Management of ocular thermal and chemical injuries, including amniotic membrane therapy

Management of ocular thermal and chemical injuries, including
amniotic membrane therapy
Robert Fish and Richard S. Davidson
Rocky Mountain Lions Eye Institute, University of
Colorado School of Medicine, 1675 N. Aurora Court,
MS F731, PO Box 6510, Aurora, CO 80045, USA
Correspondence to Richard S. Davidson, MD,
Associate Professor, Rocky Mountain Lions Eye
Institute, University of Colorado, School of Medicine,
1675 N. Aurora Court, MS F731, PO Box 6510,
Aurora, CO 80045, USA
Tel: +1 720 848 2500; fax: +1 720 848 5014;
e-mail: [email protected]
Current Opinion in Ophthalmology 2010,
21:317–321
Purpose of review
To provide a concise review of the literature regarding potential management strategies
of ocular thermal and chemical injuries.
Recent findings
After experiencing a serious ocular surface burn, either thermal or chemical, the goal of
therapy is to restore a normal ocular surface and corneal clarity. If extensive corneal
scarring and/or limbal stem cell deficiency are present, techniques such as limbal stem
cell grafting, amniotic membrane transplantation and possibly a keratoprosthesis can be
employed to help restore vision. This article will review the literature available and
discuss how these techniques have improved the prognosis of patients with serious
thermal and chemical injuries.
Summary
Ocular thermal and chemical injuries are a true ocular emergency and require immediate
and intensive evaluation and treatment. The sequelae of an ocular burn can be severe
and particularly challenging to manage. Improvements in the understanding of the
pathophysiology of a radiant energy or chemical injury as well as advancements in ocular
surface reconstruction have provided hope for patients in whom would otherwise have a
dismal visual prognosis.
Keywords
acid burn, alkali burn, amniotic membrane therapy, keratoprosthesis, ocular burn,
thermal burn
Curr Opin Ophthalmol 21:317–321
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1040-8738
Introduction
Burns to the eyelids, conjunctiva, cornea, or sclera,
whether from radiant energy or a chemical cause, are a
true ophthalmic emergency [1]. The extent of the injury
may vary but requires immediate evaluation and treatment. Ocular burns are classified based on their etiologies
with radiant energy injuries (either thermal or ultraviolet)
tending to carry a better prognosis compared with chemical exposures (acid or alkali). In general, the severity of
the injury is directly related to the duration of exposure
and the properties of the causative agent [1].
Radiant energy injuries
Radiant energy injuries may be divided into thermal or
ultraviolet exposure. The cell death that occurs from a
thermal injury is usually limited to the superficial epithelium, however, more extensive damage may sometimes
occur. When a patient presents with a radiant energy injury
it is important to thoroughly assess the extent of the ocular
damage. Careful inspection of the eyelids and ocular
surface is essential to determine the proper approach to
1040-8738 ß 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
treatment. If the eyelids are injured as a result of the burn,
it is important to determine whether or not the patient is
able to adequately close the eye (s). If voluntary closure is
not possible, then placement of a suture tarsorrhaphy may
be helpful to protect the ocular surface. In addition to
inspection of the eyelids, a complete ocular examination
should also be performed. One should assess the status of
the conjunctiva (both palpebral and bulbar) as well as
the corneal surface. Corneal epithelial defects should be
quantified and the presence or absence of an anterior
chamber reaction should also be noted.
Ultraviolet burns tend to result in a severe punctate
keratitis. Although these injuries tend not to be vision
threatening, they may be extremely painful. With frequent lubrication of the ocular surface they tend to
resolve with minimal sequelae within 24–48 h.
Treatment in the immediate period following thermal
injury should consist of frequent lubrication of the ocular
surface with a bland lubricating ointment (or artificial
tears if damage to the ocular surface is minimal)
and prevention of infection with the use of a topical
DOI:10.1097/ICU.0b013e32833a8da2
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318 Corneal and external disorders
Figure 1 Photo of severe cicatricial changes following thermal
injury (photo courtesy of Vikram D. Durairaj M.D.)
antibiotic. If a significant amount of corneal edema is
present then adding a topical steroid can be beneficial
but if this is done prior to closure of the epithelium then
one needs to observe the patient carefully for signs of
infection. If the eyelids are significantly burned then a
combination antibiotic/steroid (tobramycin/dexamethasone, Alcon Laboratories, Fort Worth, Texas, USA) ointment may also be beneficial in promoting healing and
minimizing scar formation. These patients should be
followed very closely for signs of infection and referral
to an oculoplastics specialist may also be indicated if the
patient shows signs of cicatricial eyelid changes as the eye
is healing. Figs 1 and 2 demonstrate the severe cicatricial
eyelid changes that may occur with a severe thermal
injury (photos courtesy of Vikram D. Durairaj, M.D.).
