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

Alkalis (PIM G012) Page 1 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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

Alkalis (PIM G012) Page 2 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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)

Alkalis (PIM G012) Page 3 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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

Alkalis (PIM G012) Page 4 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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

Alkalis (PIM G012) Page 5 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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

Alkalis (PIM G012) Page 6 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 7 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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; 

Alkalis (PIM G012) Page 8 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 9 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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. 

Alkalis (PIM G012) Page 10 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 11 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 12 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 13 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 (PIM G012) Page 14 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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

Alkalis (PIM G012) Page 15 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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

Alkalis (PIM G012) Page 16 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
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) 

Alkalis (PIM G012) Page 17 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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). 

Alkalis (PIM G012) Page 18 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 19 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 20 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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. 

Alkalis (PIM G012) Page 21 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

Alkalis (PIM G012) Page 22 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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., 

Alkalis (PIM G012) Page 23 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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). 

Alkalis (PIM G012) Page 24 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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

 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 

Alkalis (PIM G012) Page 25 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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. 

 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 

Alkalis (PIM G012) Page 26 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015
 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 

 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

Alkalis (PIM G012) Page 27 of 27

http://www.inchem.org/documents/pims/chemical/pimg012.htm 9/3/2015