Alkalis
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names, main trade names |
| 1.6 Main manufacturers, main 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 |
| 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 Other |
| 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 and excretion |
| 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) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL 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 |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 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 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, 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 and 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 Other |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. Additional information |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
Alkalis
International Programme on Chemical Safety
Poisons Information Monograph G012 (Group PIM)
Chemical
1. NAME
1.1 Substance
Alkalis
1.2 Group
Substances included:
Sodium hydroxide
Potassium hydroxide
Calcium hydroxide
1.3 Synonyms
Sodium hydroxide:
Caustic flake; Caustic soda;
Hydroxyde de sodium (French);
Hydroxyde de sodium, solide (French);
Hydroxyde de sodium, solutions (French);
Lewis-red devil lye;
Liquid caustic
(solutions of 45-75% sodium hydroxide in water);
Lye; Natriumhydroxid (German);
Natriumhydroxyde (Dutch); Soda lye;
Soda, caustic; Soda, hydrate;
Sodio(idrossido di); Sodium hydrate;
White caustic;
Potassium hydroxide
Caustic potash;
Caustic potash solutions;
Hydroxyde de potassium (French);
Hydroxyde de potassium, solide (French);
Hydroxyde de potassium, solutions (French);
Kaliumhydroxid (German);
Kaliumhydroxyde (Dutch); KOH;
Lye; Potassa;
Potasse caustique;
Potassio (idrossido di);
Potassium (hydroxyde de);
Potassium hydrate;
Potassium hydrate solutions;
Calcium hydroxide:
Agricultural lime; Bell mine;
Biocalc; Calcium dihydroxide;
Calcium Hydrate; Calvit;
Calvital; Carboxide;
Caustic lime; Caustic lime water;
Hydrated lime; Hydroxyde de calcium;
Kalkhydrate; Kemikal;
Limbux; Lime hydrate;
Lime milk; Lime water;
Milk of lime; Slaked lime
1.4 Identification numbers
1.4.1 CAS number
Sodium hydroxide: 1310-73-2
Potassium hydroxide: 1310-58-3
Calcium hydroxide: 1305-62-0
1.4.2 Other numbers
Sodium hydroxide, solid: UN1823 (DOT)
Sodium hydroxide, solution: UN1824 (DOT)
Sodium hydroxide NIOSH/RTECS: WB4900000
Potassium hydroxide, solid: UN1813 (DOT)
Potassium hydroxide, solution: UN1814 (DOT)
Potassium hydroxide NIOSH/RTECS: TT2100000
Calcium hydroxide NIOSH/RTECS: EW2800000
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
Alaklis are one of the most common causes of chemical
burn. On ingestion alkalis are capable of causing severe
damage and even a very small quantity may cause significant
morbidity requiring prolonged and repeated
hospitalisation.
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 both the stomach and small
intestine may be involved. The severity of injury depends on
a number of factors including the concentration of the agent,
the duration of contact and the volume ingested and the
presence of food in stomach. 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.
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.
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,
and
3) sloughing of superficial necrotic layer 2 to 4 days later.
Classification or grading of Oesophageal Burns:
First Degree: mucosa only, hyperemic odematous mucosa, may
be superficial sloughing;
Second degree: destruction of mucosa ans submucosa,
penetration into muscle layers, exudate is
present, erosions and shallow ulcers;
Third degree: full thickness injury, possible perforation,
deep ulcerations, black coagulation.
Skin burns: 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. The injury can progress over
several hours and the skin may be discoloured brown or black
within a short period of time, these factors make initial
assessment of the burn depth difficult. Also, there may be
recurring skin breakdown over a long period after the initial
injury which can complicate and delay recovery.
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 resulting in blindness.
2.2 Summary of clinical effects
Ingestion
This 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, paralytic ileus, stridor, dysphagia and shock.
Oesophageal and pharyngeal oedema may occur.
