MANAGEMENT OF CORNEAL BURN

Dr. Tjahjono D. Gondhowiardjo SpM (K) PhD

Introduction
Ocular burn represents up to 18% of ocular trauma with chemical injuries occurs in
about 12% cases of ocular trauma.1 Chemical injuries are caused by acid and alkali
agents and found mostly in working accidents. Chemical burn is considered a true
ocular emergency and causing limbal stem cell deficiency. 3 This can lead to
permanent defect if left untreated.

Common causes of chemical hazards are listed below :

Table 1 Chemical agents in ocular chemical injury

Substance Found in
Acid
Sulfuric acid Car batteries
Sulfurous acid Bleach and refrigerant
Acetic acid Vinegar
Hydrochloric acid Swimming pool
Hydrofluoric acid Glass polishing
Alkali
Ammonia Cleaning agents, fertilizers
Potassium hydroxide Caustic potash
Magnesium hydroxide Fireworks
Line White wash, cement, mortar

Acid
Acids are the agents that have a low pH. They dissociate into hydrogen ions and
anions which cause a change in pH within the eyes, denaturation,precipitation and
coagulation necrosis.3,4 The coagulated proteins therefore cause the cornea loses its
transparency and prevent penetration into deeper structures. This is believed to be the
reason made acids are less harmful that the alkali except hydrofluoric acid. The
fluoride ion can make a deep penetration despite the protein coagulation and therefore
causes anterior segment damages. 3–5

Alkali
Alkali agents are lipophilic and have a high pH. It will dissociate into hydroxyl ion
and cations. The hydroxyl ions cause saponification of fatty acids which will lead to
liquefactive necrosis, whereas the cations interact with collagen bundles and
proteoglycans causing fogging of the stroma.3,4 The damaged tissues then secrete
proteolytic enymes lead to extensive damages.

There might be an acute rise of intraocular pressure due to contraction of the cornea
and sclera. Fibrotic damage to the trabecular meshwork and debris accumulation can
cause long-term rise of intraocular pressure.1 Damage to the conjunctiva may lead to
extensive scarring, perilimbal ischemia and contracture of fornices. Loss of goblet cell
in conjunctiva makes dryness of the eyes.1,3,4

Presentation

Patient with chemical burn will come with severe pain, epiphora, blepharospasm and
decreased visual acuity. Prior to a full ophthalmic exam, the pH of both eyes should
be checked. If the pH is not in physiologic range, then the eye must be irrigated to
bring the pH to an appropriate range (between 7 and 7.2). The physical exam should
asses corneal, conjunctival and limbal involvement to classify the degree of injury.

The palpebral fissures should be checked and the fornices should be swept during the
initial exam. Both the palpebral and bulbar conjunctiva should be examined
with fluorescein under a cobalt blue light. As above, retained particulate matter can
cause persistent damage, despite irrigation. The intraocular pressure should also be
documented, as alkali injuries have been found to both acutely and chronically cause
an elevation of IOP. 1,3,4

Physical examination may reveal hazy cornea in the affected eye, corneal and
conjuctival epithelial defects, chemosis, limbal ischemia and increased IOP. Limbal
stem cell deficiency (LSCD) due to limbal ischemia will result in failure of corneal
epithelial healing, neovascularization and conjunctivalization.1,4 Extensive conjunctiva
burns can lead to symplepharon, cicatrical entropion and ectropion, and also trichiasis.
There are two major classification for corneal burns that is commonly used in daily
practice, Roper-Hall (modified Hughes) classification and Dua classification.1,4  The
Roper-Hall classification is based on the degree of corneal involvement and limbal
ischemia. The Dua classification is based on an estimate of limbal involvement (in
clock hours) and the percentage of conjunctival involvement.

