5 L bottles.
Pastueriser Cleaner Liquid: 25 L bottles.
Pastueriser Powder: 25 kg buckets.
SPA Plus: 5 L and 20 L drum.
Sun Liquid: 1L, 3L bottles.
Sun Fresh Lemon Liquid: 1L, 3L bottles.
TC Plus: 20 L drum.
Unipak G1: 4.5 kg direct dispense bottles.
Unipak G3: 4.5 kg direct dispense bottles.
Unipak G5: 4.5 kg direct dispense bottles.
Pastueriser Cleaner Liquid: 25 L bottles.
Vanosan: 25 L bottles.
1.8.4 Packaging
See above.
1.9 Physico-chemical properties
Chemical structure
NaOH, molecular weight 40.01.
Physical state
Fused solid with crystalline structure available as pellets, sticks,
flakes or lumps.
Colour
White.
pH
Of 0.05% solution about 12, of 0.5% solution about 13 and of a 5%
solution about 14.
Solubility in water and organic solvents
1g of sodium hydroxide dissolves in 0.9ml water, 0.3ml boiling water,
7.2ml absolute alcohol and 4.2ml methanol. It is also soluble in
glycerol.
Important chemical interactions
Readily absorbs carbon dioxide and water from air. Generates heat when
dissolving or when mixed with an acid. Corrosive to organic tissue and
to aluminium metal in the presence of moisture. Reacts violently with
acetaldehyde, acetic anhydride, acrolein, acrylonitrile, allyl
alcohol, allyl chloride, chlorohydrin, chloronitrotoluenes,
chlorosulphonic acid, 1,2-dichloroethylene, ethylene cyanhydrin,
glyoxal, hydroquinone, maleic anhydride, nitroethane, pentol, oleum,
phosphorous, tetrahydrofuran, trichloroethylene, water,
4-chloro-2-2methylphenol, cinnamaldehyde, cyanogen azide, diborane,
4-methyl-2-nitrophenol, 3-methyl-2-penten-4-yn-1-ol,
1,2,4,5-tetrachlorobenzene (to form 2,3,7,8-tetrachlorobenzodioxin),
1,1,1-trichloroethanol, trichloronitromethane, zinc and zirconium.
Major products of combustion/pyrolysis
Sodium hydroxide is not combustible but the solid form on mixing with
moisture or water may produce sufficient heat to ignite combustible
material. When heated to decomposition sodium oxide (Na2O) is
produced.
Boiling point
1390°C
5% solution 102°C
10% solution 105°C
20% solution 110°C
30% solution 115°C
40% solution 125°C
50% solution 140°C
Melting point
318.4°C
Density
2.13 g/cm3 at 25°C
Vapour pressure
1 mmHg at 739°C
Reactivity
Sodium hydroxide reacts vigorously with 1,2,4,5-tetrachlorobenzene
to form 2,3,7,8-tetrachlorobenzodioxin.
Mixtures with aluminium and arsenic compounds can form arsine.
Contact with some metals (such as aluminium, tin, lead and zinc)
can generate hydrogen.
1.10 Hazard/risk classification
Corrosive.
1.11 Uses
Sodium hydroxide is used to neutralise acid solutions and make sodium
salts. It is used in the manufacture of rayon, mercerised cotton,
soap, paper, aluminium, petroleum products and in metal cleaning,
electrolytic extraction of zinc, tin plating and oxide coating.
Sodium hydroxide solutions hydrolyze fats to form soaps, they
precipitate bases and most metals (as hydroxides) from aqueous
solutions of their salts.
Sodium hydroxide is a common constituent of many household and
industrial cleaners including oven cleaners and beerline cleaners. It
is present as a stabilising agent in bleach. It may also be found in
dishwasher detergents. Some paint strippers and drain cleaners contain
sodium hydroxide. It is used as a pipe line cleaner in dairies, bars
and public houses.
Small amounts of sodium hydroxide are produced as a by-product and
released into the car interior when motor car air bag systems are
activated. Air bag systems are triggered when a sensor in the bumper
sends an electrical charge to a gas generator containing sodium azide
(70 g). A chemical reaction is initiated that produces nitrogen gas
from the sodium azide.
Sodium hydroxide is present in Clinitest(R) tablets which are used by
diabetics as an in vitro semiquantitive test for glycosuria.
1.12 Toxicokinetics
1.12.1 Absorption
Sodium hydroxide is not absorbed. Alkalis act at the site of contact.
1.12.2 Distribution
Not applicable.
1.12.3 Metabolism
Not applicable.
1.12.4 Elimination
Not applicable.
1.12.5 Half-life
Not applicable.
1.12.6 Special populations
Not applicable.
2 SUMMARY
3 EPIDEMIOLOGY OF POISONING
Sodium hydroxide burns, whether dermal, ocular or gastrointestinal,
are potentially very serious and may cause severe complications
requiring repeated or prolonged hospitalisation and long term
treatment.
Ingestion
Sodium hydroxide is the most commonly ingested strong alkali. The
majority of cases of ingestion are accidental, particularly in
children (Christesen, 1994a; Clausen et al, 1995; Gandhi et al, 1989;
Edmonson, 1987; Crain et al, 1984; Grenga, 1983; Tewfik and Schloss,
1980; Lane, 1975; Ashcraft and Padula, 1974; Leape et al, 1971) where
severe effects are relatively rare but potentially devastating. Adults
may also ingest sodium hydroxide accidentally often mistaking it for
something else (Meredith et al, 1988; Chen et al, 1988; Thompson,
1987) or where it has been transferred to a different, poorly labelled
container. This may also occur in children (Friedman, 1987) Oral burns
have also occurred in a child after she put an oven cleaner pad in her
mouth (Vilogi et al, 1985).
Sodium hydroxide has been used as a means of suicide both from
drinking the solution (Winek et al, 1995; Christesen, 1994b; Arif and
Karetzky, 1991; Hendrickx et al, 1990; Rabinowitz et al, 1990;
Ferguson et al, 1989; Rubin et al, 1989; Estrera et al, 1986; Crain et
al, 1984; Cello et al, 1980; McCabe et al, 1969; Matenga et al, 1987;
Oakes et al, 1982; Okonek et al, 1981; Balasegaram, 1975) and from
ingestion of capsules filled with sodium hydroxide (Carroll et al,
1994; Nelson et al, 1983; Gill et al, 1986; Oakes et al, 1982; Lowe et
al, 1979). A number of these cases, particularly those involving
ingestion of sodium hydroxide solution have been fatal (Rabinowitz et
al, 1990; Matenga et al, 1987; Estrera et al, 1986; McCabe et al,
1969).
In a review of 214 cases of caustic ingestion (including bleach and
acids as well as alkalis), children aged five years and under,
accounted for 39% of admissions but only 8% of the burns required
treatment, whereas adults constituted 48% of admissions with 81% of
the burns requiring treatment (Hawkins et al, 1980). Of the 20
strictures reported in this study, 16 were due to ingestion of sodium
hydroxide (12 following ingestion of sodium hydroxide solution).
Clinitest(R) tablets
Ingestion of Clinitest(R) tablets may occur accidentally (O'Connor et
al, 1986; Schlatter-Lanz, 1985; Burrington, 1975; Payten, 1972;
Mallory and Schaefer, 1977) particularly by children or the elderly or
intentionally as a means of suicide (Schlatter-Lanz, 1985; Lowe et al,
1979). Often adults take the tablets with water which may reduce the
incidence of severe oesophageal injury in this group, however there is
also the risk of gastric injury. Death from an oesophago-aortic
fistula has been reported in an elderly woman who accidentally took
two tablets with tea (O'Connor et al, 1986).
Ingestion of Clinitest(R) tablets was a much more common problem in
the past. A number of cases were reported in the literature in the
1950s and 1960s (as reviewed by Lacoutre et al, 1986).
Dermal exposure
Dermal exposure to sodium hydroxide may occur following accidents in
the industrial (O'Donoghue et al, 1996; Lee and Opeskin, 1995) or
domestic setting (Lorette and Wilkinson, 1988; O'Donoghue et al,
1996). Dermal exposure to oven cleaner pads has also resulted in
injury (Vilogi et al, 1985).
Chemicals are a relatively uncommon cause of burns requiring treatment
in a burns unit, but of these, sodium hydroxide is the most commonly
implicated chemical. Of 3,251 patients admitted to a regional burns
unit 100 (3.1%) had sustained chemical burns, which accounted for
16.5% of industrial burning accidents. Alkaline materials caused 37%
of the accidents, 26% were due to sodium hydroxide, acids accounted
for 27% of the burns with hydrofluoric acid involved in half these
cases (Herbert and Lawrence, 1989). Alkali burns may initially appear
superficial which can lead to a delay in treatment.
