The document discusses chemical injuries of the cornea, including their epidemiology, causative agents, classification, stages of healing, and management strategies. Chemical injuries are usually accidental and occur most often in young men in the workplace. Alkali agents like lye and ammonia cause more severe injuries than acids. Injuries are classified from Grade I to IV based on the extent of epithelial defects, limbal ischemia, and corneal haze, with Grade IV having the poorest prognosis. Following injury, the cornea goes through stages of epithelial recovery, inflammation, neovascularization, and potential conjunctivalization before final healing. Management involves irrigation, medications, and possible surgical techniques depending on the grade and stage of healing

1. Chemical Injuries
of the Cornea
Kathryn Colby, MD, PhD
VOLUME XXVIII NUMBER 1
MARCH 2010 (MODULE 1 OF 3)
Reviewers and Contributing Editor
George A. Stern, MD, Editor for Cornea & External Disease
Kenneth M. Goins, MD, Basic and Clinical Science, Course Faculty, Section 8
Ron W. Pelton, MD, PhD, Practicing Ophthalmologists Advisory Committee for Education
FocalPoints
Consultants
Roswell R. Pfister, MD
Scheffer C.G. Tseng, MD, PhD
Clinical Modules for Ophthalmologists

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ii FOCAL POINTS : MODULE 1, 2010
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3. FOCAL POINTS : MODULE 1, 2010 1
Introduction
Chemical injuries of the cornea are ophthalmic emergen-
cies. These injuries often result in significant ocular mor-
bidity and generally strike young adults in the prime of
life. Classification schemes enable the ophthalmologist
to determine the severity of the injury and the prognosis
for the injured eye. Immediate management consists of
copious irrigation following the exposure. Effective man-
agement in the intermediate and late phases requires an
understanding of the cellular events occurring during
each phase. Appropriate medical and surgical care helps
ensure the best outcomes for these potentially blinding
injuries.
Epidemiology of Chemical Injuries
Similar to open globe injuries, most chemical injuries
occur in young men. In published series of chemical inju-
ries, approximately two-thirds of patients are men. The
visual impact of chemical injuries is magnified because
they generally occur in patients in the prime of life.
While a small percentage of chemical injuries are delib-
erately inflicted during an assault, the vast majority (90%)
are accidental. Approximately two-thirds of chemical
injuries occur in the workplace. The bulk of workplace-
related chemical injuries occur at construction sites,
Contents
Introduction 1
Epidemiology of Chemical Injuries• 1
Causative Agents 2
Classification Schemes 2
Stages of Ocular Surface Recovery
Following Chemical Injury 3
Management Strategies 4
Medical Therapies• 4
Role and Timing of Surgical Treatment•
Following Chemical Injury 6
Putting It All Together: A Case Report 8
Conclusion 9
Clinicians’ Corner 10
Financial Disclosures
The authors, reviewers, and consultants disclose the following finan-
cial relationships. Kathryn Colby, MD, PhD: (C) Alcon Laboratories,
Vistakon Johnson & Johnson Visioncare; (E) Novartis Pharmaceuticals
Corporation. D. Michael Colvard, MD, FACS: (C) Advanced Medical
Optics, Bausch & Lomb; (P) OASIS Medical. Ron W. Pelton, MD,
PhD: (L) AO-ASIF. Steven I. Rosenfeld, MD, FACS: (L) Allergan.
Scheffer C.G. Tseng, MD, PhD: (C) Bio-Tissue; (E) TissueTech;
(O, P) Bio-Tissue, TissueTech. C. Gail Summers, MD: (C) McKesson.
Albert T. Vitale, MD: (C) Bausch & Lomb Surgical.
The following contributors state that they have no significant financial
interest or other relationship with the manufacturer of any commer-
cial product discussed in their contributions to this module or with
the manufacturer of any competing commercial product: William
S. Clifford, MD; Bradley S. Foster, MD; Kenneth M. Goins, MD; Anil
D. Patel, MD; Roswell R. Pfister, MD, Eric P. Purdy, MD; George A.
Stern, MD.
C = Consultant fee, paid advisory boards or fees for attending a
meeting
E = Employed by a commercial entity
L = Lecture fees (honoraria), travel fees or reimbursements when
speaking at the invitation of a commercial entity
O = Equity ownership/stock options of publicly or privately traded
firms (excluding mutual funds)
P = Patents and/or royalties that might be viewed as creating a
potential conflict of interest
S = Grant support
Learning Objectives
Upon completion of this module,
the reader should be able to:
Describe the classification scheme and•
epidemiology of chemical injuries of the cornea
Consider management strategies for each stage of•
healing after a chemical injury of the cornea
Appraise the surgical approaches to chemical•
injuries of the cornea in acute and late phases of
management