Table 2 Roper Hall Classification

Roper Hall Classification

Grade Prognosis Cornea Conjunctiva/Limbus
I Good Corneal epithelial damage No limbal ischemia
II Good Corneal haze, iris details visible <1/3 limbal ischemia
III Guarded Total epithelial loss, stromal haze, 1/3 – ½ limbal
iris details obscured ischemia
IV Poor Cornea opaque, iris and pupil > ½ limbal ischemia
obscured

Table 3 Dua Classification

Dua Classification for

Grade Prognosis Clinical findings Conjunctiva Analogue
Involvement Scale*
I Very good 0 clock hours of limbal 0% 0/0%
involvement
II Good < 3 clock hours of limbal < 30% 0.1-3/1-29.9%
involvement
III Good Between 3-6 clock hours of 30- 50 % 3.1-6/31-50%
limbal involvement
IV Good to Between 6-9 clock hours of 50 – 75% 6.1-9/51-75%
guarded limbal involvement
V Guarded Between 9 and 12 clock 75 – 100 % 9.1-11.9/75.1-
to poor hours of limbal 99.9%
involvement
VI Very poor Total limbus (12 clock Total 12/100%
hours) involved conjunctiva
(100%)
involved
*The analogue scale represents the amount of limbal involvement in clock hours of
affected limbus/percentage conjunctival involvement (bulbar conjunctiva including
conjunctival fornices) . Dua classficiation was found to be superiorto the Roper-Hall
in prediction outcome in severe burns.

Clinical course of chemical ocular injury

Immediate phase
This happens when the chemical agents contacts the ocular surface. 4 Emergency
therapy such as immediate and extensive irrigation under topical anesthetics drop is
suggested for about 10 minutes. Irrigating contact lenses including Morgan Lens can
also be used to provide ocular irrigation and medication to the affected cornea and
conjunctiva. Ocular surface pH is checked using a urinary pH strip and continue the
irrigation until the pH normalizes to 7. The common used solutions for irrigation are
Normal Saline, Ringer Lactate, and Balanced Saline Solution.4,6

Acute Phase
The first 7 days after chemical injury are considered as acute phase. During this
phase, ocular tissues reestablish the superficial protective layer of cornea epithelium.
Enhance reepithelialization, decease inflammation and prevent infection will be
beneficial.4 Broad spectrum topical antibiotic, cycloplegic and antiglaucoma therapy
are needed.

Early reparative phase (8-20 days)

Immediate regeneration of ocular surface epithelium happens in this phase. Transition
period of ocular healing from acute to chronic may occur and lead to scaring. Stromal
ulceration often resulted from digestive enzymes activation such as collagenase,
metalloproteinase and other protease.4

Late reparative phase and sequelae (after 21 days)

This phase is characterized by completion of healing with good visual prognosis in
Grade I and II and complications with poor visual prognosis in Grade III and IV. The
late complications of chemical burns include poor vision, corneal scarring, dry eyes,
symblepharon, uveitis, cataract and other adnexal abnormalities ( lagophthalmos,
entropion, ectropion and trichiasis).1,4
Management

The goals of management in ocular chemical injuries are the removal of chemical
agent, pain, IOP and inflammation control, infection prevention and of ocular
epithelial healing. Both medical and surgical interventions are needed to restore the
damaged structures depending on the injury severity. There are several approaches to
management of ocular chemical injuries and will be presented in the tables as follow.
4,6–8

Table 4 Management approach in ocular chemical injury based on goals of management

Goals of Medical Management Surgical Management

managemen
t
Removal of  Irrigation solution Surgical debridement
the chemical  Open eyelids (±
agent speculum)
 Sterile cotton swab