Ocular burns
Most alkaline burns to the eye occur at work (Moon and Robertson,
1983; Pfister and Koshi, 1982), but domestic accidents also account
for a large proportion of ocular burns, particularly in children (Moon
and Robertson, 1983). The most severe injuries are seen in men of
working age (Nelson and Kopietz, 1987). Alkalis have also been used in
assault (Beare, 1990a). Ocular injury has also been reported from
accidental instillation of a sodium hydroxide solution into the eye
instead of a contact lens solution (Mauger, 1988) and from exposure to
sodium hydroxide in oven cleaner pads (Vilogi et al, 1985).
Motor car air bags
Small amounts of sodium hydroxide are produced as a by-product and
released into the car interior when motor car air bag systems are
activated. There have been reports of both ocular (White et al, 1995;
Smally et al, 1992; Swanson-Biearman et al, 1993; Ingraham et al,
1991) and dermal burns (Swanson-Biearman et al, 1993) following
activation of air bags during motor car accidents.
4 MECHANISM OF ACTION/TOXICITY
4.1 Mechanism
Alkalis cause liquifactive necrosis with saponification of fats and
solubilisation of proteins. There is a decrease in the collagen
content of tissue and saponification of cell membrane lipids and
cellular death. They are also hygroscopic and will absorb water from
the tissues. These effects result in adherence and deep penetration
into the tissues.
Ingestion
Alkalis cause the most severe corrosive effects on the oesophagus,
rather than the stomach as is the case with acids. However, following
deliberate ingestion of a large quantity of an alkali (as with
intentional ingestion in adults) both the stomach and small intestine
may be involved. This is particularly the case with liquid sodium
hydroxide.
Oesophageal changes can be divided into 3 stages:
1) acute necrotic phase in which cell death occurs due to coagulation
of intracellular protein,
2) intense inflammatory reaction in viable tissues surrounding the
necrotic area, thrombosis of vessels occurs,
3) sloughing of superficial necrotic layer 2-4 days later (Adam and
Birck, 1982).
Strictures form due to an intense fibroblastic reaction and
superficial granulation tissue formation that terminates with
extensive scar formation and luminal narrowing. The newly formed
collagen contracts both cirumferentially and longitudinally resulting
in oesophageal shortening and stricture formation.
Clinitest(R) tablets
The sodium hydroxide in these tablets reacts with the saliva and
liberates heat which can produce a full thickness burn of the
oesophagus. Clinitest(R) tablets also adhere to the oesophagus either
because of thermal coagulation or because of the carbon dioxide
bubbles produced from the reaction of the citric acid and sodium
hydroxide present (Burrington, 1975). Gastric injury may also occur.
Ocular burns
Alkali burns of the eye are very serious because they cause disruption
of the protective permeability barriers and rapidly penetrate the
cornea and anterior chamber. They combine with cell membrane lipids
which causes disruption of the cells and stromal mucopolysaccharides
with concomitant tissue softening. Sodium hydroxide can pass freely
through the cornea and cause damage to all layers of the cornea and to
the anterior segment structures in severe cases (Wright, 1982).
In the acute phase the following occurs: sloughing of the corneal
epithelium, necrosis of the cells of the corneal stroma and
endothelium, loss of corneal mucoid, oedema of the corneal stroma and
ciliary processes, ischaemic necrosis and oedema of the conjunctiva
and limbal region of the sclera and infiltration of inflammatory cells
into the cornea and iris. Corneal infiltration and degeneration occurs
1-3 weeks after injury (Grant and Schuman, 1993).
Alkalis cause rapid loss of corneal mucoprotein. They also bind to
corneal mucoprotein and collagen and the eye may remain alkaline
despite prolonged irrigation due to slow dissociation of hydroxyl ions
from corneal proteins. A large number of animal experiments,
particularly on rabbits, have been conducted to study alkali injury to
the eye and it is known from these experiments that in the rabbit eye
the pH of the aqueous humour can rise to 10-11 within a few minutes or
even higher in severe cases. The pH slowly falls over a period of
hours, except in extreme cases (Grant and Schuman, 1993).
Injury of the endothelium causes failure of the endothelial pump which
normally keeps the cornea deturgesced and clear. This failure causes
the corneal stroma to become oedematous and susceptible to
vascularisation and scarring.
When the protective sheath around collagen is damaged, collagenases
produced by polymorphonuclear leucocytes infiltrate the damaged area
and degrade the corneal collagen causing melting or ulceration of the
stroma, formation of descemoteceles (herniation of Descemet's
membrane) and perforation of the cornea. This phase is evident 3-7
days post-injury.
The role of injury to blood vessels remains unclear, as with other
chemical burns to the eye the blood vessels of the conjunctiva and
episclera are seen to be thrombosed immediately after exposure.
Both alkali and acid burns cause a transient rise in intraocular
pressure due to shrinkage of the eye coats. A second phase of raised
intraocular pressure may occur due to prostaglandin release and a
still later phase with glaucoma due to obstruction of aqueous outflow
caused by inflammation or synechiae.
In severely damaged untreated burns inflammatory destruction and
ulceration continues to occur for weeks or months resulting in damage
ranging from dense vascular invasion to opaque scarring and corneal
perforation.
During the recovery process, surviving keratocytes begin to form new
collagen but a decrease in available ascorbate (caused by injury to
the main source in the ciliary body) is a limiting factor in this
process. This lack of ascorbate may also render the cornea more
susceptible to attack by oxygen free radicals.
4.2 Toxic dose
The severity of injury will depend on a number of factors including
the concentration of the agent, the duration of contact and the volume
ingested. It is greatest where the pH is above 12. However, pH is not
the only factor which determines the extent to which a substance can
cause corrosive injury. Alkaline reserve (which is the amount of a
standard acid solution needed to titrate an alkali to a specified pH -
usually pH 8, the pH of normal oesophageal mucosa) has been found to
correlate better than pH with the production of caustic oesophageal
injury (Hoffman et al, 1989). Although this method is not currently
used (except internally by some manufacturers to classify products as
irritant or corrosive) it appears to be a better predictor of injury
than pH. Alkaline reserve may also be referred to as the titratable
alkaline reserve (TAR).
Solid preparations and viscous liquids are also more likely to produce
severe injury due to prolonged contact. Following ingestion of a small
amount the injury is usually limited to the oropharyngeal region and
the oesophagus. The greater the volume the greater the risk of
duodenal and gastric damage.
Several studies have been carried out in an attempt to correlate
clinical effects and injury. Gaudreault et al (1983) found that signs
and/or symptoms do not adequately predict the presence or severity of
an oesophageal lesion. Crain et al (1984) found that the presence of
two or more signs or symptoms (vomiting, drooling, stridor) may be a
reliable predictor of oesophageal injury. In the study by Nuutinen et
al (1994) prolonged drooling and dysphagia (12-24 hours) were observed
to predict oesophageal scar formation with 100% sensitivity. In the
study of 224 children (aged 0-14 years) by Clausen et al (1994)
serious complications were due to ingestion of sodium hydroxide or a
dishwasher product. Children without any signs or symptoms at the
first examination did not develop stricture or epiglottal oedema.
The study by Christesen (1995) also found that complications only
developed in children who had ingested strong alkalis (sodium
hydroxide, ammonia and dishwasher products). The author found that
children with respiratory symptoms were at greater risk of developing
complications and that liquid sodium hydroxide tended to cause more
complications than the granular form. It was also concluded that
asymptomatic patients are not at risk of complications and probably do
not require endoscopy.
Knopp (1979) reported that in patients with oral burns approximately
one third had significant oesophageal injury, whereas 2-15% of
patients with oesophageal injury had no oral burns.
Clinitest(R) tablets
Ingestion of 1 tablet is sufficient to cause oesophageal stricture.
However, ingestion of 47 tablets over 1 month by an adult caused only
gastritis and eschar formation in the lower two thirds of the stomach
with full recovery (Mallory and Schaefer, 1977).
5 FEATURES OF POISONING
5.1 Acute
5.1.1 Ingestion
Ingestion of sodium hydroxide may cause an immediate burning pain in
the mouth, oesophagus and stomach (retrosternal and epigastric pain),
with swelling of the lips. This is followed by vomiting, haematemesis,
increased salivation, ulcerative mucosal burns, dyspnoea, stridor,
dysphagia and shock. Oesophageal and pharyngeal oedema may occur.