Acute complications: These include gastrointestinal
haemorrhage and perforation of the gut (mediatinitis and
peritonitis as suggested by increasing abdominal pain,
persistent vomiting, direct and indirect tenderness and a
rigid abdominal wall). Dyspnoea and stridor may occur and in
severe cases there may be upper airway obstruction.
Aspiration can be a serious complication.
Late complications: Oesophageal stricture and pyloric
stenosis may occur as late complications. Stricture
formation usually begins to develop 14 to 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. 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 alkali rather than a solid. The small intestine may
also be involved. Oesophago-aortic fistulae and rupture of
the aorta are rare complications of corrosive ingestion.
Tracheo-oesophageal fistulae and less commonly,
broncho-oesophageal fistulae, have been reported following
ingestion of alkalis. Perforation and fistula may develop as
a consequence of invasive diagnostic procedure and treatment
(ie. oesophageal dilatation).
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.
Achlorhydria with reduced or absent intrinsic factor may also
occur.
Long-term risks: Patients with oesophageal strictures are
at significant risk for developing squamous cell carcinoma,
which can occur years after the initial injury. The vast
majority of data is on sodium hydroxide about which there
have been more reports of ingestion. The incidence of
carcinoma following oesophageal injury from sodium hydroxide
is 0.8 to 4%.
Skin exposure
Alkalis can cause deep penetrating burns and necrosis. There
is also a risk of secondary infection of the damaged skin.
Eye contact
Alkalis are responsible for some of the most severe, blinding
injuries to the eye. Urgent ophthalmological referral is
required. Even if the initial manifestations are mild, the
injuries may develop into opacification, vascularization,
ulcerations and perforations.
2.3 Diagnosis
The history of exposure to alkali vapors, solutions or
solids and the evidence of corrosive lesions on the
gastrointestinal tract (GI) tract, skin or eyes are essential
for the diagnosis. pH indicator shows alkaline reaction in
contact with affected tissues or stomach content. Chemical
identification of the toxic agent will help to fulfil the
diagnosis.
2.4 First aid measures and management principles
Ingestion:
Asymptomatic/mildly symptomatic patients: It should be
noted that oesophageal damage may occur in the absence of
oral burns. 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. Neutralising chemicals should never be
given because heat is produced during neutralisation and this
could exacerbate any injury.
Gastro-oesophagoscopy should be undertaken within 12 to 24
hours of the event to assess the extent and severity of the
injury. Endoscopy is contraindicated in patients with third
degree burns of the hypopharynx, burns involving the larynx
or those with respiratory distress. Traditionally the
endoscopist terminates the procedure at the first deep,
penetrating and/or circumferential burn because of the risk
of perforation. However some physicians now recommend the
use of flexible endoscopy to include the stomach and small
intestine (panendoscopy) regardless of the presence of second
or non-perforating third degree burns to the oesophagus. If
perforation is suspected or severe hypopharyngeal burns are
present, radiographic studies with water-soluble contrast
media may be used instead.
Patients with grade 1 oesophageal burns may be discharged
after 2 to 3 days, if they are able to take oral fluids and
semi-solids. Those with grade 2 burns should be admitted and
given parenteral nutrition. Intensive care is usually
required for patients with grade 3 burns. For discussion on
the use of steroids and antibiotics - see below.
Severely affected patients: Treatment is supportive. In
severely affected patients aggressive intervention is
essential. Urgent assessment of the airway and endoscopic
evaluation is required. A supraglottic-epiglottic burn with
erythema and oedema is usually a sign that further oedema
will occur which will lead to airway obstruction and is an
indication to evaluate for early intubation or tracheostomy.
Give plasma expanders/intravenous fluids for shock and check
and correct the acid/base balance. Abdominal and chest X-rays
need to be taken to check for perforation. Analgesia will
almost certainly be needed. Intubation and ventilation may be
necessary for patients with respiratory distress. Parenteral
feeding will be necessary. Surgical intervention may also be
required for gastrointestinal perforation or haemorrhage.