In situations where it appears that the limbal stem cells
have been damaged then treatment should proceed as
described below in the section on chemical injuries.
Chemical injuries
Like patients with a thermal injury, patients with a
chemical injury will often present with the sudden onset
of severe pain, epiphora, and blepharospasm after
exposure to the inciting agent. Patients are often male
Figure 2 Photo of same patient after surgical repair (photo
courtesy of Vikram D. Durairaj M.D.)
Figure 3 Grade 4 alkali burn 10 days after initial injury. Cornea is
beginning to show some clearing centrally, however, a significant epithelial defect and ocular surface inflammation remains
and work in an industrial setting, however, an acid or
alkali injury can also occur within the domestic and/or
assault setting. Eye protection (for those working with
chemicals) is important to minimize the risk and severity of
the exposure, but patients wearing eye protection may
still encounter significant ocular contamination. Chemicals that may be implicated in alkali injuries include
cleaning agents (sodium hydroxide), fertilizers
(ammonium hydroxide), plaster (calcium hydroxide) and
air bags (sodium hydroxide aerosol) [2,3]. Alkali substances
are lipophilic and penetrate the eye more rapidly than
acids. The basic substance can quickly deposit within the
tissues of the ocular surface causing a saponification reaction within those cells. The damaged tissues then secrete
proteolytic enzymes as part of an inflammatory response,
which leads to further damage (a process called liquefactive necrosis). Alkali substances can penetrate into the
anterior chamber as well causing cataract formation,
damage to the ciliary body and damage to the trabecular
meshwork. Due to the rapidity of this process, patients
may experience irreversible intraocular damage in as little
as 5–15 min (Fig. 3).
Acid injuries tend to be less severe due to the fact that
acids tend to cause protein coagulation in the epithelium,
which limits further penetration into the eye. The one
exception to this is hydrofluoric acid, which may rapidly
pass through cell membranes and enter the anterior
chamber of the eye [1].
The damage to the corneal and conjunctival epithelium
from an ocular burn may be so severe as to damage the
pluripotent limbal stem cells causing a limbal stem cell
deficiency (LSCD). This may lead to opacification and
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Management of thermal and chemical injuries Fish and Davidson 319
neovascularization of the cornea. An acute intraocular
pressure rise occurrence due to shrinkage and contraction
of the cornea and sclera is also possible [4]. Longer term
intraocular pressure rises can occur from accumulation of
inflammatory debris within the trabecular meshwork
as well as damage to the trabecular meshwork itself.
Damage to the conjunctiva can cause extensive scarring,
perilimbal ischemia, and contracture of the fornices. Loss
of goblet cells and conjunctival inflammation can leave
the ocular surface prone to dryness. This predisposition
to dryness along with the possibility of lid malposition
due to symblepharon formation or the formation of
a cicatricial entropion or ectropion can be particularly
problematic as well.
Initial evaluation and initial treatment
Patients suffering from a chemical injury will often
initially present to the emergency department following
exposure. Once a history of chemical exposure is
obtained, the chemical should be identified if possible
but this should not delay treatment of the patient. The
local poison control center can be contacted if unsure of
the nature of the chemical, www.aapcc.org, 1-800-2221222. The emergency department should be familiar
with the necessity of prompt evaluation and treatment
of this emergency and it should be triaged appropriately.
Immediate treatment should include copious irrigation
prior to ophthalmic evaluation. pH testing should be
done in concert with this and familiarity with the testing
strips with reference to the manufacturer’s specifications
regarding interpretation, if necessary, should be sought if
unfamiliar with how to interpret the results.