It should be noted that oesophageal damage may occur in the absence
of oral burns (Krenzelok and Clinton, 1979; Kynaston et al, 1989).
Acute complications
These include gastrointestinal haemorrhage and perforation of the gut
(suggested by increasing abdominal pain, persistent vomiting, direct
and indirect tenderness and a rigid abdominal wall).
Gastric ulcers on the greater curvature and the antrum have been
reported following ingestion of capsules filled with sodium hydroxide
(Gill et al, 1986; Carroll et al, 1994; Oakes et al, 1982; Lowe et al,
1979).
Late complications
Oesophageal stricture and pyloric stenosis may occur as late
complications. Stricture formation usually begins to develop 14-21
days after ingestion. Most strictures become manifest within the first
two months. Strictures may prevent an adequate nutritional intake and
in severe cases patients may be unable to swallow their own saliva.
Healing of oesophageal injury depends on the severity of the injury.
In the study by Di Costanzo et al (1980) first degree burns healed in
about a week, second degree burns in 20-30 days and third degree burns
within 90 days.
Gastric necrosis and stricture may occur, usually in patients who have
oesophageal injury as well. Gastric injury is more likely to occur
following ingestion of liquid sodium hydroxide than ingestion of the
solid. The small intestine may also be involved, duodenal and colonic
necrosis has also been reported with ingestion of sodium hydroxide
solution (Guth et al, 1994).
Oesophago-aortic fistulae and rupture of the aorta are rare
complications of corrosive ingestion (Ottoson, 1981).
Tracheo-oesophageal fistulae and less commonly, broncho-oesophageal
fistulae, have been reported following ingestion of alkalis (McCabe et
al, 1969; Sarfati et al, 1987; Allen et al, 1970). They have also been
reported to form as a complication of oesophageal dilatation (Mutaf et
al, 1995). The main symptoms of a tracheo-oesophageal fistula are
persistent pneumonia, choking and cyanosis while feeding.
Severe corrosive injury to the stomach may result in a small scarred
immobile stomach and in such cases small, frequent intakes of food may
be necessary to prevent dumping syndrome. Achlorhydria with reduced or
absent intrinsic factor may also occur. (Dumping syndrome is a complex
reaction thought to be secondary to excessively rapid emptying of
gastric contents into the jejunum. Clinical effects include nausea,
sweating, palpitations, syncope and diarrhoea).
Alkalis are known to increase the risk of oesophageal cancer, which
can occur years after the initial injury (Isolauri and Markkula, 1989;
Appelqvist and Salmo, 1980; Kinnman et al, 1968). The incidence of
carcinoma following oesophageal injury from sodium hydroxide is 0.8-4%
- see section 9.1.
Clinitest(R) tablets
These are easily mistaken for oral medication and can cause severe
oesophageal injury if ingested. They can become lodged in the
oesophagus and cause stricture formation. Strictures are usually short
and located at about the level of carina (Burrington, 1975). Death
from an oesophago-aortic fistula has been reported (O'Connor et al,
1986).
5.1.2 Inhalation
Pulmonary oedema may occur following inhalation of vaporised caustics.
5.1.3 Dermal
On the skin alkalis can cause severe burns. The skin is discoloured
brown or black which may make initial assessment of the injury
difficult. There may be recurring skin breakdown over a long period
(O'Donoghue et al, 1996).
It should be noted that after exposure to low concentration alkalis
the affected area may remain painless for several hours (Lorette and
Wilkinson, 1988).
5.1.4 Ocular
Sodium hydroxide is responsible for some of the most severe, blinding
injuries to the eye. There is intense pain with blepharospasm. Visual
acuity is decreased due to injury to the corneal epithelium and
corneal oedema.
In mild cases there may be sloughing of the corneal and conjunctival
epithelium. In more severe cases there may be conjunctival swelling
(chemosis) and necrosis with hazing or opacity of the cornea. There is
a rise in intraocular pressure initially as the sclera of the eye
shrinks and then due to a release of prostaglandins.
Severe burns are characterised by ischaemic necrosis. This is due to
reduced or absent blood flow as a result of thrombosed blood vessels
which leaves the conjunctiva and sclera white. If the eye has been
penetrated fibrin may be present in the anterior chamber with
infiltration of inflammatory cells. The pupil may be dilated and
unreactive due to damage to the sphincter and dilator muscles. Retinal
damage may also occur in severe ocular burns.
Assessment of the injury and a prognosis may be difficult until 48-72
hours after the exposure (Pfister and Koshi, 1982).
There may be involvement of the lids with erythema, oedema or
blistering or in severe cases ischaemic necrosis.
Late complications of severe ocular burns include: persistent oedema,
glaucoma, vascularisation of cornea, fibrous tissue scarring of
cornea, growth of vessels throughout cornea, ulceration, perforation,
permanent opacity, staphyloma, phthisis bulbi (shrinkage and wastage
of eyeball), cataract and symblepharon (adhesion between tarsal
conjunctiva and bulbar conjunctiva).
5.1.5 Other routes
No data.
5.2 Chronic toxicity
5.2.1 Ingestion
Clinitest(R) tablets
A 71 year old woman developed gastritis and eschar formation in the
lower two thirds of the stomach after accidentally ingesting 47
Clinitest(R) tablets over a period of 1 month. Her oesophagus was
normal. She made a full recovery (Mallory and Schaefer, 1977).
5.2.2 Inhalation
Obstructive airway disease has been reported following chronic
occupational exposure to sodium hydroxide mist. The patient developed
cough, dyspnoea and tachypnoea after a 20 year exposure to sodium
hydroxide. The solution was used to clean jam containers which were
boiled in it for two hours. He had a barrel chest with limited
movements and diffuse expiratory wheezing. A chest X-ray showed severe
pulmonary hyperinflation (Rubin et al, 1992).
5.2.3 Dermal
No data.
5.2.4 Ocular
No data.
5.2.5 Other routes
No data.
5.3 Systematic description of clinical effects
5.3.1 Cardiovascular
Tachycardia and hypotension may occur in patient with severe corrosive
damage to the gastrointestinal tract resulting in haemorrhage or
perforation.
Oesophago-aortic fistulae and rupture of the aorta are rare
complications of corrosive ingestion (Ottoson, 1981), they has also
been reported following ingestion of Clinitest(R) tablets (O'Connor et
al, 1984). Pericarditis may occur (McCabe et al, 1969; Matenga et al,
1987).
5.3.2 Respiration
Acute
Dyspnoea and stridor may occur and in severe cases there may be upper
airway obstruction. Recurrent atalectasis and pneumonia developed in
two adults who suffered bronchial burns after ingestion of sodium
hydroxide (Meredith et al, 1988)
Mediastinitis may occur (McCabe et al, 1969; Matenga et al, 1987;
Allen et al, 1970).
Tracheo-oesophageal fistulae and less commonly, broncho-oesophageal
fistulae, have been reported following ingestion of alkalies (McCabe
et al, 1969; Sarfati et al, 1987; Balasegaram, 1975). They have also
been reported to form as a complication of oesophageal dilatation
(Mutaf et al, 1995). The main symptoms of a tracheo-oesophageal
fistula are persistent pneumonia, choking and cyanosis while feeding.
Pulmonary oedema may occur following inhalation of vaporised caustics.
Chronic
Obstructive airway disease has been reported following chronic
occupational exposure to sodium hydroxide mist. The patient developed
cough, dyspnoea and tachypnoea after a 20 year exposure to sodium
hydroxide. The solution was used to clean jam containers which were
boiled in it for two hours. He had a barrel chest with limited
movements and diffuse expiratory wheezing. A chest X-ray showed severe
pulmonary hyperinflation (Rubin et al, 1992).
5.3.3 Neurological
Neurological effects are not expected with sodium hydroxide exposure,
except the psychiatric complications of patients requiring long-term
therapy and the effects of inability to speak or swallow.
5.3.4 Gastrointestinal
Ingestion of sodium hydroxide may cause an immediate burning pain in
the mouth, oesophagus and stomach (retrosternal and epigastric pain),
with swelling of the lips. This is followed by vomiting, haematemesis,
increased salivation, ulcerative mucosal burns and dysphagia.
Oesophageal and pharyngeal oedema may occur.
It should be noted that oesophageal damage may occur in the absence
of oral burns (Krenzelok and Clinton, 1979; Kynaston et al, 1989).