4. 2 FOCAL POINTS : MODULE 1, 2010
chemical plants, and machine factories. Safety glasses,
the best defense against chemical injuries, are unfortu-
nately no match for strong chemicals under high pressure
that characterize many industrial accidents. The remain-
ing one-third of injuries occur at home, with only a small
percentage occurring at school. In contrast to industrial
accidents, chemical injuries in the home can often be pre-
vented by the use of appropriate safety glasses.
Causative Agents
Injuries caused by alkali agents are more common and
generally more serious than those caused by acids. Alka-
lis penetrate tissue more readily than acids due to their
ability to saponify cell membranes. Strong alkali agents
can reach the anterior chamber within 15 seconds of
exposure, causing cell death and corneal hydrolysis
along the way.
Alkali agents that cause ocular injuries include ammo-
nia, lye (sodium hydroxide), potassium hydroxide, magne-
sium hydroxide, and lime. Ammonia, found in fertilizers,
refrigerants, and cleaning solutions, is especially danger-
ous because it penetrates tissues almost instantaneously
and can liberate toxic fumes when combined with water.
Lye, present in drain cleaners, is almost as dangerous as
ammonia. Potassium hydroxide, found in caustic potash,
does not penetrate as rapidly as lye and is a less com-
mon cause of serious injury. Magnesium hydroxide, found
in firework sparklers and flares, produces damage
through both chemical and thermal mechanisms. Lime,
a component of plaster, mortar, cement, and whitewash,
is the most common cause of workplace chemical inju-
ries overall. Lime’s slow speed of penetration lessens the
severity of the injury. However, solid particles of lime
can become lodged in the conjunctiva (especially the
upper palpebral conjunctiva or fornix) and can act as a
reservoir, slowly releasing damaging chemicals.
Ocular injuries are caused by multiple acid agents,
including sulfuric acid, sulfurous acid, hydrofluoric acid,
acetic acid, and hydrochloric acid. Exploding car batter-
ies are a source of sulfuric acid; these injuries can be asso-
ciated with ocular lacerations from released particulate
matter. Sulfurous acid, found in bleach and refrigerant,
penetrates more easily than other acids due to its high
lipid and water solubility. Hydrofluoric acid, used in glass
polishing and mineral refining, causes severe injury due
to the rapid penetration of the fluoride ion into the cor-
nea, which rivals that of the alkali agents. Systemic burns,
even ones involving a tiny percentage of the body’s sur-
face area (2%), can be fatal due to uncontrolled metabolic
perturbations. Acetic acid, found in vinegar and as glacial
acetic acid, generally only produces injury if the eye is
exposed to a high-concentration form for an extended
period of time. Finally, hydrochloric acid penetrates poorly
and only causes damage following prolonged exposure.
Classification Schemes
The severity of a chemical injury and its prognosis can
usually be determined based upon the initial examina-
tion. To grade an injury, the physician determines the
extent of damage to the corneal epithelium, limbus, and
conjunctiva. The presence or absence (and the magni-
tude) of limbal ischemia is noted, as is the quality of the
view through the cornea. These features are then used
to classify the injury (Table 1).
Table 1. Prognostic Features of Chemical Injury
GRADE OF INJURY CLINICAL FINDINGS PROGNOSIS
Grade I Corneal epithelial defect
No corneal haze
No loss of limbal stem cells
Excellent
Grade II Cornea mildly hazy
Focal limbal ischemia
Generally good; may have focal conjunctivalization
of cornea in area of limbal stem cell loss
Grade III Severe corneal haze limits view of anterior segment
structures
Extensive limbal ischemia with loss of most limbal
stem cells
Guarded; cornea must be repopulated with
conjunctiva; surgery needed for visual
rehabilitation
Grade IV Complete loss of corneal and proximal conjunctival
epithelium
Cornea opaque
Complete limbal ischemia and loss of all limbal
stem cells
Extremely poor; melting likely; globe salvage may
not be possible

5. FOCAL POINTS : MODULE 1, 2010 3
grade IV injuries despite aggressive medical and surgical
management.
A recently described classification scheme by Bagley
and colleagues also suggests the importance of the depth
of the corneal injury and the involvement of the corneal
endothelium in the prognosis of chemical injuries.
Stages of
Ocular Surface
Recovery Following
Chemical Injury
An understanding of the biological events that take place
following a chemical exposure will aid the clinician in
The Hughes classification scheme (as modified by
Thoft) divides chemical injuries into 4 categories. A grade I
injury involves the corneal epithelium only. In a grade I
injury, the limbal stem cells, which serve as the source of
differentiated corneal epithelium, are spared. The cornea,
although denuded of epithelium, remains clear. There is
no limbal ischemia. The prognosis for a full recovery of
normal corneal appearance and function is excellent.
A grade II injury is characterized by a partial loss of the
limbal stem cells with focal limbal ischemia. The cornea
is hazy, but anterior segment structures (iris, lens) can
still be visualized (Figure 1). The prognosis for grade II
injuries is generally good, but there may be long-term
persistent epithelial dysfunction in the area that sus-
tained stem cell loss, with focal replacement of corneal
epithelium with conjunctival epithelium (conjunctival-
ization), haze, and neovascularization.
Grade III injuries have a guarded prognosis due to com-
plete loss of the corneal epithelium and loss of most, if
not all, of the limbal stem cells (Figure 2). Up to 50% of
the limbus is frankly ischemic and corneal haze limits
visualization of the iris and lens. Following grade III inju-
ries, resurfacing of the cornea can only be accomplished
by growth of conjunctival epithelium over the corneal
stroma. While conjunctival ingrowth will restore the
tectonic stability of the globe, it does not allow for good
vision due to vascularization and scarring.
The prognosis of grade IV injuries is extremely poor.
In these injuries, there is complete loss of corneal epi-
thelium and limbal stem cells plus loss of the proximal
conjunctival epithelium (Figure 3). The injured cornea
is opaque, allowing no view into the anterior cham-
ber. More than 50% of the limbus is ischemic. With no
endogenous source of epithelium to repopulate the cor-
neal surface, sterile ulceration is a common sequela of
Figure 1 Acute grade II burn with focal (approximately
3 clock hours) of limbal stem cell loss.
Figure 2 Acute grade III burn showing extensive corneal
haze impeding visualization of the iris and limbal ischemia of
approximately 6 clock hours.
Figure 3 Acute grade IV burn with porcelainization of the
cornea and bulbar conjunctiva.