The initial ocular examination should include a basic
ophthalmic examination with attention being paid to
the examination of the fornices to ensure that there is
no remaining alkaline material such as lime or plaster
present. Sweeping the fornices with a glass rod can
sometimes aid with this assessment. Irrigation with isotonic saline or lactated Ringer’s solution should be
performed and sometimes irrigating volumes up to 20
liters or more is required to change the pH to a physiologic level. The longer irrigation is delayed, the more
irrigation volume that will likely be required as the
chemical can deposit within the tissue making it somewhat recalcitrant to irrigation. A topical anesthetic to
provide the patient with some degree of comfort may
be helpful.
One study comparing isotonic saline, lactated ringer’s
solution, normal saline with bicarbonate, and balanced
saline solution plus (BSS Plus, Alcon Laboratories, Fort
Worth, Texas, USA) noted no difference in normalization
of pH but did note more tolerance and comfort with BSS
plus [5]. A Morgan lens may also be employed to allow
more direct irrigation of the ocular surface, thereby limiting a patient’s involuntary blepharospasm from preventing irrigation of the ocular surface.
Once copious irrigation has been achieved and the pH is
neutralized, the ocular examination should proceed with
attention being paid to visual acuity, intraocular pressure,
perilimbal blanching/ischemia (paying attention to clock
hours of involvement of blanching, as well as overall
health and appearance of the corneal epithelium). Initial
pH testing should involve both eyes even if the patient
claims to only have unilateral ocular pain/irritation so that
a contralateral injury is not neglected.
Classification
Classification schemes regarding the extent of the initial
injury were initially developed in the mid 1960’s, first by
Ballen [6] and then further modified by Roper-Hall [7].
The Roper-Hall classification system was largely based
on the degree of corneal haze and the amount of perilimbal blanching/ischemia noted on a grading scale of I
(good prognosis) to IV (poor prognosis) (Table 1). Pfister
subsequently made a classification system varying from
mild, mild-moderate, moderate to severe, severe and very
severe based upon pictures and photographs demonstrating corneal haze and perilimbal ischemia [8]. Dua proposed a classification scheme based upon clock hour
limbal involvement (as opposed to ischemia) as well as
percentage of bulbar conjunctival involvement [9]. The
important thing in the clinical setting is to note the
amount of limbal, corneal and conjunctival involvement
at the time of initial injury and to document changes in
the examination as the patient is followed, however,
grading the severity may provide the patient with a
general idea of the prognosis.
Subacute medical management
Once the pH has been neutralized and the patient has
been more thoroughly examined, attention should be
directed toward treating the injuries the patient has
received. This treatment includes promoting healing of
Table 1 Classification of severity of ocular surface burns by Roper–Hall [7]
Grade
Prognosis
Cornea
Conjunctiva/limbus
I
II
III
IV
Good
Good
Guarded
Poor
Corneal epithelial damage
Corneal haze, iris details visible
Total epithelial loss, stromal haze, iris details obscured
Cornea opaque, iris and pupil details obscured
No limbal ischemia
<1/3 limbal ischemia
1/3–1/2 limbal ischemia
>1/2 limbal ischemia
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320 Corneal and external disorders
the corneal epithelium and treating the intraocular pressure if elevated. If the extent of the injury is minor,
preservative free artificial tears may be adequate to
promote reepithelization. A bandage contact lens may
provide the patient with more comfort as well. Studies
have demonstrated that oral or topical ascorbate, and
topical citrate can promote epithelial healing and limit
stromal necrosis [8]. A topical steroid may also be
employed to limit the ensuing inflammatory infiltrate
and promote healing. Use of topical steroids alone can
potentially lead to a further increase in corneoscleral melt
[10]. Davis et al. [11] evaluated patients with topical
prednisolone 0.5% in conjunction with topical ascorbate
10% and concluded that there was not an associated
increase in corneoscleral melt if topical steroids were
used until reepithelization.
If there is a large epithelial defect, use of a topical
antibiotic such as a fourth generation fluoroquinolone
for antimicrobial prophylaxis is indicated. If there is
extensive damage and necrosis, the patient may be better
served undergoing debridement of the necrotic tissue.
Following debridement there may be a role in amniotic
membrane grafting to promote epithelial regeneration
whilst suppressing perilimbal inflammation (see below
surgical management).
If the patient has an elevated intraocular pressure,
aqueous suppression is the first choice. Oral aqueous
suppression if the patient has no other contraindications
may be preferable to avoid further toxicity to the epithelium from the preservatives in the drops. This method
of treatment may also be more comfortable to the patient
as well. Cycloplegia may also improve the patient’s
comfort following the injury.