Late complications: strictures that prevent adequate
nutritional intake and do not respond to dilatation require
oesophagectomy and colonic interposition. 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.
Severe cases of alkali ingestion may result in long-term
problems and require prolonged hospitalisation and several
surgical procedures and psychological treatment is
recommended. On discharge all patients must be advised on
the possibility of late onset sequelae and advised to return
if necessary. In patients who have developed oesophageal
stricture monitoring for life is recommended because of the
risk of malignant disease.
Dermal injury: The most important therapy for dermal alkali
injuries is removal of contaminated clothes and irrigate with
copious running water. 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. The earlier the irrigation is begun the
greater the benefit. Irrigation should, therefore, be
started as soon as possible, until the slippery and soapy
sensation is no longer felt in the affected area. The
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. Referral to a burns
unit is recommended.
Ocular injury: Copious and immediate irrigation of exposed
eyes is essential. Contact lenses should be removed prior to
irrigation. Tepid water (preferably sterile) or normal
saline may be used, although other solutions have been
employed in an emergency including tap water. 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. 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. Urgent referral to an
ophthamologist is recommended.
The use of steroids in corrosive 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. The use of
steroids for corrosive injury in man is a controversial
subject which has generated a huge amount of literature (see
section 10).
Steroids are valuable in the management of laryngeal oedema,
a complication of alkali ingestion.
The main aim of steroids 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 is sometimes not 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 and may be delayed .
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.
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) infections
b) perforation of the gastrointestinal tract or secondary
mediastinitis
c) gastrointestinal bleeding
d) 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.
When to begin therapy: Once the decision has been made to
use steroids, therapy should be started within 24 to 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.
The short duration of steroid therapy should not produce a
significant reduction in intrinsic steroid production or
alter the metabolic balance.
The use of antibiotics in corrosive injury
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,
but others considered this unnecessary since the risk of
infection is low.
Adjuntive treatment
The use of H2-blockers and metoclopramide may help to prevent
secondary acid injury to the esophagus.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
Calcium hydroxide
Molecular mass: 74.1
Chemical formula: Ca(OH)2
Potassium hydroxide
Molecular mass: 56.1
Chemical formula: KOH
Sodium hydroxide
Molecular mass: 40.0
Chemical formula: NaOH
3.3 Physical properties
3.3.1 Colour
Calcium hydroxide: white/greyish-white
Potassium hydroxide: white
3.3.2 State/Form
Calcium hydroxide: solid-powder
Potassium hydroxide: deliquescent solid
3.3.3 Description
Calcium hydroxide
Melting point (decomposes): 580°C
Relative density (water = 1): 2.
Solubility in water: None
Potassium hydroxide
Boiling point: 1324°C
Melting point: 380°C
Relative density (water = 1): 2.04
Solubility in water, g/100 mL at 25°C: 110
Vapour pressure, kPa at 714°C: 0.13
Sodium hydroxide
Boiling point: 1390°C
Melting point: 318°C
Relative density (water = 1): 2.1
Solubility in water, g/100 mL at 20°C: 109
3.4 Hazardous characteristics
Calcium hydroxide
The substance decomposes on heating producing calcium oxide.
The substance is a medium strong base.
Potassium hydroxide
The substance is a strong base, it reacts violently with acid
and is corrosive in moist air toward metals such as zinc,
aluminum, tin and lead forming a combustible/explosive gas.
Rapidly absorbs carbon dioxide and water from air. Contact
with moisture or water will generate heat .
Sodium hydroxide
The substance is a strong base, it reacts violently with acid
and is corrosive in moist air to metals like zinc, aluminum,
tin and lead forming a combustible gas. Attacks some forms of
plastics, rubber and coatings.Contact with moisture or water
may generate heat.
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Alkalis are present in a number of household
products (e.g. drain cleaners, oven cleaners,
dishwasher products, some paint strippers) and are
also used in industry.