6. 4 FOCAL POINTS : MODULE 1, 2010
managing these injuries. One can divide the events into
4 phases: initial (day 0), acute (days 0 to 7), intermediate or
early repair (days 7 to 21), and late repair (after day 21).
In the weeks immediately following a chemical injury,
there is interplay of multiple events as the cornea
attempts to repair itself. These events include epithelial
regrowth and migration, collagen synthesis and degrada-
tion, and activation and migration of keratocytes.
During the first week, epithelial regrowth begins if
there are sufficient undamaged limbal stem cells to
provide a source of healthy corneal epithelium. Treat-
ment efforts are directed at encouraging this growth,
by quelling inflammation and avoiding topical medica-
tions that might damage the fragile epithelium. Kerato-
cyte activation begins in response to the injury, allowing
the initiation of collagen synthesis. Little or no collagen
breakdown occurs in the first week following injury.
Epithelial migration continues during the early repair
phase (days 7 to 21). Mild injuries may show complete
re-epithelialization during this phase, while grade II
injuries may display a focal persistent epithelial defect,
corresponding to the area of limbal stem cell destruc-
tion (Figure 4a). More severe injuries typically show little
or no re-epithelialization during this period. Eyes with
grade IV injuries typically retain their ischemic appear-
ance. Ocular surface inflammation persists as long as
the corneal surface remains denuded. Keratocytes con-
tinue to function during this phase to repair damage to
the corneal stroma. Activity of collagenases (produced
by both keratocytes and invading inflammatory cells)
peaks by day 14 to 21 while collagen synthesis contin-
ues. The relative strength of these opposing forces deter-
mines whether corneal melting will occur. Treatment
approaches in this phase attempt to maximize collagen
synthesis while minimizing collagenase activation to
reduce the risk of sterile ulceration of the cornea. Cor-
neal perforation will ensue if sterile melting cannot be
arrested. Once the corneal surface is intact, collagenase
activity decreases as does the risk of corneal melting.
The late repair phase occurs after day 21. In mild inju-
ries in which the limbal stem cell population is intact,
a normal corneal surface is re-established. Focal limbal
stem cell loss (grade II) may lead to focal conjunctivaliza-
tion of the cornea in the area of the stem cell defect (Fig-
ure 4b). For grade III injuries, delayed re-epithelialization
is the norm, although with proper medical and surgi-
cal management, eventually the corneal surface will be
repopulated with conjunctival epithelium. Grade IV inju-
ries have an extremely poor prognosis due to the com-
plete loss of limbal stem cells and adjacent conjunctiva.
Despite optimal management, these eyes often cannot
be saved.
Management Strategies
There are 3 main goals in managing a chemical injury:
enhance recovery of the corneal epithelium; augment
collagen synthesis while minimizing collagen break-
down and sterile ulceration; and control inflammation.
In severe cases, surgical treatment may be indicated.
Table 2 summarizes initial treatments based on the
grade of the injury.
Medical Therapies
Irrigation. Initial management of an acute chemical
injury is relatively straightforward. The severity of a
chemical burn is a function of both the toxicity of the
agent involved and the duration of exposure. Time is of
the essence, since chemical burns are one of the only
true ophthalmic emergencies. The eye should be copi-
ously irrigated as quickly as possible after the exposure
Figure 4 Grade II burn. a. Twenty-nine days following
grade II burn with focal thinning and impending perforation.
Tissue adhesive and a bandage contact lens were applied.
Same patient as Figure 1. b. Final result following grade II
burn with focal corneal melt, treated with tissue adhesive.
Vision 20/20 but patient complains of photophobia.
a
b

7. FOCAL POINTS : MODULE 1, 2010 5
with whatever clean fluid is available. Irrigation should
be repeated upon arrival to the hospital, since irriga-
tion at the location of the injury or in the ambulance is
often insufficient to entirely remove the offending agent.
Once irrigation is complete, the pH of the ocular surface
is checked with expanded range pH paper. If the pH has
normalized (7.0 to 7.2), then the rest of the history can be
taken and the eye examined. If the pH is still abnormal,
then irrigation should be continued and the pH measure-
ment repeated. The pH should be rechecked every 15 to
30 minutes to ensure that it remains normal. A pH that
rises after initial normalization suggests that trapped par-
ticulate matter (for example, particles of plaster) is con-
tinuing to leach chemical onto the surface of the eye.
Exam. A complete ophthalmic exam is performed, includ-
ing inspection and sweeping of the inferior and superior
fornix to remove trapped particles. Intraocular pressure
is checked, since chemical injuries may cause an acute
pressure increase. The injury is graded based upon the
extent of damage to the cornea, limbus, and conjunctiva.
In an acute chemical injury, a white “porcelainized” eye
typically denotes extensive limbal ischemia, represent-
ing severe damage. This is occasionally misinterpreted
as a mild injury by an inexperienced observer. Similarly,
a cornea that is completely denuded of epithelium will
take up fluorescein stain poorly, leading the examiner
to underestimate the initial extent of the damage. One
should also inspect the chemical safety sheet for the
agent in question. Certain agents such as hydrofluoric
acid can cause life-threatening metabolic imbalances;
patients injured by this agent need concurrent medical
evaluation.
Initial Treatment. During the acute phase of recovery
(first week after the injury), the goal is to encourage
epithelial healing while controlling inflammation and
preventing superinfection. Patients with mild injuries
(grade I) can be placed on a topical antibiotic ointment
such as erythromycin 4 times a day. A cycloplegic agent
can be given to help with comfort (cyclopentolate 2 to
3 times daily or a single dose of scopolamine given by
the examiner). Preservative-free artificial tears can also
provide comfort following a chemical injury. Even mild
chemical injuries have significant associated inflamma-
tion, and we would typically give topical corticosteroids,
usually prednisolone acetate 1% 4 times a day, with a
rapid taper to off once the corneal epithelium is healed.
Patients with mild chemical injuries are followed every
1 to 2 days until the ocular surface is stable. Patients
may experience ocular discomfort even months after a
relatively minor chemical injury. Supportive measures
such as lubrication and treatment of any associated
Table 2. Initial Treatment Paradigms Based on Grade of Injury
GRADE OF INJURY RECOMMENDED TREATMENT
Grade I Topical antibiotic ointment (erythromycin or similar) qid
Prednisolone acetate 1% qid
Preservative-free artificial tears as needed
Consider short-acting cycloplegia (cyclopentolate tid or a single drop of scopolamine)
Grade II Topical antibiotic drop (fluoroquinolone) qid
Prednisolone acetate 1% hourly while awake (first 7–10 days); taper corticosteroids if epithelium not healed by
day 10–14
Atropine sulfate bid
Sodium ascorbate drops (10%) hourly while awake
Vitamin C, 2 grams po qid
Doxycycline, 100 mg po bid
Preservative-free artificial tears as needed
Oral pain medicines as needed
Progestational steroids (1% medroxyprogesterone) qid if epithelial defect persists after day 10
Debridement of necrotic epithelium as needed
Application of tissue adhesive as needed
Grade III As for grade II
Amniotic membrane considered if epithelial healing halts
Grade IV As for grades II/III
Early surgery (amniotic membrane, advancement of posterior conjunctiva) usually necessary given severity of
ocular surface damage

