PART 4 CORNEA AND OCULAR SURFACE DISEASES
SECTION 8 Trauma
Acid and Alkali Burns
Naveen K. Rao, Michael H. Goldstein
Definition: Chemical exposure to the eye resulting in trauma ranging
from mild irritation to severe damage of the ocular surface and anterior
segment with permanent vision loss.
Key features
■ Alkali burns are typically more severe than acid burns.
■ Acute management should be directed at eliminating the causative
agent.
■ Initial evaluation includes assessment of degree of corneal
epithelial injury, corneal opacity, and limbal ischemia.
Associated features
■ Limbal stem cell deficiency, corneal opacification, corneal
perforation, glaucoma, symblepharon, cicatricial entropion,
trichiasis, fibrovascular pannus
INTRODUCTION
Chemical exposure to the eye can result in trauma ranging from mild
irritation to severe damage of the ocular surface and anterior segment
with permanent vision loss. Chemical burns constitute between 7.7%
and 18% of all ocular trauma.1–4 The majority of victims are young
men.5–7 Injuries usually occur accidentally at work or at home, but also
may occur deliberately from assault.5–9 Many victims report not wear-
ing proper eye protection at the time of the injury.7 In the household
setting chemicals abound, in the form of solutions in automobile bat-
teries, pool cleaners, detergents, ammonia, bleach, and drain cleaners.
Although most injuries are mild with minimal sequelae, severe cases
present a management challenge (Fig. 4-26-1).
296 Fig. 4-26-1  Complete corneal vascularization and opacification in patient with
previous alkali injury. (Courtesy of Anthony J. Aldave, MD.)
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4.26 
ALKALI INJURIES
Alkali injuries occur more frequently than acid injuries and are more
severe.1,5–8 Common causes of alkali injury include lime (Ca(OH)2), lye
(NaOH or KOH), and ammonia (NH3).5,7,10 Alkalis penetrate more
readily into the eye than acids, damaging stroma and endothelium as
well as intraocular structures such as the iris, lens, and ciliary body.
Lime, found in cement and plaster, is the most common cause of alkali
injury. Damage from lime injury is limited, however, due to precipita-
tion of calcium soaps that limit further penetration. Lye and ammonia
are associated with the most severe alkali injuries. Ammonia can be
detected in the anterior chamber with a rise in aqueous humor pH
within seconds of exposure.11,12 Irreversible intraocular damage has
been noted to occur at aqueous pH levels of 11.5 or greater.13
ACID INJURIES
Acids cause superficial damage but generally cause less severe ocular
injury than alkalis, as the immediate precipitation of epithelial proteins
offers some protection by acting as a barrier to intraocular penetra-
tion.14 Very strong or concentrated acids, however, can penetrate the
eye just as readily as alkaline solutions. Sulfuric (H2SO4), sulfurous
(H2SO3), hydrochloric (HCl), nitric (HNO3), acetic (CH3COOH), formic
(CH2O2), and hydrofluoric (HF) acids are frequent causes of acid
burns.10 The most common cause is sulfuric acid, which is commonly
found in industrial cleaners and automobile batteries. Hydrofluoric acid
causes the most serious acid injuries due to its low molecular weight,
which allows easier penetration through the stroma.15 The injury may
be compounded by thermal burns from heat generated by the acid’s
reaction with water on the corneal tear film.16
PATHOPHYSIOLOGY
The severity of ocular injury from alkali or acid is related to the type of
chemical, the concentration of the solution, the surface area of contact,
the duration of exposure, and the degree of penetration. The hydroxyl
ion (OH−) of alkaline solutions saponifies fatty acids in cell membranes
leading to cell lysis, with subsequent hydrolysis and denaturation of
proteoglycans and stromal collagen.17,18 The hydrogen ion (H+) of acidic
solutions alters the pH, while the anion causes protein binding and
precipitation in the corneal epithelium and superficial stroma.19 This
protein precipitation produces the typical ground glass appearance of
the epithelium and acts as a barrier to further penetration. If penetra-
tion of either alkali or acid occurs, the hydration of glycosaminoglycans
