Chemical (Alkali and Acid) Injury of The Conjunctiva and Cornea - EyeWiki

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Chemical (Alkali and Acid) Injury of the

Conjunctiva and Cornea
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Danielle Trief, MD MSc (/User%3ADanielle.trief), James Chodosh MD

Original article (/w/index.php?
contributed by title=User%3AJames_Chodosh_MD&action=edit&redlink=1), Kathryn
(/Property%3AAuthors): Colby MD (/w/index.php?
title=User%3AKathryn_Colby_MD&action=edit&redlink=1)
Danielle Trief, MD MSc (/User%3ADanielle.trief) and Maria A. Woodward,
All contributors:
MD (/User%3AMaria.A.Woodward)
Assigned editor: Maria A. Woodward, MD (/User%3AMaria.A.Woodward)
Assigned status Up to Date by Maria A. Woodward, MD
Review:
(/User%3AMaria.A.Woodward) on February 17, 2017.
cal (Alkali and Acid) Injury of the Conjunctiva and Cornea

Classification and external resources
[1] (http://en.wikipedia.org/wiki/ICD-10_Chapter_T)26.6
sification_of_Diseases_and_Related_Health_Problems)-10
(http://apps.who.int/classifications/icd10/browse/2010/en#/T26.6)
http://eyewiki.aao.org/Chemical_(Alkali_and_Acid)_Injury_of_the_Conjunctiva_and_Cornea 1/15
372.06 (http://www.icd9data.com/getICD9Code.ashx?
sification_of_Diseases_and_Related_Health_Problems)-9
icd9=372.06)
Chemical (alkali (http://en.wikipedia.org/wiki/Alkali) and acid (http://en.wikipedia.org/wiki/Acid)) injury of

the conjunctiva (http://en.wikipedia.org/wiki/Conjunctiva) and cornea (http://en.wikipedia.org/wiki/Cornea)
is a true ocular emergency and requires immediate intervention. Chemical injuries to the eye can produce
extensive damage to the ocular surface and anterior segment leading to visual impairment
(http://en.wikipedia.org/wiki/Visual_impairment) and disfigurement
(http://en.wikipedia.org/wiki/Disfigurement). Early recognition and treatment ensures the best possible
outcome for this potentially blinding (http://en.wikipedia.org/wiki/Blindness) condition.
Contents
1 Disease Entity
1.1 International Classification of Diseases
1.2 Epidemiology
1.3 Etiology
1.4 Pathophysiology
1.4.1 Alkali
1.4.2 Acids
1.5 Primary prevention
2 Diagnosis
2.1 History
2.2 Physical examination
2.3 Symptoms
3 Management
3.1 Irrigation
3.2 Medical therapy
3.2.1 Standard Treatments
3.2.2 Other Treatments:
3.3 Surgical Treatments
3.4 Recommended Treatment
3.4.1 Grade I
3.4.2 Grade II
3.4.3 Grade III
3.4.4 Grade IV
3.5 Stages of Ocular Recovery
3.6 Follow up
3.7 Other long term complications
3.7.1 Glaucoma
3.7.2 Dry eye
3.7.3 Damage to the eyelids or palpebral conjunctiva
4 Additional Resources
5 References
Disease Entity
International Classification of Diseases
ICD-9-CM (http://en.wikipedia.org/wiki/ICD-9#ICD-9) 940.2 alkaline chemical burn to cornea and