Acute complications
These include gastrointestinal haemorrhage and perforation of the gut
(suggested by increasing abdominal pain, persistent vomiting, direct
and indirect tenderness and a rigid abdominal wall).
Gastric ulcers on the greater curvature and the antrum have been
reported following ingestion of capsules filled with sodium hydroxide
(Gill et al, 1986; Carroll et al, 1994; Oakes et al, 1982; Lowe et al,
1979).
Late complications
Oesophageal stricture and pyloric stenosis may occur as late
complications. Stricture formation usually begins to develop 14-21
days after ingestion. Most strictures become manifest within the first
two months. Strictures may prevent an adequate nutritional intake and
in severe cases patients may be unable to swallow their own saliva.
Healing of oesophageal injury depends on the severity of the injury.
In the study by Di Costanzo et al (1980) first degree burns healed in
about a week, second degree burns in 20-30 days and third degree burns
within 90 days.
Gastric necrosis and stricture may occur, usually in patients who have
oesophageal injury as well. Gastric injury is more likely to occur
following ingestion of liquid sodium hydroxide than ingestion of the
solid. The small intestine may also be involved, dudodenal and colonic
necrosis has also been reported with ingestion sodium hydroxide
solution (Guth et al, 1994).
Oesophago-aortic fistulae and rupture of the aorta are rare
complications of corrosive ingestion (Ottoson, 1981).
Tracheo-oesophageal fistulae and less commonly, broncho-oesophageal
fistulae, have been reported following ingestion of alkalies (McCabe
et al, 1969; Sarfati et al, 1987; Allen et al, 1970). They have also
been reported to form as a complication of oesophageal dilatation
(Mutaf et al, 1995). The main symptoms of a tracheo-oesophageal
fistula are persistent pneumonia, choking and cyanosis while feeding.
Severe corrosive injury to the stomach may result in small scarred
immobile stomach and in such cases small, frequent intakes of food may
be necessary to prevent dumping syndrome (Meredith et al, 1988.
Achlorhydria with reduced or absent intrinsic factor may also occur.
(Dumping syndrome is a complex reaction thought to be secondary to
excessively rapid emptying of gastric contents into the jejunum.
Clinical effects include nausea, sweating, palpitations, syncope and
diarrhoea).
Alkalis are known to increase the risk of oesophageal cancer, which
can occur years after the initial injury (Isolauri and Markkula, 1989;
Appelqvist and Salmo, 1980; Ti, 1983; Hopkins and Postlethwait, 1981;
Benirschke, 1981; Kinnman et al, 1968). The incidence of carcinoma
following oesophageal injury from sodium hydroxide is 0.8-4% - see
section 9.1.
Clinitest(R) tablets
These are easily mistaken for oral medication and can cause severe
oesophageal injury if ingested. They can become lodged in the
oesophagus and cause stricture formation. Strictures are usually short
and located at about the level of carina (Burrington, 1975), they
generally take. Gastric ulcerations have also been reported (Oakes et
al, 1982). A 71 year old woman developed gastritis and eschar
formation in the lower two thirds of the stomach after accidentally
ingesting 47 Clinitest(R) tablets over a period of 1 month. Her
oesophagus was normal. She made a full recovery (Mallory and Schaefer,
1977). Death from an oesophago-aortic fistula has been reported
(O'Connor et al, 1986).
5.3.5 Hepatic
Jaundice with an elevated alkaline phosphatase concentration has been
reported in a fatal case of sodium hydroxide ingestion. The authors
postulated that biliary obstruction due to oedema, following burns of
the ampulla as a possible explanation for this finding (Matenga et al,
1987).
5.3.6 Urinary
No data.
5.3.7 Endocrine and reproductive system
No data.
5.3.8 Dermatological
Sodium hydroxide causes deep penetrating burns and necrosis. The skin
is discoloured brown or black which may make initial assessment of the
injury difficult. There may be recurring skin breakdown over a long
period (O'Donoghue et al, 1996).
Dermal alkali injuries differ from those of other burns for a number
of reasons:
* The injury may be painless and not be immediately evident. This
initial lack of pain may lead to a delay in treatment.
* Injury can progress over several hours.
* Also initial assessment of the burn depth may be difficult
because the skin may be discoloured brown or black within a short
period of time.
5.3.9 Eye, ears, nose and throat
Ocular
Sodium hydroxide is responsible for some of the most severe, blinding
injuries to the eye. There is intense pain with blepharospasm. Visual
acuity is decreased due to injury to the corneal epithelium and
corneal oedema.
In mild cases there may be sloughing of the corneal and conjunctival
epithelium. In more severe cases there may be conjunctival swelling
(chemosis) and necrosis with hazing or opacity of the cornea. There is
a rise in intraocular pressure initially as the sclera of the eye
shrinks and then with a release of prostaglandins.
Severe burns are characterised by ischaemic necrosis. This is due to
reduced or absent blood flow as a result of thrombosed blood vessels
which leaves the conjunctiva and sclera white. If the eye has been
penetrated fibrin may be present in the anterior chamber with
infiltration of inflammatory cells. The pupil may be dilated and
unreactive due to damage to the sphincter and dilator muscles. Retinal
damage may also occur in severe ocular burns.
Assessment of the injury and a prognosis may be difficult until 48-72
hours after the exposure (Pfister and Koshi, 1982).
There may be involvement of the lids with erythema, oedema or
blistering or in severe cases ischaemic necrosis.
Late complications of severe ocular burns include: persistent oedema,
glaucoma, vascularisation of cornea, fibrous tissue scarring of
cornea, growth of vessels throughout cornea, ulceration, perforation,
permanent opacity, staphyloma, phthisis bulbi (shrinkage and wastage
of eyeball), cataract and symblepharon (adhesion between tarsal
conjunctiva and bulbar conjunctiva).
5.3.10 Haematological
Neutropaenia and thrombocytopenia have been reported in a fatal case
of sodium hydroxide ingestion (Matenga et al, 1987).
5.3.11 Immunological
No data.
5.3.12 Metabolic
5.3.12.1 Acid-base disturbances
Lactic acidosis may occur in severe cases due to tissue damage and
shock (Okonek et al, 1981).
5.3.12.2 Fluid and electrolyte disturbances
None.
5.3.12.3 Other
None.
5.3.13 Allergic reactions
No data.
5.3.14 Other clinical effects
None.
5.4 At risk groups
5.4.1 Elderly
Since the elderly are not involved in occupations involving sodium
hydroxide they are at less risk of exposure. However they may still be
exposed in the domestic setting or from motor car air bags. Accidental
ingestion of Clinitest(R) tablets is also a problem in this age group.
5.4.2 Pregnancy
Not applicable.
5.4.3 Children
Children are at particular risk of exposure to sodium hydroxide in the
home where they may sustain dermal, ocular or gastrointestinal injury.
Ocular injury has been reported in a child following activation of an
motor car air bag (Ingram et al, 1991). Children are also at risk from
accidental ingestion of Clinitest(R) tablets.
5.4.4 Enzyme deficiencies
Not applicable.
5.4.5 Enzyme induced
Not applicable.
5.4.6 Occupations
There is a risk of exposure to sodium hydroxide in a number of
occupations including chemical workers, those involved in the
manufacture of sodium hydroxide and cleaners using sodium hydroxide
containing products.
5.4.7 Others
Dermal (Swanson-Biearman et al, 1993) and ocular (White et al, 1995;
Smally et al, 1992; Swanson-Biearman et al, 1993) burns have been
reported from exposure to sodium hydroxide following activation of
motor car air bags.
6 MANAGEMENT
6.1 Decontamination
Ingestion
Gastric lavage and emesis are contraindicated because of the risks of
further injury on re-exposure of the oesophagus. Nasogastric
aspiration of the stomach contents is probably less effective for
ingestion of alkali than for acids, since alkalis tend to damage the
oesophagus rather than the stomach. Oral fluids should be given (Homan
et al, 1994) unless there is evidence of severe injury. Neutralising
chemicals should never be given because heat is produced during
neutralisation and this could exacerbate any injury (Rumack and
Burrington, 1977).
Ingestion of Clinitest(R) tablets
Orange juice or milk should be given to drink as soon as possible
after ingestion of a Clinitest(R) tablet as this reduces the rate of
release of heat of reaction. Water should be given if milk is not
available. Even late administration of diluents may be beneficial
because of the non-uniform break up of tablets (Lacoutre et al, 1986).