leads to loss of stromal clarity. Loss of proteoglycans from the stroma
results in shrinkage of collagen and can lead to an acute rise in intraoc-
ular pressure due to distortion of the trabecular meshwork.20 The
release of prostaglandins also contributes to the rise in intraocular pres-
sure following alkali and acid injuries.19,21,22 Chemical penetration into
the eye may acutely damage stromal keratocytes, stromal nerve end-
ings, corneal endothelium, iris, trabecular meshwork, and ciliary
body.17,19
In addition to corneal and intraocular injury, chemical burns result
in damage to the conjunctiva, limbus, and eyelids.23 Damage to palpe-
bral and bulbar conjunctiva can lead to loss of goblet cells and chronic
dry eye disease.17 Ischemic necrosis of the conjunctiva induces loss of
vascularization at the limbus and loss of limbal stem cells, as well
as infiltration of leukocytes.17,19,24 Damage to the corneal epithelium
with injury solely to Bowman’s layer and anterior stroma may lead to
recurrent corneal erosions. Damage to the limbal stem cells, however,
can result in persistent corneal epithelial defects, conjunctivalization of
the cornea, presence of goblet cells within the corneal epithelium, and
superficial and deep neovascularization.19,23 Late sequelae of severe
burns include cicatrization of the conjunctiva with symblepharon for-
mation and entropion.19 Coagulation of the posterior lid margin may
cause posterior displacement of meibomian gland orifices with
trichiasis.17
After a chemical burn, breakdown of the blood–aqueous barrier may
result in a severe fibrinous inflammatory reaction. Damage to the cili-
ary body epithelium can cause decreased secretion of ascorbate, result-
ing in impaired keratocyte collagen synthesis and deficient stromal
repair, because ascorbate is a cofactor in the rate-limiting step in col-
lagen synthesis.25
Within 12–24 hours of injury, conjunctival necrosis and hydrolysis
of cellular and extracellular proteins produce chemotactic inflamma-
tory mediators that stimulate the infiltration of the peripheral cornea
with neutrophils.1,17,26 The neutrophils potentiate surface inflamma-
tion and release a variety of degradative enzymes such as
N-acetylglucosaminidase and cathepsin-D.24 Damage to the corneal
stroma and subsequent ulceration is mediated by the interaction
among keratocytes, epithelial cells, and neutrophils. Stromal repair is
marked by a balance between collagen synthesis and degradation.27
Keratocytes are multipotent cells capable of producing new type I col-
lagen as well as type I collagenase, a matrix metalloproteinase (MMP).28
MMPs are enzymes that can degrade matrix macromolecules such as
collagen. The three major groups of MMPs include collagenases, gela-
tinases, and stromelysins.27 Keratocyte activity may be regulated by
cytokines from epithelial cells, inflammatory cells, and other kerato-
cytes. A close interaction exists between keratocytes and the overlying
epithelial cells; type I collagenase production by keratocytes is both
stimulated and inhibited by epithelial cytokines.29,30
CLINICAL COURSE
McCulley divided the clinical course of chemical injury into four dis-
tinct phases: immediate, acute (0–7 days), early reparative (7–21 days),
and late reparative (after 21 days).16 Clinical findings immediately fol-
lowing chemical exposure can be used to assess the severity and prog-
nosis of the injury. The Roper–Hall modification of the Hughes
classification system provides a prognostic guideline based on corneal
appearance and extent of limbal ischemia.7,31,32 In Grade I injury, there
is corneal epithelial damage, no corneal opacity, no limbal ischemia,
and a good prognosis. In Grade II injury, the cornea is hazy but iris
details are visible. There is ischemia involving less than one-third of
the limbus, and the prognosis is good. In Grade III injury, there is total
epithelial loss, stromal haze obscuring iris details, ischemia of one-
third to one-half of the limbus, and the prognosis is guarded. In Grade
IV injury, the cornea is opaque with no view of the iris or pupil, the
ischemia is greater than one-half of the limbus, and the prognosis is
poor.