8. 6 FOCAL POINTS : MODULE 1, 2010
meibomian gland dysfunction or dry eye will help return
the ocular surface to its pre-injury state.
For burns of grade II and above, the importance of
intensive topical corticosteroids in the acute phase can-
not be overemphasized. There is concern that topical
corticosteroids can exacerbate corneal melting. While
this is true in the later stages of chemical injury man-
agement, in the acute stage topical corticosteroids are
very beneficial for controlling the severe inflammatory
sequelae and should be used in an appropriately aggres-
sive fashion. Corneal melting from activation of corneal
collagenases typically does not begin before 10 to 14 days
after the injury. Therefore, the first week represents a
window in which corticosteroids can and should be used
to quell the raging inflammation and give the ocular sur-
face a chance to heal. For grade II burns and above, we
typically use prednisolone acetate 1% hourly while the
patient is awake.
Additional considerations include the following:
Long-acting cycloplegia (ie, atropine sulfate 2 times•
daily) is beneficial.
Oral narcotics are often required for pain control.•
A stronger topical antibiotic (such as a fluoroqui-•
nolone) is given at least 4 times daily to reduce the
risk of bacterial superinfection.
Topical sodium ascorbate (10%) and oral vitamin C•
supplementation are given to promote collagen syn-
thesis. Ascorbate, a cofactor in the rate-limiting step of
collagen synthesis, may be depleted following a chemi-
cal injury. Animal data suggests that ascorbate admin-
istration may reduce corneal ulceration.
Oral tetracycline derivatives are given to reduce the•
risk of ulceration due to their inhibitory effects on cor-
neal matrix metalloproteinases. They may also help to
reduce ocular surface inflammation.
Preservative-free tear supplements may be adminis-•
tered as needed.
Glaucoma medications (topical or oral) are prescribed•
if the intraocular pressure is elevated.
There is little role for topical nonsteroidal agents in•
a severe chemical injury. Their anti-inflammatory
power is dwarfed by that of the recommended topical
corticosteroids and they have the potential to cause
issues with epithelial healing.
Similarly, bandage contact lenses are of marginal util-•
ity in the acute management of chemical burns, as the
eye is usually too inflamed to tolerate a foreign body
on its surface.
Monitoring and Follow-Up. Patients with severe chem-
ical injuries (grade II and above) should be followed
daily initially. If there is a concern about compliance,
consideration should be given to inpatient admission.
Once epithelial healing is progressing, then follow-up
visits can be reduced accordingly. However, it is impor-
tant to maintain close observation while patients remain
on topical corticosteroids.
The real “art” of managing chemical burns comes
after the first week. For milder injuries (grade I and less
severe grade II), epithelial regrowth within the first 7 to
10 days is typical. Once epithelial regrowth is progress-
ing, topical corticosteroids can be tapered, with cessa-
tion of therapy once the epithelium is completely intact
and the eye is quiet. Lubrication and management of co-
existing dry eye and meibomian gland dysfunction will
help with post-injury discomfort.
For more severe grade II injuries and all grade III inju-
ries, complete epithelial healing usually takes longer
than 10 days. At this point, the risk of corneal melting
increases due to the shift towards collagen breakdown
at the expense of collagen synthesis. Topical corticoster-
oids must be tapered if the epithelium is not intact. Low-
dose corticosteroids (prednisolone acetate 1% once or
twice daily) may be continued if the patient is followed
closely, because corneal melting can occur precipitously
in these patients. In place of corticosteroids, topical pro-
gestational steroids such as 1% medroxyprogesterone
can be started to provide some anti-inflammatory effect
without inducing corneal melting. Other medicines are
continued. If epithelial healing falters or comes to a com-
plete halt or progressive corneal melting occurs, then
one must resort to the surgical maneuvers described in
the next section.
In grade IV injuries, medical therapy alone will not
restore the epithelial integrity of the eye, and surgery is
virtually always required. One may begin medical man-
agement initially to quiet the eye, but with the knowl-
edge that this is purely a temporizing measure.
Role and Timing of Surgical Treatment
Following Chemical Injury
Debridement. Mild chemical injuries rarely require sur-
gery for management. More severe grade II injuries may
require focal debridement of necrotic corneal or conjunc-
tival epithelium. This should be done as early as possible,
because the necrotic tissue serves as a source of inflam-
matory mediators that can inhibit re-epithelialization.
Necrotic corneal epithelium can be removed at the slit
lamp with surgical sponges. Extensive necrotic conjunc-
tiva can be excised with scissors using topical anesthesia
with the aid of a slit lamp or under an operating micro-
scope. Occasionally grade II injuries show focal corneal
melting that can usually be managed with the appli-

9. FOCAL POINTS : MODULE 1, 2010 7
cation of cyanoacrylate tissue adhesive covered with a
bandage contact lens.
Grade III injuries often require surgery for both acute
and long-term management. In the acute phase, necrotic
tissue should be debrided whenever needed, for the rea-
sons detailed above.
Restoration of the Corneal Surface. If epithelium
(either corneal or conjunctival) does not begin to grow
in to cover the cornea or if regrowth begins but then fails
to progress, placement of an amniotic membrane within
the first several weeks after the injury may be useful.
Amniotic membrane has anti-inflammatory properties
and can provide a scaffold for the regrowth of epithe-
lium. It can be sutured (using either 10.0 Vicryl or 10.0
nylon) or glued (using Tisseel fibrin glue) into place.
Amniotic membrane on a conformer ring (ProKera, Bio-
Tissue, Miami, FL) can also be used in this setting, often
with a tarsorrhaphy to prevent dislocation of the mem-
brane. However, despite the useful properties of amniotic
membrane in this setting, it does not replace limbal stem
cells, but may allow conjunctival epithelium to grow in
to cover the cornea. In severe injuries, one often must
be satisfied, in the short-term at least, with an eye that
is resurfaced by vascularized, conjunctival epithelium.
While this is not compatible with good vision, at least
this restores tectonic stability to the eye and eliminates
the risk of progressive corneal melting.
ONLINE VIDEO:
Amniotic Membrane in Acute Chemical Burn, 8 min 26 sec
ONLINE VIDEO:
Use of Sutureless Amniotic Membrane, 1 min 25 sec
Some clinicians advocate the use of amniotic mem-
brane transplantation acutely in all serious chemical
injuries (grade II and above). In our hospital, we gen-
erally reserve amniotic membrane for chemical inju-
ries that do not respond to initial medical management.
Amniotic membrane is a useful adjunct, but it is quite
expensive and not covered by some insurers in our area,
so we prefer to limit its use to situations in which we
know it is required.
The same management strategies can be used in
grade IV injuries, although the complete destruction of
the limbal stem cell population and limbal conjunctiva
makes it unlikely that they will be successful. Mobiliza-
tion and advancement of more posterior conjunctiva and
Tenon’s capsule can be used to bring healthy tissue into
the damaged area and may increase the likelihood of ini-
tial stabilization of these badly damaged globes.
Eyelid issues such as malpositions or trichiasis may
accompany severe chemical injuries and need to be
addressed to prevent further damage to the cornea and
inhibition of epithelial healing.
Ongoing Suppression of Inflammation. Once the cor-
neal surface has been restored, either with corneal
epithelium in less severe burns, or with conjunctival
epithelium in more severe burns, the frequency of fol-
low-up can be reduced. Severely burned eyes will benefit
from ongoing suppression of inflammation with low-
dose corticosteroids or topical cyclosporine. Bland oph-
thalmic ointment and preservative-free artificial tears
will help improve ocular comfort.
Stem Cell Transplantation. Following a severe unilateral
chemical injury in which there has been loss of most
or all of the limbal stem cell population, one can con-
sider an autologous limbal stem cell transplant from the
patient’s other eye, described in detail by Nordlund et al.
Caution should be exercised if the other eye was dam-
aged as well, since even mild injuries can deplete the
stem cell reserve to the point that harvesting some of
the stem cells may lead to the surface epitheliopathy in
the good eye.
If the original injury was bilateral or there is concern
about the viability of the stem cell population in the
good eye, then there are several options. One can con-
sider a living-related stem cell graft from a family mem-
ber or a cadaveric donor. Both of these require systemic
immunosuppression, which adds to the complexity of
postoperative management. Cultured buccal mucosa has
shown some utility in this situation, although again, like
amniotic membrane alone, buccal mucosa does not con-
tain limbal stem cells. A novel approach involves the use
of the patient’s own limbal stem cells that have been
expanded in culture in vitro and then transplanted back
on to the injured eye. This allows harvesting of a much
smaller amount of limbal stem cells, which can be useful
when one is unsure of the status of the stem cell popula-
tion in the good eye.
Additional Measures and Follow-Up. Once the health of
the ocular surface has been restored, then a corneal trans-
plant can be considered if needed. Supportive measures
including concurrent amniotic membrane transplanta-
tion and suture tarsorrhaphy may also be performed to
promote epithelial healing of the corneal transplant. The
graft should be secured with interrupted sutures (rather
than with a running suture) to allow selective suture
removal if corneal neovascularization ensues. Postoper-
ative management includes topical steroids, antibiotics

