Alkalis (PIM G012)

http://www.inchem.org/documents/pims/chemical/pimg012.htm#PartTitle:7. TOXICOLOGY[9/3/2015 2:57:26 PM]

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
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 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
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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)
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 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
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 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
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 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; 
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 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:

 
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 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
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 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
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 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

 
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 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
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 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
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 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
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 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"
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 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%.
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 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
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 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
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 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
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 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).
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 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

 Adam JS and Birck HG. (1982) Pediatric caustic ingestion. 

 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
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 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.

 Pediatrics 71 (5):767-770

 

 Haller JA, Andrews HG, White JJ, Tamer MA and Cleveland WW. (1971) 

 Pathophysiology and management of acute corrosive burns of the

 esophagus: results of treatment in 285 children. J Pediatr Surg 6

 (5):578-584

 

 Hawkins DB, Demeter MJ and Barnett TE. (1980) Caustic ingestion:

 controversies in management. A review of 214 cases. Laryngoscope

 90:98-109

 

 Herbert K and Lawrence JC. (1989) Chemical burns. Burns 15

 (6):381-384

 

 Howell JM, Dalsey WC, Hartsell FW and Butzin CA. (1992) Steroids

 for the treatment of corrosive esophageal injury: a statistical

 analysis of past studies. Am J Emerg Med 10:421-425

 

 Isolauri J and Markkula H. (1989) Lye ingestion and carcinoma of

 the oesophagus. Acta Chir Scand 155:269-271

 

 Kinnman J, Shin HI and Wetteland P. (1968) Carcinoma of the

 oesophagus after lye ingestion. Report of a case in 15 year old

 Korean male. Acta Chir Scand 134:489-493

 

 Klein-Schwartz W and Oderda GM. (1983) Management of corrosive

 ingestions. Clin Toxicol Consult 5 (2):39-55

 

 Knopp R. (1979) Caustic ingestions. JACEP 8:329-336

 

 Meredith TJ. (1996) Corrosive ingestion: how should it be

 managed? XVII International Congress of the EAPCCT Marseille June

 4-7 1996

 

 Middlekamp JN, Ferguson TB, Roper CL and Hoffman FD. (1969) The

 management and problems of caustic burns in children. J Thorac

 Cardiovasc Surg 57:341-347

 

 Moazam F, Talbert JL, Miller D and Mollitt DL. (1987) Caustic

 ingestion and its sequelae in children. South Med J

 80:187-190

 

 Nuutinen M, Uhari M, Karvali T and Kouvalainen K. (1994)

 Consequences of caustic ingestions in childeren. Acta Paediatr

 83:1200-1205

 

 Oakes DD, Sherck JP and Mark JBD. (1982) Lye ingestion. Clinical

 patterns and therapeutic implications. J Thorac Cardiovasc Surg

 83:194-204

 

 OœDonoghue JM, Al-Ghazal SK and McCann JJ. (1996) Caustic soda

 burns to the extremities: difficulties in management. BJCP 50

 (2):108-109

 

 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. 

 Laryngoscope 106 (Suppl 78):1-12

 

 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

 formation. J Pediatr Surg 24 (2):171-173

 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

 
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 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)

 

 See Also:

 Toxicological Abbreviations