Ocular
Copious and immediate irrigation of exposed eyes is essential. Water
(preferably sterile) or normal saline may be used, although other
solutions have been employed in an emergency including tap water,
Hartmans solution and universal buffer solution. Particulate matter
should be removed with cotton wool buds or forceps. The pH of the
cornea and irrigating fluid from the eye should be monitored with
universal indicator paper. Irrigation should be continued until the pH
of the eye is normal and remains so for 2 hours.
Pain and blepharospasm may make irrigation difficult and the use of
anaesthetic drops (e.g. amethocaine, lignocaine) may be needed to
facilitate thorough irrigation. A lid speculum may be used if
required. It is essential that the whole eye is irrigated including
under the upper and lower lids. The use of an irrigating contact lens
or an anterior chamber tap (paracentesis) have also been recommended
(Nelson and Kopietz, 1987; Pfister and Koshi, 1982).
Dermal
All contaminated clothing must be removed. Copious irrigation of the
skin should be commenced immediately. If an extensive area has been
exposed whole body irrigation should be undertaken preferably using a
high-flow shower unit. The burnt areas should then be covered with wet
compresses during transfer to hospital (Herbert and Lawrence, 1989).
See supportice care for further details.
6.2 Supportive care
Ingestion
Asymptomatic/mildly symptomatic patients
It should be noted that oesophageal damage may occur in the absence
of oral burns (Krenzelok and Clinton, 1979; Kynaston et al, 1989).
These patients must be admitted for observation until the extent of
the injury (if any) can be determined. Oral fluids may be given if the
patient is willing to drink. Oral feeding should be maintained if the
patient is able to tolerate it, otherwise tube feeding or parenteral
nutrition should be provided. On discharge all patients must be
advised on the possibility of late onset sequelae and advised to
return if necessary.
Severely affected patients
Treatment is supportive. In severely affected patients aggressive
intervention is essential (Meredith et al, 1988; Hendrickx et al,
1990; Andreoni et al, 1995). Urgent assessment of the airway and
endoscopic evaluation is required (see section 6.6 Investigations). A
supraglottic-epiglottic burn with erythema and oedema is usually an
sign that further oedema will occur which will lead to airway
obstruction and is an indication for early intubation or tracheostomy
(Meredith et al, 1988). See section 6.7 Management controversies.
Give plasma expanders/intravenous fluids for shock and check and
correct the acid/base balance. Analgesia will almost certainly be
needed. Intubation and ventilation may be necessary for patients with
respiratory distress. Appropriate antibiotic therapy should be given
if necessary. Parenteral feeding will be necessary.
Late complications
Strictures that prevent adequate nutritional intake and do not respond
to dilatation require oesophagectomy and colonic interposition.
Oesophageal strictures which result in a lumen >10mm do not impede
normal life and should not require intervention (Sarfati et al, 1987).
Surgical intervention may also be required for gastrointestinal
perforation or haemorrhage.
There may be loss of speech and inability to swallow as a result of
severe corrosive injury. Speech and swallowing rehabilitation is a
complex subject and is discussed by Shikowitz et al (1996) with
description of the surgical techniques used and the tools used to
determine the success of the reconstruction.
Severe cases of sodium hydroxide ingestion may result in long-term
hospitalisation and repeated surgical procedures. Psychological
support is recommended.
Ocular
After irrigation further treatment is aimed at preventing optic nerve
damage from raised intraocular pressure and to protect the cornea from
ulceration, perforation and infection (Nelson and Kopietz, 1987).
Raised intraocular pressure can be managed with topical beta-blockers
(e.g timolol).
Broad spectrum antibiotic drops (e.g. gentamicin, chloramphenicol) are
recommended in cases of epithelial damage. Delayed epithelial healing
is common after severe alkali burns and the use of 'bandage' soft
contact lenses have been recommended to speed up the process (Nelson
and Kopietz, 1987; Pfister and Koshi, 1982). Mydriatic drops, such as
atropine, may alleviate pain but a short acting mydriatic may be
better, particularly in the elderly who are at risk of glaucoma from
mydriasis (Beare, 1990b).
In the long-term care of chemical injuries to the eye the main problem
is dry eyes due to damage to the Meibomian glands, presence of mucin-
secreting globlet cells on the eye surface or scarring of the tear
ducts. The use of tear film substitutes (e.g. hypromellose drops) may
be beneficial in such cases. Chronic glaucoma and recurrent epithelial
breakdown are other common problems and make patients with alkali
damaged corneas poor candidates for corneal grafting.
Corneal grafting should not be attempted until 12-18 months after the
injury once the inflammatory response has settled. The failure rate is
high, about 50-70% (Pfister and Koshi, 1982) because of the reasons
stated above. In cases where grafting fails a keratoprosthesis is a
last resort but this has a high complication and failure rate (Pfister
and Koshi, 1982).
Plastic surgery may be required for correction of other problems
including cicatricial lid deformities, trichiasis (ingrowing
eyelashes) and symblepharon.
See also section 6.7 Management Controversies.
Dermal
On arrival at hospital analgesia, oxygen therapy and intravenous fluid
replacement should be commenced if the clinical condition of the
patient warrants it. Assessment of the depth and extent of injury is
not reliable at an early stage.
The most important therapy for dermal alkali injuries is prolonged
copious irrigation. This effectively cleanses the wound of unreacted
chemical, dilutes the chemical already in contact with tissue and
restores tissue water lost to the hygroscopic effect of alkalis
(Leonard et al, 1982). The earlier the irrigation is begun the greater
the benefit. Irrigation should, therefore, be started as soon as
possible and continued, in hospital, until the pH of the skin is no
longer alkaline. In the 273 cases reported by Bomberg et al (1965)
irrigation was continued for between 6 hours and 6 days (mean 24
hours). In this study, irrigation was shown to reduce the length of
stay in hospital, the time to grafting and the number of cases
requiring surgery.
Irrigation of the injury site at the scene of the accident has also
been shown to decrease the incidence of full thickness skin loss and
to significantly reduce hospital stay and morbidity (Leonard et al,
1982).
Testing the pH of the skin immediately after irrigation may be
misleading. It is recommended that 15 minutes elapse before this is
undertaken to allow residual alkali to diffuse up from the deeper
regions of the dermis (Herbert and Lawrence, 1989; O'Donoghue et al,
1996).
Spontaneous separation of the eschar (the slough produced by a burn)
following a chemical burn takes about 30 days, which is much longer
than with thermal burns. Waiting for this to occur prolongs treatment
and O'Donoghue et al (1996) recommend irrigation followed by early
excision of the injury site followed by immediate skin grafting for
the best results. (Debridement is the removal of foreign material or
dead skin from or adjacent to a traumatic or infected lesion until
healthy tissue is exposed).
Referral to a burns unit is recommended.
6.3 Monitoring
Ingestion/dermal exposure
In severely affected patients it will be necessary to monitor the
airway and respiratory status and blood gases. The patient should also
be monitored for signs of shock.
Ocular exposure
Intraocular pressure should be monitored.
6.4 Antidotes
None relevant.
6.5 Elimination techniques
None relevant.
6.6 Investigations
Ingestion
Abdominal and chest X-rays need to be taken to check for perforation.
Endoscopic examination
If facilities allow gastro-oesophagoscopy should be undertaken to
assess the extent and severity of the injury. This procedure can be
safely undertaken within 9-96 hours of the ingestion. It should be
avoided 5-15 days post-ingestion because this is the time period over
which the tissues slough and there is increased risk of perforation.
Endoscopy is contraindicated in patients with third degree burns of
the hypopharynx, burns involving the larynx or those with respiratory
distress. Where there is complete obliteration of the oesophageal
lumen the procedure should be terminated and repeated 48 hours later
(Ali Zargar et al, 1991).
Traditionally the endoscopist terminates the procedure at the first
deep, penetrating and/or circumferential burn because of the risk of
perforation. However with a flexible endoscopy the stomach and small
intestine (panendoscopy) can be examined regardless of the presence of
second or non-perforating third degree burns to the oesophagus (Ford,
1991). Ali Zargar et al (1991) recommend examination of the stomach
and the first part of the duodenum.
Pharyngolaryngoscopy and bronchoscopy are also recommended in severely
affected patients. Laparotomy evaluation of the gastrointestinal tract
beyond the oesophagus may also be indicated if there are second or
third degree circumferential burns of the oesophagus (Meredith et al,
1988).
Oesophageal burns are generally classified by the following
description (Ford, 1991):
* first degree - erythema and oedema.