These patients will require close follow up after the
initial injury for management of possible sequelae including potential corneal ulceration/perforation, secondary
open angle glaucoma, corneal scarring, limbal stem cell
deficiency, conjunctival scarring/symblepharon, dry eye,
and exposure due to lid malposition from cicatricial
changes.
Surgical management of ocular surface
damage
Surgical management of an ocular burn is directed
towards the initial debridement of necrotic material
and, if necessary, the application of topical adhesives
or tectonic grafting (in the setting of a perforated corneal
ulcer), replacing devitalized limbal stem cells, restoring
the corneal clarity and transparency, and addressing lid
malposition/lagophthalmos as well as treating glaucoma.
The surgical management of lid malposition and glaucoma extend beyond the scope of this article.
In recent years, advancements have been made in limbal
stem cell transplantation, adjunctive usage of amniotic
membrane and, in severe cases, placement of a keratoprosthesis. The improvements made in these areas have
provided patients with hope of visual rehabilitation in
cases that would have previously been given a very
poor prognosis dooming them to a life of disability and
dependency.
Amniotic membrane transplantation (AMT) helps to
restore the conjunctival surface and reduce limbal
stromal inflammation and can be used in both the acute
and chronic setting following a chemical or thermal
injury [12–14] Meller et al. [14] reported on 13 eyes of
11 patients receiving AMT within 2 weeks following
conventional medical therapy. They noted epithelialization in 11 of 13 eyes, and only those eyes with grade IV
burns experienced limbal stem cell deficiency (LCSD).
AMT can be used in the clinical setting of ocular surface
reconstruction, healing an epithelial defect, improving
limbal stem-cell function (disruption of the limbal barrier with irregular epithelial surface or visually significant
corneal scarring), and symptomatic pain relief. Tejwani
reported a 92.9% success in healing epithelial defects,
84.6% success in symptomatic relief, 63.5% success in
ocular surface reconstruction and 63.3% success in
improving limbal stem cell function in a retrospective
case review of patients with alkali injuries undergoing
AMT either in the acute or chronic setting after the
initial injury [12]. Tseng et al. [13] reported four patients
with mild LCSD due to chemical burns and showed
significant postoperative improvement following AMT.
In patients with total LCSD, there were eight patients
undergoing staged AMT followed by autologous limbal
stem cell transplantation (ALT) and penetrating
keratoplasty (PKP) of which seven out of eight experienced an improvement in visual acuity, whereas one
experienced a worsened visual acuity. Gomes et al.
[15] reported the usage of AMT alone in patients with
partial LCSD and in concert with ALT for those with
total LSCD in patients with chemical burn. They
reported 90% of patients showed an improvement in
their visual acuity.
Ocular surface restoration with AMT has the advantage
of creating an environment with reduced perilimbal
inflammation; promoting healthy epithelium with
reduced corneal neovascularization and may set the
patient up for successful future ALT and/or PKP if
stromal scarring remains. The downside of autologous
limbal stem cell transplantation is the need for systemic
immunosuppression.
In those patients in whom it ultimately does not become
possible to restore corneal clarity and a normal ocular
surface, a keratoprosthesis remains a viable option. A long
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Management of thermal and chemical injuries Fish and Davidson 321
discussion preoperatively regarding the risks of this
procedure and the need for regular follow up and adherence to an intensive daily eye drop regimen should take
place prior to performing the surgery. A patient with
unilateral ocular involvement may not be ready for or
motivated to undergo such a procedure, and may be
setting himself or herself up for a complicated and
undesirable postoperative course. In the proper setting,
however, keratoprosthesis placement can be a truly
vision-saving procedure.
The Boston Type I keratoprosthesis study group found
89% (17/19) anatomical retention in patients with a
chemical burn, results similar to those patients who
experienced multiple graft rejections, with slightly
improved visual acuity results – 94% BCVA more than
20/200 (16/19) [16]. Bradley et al. [17] reported similar
results with three alkali burn patients experiencing 100%
anatomical retention and 100% visual acuity more than
20/200. The complications of a keratoprosthesis placement include infection, corneal melt, glaucoma, as well as
formation of a retroprosthetic membrane. Monitoring for
postoperative glaucoma has proved particularly challenging with no reliable way of checking intraocular pressure
to date. Some surgeons will place a tube shunt at the time
of keratoprosthesis placement in anticipation of this
problem. We currently will keep our patients on a topical
antibiotic drop regimen indefinitely. We choose to use a
fourth generation fluoroquinolone and reserve vancomycin or other fortified antibiotic drops for cases of infectious ulcerative keratitis/melt should they arise.