10. 8 FOCAL POINTS : MODULE 1, 2010
membrane was sutured over the cornea and proximal
conjunctiva on day 12. Epithelial healing was first noted
25 days after the injury (Figure 6) and melting did not
occur. Six weeks following the injury, a small epithelial
defect remained without thinning. The superior conjunc-
tiva remained ischemic (Figure 7). Ten weeks following
the injury, the surface was completely intact (although
covered by conjunctiva), with 20/400 vision and a nor-
mal intraocular pressure (Figure 8). Prednisolone acetate
(1%) was continued once daily. The patient was unable
to return to her occupation due to her poor vision in
this eye and reduced stereopsis, and she sought career
retraining during this time.
The eye was allowed to quiet during the months follow-
ing the injury. Neovascularization progressed, reducing
and possibly cyclosporine. Occasionally restoration of
the ocular surface is enough to allow acceptable vision,
however, and a penetrating keratoplasty is not required
(see below).
Permanent Boston keratoprostheses have been used
in chemical burn patients with reasonable success. This
type of device is especially useful in bilateral severe
burns, because its success is not dependent upon limbal
stem cell function and it does not require the use of sys-
temic immunosuppression.
Putting It All Together:
A Case Report
A healthy, 27-year-old chef presented to the Massachu-
setts Eye and Ear Infirmary after a high-pressure ammo-
nium chloride burn to the right eye. Her eye was irrigated
at work immediately after the injury. Ocular pH upon
arrival was 7.1. Further irrigation was performed; the pH
remained stable. Vision was count fingers and intraocu-
lar pressure was 18. Slit-lamp exam revealed virtually
complete limbal ischemia (Figure 5) and loss of all proxi-
mal conjunctival epithelium, consistent with a grade IV
injury. The left eye was uninjured. Hourly 1% predni-
solone acetate was started, along with topical antibiot-
ics, atropine, and 10% sodium ascorbate. Oral vitamin C
(2 grams daily) and doxycycline (100 mg twice daily) were
begun. She was followed daily. She did not tolerate the
doxycycline, which was discontinued.
By day 10, there was no epithelial healing and corti-
costeroids were tapered to 4 times daily. An amniotic
Figure 7 Six weeks following injury; epithelial healing is
progressing, with a small central epithelial defect remain-
ing without corneal thinning. Superior conjunctiva remains
ischemic in appearance.
Figure 5 Acute grade IV burn from high-pressure ammo-
nium chloride injury at work.
Figure 6 Twenty-five days following injury, 13 days following
amniotic membrane transplantation.

11. FOCAL POINTS : MODULE 1, 2010 9
postoperative course was uneventful. Five months after
reconstructive surgery, vision was 20/70 uncorrected
with an intact corneal epithelium and a white and quiet
eye (Figure 10). No further surgery was recommended.
Conclusion
With appropriate management, it is possible to restore
vision to all but the most severely burned eyes. While
our current understanding of these injuries allows us to
save many of these eyes, more work is needed to improve
the prognosis of grade IV injuries. Ongoing animal and
human research is investigating the use of novel topi-
cal agents to reduce angiogenesis, inhibit inflammation,
promote repair, and reduce the risk of corneal melting.
Efforts at preventing ocular chemical burns are equally
important and deserve emphasis.
Kathryn Colby, MD, PhD, is a practicing cornea spe-
cialist at Massachusetts Eye and Ear Infirmary and
Children’s Hospital, Boston, and an assistant professor
of ophthalmology at Harvard Medical School, Boston,
Massachusetts.
vision to counting fingers, but the eye remained tectoni-
cally stable (Figure 9) with a normal intraocular pres-
sure. One year after the original injury, the patient was
ready to proceed with ocular surface reconstruction. A
superficial keratectomy and conjunctival resection was
performed OD. Two limbal stem cells grafts were har-
vested from the left eye and sutured into place on the
right eye. An amniotic membrane was sutured into place
over the right cornea and proximal conjunctiva. Her
Figure 9 One year following injury, immediately before ocu-
lar surface reconstruction. Vision is hand motion.
Figure 10 Five months following ocular surface reconstruc-
tion. Vision is 20/70.
Figure 8 Ten weeks following grade IV injury; the ocular
surface is conjunctivalized, but intact.