* second degree - erythema, blistering, superficial ulceration,
fibrinous exudate.
* third degree - erythema, deep ulceration, friability, eschar
formation, perforation.
First degree burns do not cause strictures, second degree burns result
in strictures in 15-30% of cases but third degree injury results in
stricture formation in over 90% of cases (Howell, 1986).
Follow up appointments should be made on discharge because of the risk
of delayed damage and the patient should be advised to return in the
meantime if there is any evidence of oesophageal stricture (suggested
by vomiting, weight loss, bloating and anorexia). Patients who develop
strictures will require monitoring for life for the development of
malignant disease of the oesophagus.
Ocular
Ophthalmological referral is essential for alkali burns to the eye.
Visual acuity and intraocular pressure should be checked if possible.
The eye stained with fluorescein since this will reveal the full
extent of conjunctival and corneal epithelial loss (Beare, 1990b).
6.7 Management controversies
Ingestion
Management of severe corrosive injury
Although it is agreed that the aim of initial management is the
prevention of strictures, there is no consensus on the management of
severe corrosive injury to the oesophagus and stomach. A number of
very useful reviews have been published on the subject (Shaffer et al,
1994; Andreoni et al, 1995; Ford, 1991; Moore, 1986; Postlethwait,
1983; Klein-Schwartz and Oderda, 1983; Knopp, 1979). There is no
question of the value of endoscopic investigation to determine the
extent and severity of the injury although there is some debate on the
relative usefulness of different types of endoscope (rigid and
flexible). Some authors recommend early aggressive treatment (Andreoni
et al, 1995; Hendrickx et al, 1990; Meredith et al, 1988; Gossot et
al, 1987; Thompson, 1987; Estrera et al, 1986; Kirsh et al, 1978;
Allen et al, 1970) while others recommend more conservative therapy
(Ribet et al, 1990), particularly in children (Gandhi et al, 1989;
Rappert et al, 1993; Gundogdu et al, 1992).
Oesophagogastrectomy or gastrectomy (partial or total) has been
recommended for large areas of necrosis to prevent perforation and
subsequent peritonitis or mediastinitis. In practice this will only be
necessary in a small number of patients. In the experience of Gossot
et al (1987), which includes ingestion of acids as well as alkalies, a
necrotic stomach always leads to perforation. There is also the risk
of fistula formation which can occur between the oesophagus and the
trachea, bronchus or aorta. Gossot et al (1987) found a high mortality
rate with oesophagectomy performed transthoracically (76%) and
recommend the removal of a necrotic oesophagus by a transhiatal blunt
dissection and stripping technique. In the small number of patients on
which this was performed the mortality rate was 38%. The authors
suggest that the avoidance of thoracotomy may prevent the occurrence
of tracheobronchial lesions.
Meredith et al (1988) recommend gastrostomy with placement of a string
to guide future dilatations for patients not undergoing gastrectomy or
oesophagogastrectomy. Early implacement of a intraluminal stent has
also been recommended to prevent the formation of strictures (Estrera
et al, 1986; Wijburg et al, 1989).
Gandhi et al (1989) recommend the use of string-guided oesophageal
dilatation with endoscopically guided steroid injection as a safe and
reliable method for the treatment of oesophageal strictures in
children. In these cases there was no need for oesophageal replacement
or resection in most patients. In the study by Gundogdu et al (1992)
it was found that conservative treatment of strictures was more
successful in children under 8 years of age.
The use of steroids and antibiotics in the management of corrosive
oesophageal injury
Steroids have an anti-inflammatory effect and decrease fibroblastic
activity and scar tissue formation. Animal data has demonstrated that
strictures formed in subjects given steroids have been less well
structured with fewer inflammatory changes and less fibrin deposition
(Spain et al, 1950; Rosenberg et al, 1953). The use of steroids for
corrosive injury in man is a controversial subject which has generated
a huge amount of literature.
Middlekamp et al (1969) reported thirty-two cases of oesophageal burns
due to alkali injury, none of the patients with first degree burns
(nineteen cases) developed oesophageal stricture. One patient (out of
six) with second degree burns and all patients with third degree burns
(seven) developed oesophageal stricture.
In a study by Anderson et al (1990) on the use of steroids in children
with corrosive injury of the oesophagus, of one hundred and thirty-one
children sixty had oesophageal burns. Of these burns, fifty-five were
caused by known agents, 91% of which were alkaline. Oesophageal
stricture developed in ten of the thirty-one children treated with
steroids and in eleven of the twenty-nine controls. Nine of the ten
patients in the steroid group had third degree burns and one had
second degree injuries, all eleven patients in the control group had
third degree burns. Twenty-one patients given steroids and eighteen
controls did not develop strictures, of these children all but one had
first or second degree injuries.
Several authors have found that it is the depth of the initial burn
rather than the initial treatment which determines the outcome
(Anderson et al, 1990; Moazam et al, 1987; Webb et al, 1970; Oakes et
al, 1982).
The main aim of the management of alkali injury is to reduce stricture
formation. The role of steroids in alkali injury is still the subject
of much debate, however most authors agree that patients with first
degree burns do not require steroids since these burns usually heal
without stricture formation. The difficulty here is determining the
severity of the injury from oesophagoscopy since it is difficult to
determine the depth of the burn and the endoscope cannot be passed
beyond the first identified burn due to the risk of perforation. Some
burns are so severe and extensive that strictures may develop despite
steroid therapy (Haller et al, 1971) and may be delayed (Middlekamp et
al, 1969).
In summary, steroids are probably most effective for second degree or
moderately severe burns (Klein-Schwartz and Oderda, 1983; Hawkins et
al, 1980; Webb et al, 1970). They are not necessary for first degree
burns and appear to be ineffective in preventing stricture formation
following third degree burns. However, there is no clinical evidence
that steroid therapy is more effective than non-steroid therapy in
reducing oesophageal stricture in any patient, even those with second
degree burns. Some authors believe there is no place for steroid
therapy in the management of corrosive injury (Wijburg et al, 1989; Di
Costanzo et al, 1980). As Oakes et al (1982) state, clinicians should
not feel compelled to institute steroid therapy for caustic
oesophagitis simply because it is considered 'standard therapy'.
Contraindications and problems in steroid therapy
It should be noted that there are definite contraindications to the
use of steroids, these are as follows:-
a) active infection
b) perforation of the gastrointestinal tract or secondary
mediastinitis
c) significant gastrointestinal bleeding
d) history of or active ulcer
Steroids depress the immune system and as a result the patient is more
susceptible to infection. Also steroids may mask the signs and
symptoms of infection as well as those of perforation and peritonitis.
Steroid therapy may also result in a thin-walled oesophagus vulnerable
to perforation due to reduced wound healing and scar formation
(Cardona and Daly, 1971).
When to begin therapy
Once the decision has been made to use steroids therapy should be
started within 24-48 hours of the injury because the major
inflammatory insult occurs within the first 48 hours and after this
time steroids have little antifibroblastic activity. Therapy started
later may reduce scar formation but all evidence indicates that the
best results are obtained with early institution of therapy (Haller et
al, 1971). The short duration of steroid therapy should not produce a
significant reduction in intrinsic steroid production or alter the
metabolic balance.
Antibiotics
Antibiotics should be used in all patients with evidence of infection.
Some authors suggest that prophylactic antibiotics should be given in
patients on steroid therapy (Howell et al, 1992; Hoffman et al, 1990;
Adam and Birck, 1982), but others considered this unnecessary (Wijburg
et al, 1989; Klein-Schwartz and Oderda, 1983; Wijburg et al, 1985)
since the risk of infection is low (Knopp, 1979).
Lathyrogens
Lathyrogens are drugs which decrease the strength of collagen fibres
through interruption of the covalent crosslinks between newly formed
collagen molecules. Although animal data has demonstrated that
lathyrogens are effective in preventing stricture formation (Butler et
al, 1977) their efficacy in man is as yet undetermined (Moore, 1986).
Ocular burns
A number of substances have been investigated in the treatment of
alkali burns of the eye with the aim of reducing the severity of
damage.
Ascorbate (ascorbic acid)
Ascorbate is required for the formation of collagen and production is
reduced when the ciliary body is damaged by alkali burns. It may also
act as a scavenger of free radicals released by the infiltrating
polymorphonuclear leucocytes.