conjunctiva, 940.3 acid chemical burn to the cornea and conjunctiva, 372.06 chemical conjunctivitis
ICD-10-CM (http://en.wikipedia.org/wiki/ICD-10-CM) T26.60XA Corrosion of cornea and conjunctival sac,
unspecified eye, initial encounter.
Epidemiology
Chemical injuries to the eye represent between 11.5%-22.1% of ocular traumas.[1]About two thirds of
these injuries occur in young men. The vast majority occur in the workplace as a result of industrial
accidents. A minority of injuries occur in the home or secondary to assault. Alkali materials are found
more commonly in building materials and cleaning agents and occur more frequently than acid injuries.[2]
Etiology
Chemical injuries occur as a result of acid, alkali, or neutral (http://en.wikipedia.org/wiki/Neutral) agents.
Common causes of alkali and acid injuries are listed below.[2][3]
(/File%3AAcid_injuries.png)
(/File%3AAlkaliinjuries.png)
Pathophysiology
Alkali
Alkali agents are lipophilic (http://en.wikipedia.org/wiki/Lipophilic) and therefore penetrate tissues more
rapidly than acids. They saponify (http://en.wikipedia.org/wiki/Saponify) the fatty acids
(http://en.wikipedia.org/wiki/Fatty_acids) of cell cell membranes
(http://en.wikipedia.org/wiki/Cell_membranes), penetrate the corneal stroma and destroy proteoglycan
(http://en.wikipedia.org/wiki/Proteoglycan) ground substance and collagen
(http://en.wikipedia.org/wiki/Collagen) bundles. The damaged tissues then secrete proteolytic
(http://en.wikipedia.org/wiki/Proteolytic) enzymes (http://en.wikipedia.org/wiki/Enzymes), which lead to
further damage.[4][5]
Acids
Acids are generally less harmful than alkali substances. They cause damage by denaturing
(http://en.wikipedia.org/wiki/Denaturation) and precipitating proteins in the tissues they contact. The
coagulated (http://en.wikipedia.org/wiki/Coagulation) proteins act as a barrier to prevent further
penetration (unlike alkali injuries).[5] The one exception to this is hydrofluoric
(http://en.wikipedia.org/wiki/Hydrofluoric_acid) acid, where the fluoride ion rapidly penetrates the
thickness of the cornea and causes significant anterior segment destruction.[6]
Primary prevention
Since the majority of injuries occur at work, protective eye shields
(http://en.wikipedia.org/wiki/Eye_protection) are mandatory when handling potentially corrosive
(http://en.wikipedia.org/wiki/Corrosive) substances (OSHA regulation, 1910.133
(http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=9778)).
However, even protective goggles are no match for chemicals under high pressure.
Diagnosis
History
The severity of ocular injury depends on four factors: the toxicity (http://en.wikipedia.org/wiki/Toxicity) of
the chemical, how long the chemical is in contact with the eye, the depth of penetration, and the area of
involvement. It is therefore critical to take a careful history to document these factors. The patient should
be asked when the injury occurred, whether they rinsed their eyes afterwards and for how long, the
mechanism of injury (was the chemical under high pressure?), the type of chemical that splashed in the
eye, and whether or not they were wearing eye protection. If available, it is helpful to obtain the packaging
of the chemical. There is often product information on this packaging including chemical composition. If
this information is not immediately available, chemical information can be found by contacting the local
poison control center at aapcc (http://www.aapcc.org) or 1 800-222-1222.
Physical examination
Prior to a full ophthalmic exam, the pH (http://en.wikipedia.org/wiki/PH) of both eyes should be checked. If
the pH is not in physiologic range, then the eye must be irrigated to bring the pH to an appropriate range
(between 7 and 7.2). It is recommended to wait at least five minutes after irrigation before checking the
pH to ensure that the pH does not rise or fall secondary to retained particulate matter.
The physical exam should be used to assess the extent and depth of injury (see classification schemes
below). Specifically, the degree of corneal (http://en.wikipedia.org/wiki/Cornea), conjunctival
(http://en.wikipedia.org/wiki/Conjunctival) and limbal (http://en.wikipedia.org/wiki/Corneal_limbus)
involvement should be documented, as it can be used to predict ultimate visual outcome.[7]
The palpebral fissures (http://en.wikipedia.org/wiki/Palpebral_fissure) should be checked and the fornices
should be swept during the initial exam. Both the palpebral and bulbar conjunctiva should be examined
with fluorescein (http://en.wikipedia.org/wiki/Fluorescein) under a cobalt blue light. As above, retained
particulate matter can cause persistent damage, despite irrigation. The intraocular pressure
(http://en.wikipedia.org/wiki/Intra-ocular_pressure) should also be documented, as alkali injuries have
been found to both acutely and chronically cause an elevation of IOP.[8]
Two major classification schemes for corneal burns are the Roper-Hall (modified Hughes) classification[9]
[10] and the Dua classification.[11] The Roper-Hall classification is based on the degree of corneal
involvement and limbal ischemia. The Dua classification is based on an estimate of limbal involvement (in
clock hours) and the percentage of conjunctival involvement. In a randomized controlled trial
(http://en.wikipedia.org/wiki/Randomized_controlled_trial) of acute burns, the Dua classification was
found to be superior to the Roper-Hall in predicting outcome in severe burns.[7] However, both
classification schemes are commonly employed in daily practice.
(/File%3ABurnlegend2.JPG)
Symptoms
The most common symptoms are severe pain, epiphora