12. 10 FOCAL POINTS : MODULE 1, 2010
Clinicians’Corner
1. Following a chemical injury, what is the preferred
method for irrigating the eye? Does the chemical
agent dictate the method?
Dr. Pfister: At the site of the injury, any clean source of
water can be used to lavage the eye, but ideally a bottle of
solution is already prepared for such emergencies. In the
emergency room, hand-held irrigation from intravenous
tubing is sufficient, but it is much more effective and
efficient to insert a contact lens with a fitting to accom-
modate the IV tubing (Morgan lens), delivering fluid into
the eye continuously over a 2-hour period.
Alkali and acid chemical injuries are best lavaged with
Ringer’s lactate solution, although most sterile isotonic
irrigants are acceptable. The pultaceous character of lime
(calcium hydroxide) often requires bulk removal with a
cotton-tipped applicator, facilitated by intermittent irri-
gation with a solution of EDTA, 0.01 M. EDTA should not
be used as a long-term irrigant because, in the presence
of an epithelial defect, penetration to endothelium might
well add additional damage by calcium chelation.
Dr. Tseng: For liquid chemicals, irrigation with clean
water or saline is usually sufficient if the conjunctival cul-
de-sac is well rinsed. This can be hard to achieve because
of the patient’s blepharospasm and pain. To circumvent
this concern, a Morgan lens is a good choice. For solid
chemicals (especially pressurized), including cement, sim-
ple irrigation is insufficient. All embedded debris needs to
be removed by forceps and if necessary by surgery.
2. Following irrigation, what is your immediate man-
agement of a grade II to IV alkali injury?
Dr. Pfister: Topical antibiotics and mydriatics/cyclople-
gics are “de rigeuer” shortly after the injury. The use
of a topical corticosteroid to suppress the inflammatory
response is controversial, but if a topical corticosteroid is
used, it must not be continued for more than 7 to 10 days
after the injury to avoid inhibition of wound repair and
Clinicians’ Corner provides additional viewpoints on
the subject covered in this issue of Focal Points. Con-
sultants have been invited by the Editorial Review
Board to respond to questions posed by the Acade-
my’s Practicing Ophthalmologists Advisory Committee
for Education. While the advisory committee reviews
the modules, consultants respond without reading the
module or one another’s responses. –Ed.

13. FOCAL POINTS : MODULE 1, 2010 11
of amniotic membrane over the cornea and conjunctiva
to determine the best fit. For fixation I place 4 vertical
mattress 9-0 Vicryl sutures through the amniotic mem-
brane and episclera in each quadrant at the limbus. I
use the remaining skirts of amniotic membrane to line
the cul-de-sacs, passing 8-0 Vicryl suture through the
upper and lower lids, temporally and nasally, to secure
the membrane to the conjunctival reflection. I can place
additional sutures, where needed, to further secure the
membrane in place.
When the acute process has subsided, I perform a sec-
ond, more definitive operation with amniotic membrane
as a base. These are my steps. (1) Resect any corneal pan-
nus and allow it to retract 4 to 6 mm from the limbus.
(2) Cut amniotic membrane to fit this corneoscleral
defect and use sutures and biologic adhesive (Tisseel) to
secure to the episclera. (3) Harvest 2 or 3 patches of cor-
neal stem cells, if available, from the patient’s other eye
or use patches from a blood relative or cadaver, in that
order of desirability. (4) Secure the stem cell patches at
the limbus using 10-0 nylon sutures through amniotic
membrane into the episclera.
Dr. Tseng: I use amniotic membrane whenever the epi-
thelium is not healing (if the defect is mostly within
the cornea), or if the defect involves most of the lim-
bus or beyond. In general, to resurrect the remaining
stem cells, the surgeon should transplant amniotic mem-
brane within 7 to 10 days. One layer of cryopreserved
amniotic membrane serves as a biological bandage cov-
ering cornea and involved conjunctiva, using a perilim-
bal 10-0 nylon purse-string suture. Alternatively, this
technique can now be simplified by insertion of a Pro-
Kera device (Bio-Tissue, Miami, FL), which is amniotic
membrane stretched across a symblepharon ring. If the
defect involves the fornix or tarsal conjunctiva, mem-
brane is best to be sutured from lid margin to lid margin
by anchoring sutures from the fornix through the lid
and tied across a bolster.
4. What is your management of corneal melting fol-
lowing chemical injury? What about descemeto-
cele or perforation?
Dr. Pfister: Corneal ulceration after chemical injury is
the result of destruction of both the devitalized and
acceleration of ulceration. In chemical injuries, inflam-
matory cell suppression must be balanced against dimin-
ished host keratocyte and fibroblast cell repair.
Treatment with EDTA, cysteine, or acetylcysteine has
been advocated as prevention against corneal ulceration,
based on their ability to inhibit metalloproteinases. Met-
alloproteinases act by degrading native and denatured
collagen, hence promoting ulceration.
Animal research has shown that topical 10% ascor-
bate and 10% citrate dramatically reduce the frequency
of corneal ulceration by inhibiting the effects of neutro-
phils and enhancing normal collagen synthesis. A combi-
nation of citrate and ascorbate, both 10%, results in only
a 4% incidence of corneal ulcer in animal eyes. Clinical
studies in humans bear out this favorable effect, espe-
cially in grade III or higher alkali injuries.
Dr. Tseng: My initial management is topical cortico-
steroids q2h, prophylactic antibiotics (preferably a fluo-
roquinolone) tid, oral vitamin C 2 grams/day, and oral
doxycycline 100 mg qd. Most important is to document
the extent of fluorescein-stained epithelial defects includ-
ing the cornea, limbus, and conjunctiva (from lid margin
to lid margin), and look for blanching of blood vessels,
indicating ischemia. This should be repeated in less than
1 week to determine whether there is acceptable healing
or an increase in ischemia, which frequently will take a
few days to weeks to become obvious.
3. What are the indications and timing for the use of
amniotic membrane? Describe your technique of
amniotic membrane transplantation.
Dr. Pfister: Amniotic membrane is commonly used in the
early phases after chemical injury to suppress the initial
inflammatory process and later to additionally create a
new substrate upon which epithelium can migrate. It
can be performed within a week or 2 of injury, but could
also be performed several weeks or even months later.
Later, amniotic membrane is commonly used in conjunc-
tion with stem cell transplants to encourage reformation
of an intact epithelial layer. It has been shown that, in
the absence of corneal stem cells, amniotic membrane
alone cannot heal the corneal epithelial surface.
My technique is to prepare the ocular surface by
removing any loose epithelial tissue. I place a large piece