4.2 High risk circumstance of poisoning
4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
5.1 Oral
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 both the stomach and small intestine
may be involved. The severity of injury depends on a number
of factors including the concentration of the agent, the
duration of contact and the volume ingested and the presence
of food in stomach. 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.
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.
5.2 Inhalation
Not relevant.
5.3 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. The injury can progress over several
hours and the skin may be discoloured brown or black within a
short period of time, these factors make initial assessment
of the burn depth difficult. Also, there may be recurring
skin breakdown over a long period after the initial injury
which can complicate and delay recovery (OœDonoghue et al.,
1996).
5.4 Eye
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 resulting
in blindness.
5.5 Parenteral
Not relevant.
5.6 Other
Not relevant.
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 and excretion
7. TOXICOLOGY
7.1 Mode of action
Alkalis cause liquifactive necrosis with saponification
of fats and solubilisation of proteins, they are also
hygroscopic and will absorb water from the tissues. These
effects result in adherence and deep penetration into the
tissues.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
7.2.1.2 Children
Children are commonly reported to
ingest corrosive substances but severe
effects are relatively rare. Several studies
have been carried out in children in an
effort 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 another study, prolonged drooling
and dysphagia (12 to 24 hours) were observed
to predicted oesophageal scar formation with
100% sensitivity (Nuutinen et al., 1994). In
a study of 224 children (aged 0 to 14 years)
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 (Clausen et al., 1994).
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)
7.3 Carcinogenicity
7.4 Teratogenicity
7.5 Mutagenicity
7.6 Interactions
8. TOXICOLOGICAL 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
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
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
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
This 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,
paralytic ileus, stridor, dysphagia and shock.
Oesophageal and pharyngeal oedema may occur.
Acute complications: these include gastrointestinal
haemorrhage and perforation of the gut leading to
mediastinitis nad peritonitis (suggested by increasing
abdominal pain, persistent vomiting, direct and
indirect tenderness and a rigid abdominal wall).
Dyspnoea and stridor may occur and in severe cases
there may be upper airway obstruction. Aspiration can
be a serious complications.
Late complications: oesophageal stricture and
pyloric stenosis may occur as late complications.
Stricture formation usually begins to develop 14 to 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.
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 alkali rather than a solid. The small
intestine may also be involved. Oesophago-aortic
fistulae and rupture of the aorta are rare
complications of corrosive ingestion.
Tracheo-oesophageal fistulae and less commonly,
broncho-oesophageal fistulae, have been reported
following ingestion of alkalis. Perforation and
fistula may develop as a consequence of invasive
diagnostic procedure and treatment (ie. oesophageal
dilatation).
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. Achlorhydria with reduced
or absent intrinsic factor may also occur.
Long-term risks: alkalis are known to increase the
risk of oesophageal cancer, which can occur years
after the initial injury (Appelqvist and Salmo, 1980;
Benirscke, 1981; Isolauri and Markkula, 1989; Kinnman
et al., 1968). The vast majority of data is on sodium
hydroxide about which there have been more reports of
ingestion. The incidence of carcinoma following
oesophageal injury from sodium hydroxide is 0.8 to 4%.
9.1.2 Inhalation
Not relevant
9.1.3 Skin exposure
Alkalis can cause deep penetrating burns and
necrosis. There is also a risk of secondary infection
of the damaged skin.
9.1.4 Eye contact
Alkalis are responsible for some of the most
severe, blinding injuries to the eye. Urgent
ophthalmological referral is required.
9.1.5 Parenteral exposure
Not relevant
9.1.6 Other
Not relevant
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
See Section 9.1
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 Other
9.4.7 Endocrine and reproductive systems
9.4.8 Dermatological
9.4.9 Eye, ear, 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 and 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 Other
9.6 Summary
10. MANAGEMENT
10.1 General principles
Ingestion:
Asymptomatic/mildly symptomatic patients: It should be
noted that oesophageal damage may occur in the absence of
oral burns. 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 may be given 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.