(http://en.wikipedia.org/wiki/Epiphora_(medicine)), blepharospasm
(http://en.wikipedia.org/wiki/Blepharospasm), and reduced visual acuity
(http://en.wikipedia.org/wiki/Visual_acuity).
Management
Irrigation
Early irrigation is critical in limiting the duration of chemical
exposure. The goal of irrigation is to remove the offending
substance and restore the physiologic pH. It may be necessary
to irrigate as much as 20 liters to achieve this. To optimize
patient comfort and ensure effective delivery of the irrigating
solution, a topical anesthetic is generally administered. An
eyelid speculum or Morgan Lens®
(http://en.wikipedia.org/wiki/Morgan_Lens) (MorTan, Missoula
MT) can be used to keep the eye open, while the irrigating
solution is delivered through IV tubing. There has been some
debate on the most effective irrigating solutions. A study by
Herr et al. compared Normal Saline (NS)
(http://en.wikipedia.org/wiki/Saline_(medicine)), Normal Saline
with Bicarbonate (NS + Bicarb), Lactated Ringer’s solution (LR)
(http://en.wikipedia.org/wiki/Lactated_ringer), and Balanced
Saline Solution
(http://en.wikipedia.org/wiki/Balanced_salt_solution) Plus (BSS (/File%3AIrrigation,people.JPG)
Plus, Alcon Laboratories, Fort Worth, TX) irrigating solutions to
investigate which solution optimized patient comfort. They
found that patients tolerated and preferred BSS irrigation
compared to NS, NS + Bicarb, and LR.[12] In experiments in
rabbit eyes following sodium hydroxide (http://en.wikipedia.org/wiki/NaOH) injury, a borate buffer solution
(http://en.wikipedia.org/wiki/Borate_buffered_saline) called Cedderroth eye wash
(http://en.wikipedia.org/wiki/Cederroth) (Cedderroth Industrial Products, Upplands Vaasby Sweden) and a
Diphthorine and Previn solution (Prevor, Cologne Germany) more efficiently normalized the pH compared
to saline and phosphate buffer solutions (http://en.wikipedia.org/wiki/Phosphate_buffered_saline).[13] Of
course, early irrigation is paramount to limiting the duration of chemical exposure. If clean water is
available at the site of injury and a standard irrigating solution is not, then the eyes should immediately be
washed out with water.[14][15]
Medical therapy
Patients with mild to moderate injury (Grade I and II) have a good prognosis and can often be treated
successfully with medical treatment alone. The aims of medical treatment are to enhance recovery of the
corneal epithelium and augment collagen synthesis, while also minimizing collagen breakdown and
controlling inflammation.[3]
Standard Treatments
Antibiotics- A topical antibiotic ointment like erythromycin ointment

(http://en.wikipedia.org/wiki/Erythromycin) four times daily can be used to provide ocular lubrication and
prevent superinfection. Stronger antibiotics (e.g. a topical fluoroquinolone
(http://en.wikipedia.org/wiki/Fluoroquinolone)) are employed for more severe injuries (e.g. Grade II and
above).
Cycloplegic agents such as atropine (http://en.wikipedia.org/wiki/Atropine) or cyclopentolate
(http://en.wikipedia.org/wiki/Cyclopentolate) can help with comfort.
Artificial tears- and other lubricating (http://en.wikipedia.org/wiki/Artificial_tears) eye drops, preferably
preservative free, should be used generously for comfort.
Steroid drops- In the first week following injury, topical steroids (http://en.wikipedia.org/wiki/Steroids) can
help calm inflammation and prevent further corneal breakdown.[14] In mild injuries, topical prednisolone
(http://en.wikipedia.org/wiki/Prednisolone) (Predforte) can be employed four times daily. In more severe
injuries, prednisolone can be used every hour. After about one week of intensive steroid use, the steroids
should be tapered because the balance of collagen synthesis vs. collagen breakdown may tip
unfavorably toward collagen breakdown.[16]
Other Treatments:
Ascorbic acid- is a cofactor (http://en.wikipedia.org/wiki/Cofactor_(biochemistry)) in collagen synthesis
and may be depleted following chemical injury. Ascorbic acid (http://en.wikipedia.org/wiki/Ascorbic_acid)
can be used as a topical drop (10% every hour) or orally (two grams, four times daily in adults). In one
study, severe alkali burns in rabbit eyes were associated with reduced ascorbic acid levels in the aqueous
humor (http://en.wikipedia.org/wiki/Aqueous_humor). This reduction correlated with corneal stromal
ulceration and perforation. Systemic administration of Vitamin C (http://en.wikipedia.org/wiki/Vitamin_C)
helped promote collagen synthesis and reduce the level of ulceration.[17]Care must be taken in patients
with compromised renal function because high levels of Vitamin C are potentially toxic to the kidneys.[18]
Doxycycline- acts independently of its antimicrobial properties to reduce the effects of matrix
metalloproteinases (MMPs) (http://en.wikipedia.org/wiki/Matrix_metalloproteinase), which can degrade
type I collagen. The tetracycline (http://en.wikipedia.org/wiki/Tetracycline) class inhibits MMPs by
restriction of the gene expression of neutrophil collagenase and epithelial gelatinase, suppression of
alpha 1 antitrypsin degradation and scavenging reactive oxygen species, thereby reducing ocular surface
inflammation.[19][20]
Citrate drops- histological sections of cornea from alkali burns reveal an intense polymorphonuclear
infiltrate (PMN) (http://en.wikipedia.org/wiki/Polymorphonuclear_neutrophil).[21] PMNs provide a major
source of proteolytic enzymes, which can dissolve the corneal stromal collagen. Deficiency in calcium
inhibits the PMNs from granulating and releasing proteolytic enzymes. Citrate
(http://en.wikipedia.org/wiki/Citrate) is a potent chelator (http://en.wikipedia.org/wiki/Chelator) and can
therefore decrease proteolytic activity. Citrate also appears to inhibit collagenases.[22][23]
1% Medroxyprogesterone- is a progestational (http://en.wikipedia.org/wiki/Progesterone) steroid and
has less anti-inflammatory potency than corticosteroids, but has a minimum effect on stromal repair.
Medroxyprogesterone (http://en.wikipedia.org/wiki/Medroxyprogesterone) can therefore be substituted for
cortical steroids after 10-14 days of steroid treatment.[2][24]
Platelet rich plasma eye drops- have been found to be rich in growth factors and platelet rich plasma
eye drops (http://en.wikipedia.org/wiki/Platelet_Rich_Plasma) can lead to faster epithelialization for
certain classes of burns.[25]
Surgical Treatments
Debridement of necrotic epithelium- should be performed as early as possible because necrotic