Animal experiments with systemic and topical ascorbate has produced
conflicting results (Grant and Schuman, 1993; Pfister, 198; Pfister et
al, 1982). Wright (1982) suggests the use of 10% sodium ascorbate
drops hourly by day for 4-6 weeks. Systemic ascorbate may also be
given (1g daily), but topical ascorbate is favoured over systemic
because damage to the ciliary epithelium impairs transport of
ascorbate across the blood-aqueous barrier.
Collagenase inhibitors
These have been used because there is evidence that collagenases
released by infiltrating polymorphonuclear leucocytes can cause the
breakdown of corneal stroma. Various agents have been tried including
cysteine, acetylcysteine, sodium and calcium EDTA, penicillamine.
Animal experiments have produced conflicting results (Wright, 1982;
Grant and Schuman, 1993) and there are currently no recommendations
for the use of collagenase inhibitors in alkali injury to the eye.
Sodium citrate
Citrate is thought to prevent the degranulation of polymorphonuclear
leucocytes and thereby reduce the production of free radicals and
proteolytic enzymes, and it has been suggested that the use of topical
10% citrate may be beneficial in the treatment of alkali-induced
corneal ulcers (Pfister et al, 1988).
Steroids
Steroid therapy in the treatment of alkali-induced ocular injury is
controversial. Is should only be considered for the treatment of
severe burns. Wright (1982) suggests topical steroid therapy in cases
of severe burns but only where stromal melting is absent and then to
change to a collagenase inhibitor such as sodium citrate. However,
clinical data to support their use is lacking and Pfister and Koshi
(1982) advise avoiding topical steroids where possible because they
interfere with the healing process.
Prostaglandin inhibitors
Prostaglandins are important in the recruitment of polymorphonuclear
leucocytes but an effective topical prostaglandin preparation is not
readily available and data on the benefit of such therapy is lacking.
Numerous other treatments have been recommended (as reviewed in Grant
and Schuman, 1993) but with no outstanding success.
7 CASE DATA
Literature
Case 1: Accidental ingestion, child
A 16 month old female refused to drink and began drooling after
ingesting the residue of a sodium hydroxide solution which the mother
had been using for cleaning. She vomited several times with the
vomitus containing a small amount of blood. The pharynx was red and
there was slight bleeding of the upper gums. The chest was initially
clear but 90 minutes after admission inspiratory and expiratory
wheezes were present and a chest X-ray suggested aspiration pneumonia.
At 15 hours post-ingestion laryngoscopy and oesophagoscopy were
performed. The false cords and epiglottis were found to be red and
oedematous. The cricopharyngeus was ulcerated and bleeding. The
oesophageal mucosa was bleeding and circumferential second and third
degree burns were present. The child required intubation and
ventilation and was started on methylprednisolone and ampicillin.
Ventilatory support was necessary for three weeks. Subsequent
laryngoscopy revealed laryngeal oedema and burns which resulted in
laryngeal stenosis. An oesophagoscopy at five weeks post-ingestion
revealed oesophageal narrowing. A barium swallow showed multiple
oesophageal strictures and hypoperistalsis of the proximal segment of
the oesophagus. The child required nine oesophageal dilatations, and
was eventually able to take oral feedings. She was discharged one year
after the ingestion (Klein-Schwartz and Oderda, 1983).
Case 2: Accidental ingestion, fatal
A 14 year old boy took a sodium hydroxide solution (30%) in to his
mouth. He immediately spat it out. He drank some milk and water and
vomited. On arrival about 30 minutes later he had retrosternal pain
and had difficulty swallowing. He was given antibiotics and steroids.
Oesophagoscopy was performed two days later and revealed mucosal
lesions in the upper oesophagus. He began to improve and was able to
take mashed food orally. He then began to develop difficulty in
swallowing and a X-ray on day 23 revealed a stricture at the level of
the carina of trachea. On the 38th day oesophagoscopy with dilatation
of the stricture was performed. About 2 hours later he suffered
immediate retrosternal pain. An X-ray showed perforation of the
stricture. This was sown up via a left side thoracotomy. Serious
inflammatory changes were observed with mediastinal emphysema and a
purulent pleuritis. A nasogastric tube and three drains were left in
place. On the 44th day after ingestion profuse bleeding was observed
through the nasogastric tube and drains was noted. He became shocked
and the decision was made to operate. He suffered a cardiac arrest
while general anaesthetic was being given. A right side thoracotomy
showed a 4-5 mm rupture of the descending part of the aorta with
bleeding into the left pleura. After cardiac massage, blood
transfusion and repair of the rupture he stabilised. Part of the
oesophagus was removed due to inflammation. On day 52 another
haemorrhage occurred. He was operated on again and the haemorrhage was
seen to arise from the aortic rupture. The aorta wall was fragile and
could not be repaired. The patient died on the operating table. A
purulent mediastinitis, bilateral purulent pleuritis, lung atalectasis
and pericarditis were observed at postmortem (Ottoson, 1981).
Case 3: Accidental ingestion, adult
A 19 year old male vomited immediately after ingestion of 2 mouthfuls
of sodium hydroxide. He had drunk it thinking it was wine. He was seen
in hospital within 6 hours. He had deep oral and hypopharyngeal burns,
full thickness necrosis of the entire oesophagus and stomach and
mucosal burns of the bronchus. He required an emergency treacheostomy
and oesophagogastrectomy with establishment of a cervical
oesophagostomy. A chimney jejunostomy was constructed to provide
access for enteral feeding. His post-operative course was complicated
by recurrent atelectasis and pneumonia secondary to the bronchial
burns, bowel obstruction and wound complications. He was discharged 6
weeks after the incident with a tracheostomy and jejeunostomy. He
developed dense scarring and stenosis of the hypopharynx which
required multiple laser excisions to restore pharyngeal lumen. After 9
months he underwent oesphagagogastric reconstruction with an
antiperistaltic left colon interposition from the hypopharynx to the
duodenum. Supraglottic scarring required further laser excisions and
dilatations over the next 18 months. More than 2 years after the
event, he was eating a normal diet and speaking clearly but still
occasionally required dilatation of the pharynx (Meredith et al,
1988).
This patient was one of nine individuals (aged 15-25 years) who
sustained severe corrosive injury to the stomach and oesophagus after
drinking sodium hydroxide solution in mistake for wine. The solution
had been kept in the fridge for the making of pretzels. The container
resembled a wine bottle and was labelled in German (Meredith et al,
1988; Chen et al, 1988; Thompson, 1987).
Case 4: Clinitest(R) ingestion, fatal
A 77 year old partially deaf diabetic woman accidentally swallowed 2
Clinitest(R) tablets. There was no evidence of oropharyngeal
ulceration. She was given milk to drink and discharged the next day.
She returned 2 weeks later with increasing dysphagia and could only
swallow fluids. An endoscopy revealed an oesophageal stricture. She
died three days later after a massive haematemesis. Postmortem
revealed an ulcer in the upper oesophagus which had penetrated and
perforated the aortic wall to form a oesophago-aortic fistula. There
was no evidence of pharyngeal or gastric ulceration (O'Connor et al,
1984).
Case 5: Clinitest(R) ingestion, child
A 17 month old child was brought to hospital because of increasing
dysphagia of 2 weeks duration. Clinitest(R) tablets were kept in the
home. A barium swallow revealed a short oesophageal stricture.
Repeated dilatation were of no lasting benefit even after gastrostomy
and passage of a string through the oesophagus. After 19 dilatations
in 3 months she underwent resection and primary anastomosis.
Post-operatively she required 8 dilatations over 12 months before she
could eat normally (Burrington, 1975).
Case 6: Ingestion of encapsulated sodium hydroxide
A 31 year female was admitted to hospital after ingestion that day of
3 gelatin capsules which she had filled with sodium hydroxide drain
cleaner. She complained of abdominal cramping. Endoscopy revealed
ulcerative, exudative oesophagitis in the mid to distal region. There
were three deep ulcers along the greater curvature of the stomach with
black necrotic debris in the centre. She was given antibiotics and
corticosteroids and discharged after 7 days. One month after ingestion
she returned with haematemesis and melaena. Endoscopy revealed
persistence of the ulcers in the stomach, one had evidence of recent
bleeding. She discharged herself after 4 days. Similar gastric
ulceration was observed in another patient who ingested four capsules
of the same drain cleaner. These had healed by 6 weeks post-ingestion
(Gill et al, 1986).