Gastro-oesophagoscopy should be undertaken within 12 to 24
hours of the event to assess the extent and severity of the
injury. Endoscopy is contraindicated in patients with third
degree burns of the hypopharynx, burns involving the larynx
or those with respiratory distress. Traditionally the
endoscopist terminates the procedure at the first deep,
penetrating and/or circumferential burn because of the risk
of perforation. However some physicians now recommend the
use of flexible endoscopy to include the stomach and small
intestine (panendoscopy) regardless of the presence of second
or non-perforating third degree burns to the oesophagus
(Ford, 1991; Meredith, 1996). If perforation is suspected or
severe hypopharyngeal burns are present, radiographic studies
with water-soluble contrast media may be used instead.
Patients with grade 1 oesophageal burns may be discharged if
they are able to take oral fluids. Those with grade 2 burns
should be admitted and given parenteral nutrition. Intensive
care is usually required for patients with grade 3 burns. A
laparotomy may be required if there is evidence of gastric
injury or the gastric pH is persistently alkaline (Meredith,
1996). For discussion on the use of steroids and antibiotics
- see below.
Severely affected patients: Treatment is supportive. In
severely affected patients aggressive intervention is
essential. Urgent assessment of the airway and endoscopic
evaluation is required. A supraglottic-epiglottic burn with
erythema and oedema is usually a sign that further oedema
will occur which will lead to airway obstruction and is an
indication for early intubation or tracheostomy.
Give plasma expanders/intravenous fluids for shock and check
and correct the acid/base balance. Abdominal and chest X-rays
need to be taken to check for perforation. Analgesia will
almost certainly be needed. Intubation and ventilation may be
necessary for patients with respiratory distress. Parenteral
feeding will be necessary.
Late complications: strictures that prevent adequate
nutritional intake and do not respond to dilatation require
oesophagectomy and colonic interposition. In the case of
oesophageal strictures a lumen >10mm does not impede normal
life and should not require intervention. 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 alkali ingestion may result in long-term
problems and require prolonged hospitalisation and several
surgical procedures and psychological treatment is
recommended. On discharge all patients must be advised on
the possibility of late onset sequelae and advised to return
if necessary. In patients who have developed oesophageal
stricture monitoring for life is recommended because of the
risk of malignant disease.
Dermal injury: The most important therapy for dermal alkali
injuries is removal of contaminated clothes and irrigate with
copious running water. 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. The earlier the irrigation is begun the
greater the benefit. Irrigation should, therefore, be
started as soon as possible. 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; OœDonoghue
et al., 1996). Referral to a burns unit is recommended.
Ocular injury: 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. 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. 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. Urgent referral to an
ophthamologist is recommended.
The use of steroids in corrosive 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. 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 another study 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
(Anderson et al., 1990).
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; Oakes et al., 1982; Webb et el., 1970).
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 is
sometimes not 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).
Steroids are valuable in the management of laryngeal oedema,
a complication of alkali ingestion.
In summary, steroids are probably most effective for second
degree or moderately severe burns (Hawkins et al., 1980;
Klein-Schwartz and Oderda, 1983; 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 (Di Costanzo et al., 1980; Wijburg et al., 1989). 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 to 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.
The use of antibiotics in corrosive injury
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
(Adam and Birck, 1982; Howell et al., 1992), but others
considered this unnecessary (Klein-Schwartz and Oderda,
1983; Wijburg et al., 1989) since the risk of infection is
low (Knopp, 1979).
Adjuntive treatment
The use of H2-blockers and metoclopramide may help to prevent
secondary acid injury to the esophagus (Haddad, 1998).
10.2 Life supportive procedures and symptomatic/specific treatment
See section 10.1
10.3 Decontamination
Gastric lavage and emesis are contraindicated because
of the risks of further injury on re-exposure of the
oesophagus.