(http://en.wikipedia.org/wiki/Necrotic_tissue) tissue serves as a source of inflammation and can inhibit
epithelialization.[3]
Conjunctival/Tenon’s transposition (Tenonplasty)- in Grade IV burns, anterior segment necrosis can result
from loss of limbal vascular blood supply. In severe limbal ischemia
(http://en.wikipedia.org/wiki/Ischemia), a sterile corneal ulceration can ensue. After removal of necrotic
tissue, a tenonplasty (advancement of the conjunctiva and Tenon’s to the limbus) can be employed to
reestablish limbal vascularity and facilitate re-epithelialization.[26]
Amniotic membrane transplantation (AMT)- the
purpose of AMT
(http://eyewiki.aao.org/Amniotic_Membrane_Transplant)
is to rapidly restore the conjunctival surface and to
reduce limbal and stromal inflammation. The benefits are
thought to be two fold: physical and biological. Physically,
AMT has been shown to improve patient comfort by
reduction of eyelid friction. Numerous studies have found
a reduction in pain following AMT for moderate to severe
burns.[27][28] Through its physical actions, AMT may also
prevent symblepharon
(http://en.wikipedia.org/wiki/Symblepharon) formation.
Amniotic membrane is also felt to have biologic effects.
[29] It expresses TGFB1
(http://en.wikipedia.org/wiki/TGF_beta_1) and epidermal (/File%3AStage_IV_chemical_burn_with_tex