14. 12 FOCAL POINTS : MODULE 1, 2010
Clinicians’Corner
a melt. Both a neurotrophic state and ischemia can be
aggravated by limbal stem cell deficiency. However, the
stem cell deficiency tends to bring in conjunctivalization
with vascularization, which can prevent a melt.
5. What are the best ways to prevent symblepharon?
Dr. Pfister: If extensive alkali or acid injury of the con-
junctiva occurs, especially involving the cul-de-sacs, then
some degree of symblepharon is inevitable. Tradition-
ally a glass rod was used to separate raw conjunctival
surfaces shortly after the injury, only to have fibrin-
ous exudates tend to reform adhesions. Placement of a
thin plastic wrap, lining the cul-de-sacs, and suturing it
through the eyelid has been supplanted with amniotic
membrane sutured in a similar fashion, further limit-
ing the formation of symblephara. Lateral contraction
of subconjunctival scar, formed from fibrocytes invading
conjunctiva as part of the healing process, can obliterate
the cul-de-sacs and make visual rehabilitation very dif-
ficult. Amniotic membrane contains anti-inflammatory
factors, possibly limiting this propensity to scar.
Dr. Tseng: The best way to prevent symblepharon is to
perform amniotic membrane transplantation within the
first 10 days after injury. For patients with ischemia,
Tenonplasty is the only way to avoid symblepharon. For
those without ischemia and beyond 10 days from injury,
when granulation tissue is formed around the conjuncti-
val epithelial defect, prompt subconjunctival injection of
triamcinolone acetonide is effective in preventing sym-
blepharon. After a certain stage, there is no effective way
to prevent symblepharon.
6. Is there a role for topical cyclosporine to control
dry eye following chemical injury?
Dr. Pfister: Dry eye developing after chemical injury is
the consequence of destruction of goblet cells of the con-
junctiva and cicatricial closure of aqueous and lipid tear
gland orifices onto the surface of the conjunctiva. Unless
dry eye was present prior to the injury, it is difficult to
know how cyclosporine might improve tear dynamics
after chemical injury. Preservative-free artificial tears,
ointments, and gels would improve dry eye conditions,
but only by adding fluid to the eye. It is possible that top-
ical mucomimetics might improve mucus production—a
matter worthy of trial.
vital tissue framework of the cornea. Inflammatory cells
(principally polymorphonuclear cells, PMN) discharging
enzymes, including collagenases as well as superoxide
radicals, act as the proximal effecting agent. Although
EDTA, cysteine, and acetylcysteine inhibit collagenases,
they do not affect the PMN itself, allowing it to con-
tinue to produce degrading enzymes. A more direct and
orthomolecular approach is to employ 10% citrate (neu-
tralized) every hour, 14 hours a day to inhibit all activi-
ties of PMNs including chemoattraction, degranulation,
enzyme activation, and superoxide radical production. In
animals, this approach has lead to a significant statistical
reduction in corneal ulceration.
Topical drops prepared as a 25% to 40% solution, from
the patient’s own serum, can be helpful in closing persis-
tent epithelial defects and limiting ulceration. However,
when there is a total absence of stem cells, then serum
drops are not likely to result in epithelial closure.
Descemetocele or perforation is the end result of loss
of most or all corneal stroma in a localized area, hence
treatment is often the same for both. If the adjacent tis-
sues are not vascularized and are of good quality, then an
acceptable approach is immediate closure of the leak by
cyanoacrylate adhesive, covered by a contact lens. When
the adjacent tissues are of poor quality or are vascular-
ized, a surgical course is advised. Cleaning the wound of
necrotic and devitalized tissues is followed by placement,
and suture, of a lamellar graft into the stromal defect site
and then covering the entire cornea with fresh amniotic
membrane, sutured at the limbus. Alternately, suturing
layers of amniotic membrane into the ulcer bed, and cov-
ering with amniotic membrane, is acceptable. I favor the
former to achieve immediate and strong establishment
of ocular integrity.
Dr. Tseng: A severe neurotrophic state and ischemia are
the major causes of corneal or scleral melt in chemical
injury. For the former, the management starts with punc-
tal occlusion followed by autologous serum drops and a
bandage contact lens. If these treatments do not yield
improvement, one should move to amniotic membrane,
if within the first 10 days post-injury, or to tarsorrhaphy.
For the latter, a Tenonplasty is done to correct ischemia, at
the same time using amniotic membrane to promote epi-
thelialization. If a persistent epithelial defect has not led
to a corneal melt, another temporizing measure is to glue
a hard contact lens onto the corneal surface to prevent

