CHEMICAL

BURNS

105

CHEMICAL BURNS
 Ocular chemical burns are common and are
serious ocular emergencies that require
immediate and intensive evaluation and care.

 Chemicals penetrate the eye rapidly damaging

structures and causing severe injury.

 The goal of treatment is to restore the normal

ocular surface anatomy and function.
106

1
 CHEMICAL BURNS
 Etiological Classification
1. Accidental 2. Self Inflicted
• Home 3. Occupational
• Hair Salons • Work place accidents
• Assaults • Work shops
• In nature • Laboratories

107

TYPES OF CHEMICALS
•Most severe
ALKALIES
injuries –
rapid
penetration

•Least severe
ACID
injuries – less
penetrating
than alkalies

• Neutral pH
IRRITANTS
• More
discomfort
than damage 108

2
CHEMICAL BURNS
Alkali Chemical
 Calcium hydroxide/Lime
(cement)
 Hair gel
 Hair relaxer
 Manchineel tree sap
 Ammonia (fertilizers)
 Lye (drain cleaners)
 Potassium & Magnesium
Hydroxide
Acidic Chemicals
 Sulfuric Acid (battery acid,
industrial cleaner)
 Acetic Acid (vinegar)
 Hydrochloric Acid
 Sulfurous Acid (bleach,
refrigerant)
109

CHEMICAL BURNS
 Irritants (normal pH)
• Household detergents
• Pepper spray
 Fumes
 Thermal
 Radiation
Chemical burns with acid can cause patients
to experience irreversible intraocular damage
in as little as 5–15 minutes.
110

3
 CHEMICAL BURNS
PATHOPHYSIOLOGY
Acids Alkali
 Acids are generally less harmful  Alkali agents are lipophilic and
than alkali substances. They cause therefore penetrate tissues
damage by denaturing and more rapidly than acids.
precipitating proteins in the tissues They saponify the fatty acids of
they contact. The coagulated cell cell membranes, penetrate
proteins act as a barrier to prevent the corneal stroma and destroy
further penetration (unlike alkali proteoglycan ground substance
injuries). The one exception to this and collagen bundles. The
is hydrofluoric acid, where the damaged tissues then
fluoride ion rapidly penetrates the secrete proteolytic enzymes,
thickness of the cornea and causes which lead to further damage.
significant anterior segment
destruction. 111

CHEMICAL BURNS
Clinical Presentation
 Sudden onset of severe pain
 Epiphora (excessive tearing)
 Blepharospasm (involuntary tight closure of the
eyelids)

Chemical Burns Illicit An

Emergency Response

112

4
 First Aid
Treatment

113

MANAGEMENT OF
CHEMICAL BURNS
Main Goals:
 Remove causative agent
 Promote ocular surface healing
 Control inflammation
 Prevent infection
 Control IOP

114

5
MEDICAL MANAGEMENT
 Flush eye with water.
• Cover healthy eye during flushing. Lead the water
jet from inner angle of eye to outer angle of eye.
Clean for at least 30 min under clear water.

115

MEDICAL MANAGEMENT
 Ophthalmologic Examination
• Visual Acuity (utilise a drop of topic anaesthetic if
needed to relieve pain)
• Slit Lamp assessment
• History of Injury
• Health History
• Classification
• Treatment

116

6
Classifications

117

TREATMENT
 Follow-up care should occur within 24 hours
after patient discharge.
• Topical antibiotics
• Cycloplegics (Atropine 1% reduces cilliary spasm and
pain; prevents posterior synechiae)
• Topical Lubricants (2hrly facilitates corneal healing and
minimises scarring)
• Anti-inflammatory (7-10 days then tapered reduces
inflammation)
• Ascorbic acid (Vit-C)
• IOP (Timolol 0.5%, Brimonidine 0.1%)
• Patch if necessary
118

7
TREATMENT
Nurse Management
 The severity of ocular injury depends on four factors:
the toxicity of the chemical, how long the chemical is in
contact with the eye, the depth of penetration, and the
area of involvement.
 It is therefore critical to take a careful history to
document these factors. The patient should be asked
when the injury occurred, whether they rinsed their eyes
afterwards and for how long, the mechanism of injury
(was the chemical under high pressure?), the type of
chemical that splashed in the eye, and whether or not
they were wearing eye protection. If available, it is
helpful to obtain the packaging of the chemical.
119

COMPLICATIONS
Primary
 Conjunctival inflammation
 Corneal abrasions
 Corneal haze and edema
 Acute rise in IOP.
 Corneal melting and
perforation
Secondary
 Secondary glaucoma
 Secondary cataract
 Conjunctival scarring
 Corneal thinning and perforation
 Corneal scarring and
vascularisation
 Corneal ulceration
 Complete globe atrophy (phthisis
bulbi) 120

8
PREVENTIONS

Eye Safety

121

QUESTIONS

122