10.4 Enhanced elimination
See section 10.1
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote.
10.5.2 Children
There is no specific antidote.
10.6 Management discussion
See section 10.1
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
12. Additional information
12.1 Specific preventive measures
Rescuers, first-aid personnel and medical professionals
should use appropriate protective clothing/gloves and where
necessary employ respiratory protection.
12.2 Other
13. REFERENCES
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Ann Otol Rhinol Laryngol 91:656-658
Anderson KD, Rouse TM and Randolph JGH. (1990) A controlled trial
of corticosteroids in children with corrosive injury of the
oesophagus. N Eng J Med 323 (10):637-640
Appelqvist P and Salmo M. (1980) Lye corrosion carcinoma of the
oesophagus. A review of 63 cases. Cancer 45:2655-2658
Benirscke K. (1981) Time bomb of lye ingestion? Am J Dis Child
135:17-18
Cardona JC and Daly JF. (1971) Current mangement of corrosive
esophagitis. An evaluation of results of 239 cases. Ann Otol
80:521-527
Clausen JO, Nielsen TLF and Fogh A. (1994) Admission to Danish
hospitals after suspected ingestion of corrosives. A nationwide
survey (1984-1988) comprising children aged 0-14 years.
Dan Med Bull 41:234-237
Crain EE, Gershel JC and Mezey AP. (1984) Caustic ingestions.
Symptoms as predictors of esophageal in jury. Am J Dis Child
138:863-865
Di Costanzo J, Noirclerc M, Jouglard J, Escoffier JM, Cano N,
Martin J and Gauthier A. (1980) New therapeutic approach to
corrosive burns of the upper gastrointestinal tract. Gut
21:370-375
Ford M. (1991) Alkali and acid injuries of the upper
gastrointestinal tract. Contemporary management in critical care 1
(3):225-249 Tobin MJ and Grenvik A (eds). Churchill
Livingstone
Gaudreault P, Parent M, McGuigan MA, Chicoine L and Lovejoy FH.
(1983) Predicability of eosophageal injury from signs and
symptoms: a study of caustic ingestions in 378 children.
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Haller JA, Andrews HG, White JJ, Tamer MA and Cleveland WW. (1971)
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Herbert K and Lawrence JC. (1989) Chemical burns. Burns 15
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Howell JM, Dalsey WC, Hartsell FW and Butzin CA. (1992) Steroids
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Isolauri J and Markkula H. (1989) Lye ingestion and carcinoma of
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Kinnman J, Shin HI and Wetteland P. (1968) Carcinoma of the
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Klein-Schwartz W and Oderda GM. (1983) Management of corrosive
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Knopp R. (1979) Caustic ingestions. JACEP 8:329-336
Meredith TJ. (1996) Corrosive ingestion: how should it be
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4-7 1996
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OœDonoghue JM, Al-Ghazal SK and McCann JJ. (1996) Caustic soda
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Shikovitz MJ, Levy J, Villano D, Graver LM and Pochaczevsky R.
(1996) Speech and swallowing rehabilitation following devastating
caustic ingestion: techniques and indicators for success.
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Webb WR, Koutras P, Ecker RR and Sugg WL. (1970) An evaluation
of steroids and antibiotics in caustic burns of the esophagus.
Ann Thorac Surg 9:95-102
Wijburg FA, Heymans HSA and Urbanus NAM. (1989) Caustic
esophageal lesions in childhood: prevention of stricture
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Medical Toxicology Unit,
Guyœs and St Thomasœ Trust
Avonley Road, London SE14 5ER, UK
Date: November, 1997
Review: As for author. 1997
Peer review: INTOX meeting, March 1998, London, UK
(Members of group: Drs G. Allridge, L.
Lubomovir, R. Turk, C. Alonso, S. de Ben, K.
Hartigan-Go, N. Bates)
Editor: Dr M.Ruse (September, 1998)