In the acute phase during the first week, Grade I injuries heal while
Grade II injuries slowly recover corneal clarity. Grade III and IV injuries
have little or no re-epithelization, with no collagenolysis or vasculariza-
tion. Intraocular pressure may be elevated due to inflammation and
mechanical distortion of the trabecular meshwork, or decreased due to
ciliary body damage.33 During the early reparative phase, re-epithelization
is completed in Grade II injury with clearing of opacification. In more
severe cases, delayed or arrested re-epithelization may occur. Keratocyte
proliferation occurs with production of collagen and collagenase, result-
ing in progressive thinning and potential for perforation.33
In the late reparative phase, re-epithelization patterns divide injured
eyes into two groups. In the first group, epithelization is complete or is
nearly complete with sparing of limbal stem cells. Corneal anesthesia,
goblet cell and mucin abnormalities, and irregular epithelial basement
membrane regeneration may persist. In the second group, limbal stem
cell damage is present, resulting in corneal re-epithelization by con-
junctival epithelium. This group has the worst prognosis with severe
ocular surface damage characterized by vascularization and scarring,
goblet cell and mucin deficiency, and recurrent or persistent erosions.33
Ocular surface abnormalities may be exacerbated by symblepharon
formation, cicatricial entropion, and trichiasis.19,23 A fibrovascular pan-
nus results if ulceration does not occur, compromising visual
rehabilitation.
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THERAPY
4.26 
Immediate Phase
Since the area and duration of contact determines the extent of subse-
quent injury and prognosis, immediate copious irrigation upon expo-
Acid and Alkali Burns
sure is of paramount importance.12 Irrigation should be continued for
at least 15 minutes with at least 1 liter of irrigant, until the pH of the
ocular surface reaches neutrality. Currently available solutions include
normal saline, borate-buffered saline, balanced salt solution, phosphate-
buffered saline, lactated Ringer’s, and amphoteric solutions that aim to
chelate acids and alkalis and create a reverse osmotic gradient to draw
chemicals out of the cornea.12,34,35 Some authors discourage the use of
phosphate-buffered saline, which may lead to precipitation of calcium
in the corneal stroma.35 Borate-buffered saline and amphoteric solu-
tions were found to be most effective in reducing aqueous humor pH
after an alkali burn.34,35 Normal saline and tap water were found to be
intermediately effective, and phosphate buffered saline and lactated
Ringer’s were found to have the least effective buffering capacity.35,36 If
access to commercial irrigating solutions is not immediately available,
tap water should be used, despite the fact that it is hypoosmolar and
may contribute to corneal edema.12 If an acid burn is suspected, a base
should never be used for irrigation in an effort to neutralize the acid. A
retained reservoir of chemical in the fornices should be suspected if
neutrality cannot be achieved, especially with exposure to lime, which
can be embedded in the fornices and the upper tarsal conjunctiva.33
Eversion of the lids and removal of particulate matter should be per-
formed; a cotton tipped applicator soaked in EDTA 1% may help with
the removal of stubborn lime particles.37 Necrotic corneal and conjunc-
tival tissue should be debrided to promote re-epithelization, as this
debris provides a stimulus for continued inflammation with recruit-
ment of neutrophils and MMP production.37
Acute and Reparative Phases
After irrigation, all efforts should be made to promote epithelial wound
healing, prevent infection, reduce inflammation, minimize ulceration,
and control intraocular pressure. Topical antibiotics should be used if
there is any corneal epithelial defect. Topical and systemic ocular hypo-
tensive medications may be needed. Better outcomes can be expected
with prompt re-epithelization, while delayed or absent re-epithelization
may require surgical intervention. Bandage contact lenses may be used
to promote epithelial healing. Intensive topical corticosteroid therapy
every 1–2 hours in the first 1–2 weeks decreases the inflammatory
response that can delay epithelial migration, and thus helps enhance
re-epithelization in the early phases of injury.7,38 Corticosteroid use in
the first 10 days of injury has no adverse effect on outcome with little
risk of sterile ulceration.39 Prolonged use of corticosteroids, however,
can be deleterious since corticosteroids can blunt stromal wound repair
by decreasing keratocyte migration and collagen synthesis.40 Beyond 2
weeks at the peak of the early reparative phase, suppression of kerato-
cyte collagen production by continued use of corticosteroids may offset
the benefits of inflammatory suppression and lead to stromal ulcera-
tion.40,41 Corticosteroid use should, therefore, be stressed in the first 2
weeks with subsequent taper as dictated by clinical exam. Medroxypro-
gesterone 1% is a synthetic progestogenic steroid which has weaker
anti-inflammatory activity than corticosteroids. Medroxyprogesterone
inhibits collagenase, but unlike corticosteroids, it minimally suppresses
stromal wound repair.40 As such, medroxyprogesterone can be substi-
tuted for corticosteroid after 10–14 days if worsening ulceration is of
concern.