Case 7: Dermal exposure, fatal
A 32 year old man was working in an area of a plant were hot sodium
hydroxide was being used. It is thought that he was accidentally
exposed to a spray and aerosol of the alkali which caused him to run
for the shower. Before he reached it he fell or collapsed into a pool
of sodium hydroxide. He was found next to the shower face down. He was
turned over and sprayed with copious amounts of water but was found to
be dead. A postmortem was performed 40 hours later but chemical damage
was observed to be progressing 3 days later, just prior to the
funeral. At postmortem the cotton clothing was found to be in good
condition but the leather gloves and boots were badly disintegrated.
The left boot had dissolved, only the steel toe cap and sole remained.
There were severe burns present, in some cases with total soft tissue
destruction down to the bone. Both eyes were severely damaged with
perforation of one. On the left side of the neck the skin and fat was
totally absent revealing the underlying muscles and vasculature. The
left side of the body was most severely damaged. There were some
changes to the respiratory tract indicating a minor degree of
inhalation. There was extensive epithelial loss of the tongue and the
stomach wall was found to be neutral indicating ingestion of a small
amount of alkali. In a re-enactment of the accident it was found that
the time taken for work boots to become damaged to the same degree as
the victim's under similar circumstances was about 13 minutes (Lee and
Opeskin, 1995).
Case 8: Dermal exposure requiring skin graft
A 20 year old patient presented 2 hours after accidentally spraying
herself in the face with an oven cleaner containing 4% sodium
hydroxide. She had removed the excess liquid but did not irrigate the
area. She did not experience any pain until nearly 2 hours later. On
examination she was in moderate distress with no ocular involvement.
The right side of her face was erythematous and blistering in a
serpiginous pattern extending from the infraorbital rim to the body
and angle of her mandible. The area of the right cheek had a bronze
discolouration. The body surface area involved was about 2%. The area
was irrigated for 60 minutes. Despite this the burn continued to show
signs of third degree burn involvement. She was transferred to a burns
unit and underwent surgical debridement and skin graft. Follow up six
weeks later revealed good healing and no complications (Lorette and
Wilkinson, 1988).
Case 9: Ocular injury
A 31 year man had sodium hydroxide blown into his amblyopic left eye
after an explosion caused by placing solid sodium hydroxide into a
plugged drain. He washed the eye immediately in a shower and arrived
at hospital within 5 minutes. On examination the cornea was opaque and
the lower two thirds of the conjunctiva was ischaemic. Topical
irrigation was repeated and he was transferred to the operating room
where intraocular irrigation was commenced. About 100-120ml of
Ringer's solution was used in this procedure over 90 minutes. At this
time the cornea was slightly clearer. Methylprednisolone was given by
retobulbar and subconjunctival injection. Continuous slow topical
irrigation was continued for a further 24 hours. On the first
post-operative day visual acuity was present to light, intraocular
pressure was high and a cataract was present. Topical antibiotics,
systemic and topical corticosteroids and carbonic anhydrase inhibitors
were given. Two weeks after the injury aspiration-irrigation of the
cataract was undertaken with an improvement in visual acuity.
Acetylcysteine drops were used and a soft contact lens was put in
place. He was discharged three weeks after the injury but returned
three days later with severe pain, hypopyon and hyphema. The cornea
ulcerated and perforated 27 days after the injury. The perforation was
repaired with a corneoscleral free hand graft. Despite the presence of
light perception the eye was enucleated at the patient's request 70
days after the injury (Burns and Hikes, 1979).
Internal cases
1) A 63 year old male died within 1 hour of admission after ingestion
of sodium hydroxide. He had ingested 10 teaspoons in a glass of water.
He developed pain in the mouth and chest and was given milk to drink.
On postmortem the pH of the stomach contents was 13.4. There was
blue-black discolouration of the mucosa from the lips to the pylorus.
There was no perforation, but milk was found in the lungs (NPIS
(London) 75/8481).
2) A 44 year old male was admitted to hospital after ingestion of 6
tablespoons of sodium hydroxide in a pint of water. He had severe
burns to the lips, mouth and pharynx. Twelve hours after admission he
developed laryngeal stricture and a tracheostomy was performed. His
condition remained satisfactory and the tracheostomy was removed three
days later. Four days after this he developed haematemesis and
continued to vomit blood for a month. He required 34 pints of blood by
transfusion. He began to improve after this time with occasional
diarrhoea. He then lost a stone in weight and developed electrolyte
problems, particularly hypokalaemia. It was thought he may have
developed a gastro-colic fistula. A gastro-graffin swallow revealed
narrowing of the oesophagus and of the distal part of the stomach with
dye passing straight through into the ascending colon via a
gastric-colonic fistula. Seven days after this a laparotomy was
performed and a feeding jejunostomy tube inserted into the jejunum. He
began to maintain his weight. About two weeks after this a barium meal
confirmed the presence of the fistula and he was started on oral
fluids. Three days later he complained of abdominal pain after
ingestion of soup. There was abdominal tenderness and rigidity. A
laparotomy revealed free fluid in the right para-colic gutter with an
inflamed appendix. An appendectomy and partial gastrectomy were
performed. Post-operatively he recovered well and was started on oral
fluids. Three weeks later he developed another episode of severe
abdominal pain. He deteriorated and another laparotomy showed a closed
duodenal perforation. His condition remained poor with pyrexia,
tachycardia and hypotension. Septicaemia was diagnosed and he was
continued on ampicillin and IV fluids. He continued to deteriorate and
died 3 days after the last operation, 94 days post-ingestion (NPIS
(London) 73/9664)
8 ANALYSIS
8.1 Agent/toxin/metabolite
Not relevant.
8.2 Sample containers to be used
8.3 Optimum storage conditions
8.4 Transport of samples
8.5 Interpretation of data
8.6 Conversion factors
8.7 Other recommendations
9 OTHER TOXICOLOGICAL DATA
9.1 Carcinogenicity
Alkalis are known to increase the risk of oesophageal cancer, which
can occur years after the initial injury (Isolauri and Markkula, 1989;
Ti, 1983; Hopkins and Postlethwait, 1981; Benirschke, 1981; Appelqvist
and Salmo, 1980; Kinnman et al, 1968). The incidence of carcinoma
following oesophageal injury from sodium hydroxide is 0.8-4%. Of the
fifteen patients (age range 38-83) in the study by Isolauri and
Markkula (1989) twelve had accidentally swallowed sodium hydroxide at
the age of two or three years, one at fifteen years and one at
twenty-three years of age. The time between ingestion and the
diagnosis of oesophageal cancer was 22-81 years. Appelqvist and Salmo
(1980) describe similar results, out of sixty patients with
oesophageal cancer for which the time of ingestion was known,
fifty-two had ingested the sodium hydroxide at the age of ten years or
younger.
9.2 Genotoxicity
No data.
9.3 Mutagenicity
9.4 Reprotoxicity
No data.
9.5 Teratogenicity
No data.
9.6 ADI
The acceptable daily intake is not determined.
9.7 MRL
9.8 AOEL
9.9 TLV
TLV = 2 mg m-3.
long term exposure limit = 5 mg m-3 (EH 40/95).
9.10 Relevant animal data
Leape et al (1971) demonstrated that 5ml of a 30.5% solution of sodium
hydroxide was uniformly fatal when introduced into a cat's oesophagus,
even if neutralised 3 seconds later. Exposure of cat oesophagus to
8.3% sodium hydroxide for 30 seconds resulted in destruction of the
superficial layer of squamous mucosa along with submucosal and
transmural thrombosis in blood vessels (Ashcraft and Padula, 1974).
9.11 Relevant in vitro data
10 ENVIRONMENTAL DATA
10.1 Ecotoxicological data
No data.
10.2 Behaviour
No data.
10.3 Biodegradation
No data.
10.4 Environmentally important metabolites
None.
10.5 Hazard warnings
10.5.1 Aquatic life
10.5.2 Bees
10.5.3 Birds
10.5.4 Mammals
10.5.5 Plants
10.5.6 Protected species
10.6 Waste disposal data
Sodium hydroxide may occur in waste from the following industries:
soaps, cleaning compounds, pulp and paper, petroleum, mineral and
vegetable oils, leather, dyes and textile dyeing, cotton, coal
distillation, etc.
Author
Nicky Bates
National Poisons Information Service (London Centre)
Medical Toxicology Unit
Guy's & St Thomas' Hospital Trust
Avonley Road
London
SE14 5ER
UK
This monograph was produced by the staff of the London Centre of the
National Poisons Information Service in the United Kingdom. The work
was commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review was undertaken by the Directors of the UK National Poisons
Information Service.
June 1996
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