Pain control  Topical anesthetic

drops (proparacaine
HCl 0.5%,
tetracaine HCl
0.5%)
 Systemic analgesics
(NSAIDs,
narcotics)
 Cycloplegic agents
(0.25% atropine
sulfate or
cyclopentolate)
Intraocular  Carbonic anhydrase  Trabeculectomy
pressure inhibitor  Glaucoma Seton valve
control  Betaadrenergic placement Promote
blocker
Inflammation  Topical
control corticosteroids
(prednisolone
acetate 1%,
fluorometholone
acetate 0.1%) 
four times daily in
mild injury and
every hour in
severe injury for
about 1 week  tap
off
 Progestational
steroids (topical,
subconjunctival,
systemic
medroxyprogestero
ne)  substitution
for cortical steroids
after 10-14 days of
steroid treatment
 NSAIDs
(diclofenac sodium,
ketorolac)
 Citrate  decrease
proteolytic activity

Infection  Topical ophthalmic

prevention antibiotic
drops/ointment
 (erythromycin,
bacitracin,
gentamicin,
Neosporin)
 Tetatus
immunization
Promote  Artificial tear • Conjunctival/Tenon’s advancement
ocular supplements • Limbal stem cell transplant
epithelial  Ascorbic acid  • Conjunctival/mucous membrane
healing cofactor in collagen transplant
synthesis • Amniotic membrane transplant
 Bandage soft • In vitro corneal stem cells transplant
contact lenses • Symblepharon lysis (±limbal

 Temporary transplantation)

amniotic membrane • Keratoprosthesis

patch  Osteodontokeratoprosthesis

Table 5 Management approach of ocular chemical injury based on the injury grades (Ropper Hall
Classification)

Ropper Hall Management

Classificatio
n
Grade I  Topical antibiotic ointment
 Prednisolom acetate 1% four times daily
 Preservative free artificial tears as needed
 Short cycloplegic (cyclopentolate) three times daily to
control the pain

Grade II  Topical antibiotic drop (fluoroquinolone) four times daily

 Prednisolone acetate 1% hourly while awake for the first 7-10
days. Consider tapering the steroid if the epithelium has not
healed by day 10-14. If an epithelial defect persists after day
10, consider progestational steroids (1%
medroxyprogesterone four times daily)
 Long acting cycloplegic (atropine)
  Oral Vitamin C, 2 grams four times a day
 Doxycycline, 100 mg twice a day (avoid in children)
 Sodium ascorbate drops (10%) hourly while awake
 Preservative free artificial tears as needed
 Debridement of necrotic epithelium and application of tissue
adhesive as needed

Grade III  As for Grade II

 Consider amniotic membrane transplant (ideally performed
within the first week of injury)

Grade IV  As for Grade II/III

 Early surgery is usually necessary. For significant necrosis, a
Tenonplasty

Surgical Treatments

Debridement of necrotic epithelium

This management should be performed in early phase to facilitate epithelialization.
Anterior segment necrosis can happen from loss of limbal blood supply. After
removal of necrotic tissue, a tenonplasty can help to restore limbal vascularization.1,3

Amniontic membrate transplantation (AMT)

AMT can rapidly restore the surface of conjunctiva and reduce inflammation in limbal
and stroma. Physically, AMT has been shown to reduce eyelid friction hence
improving patient comfort and prevent symblepharon formation. Moreover, amniotic
membrane is rich in TGFB1 and epidermal growth factor expression that can enhance
wound healing.1 It has also been found to have anti-inflammatory, prevent scarring
and neovascularization.

Limbal stem cell transplant

Most of the ocular chemical injuries resulted in limbal stem cell deficiency (LSCD).
Limbal autograft can be used from the healthy contralateral eye in one eye injury
(autograft) or from other living donors (allograft). Methods of transplantation can
vary from conjunctival limbal to keratolimbal.

Cultivated oral mucosal epithelial transplantation (COMET)

The cells are harvested from patient’s buccal mucosa to promote re-epithelialization
and reduce inflammation. No systemic immunosuppression agent is needed.

Boston Keratoprosthesis
This technique can be used in chronic inflammation and scarring cases. It also doesn’t
need systemic immunosuppression because of it is independent of stem cell function.8

References

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