Topical ascorbate 10% drops every 2 hours, topical citrate 10% drops
every 2 hours, and systemic ascorbate (2000 mg per day in divided
doses) replenish levels depleted from the aqueous following alkali
injury.7 Ascorbate is a cofactor in the rate-limiting step of collagen syn-
thesis and has been shown to decrease the incidence of stromal ulcera-
tion.42 Citrate is a calcium chelator that decreases intracellular calcium
levels of neutrophils and thus impairs chemotaxis, phagocytosis, and
release of lysosomal enzymes.43 Applied topically, citrate has been
shown to reduce corneal ulceration and perforation.44 Tetracyclines
have been shown to offer protection against collagenolytic degradation.
Proposed mechanisms for MMP inhibition include suppression of neu-
trophil collagenase and epithelial gelatinase gene expression, inhibition
of α1-antitrypsin degradation, and scavenging of reactive oxygen spe-
cies.27 Topical amniotic membrane suspension has been found to be 297
more effective than serum tears and preservative-free artificial tears in
 speeding epithelial recovery in animal models.45,46 In addition, topical
4 and subconjunctival bevacizumab as well as subconjunctival triamci-
nolone have been reported to decrease corneal neovascularization after
alkali burns in animals.47,48
Cornea and Ocular Surface Diseases
Surgical Therapy
Surgical interventions that may help stabilize the ocular surface after
severe chemical injury include tarsorrhaphy, tenonplasty, limbal stem
cell transplantation, and amniotic membrane transplantation. Tenon-
plasty attempts to re-establish limbal vascularity in Grade IV injury
and to promote re-epithelization.49 In this procedure, all necrotic con-
junctival and episcleral tissues are excised, Tenon’s capsule is bluntly
dissected, and the resultant flap with its preserved blood supply is
advanced to the limbus. Limbal stem cell transplantation attempts to
restore the normal corneal epithelial phenotype. In the technique
described by Kenyon and Tseng, two 8 mm crescents of peripheral cor-
neal limbal epithelium with a section of conjunctiva from either the
patient’s uninjured eye (conjunctival limbal autograft, CLAU) or that of
a close relative (living-related conjunctival limbal allograft, LR-CLAL)
are harvested and secured to the host bed.50,51 In vitro amplification of
limbal stem cells has been successful when there is limited tissue avail-
able for harvesting, as in the case of bilateral chemical burns.19
Amniotic membrane is the innermost layer of the placenta and con-
sists of a stromal matrix, a thick basement membrane, and a single
epithelial layer. Amniotic membrane has been shown to promote epi-
thelization and reduce ocular surface inflammation, vascularization,
and scarring. Amniotic membrane transplantation (AMT) has been
found to reduce proteolytic activity, increase goblet cell density, and
downregulate conjunctival and corneal fibroblasts.52–55 These actions
are beneficial in restoring the ocular surface, especially in Grade II and
III chemical burns, and may be considered in the acute or reparative
phases.55,56 AMT for Grade IV injury may be limited due to stem cell
loss and ischemia; however, when used in conjunction with limbal
stem cell transplantation, AMT may provide a substrate for stem cell
proliferation and re-epithelization.52,56,57 If surgical amniotic membrane
placement in the operating room is either not possible or impractical,
a sutureless amniotic membrane patch is commercially available
preloaded in a symblepharon ring and can be easily inserted in the
office or at the bedside.58
Penetrating keratoplasty for visual rehabilitation after chemical
injury can be fraught with complications. Prognosis is poor in the set-
ting of glaucoma, hypotony, limbal stem cell dysfunction, conjunctival
Access the complete reference list online at
298
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cicatrization, entropion, and trichiasis.19 If intraocular complications
are minimized in the setting of an optimized ocular surface and limited
deep stromal vessels, penetrating keratoplasty may be performed with
favorable results. A large-diameter penetrating keratoplasty with or
without donor limbal tissue may be considered in the acute and chronic
setting.59–61 Transplant of the cornea provides tectonic support in the
event of an impending perforation, while the limbal stem cells of the
donor address ocular surface issues.59,60 Staged surgery with limbal
stem cell transplantation followed by penetrating keratoplasty at least
6 weeks later has been shown to significantly decrease the likelihood of
corneal graft failure.62
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we choose? Graefes Arch Clin Exp Ophthalmol 2006;244:845–54.
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