Acknowledgement
Management of ocular thermal and chemical injuries, including amniotic
membrane transplantation are done by R.F. and R.S.D.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 324).
1 Tuft SJ, Shortt AJ. Surgical rehabilitation following severe ocular burns. Eye
(Lond.) 2009; 23:1966–1971.
The Tuft and Shortt article is a concise review of the appropriate treatment options
in both the acute and long-term setting for ocular surface burns. It explores the
various ocular surface reconstruction techniques available such as limbal stem cell
grafting and keratoprosthesis placement.
2
Pfister R, Pfister D. Alkali injuries of the Eye, Chapter 103 1285–1293.
Cornea, 2nd ed. In: Krachmer JH, Mannis MJ, and Holland EJ, editors.
Philadelphia, Elsevier Mosby, 2005.
3
Stein JD. ‘Air bags and ocular injuries.’ Transactions of the American
Ophthalmological Society (0065-9533), 1999; 97, p. 59.
4
Paterson CA, Pfister RR. Intraocular pressure changes after alkali burns. Arch
Ophthalmol 1974; 91:211–218.
5
Herr RD, White GL, Bernhisel K, Mamalis N, et al. Clinical comparison of ocular
irrigation fluids following chemical injury. Am J Emerg Med 1991; 9:228–231.
6
Ballen PH. Treatment of chemical burns of the eye. Eye, Ear, Nose and Throat
Monthly 1964; 43:57–58.
7
Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc UK 1965;
85:631–653.
8
Pfister RR. Chemical injuries of the eye. Ophthalmology 1983; 90:1246–
1253.
9
Dua HS, King AJ, Joseph A. A new classification of ocular surface burns. Br J
Ophthalmol 2001; 85:1379–1383.
10 Donshik PC, Berman MB, Dohlman CH, et al. Effect of topical corticosteroids
on corneal ulceration in alkali-burned corneas. Arch Ophthalmol 1978;
96:2117–2120.
11 Davis AR, Ali QH, Aclimandos WA, Hunter PA. Topical steroid use in the
treatment of ocular alkali burns. Br J Ophthalmol 1997; 81:732–734.
Conclusion
Overall, patients experiencing an ocular burn will need a
thorough and immediate evaluation and intensive treatment. Advances in understanding of the pathophysiology
of the injury have led to improvements in treatment in
the acute setting such as employment of topical ascorbate
and citrate, as well as surgical treatment in the subacute
and chronic settings with AMT, ALT with or without
PKP and ultimately keratoprosthesis placement, if
necessary. The goal of treatment is restoration of the
normal ocular surface anatomy and lid position, control of
glaucoma, and restoration of corneal clarity once this has
been achieved.
12 Tejwani S, Kolari RS, Sangwan VS, Rao GN. Role of amniotic membrane graft
for ocular chemical and thermal injuries. Cornea 2007; 26:21–26.
13 Tseng SC, Prabhasawat P, Barton K, et al. Amniotic membrane transplantation
with or without limbal allografts for corneal surface reconstruction in patients
with limbal stem cell deficiency. Arch Ophthalmol 1998; 116:431–441.
14 Meller D, Pires RTF, Mack RJS, Figueiredo F, et al. Amniotic membrane
transplantation for acute chemical or thermal burns. Ophthalmology 2000;
107:980–990.
15 Gomes JAP, Santos MS, Cunha MC, et al. Amniotic membrane transplantation for partial and total limbal stem cell deficiency secondary to chemical
burn. Ophthalmology 2003; 110:466–473.
16 Zerbe BL, Belin MW, Ciolino JB, Boston Type I Keratoprosthesis Study
Group. Results from the Multicenter Boston Type I Keratoprosthesis Study.
Ophthalmology 2006; 113:1779–1784.
17 Bradley JC, Hernandez EG, Schwab IR, Mannis MJ. Boston type I keratoprosthesis: The University of California Davis Experience. Cornea 2009;
28:321–327.
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