This document discusses chemical injuries to the eye. It describes the types of chemicals that can cause injuries, including acids and alkalis found in industrial and domestic settings. The pathology of chemical injuries is explained, noting how alkalis and acids damage ocular tissues differently. Clinical features include ulceration, limbal ischemia, and complications like symblepharon. Treatment involves immediate irrigation at the injury site, then continued irrigation, antibiotics, and steroids in the hospital. Promoting epithelialization and limiting further damage are priorities in management. Prevention emphasizes public education, industrial safety precautions, and identifying the chemical involved.

1. Chemical Injuries
Dr Meseret E.

2. Scope
 Types of chemicals and where they occur
 Pathology of chemical injuries
 Clinical features and complications
 Treatment
 Prevention

3. Introduction
 constitute the true emergencies – ie
appropriate immediate management may be
the single most important factor in
determining the outcome.

4. Types of chemicals
 Chemicals may be solid, liquid or gas
 They can be characterized as acidic or
alkaline, and organic or inorganic.

5. Where do chemical injuries occur?
 industrial – construction sites, factories
 home – domestic violence
 agricultural settings – fertilizer, pesticides
 leisure – car batteries
 war – all the above and more!

6. Alkalis
 ammonium hydroxide – fertilizer and
chemical plants
 sodium hydroxide (lye/caustic soda) –
cleaning industrial pipes, tanks and utensils
 potassium hydroxide (caustic potash)
 calcium hydroxide – lime, plaster, cement,
white wash
 magnesium hydroxide - fireworks

7. Acids
 Sulphuric acid – car batteries, industry
 Sulphurous acid – refrigerant, bleach,
preservative for fruits and vegetables
 Hydrochloric acid - used in swimming pools
as muriatic acid in weaker concentrations
 Chromic acid - used as a cleaning agent, for
laboratory glassware and in the chrome
plating industry

8. ALKALI BURNS:
 OH ion s pH saponification of fatty acids in
cell membrane cell death
 penetrate corneal stroma destroy
proteoglycans and collagen hydration
+damage to collagen fibrils
 Combine with cellular elements
(glycosaminoglycans) to form soluble
compounds further penetration & tissue
damage

9. ACID BURNS:
 Less severe
 Coagulation of proteins in epith+ superficial
stroma BARRIER no further damage
 Fewer stromal & intraocular complications

10. Pathology - clinical effects
 Epithelial defects – risk of infection
 Limbal ischemia – poor healing
 Loss of goblet cells – unstable tear film
 Coagulation in blood vessels - ischemia
 Damage to the accessory lacrimal glands -
dry eyes
 Lacrimal duct stenosis – epiphora
 Damage to the eyelids (ectropion/entropion)
– trichiasis or dry eye
 Cosmetic effect

11. Clinical features
 Ulceration of the lids, cornea and conjunctiva
 Limbal ischemia
 Subconjunctival hemorrhage
 Hazy, swollen cornea
 IOP may by high or low
 uveitis
 cataract

12. • Clear cornea
Grade I (excellent prognosis)
• Limbal ischaemia - nil
• Cornea hazy but visible
iris details
Grade II (good
prognosis)
• Limbal ischaemia < 1/3
• opaque cornea
(no iris details visible)
Grade III (guarded
prognosis)
• Limbal ischaemia –
1/3 to 1/2
• Opaque cornea
Grade IV (very poor
prognosis)
• Limbal ischaemia > 1/2

13. Complications
 Symblepharon – adhesion between bulbar and
tarsal conjunctiva
 Ectropion - exposure keratitis, Entropion/trichiasis –
corneal scarring by lashes
 Epiphora – lid malposition, lacrimal duct stenosis
 Persistent corneal epithelial defect
 Corneal neovascularization or scar
 Secondary glaucoma
 Posterior synechiae
 Cataract

14. Treatment – at injury site
 Rx within the first 2-3 minutes is the most
important
 Irrigation at the site of injury – dilutes and
washes out chemical. Open the eyes
 patient be rapidly transported to a medical
facility

15. Treatment – hospital
Immediate
 Check pH
 Repeat irrigation with n/saline. Use IV line
 Remove visible particles after double eversion
 Continue till pH neutral or for 30 minutes
 Monitor pH of the conjunctival cul-de-sac every 10 to
15 minutes for another 60 minutes to ensure that
residual material does not turn the pH basic again
 Topical antibiotic + cycloplegic (ex. Atropine)
 Steroids for 7-10 days
 Refer to the ophthalmologist

16. TREATMENT Contd:
PROMOTE EPITHELIALIZATION:
 Tear substitutes and lubricants
 Punctal occlusion in severe DES
 Lid closure (taping, pressure patch, tarsorrhaphy)
 Therapeutic soft contact lens
 Fibronectin, EGF- investigational

17. TREATMENT Cont’d:
LIMIT ULCERATION AND SUPPORT
REPAIR:
 Minimize steroid use >10days
 Ascorbate, citrate
 Tissue adhesive and soft contact lens
 Conjuctival flap
 Keratoplasty

18. Prevention
 Public education – about prevention and
early management
 Industrial safety precautions – eye protection,
equipment for immediate irrigation
- first aid
- rapid identification of the chemical ( bring
container to hospital, package labels and
inserts)
 Toxicology and poison control centers