15. FOCAL POINTS : MODULE 1, 2010 13
then clear-cut evidence of stem cell deficiency is present
and stem cell transplantation should be contemplated.
Naturally, all other potential causes of a persistent epi-
thelial defect must be eliminated.
The inflammatory response and mediators excited
by chemical injuries is severe and long lasting. Prior
data showed that waiting 18 months to perform corneal
transplantation improved the outcome by allowing the
inflammatory process to diminish. This delay might also
reduce the incidence of immune rejection in these high-
risk patients by reducing the number of immunoreac-
tive cells.
Dr. Tseng: For transplantation of either autologous (in
the form of conjunctival limbal autograft) or allogenic
(in the form of keratolimbal allograft) limbal stem cells,
transplantation is best performed when inflammation is
under control. Therefore, one should avoid performing
stem cell transplantation during the acute stage. Even at
the chronic stage, measures should be taken to restore
the ocular surface before such transplantation. For
example, all abnormalities of the lid margin, tarsus, and
lashes should be corrected; blinking should be restored
by symblepharon lysis and fornix reconstruction; and
dry eye linked to neurotrophic state should be effectively
managed. Except for such emergent situations as corneal
melt or perforation, when corneal transplantation may
be performed in the acute (inflamed) stage of chemical
injury to provide tectonic support, it should be deferred
for several months after limbal stem cell transplantation
corrects limbal stem cell deficiency.
9. When is a keratoprosthesis indicated? What ker-
atoprosthesis do you prefer following chemical
injuries?
Dr. Pfister: Over the years our success with conventional
corneal transplantation has improved considerably by
control of inflammation, maintenance of stromal integ-
rity, and stem cell transplantation. Nevertheless, kerato-
prostheses serve an important population of patients who
have not benefited from conventional corneal transplan-
tation. Keratoprostheses are considered as a last resort
after chemical injury when repeated corneal transplan-
tation fails on 2 or more occasions.
The Dohlman keratoprosthesis has the longest record
of success using a standardized protocol. There is 1 type
Dr. Tseng: No. Dry eye is caused by a neurotrophic state
following chemical burns. The chronic inflammation
caused by chemical burns is not lymphocytic.
7. When is cicatricial entropion commonly seen and
how do you manage this? Can it be prevented?
Dr. Pfister: Cicatricial entropion is commonly encoun-
tered weeks to months after the injury as scar tissue
near the tarsal conjunctival surface contracts, causing
inward rotation of the lid margin. Often this is associ-
ated with symblephara between the eyelid and eyeball.
In milder cases, lysis of symblephara and lining the raw
surfaces with buccal mucosa or amniotic membrane
might release the pressures of lid rotation and reduce
their reformation. More severe cases additionally require
splitting the eyelid at the gray line and advancing the
tarsus ahead of the eyelashes. Lysis of symblephara and
lining the conjunctival surface with amniotic membrane
offers the best opportunity for minimizing entropion.
Dr. Tseng: Cicatricial entropion is a late (several months)
complication of chemical burns that occurs when fornix
or tarsal injury has not been appropriately managed in
the acute stage. It can be prevented only by the measures
advised above including AMT, Tenonplasty, and control
of inflammation. Once formed at the chronic stage, cica-
tricial entropion can gradually cause corneal blindness;
hence, it should be surgically corrected by amniotic
membrane transplantation with or without oral mucosal
graft depending on the severity.
8. What is the proper timing of limbal stem cell trans-
plantation and corneal transplantation following
chemical injury?
Dr. Pfister: Successful limbal stem cell transplantation is
dependent on an intact episcleral vascular system, evi-
denced by the absence of necrosis or whitening of peril-
imbal tissues. Revascularization of these tissues normally
takes several weeks, allowing time to determine the true
extent of stem cell damage. It is very important to record
perilimbal fluorescein staining at the time of injury,
indicating stem cell loss. Whatever damage to stem cells
might have occurred, time should be allowed to give sur-
viving cells an opportunity to recover. When a persis-
tent epithelial defect is present for a period of 2 weeks
or more, despite conservative efforts to heal epithelium,

16. 14 FOCAL POINTS : MODULE 1, 2010
Clinicians’Corner
odonto-keratoprosthesis (OOKP) procedure followed by
Dohlman’s KPro device (also called the Boston K-Pro,
developed at Massachusetts Eye and Ear Infirmary).
Roswell R. Pfister, MD, is a practicing ophthalmolo-
gist, Pfister Vision Correction Center, Birmingham,
Alabama.
Scheffer C.G. Tseng, MD, PhD, is director, Ocular Sur-
face Center, medical director, Ocular Surface Research &
Education Foundation, and director, R & D, TissueTech,
Miami, FL.
for an eye with normal tear film, and another type for a
dry eye. There are significant complications potentially
developing after the surgery, in addition to the inability
to reliably measure intraocular pressure. Despite this,
recent developments have significantly improved the
prognosis so that many patients have now been followed
for years with acceptable vision.
Dr. Tseng: A keratoprosthesis can be considered fol-
lowing chemical injury when ischemia is absent and
inflammation is at a chronic stage. The best indica-
tion is for eyes where the ocular surface cannot be
restored (eg, severe dry eye, intense inflammation, or
keratinization). For chemical burns, I prefer the osteo-
Wagoner MD, Kenyon KR. Chemical injuries. In: Shingleton
BJ, Hersh PS and Kenyon KR, eds. Eye Trauma. St Louis, MO:
Mosby; 1991:79–94.
Wagoner MD, Al-Swailem S, Al-Jastaneiah S, Kenyon KR.
Chemical injuries of the eye. In: Miller JW, Azar DT, Blodi B,
eds. Principles and Practice of Ophthalmology, 3rd ed. Philadel-
phia: WB Saunders; 2008:761–772.
Yaghouti F, Nouri M, Abad JC, Power WJ, Doane MG, Dohlman
CH. Keratoprosthesis: preoperative prognostic categories.
Cornea. 2001;20:19–23.
Zerbe BL, Belin MW, Ciolino JB; Boston Type 1 Keratoprosthe-
sis Study Group. Results from the multi-center Boston Type I
keratoprosthesis study. Ophthalmology. 2006;113:1779.
Related Academy Materials
Chemical injuries. In: External Disease and Cornea. Basic and
Clinical Science Course, Section 8, 2009–2010.
Nordlund ML, Brilakis HS, Holland EJ. Surgical Techniques for
Ocular Surface Reconstruction. Focal Points, Clinical Modules for
Ophthalmologists, Module 12, 2006.
Suggested Reading
Bagley DM, Casterton PL, Dressler WE, et al. Proposed new
classification scheme for chemical injury to the human eye.
Regul Toxicol Pharmacol. 2006;45:206–213.
Barouch F, Colby KA. Evaluation and initial management of
patients with ocular and adnexal trauma. In: Miller JW, Azar
DT, Blodi B, eds. Principles and Practice of Ophthalmology, 3rd ed.
Philadelphia: WB Saunders; 2008:5071–5092.
Holland EJ, Croasdale CR. Epithelial transplantation for the
management of severe ocular surface disease. In: Brightbill
FS, ed. Corneal Surgery: Theory, Technique & Tissue, 3rd ed.
St. Louis, MO: Mosby; 2009:488–499.
Hosseini H, Nejabat M, Mehryar M, Yazdchi T, Sedaghat A,
Noori F. Bevacizumab inhibits corneal neovascularization in
an alkali burn induced model of corneal angiogenesis.
Clin Experiment Ophthalmol. 2007;35:745–748.
Pfister RR. Chemical trauma. In: Foster CS, Azar DT, Dohlman
CH, eds. Smolin and Thoft’s The Cornea, 4th ed. Philadelphia, PA:
Lippincott, Williams and Wilkins; 2005:781–796.
Tejwani S, Kolari RS, Sangwan VS, Rao GN. Role of amniotic
membrane graft for ocular chemical and thermal injuries.
Cornea. 2007;26:21–26.
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