growth factor
(http://en.wikipedia.org/wiki/Epidermal_growth_factor),
which have roles in wound healing.[30][31] It has also been
found to have anti-inflammatory properties.[32][33][34] Taken together, these biological effects may dampen
inflammation, promote epithelial growth, prevent scarring and prevent neovascularization
(http://en.wikipedia.org/wiki/Neovascularization). New delivery devices like ProKera® (Bio-Tissue, Miami,
Florida), which consists of a piece of cryopreserved (http://en.wikipedia.org/wiki/Cryopreserved) amniotic
membrane clipped into a dual ring system, like a symblepharon ring, allows rapid and sutureless
placement of amniotic membrane.[35] A recent Cochrane review found only one randomized controlled
trial of amniotic membrane for treatment of chemical ocular burn in the first seven days following injury.[1]
Patients with moderate burns were found to have a significantly better visual acuity following AMT
compared to medical therapy alone.[36] However, this was an unmasked trial and there were uneven
baseline characteristics of the control and treatment eyes.[1] While case series and reviews show great
promise of AMT in the treatment of chemical burns, conclusive evidence is still lacking.
Limbal stem cell transplant- Much of the damage following chemical injuries results from limbal
ischemia and the subsequent loss of stem cells capable of repopulating the corneal epithelium. Limbal
stem cell transplants
(http://eyewiki.aao.org/Application_of_Stem_Cells_for_Regenerative_Therapy_in_Cornea) have been
employed to replace this critical group of cells. Limbal stem cells are located at the base of the limbal
epithelium and are responsible for repopulation of cells in the corneal epithelium and inhibition of
conjunctival growth over the cornea.[37] Limbal autografts (http://en.wikipedia.org/wiki/Autograft) can be
used from the healthy contralateral eye if only one eye is injured in a chemical burn.[38] When both eyes
are injured, transplants have been attempted from living related donors. In a recent study from China, a
portion of the limbus of HLA matched living related donors (allograft)
(http://en.wikipedia.org/wiki/Allograft) was transplanted following chemical injury. Patients experienced a
reduction in vascularity, improved corneal opacity and corneal epithelialization without the need for
systemic immunosuppression.[37] Another option is to use cadaveric donors. This requires systemic
immunosuppression.[39] When possible, limbal stem cell transplantation should be delayed until ocular
surface inflammation has quieted.[40][41]
Cultivated oral mucosal epithelial transplantation (COMET)- can also be used to promote re-
epithelialization and reduce inflammation in corneal burns. The cells are harvested from the patient’s own
buccal mucosa (http://en.wikipedia.org/wiki/Buccal_mucosa) so that systemic immunosuppression is not
necessary.[42][43]
Boston Keratoprosthesis- Severe chemical injury leads to chronic inflammation and scarring, making
visual recovery challenging. In cases with severe inflammation, limbal stem cell transplants and corneal
transplants do not survive. In these most difficult cases, the Boston Keratoprosthesis
(http://eyewiki.aao.org/Boston_Keratoprosthesis_(KPro)) can be used. Because it is independent of stem
cell function, it does not require systemic immunosuppression.[44]
Recommended Treatment
While there is variability in treatment strategies of chemical burns, most authors recommended a graded
approach depending on the severity of injury. Mild burns (Roper-Hall grade I) respond well to medical
treatments and lubrication, while more severe burns necessitate more intensive medical therapies and
surgery. Below is a paradigm for the initial treatment of chemical injury based on the Roper-Hall grade of
injury.[3][45]
Grade I
Topical antibiotic ointment (erythromycin ointment or similar) four times a day
Prednisolone acetate 1% four times a day
Preservative free artificial tears as needed
If there is pain, consider a short acting cycloplegic like cyclopentolate three times a day
Grade II
Topical antibiotic drop like fluoroquinolone four times daily
Prednisolone acetate 1% hourly while awake for the first 7-10 days. Consider tapering the steroid if
the epithelium has not healed by day 10-14. If an epithelial defect persists after day 10, consider
progestational steroids (1% medroxyprogesterone four times daily)
Long acting cycloplegic like atropine
Oral Vitamin C, 2 grams four times a day
Doxycycline, 100 mg twice a day (avoid in children)
Sodium ascorbate drops (10%) hourly while awake
Preservative free artificial tears as needed
Debridement of necrotic epithelium and application of tissue adhesive as needed
Grade III
As for Grade II
Consider amniotic membrane transplant/Prokera placement. This should ideally be performed in the
first week of injury. Experienced surgeons have emphasized placement of the amniotic membrane to
cover the palpebral conjunctiva by suturing to the lids in the operating room, not just covering the
cornea and bulbar conjunctiva.
Grade IV
As for Grade II/III
Early surgery is usually necessary. For significant necrosis, a Tenonplasty can help reestablish limbal
vascularity. An amniotic membrane transplant is often necessary due to the severity of the ocular
surface damage.
Stages of Ocular Recovery

Stages of ocular recovery following chemical injury- [3][6]
(/File%3ARepairstagesofbur.png)
(/File%3AGrade_II_burn,_thinning,_impending_perf.png)
(/File%3AGrade_II_burn,_focal_conjunctivalization.png)
(/File%3ABurnrecoverylegend.JPG)
Figure E Figure F
*Images courtesy of Dr. Kathryn Colby (Massachusetts Eye and Ear Infirmary)
Follow up
With severe chemical burns, patients should initially be followed daily. If there is concern for compliance
with medication or if the patient is a child, one should consider inpatient admission. Once the health of the
ocular surface has been restored, follow up can be spread apart. However, even in the healthiest
appearing eyes, patients need long term monitoring for glaucoma (http://eyewiki.aao.org/Primary_Open-
Angle_Glaucoma) and dry eye (http://eyewiki.aao.org/Dry_Eye_Syndrome) as below.
Other long term complications

Glaucoma
Glaucoma is quite common following ocular injury, ranging in frequency from 15%-55% in patients with
severe burns.[8] The mechanism of glaucoma is multifactorial and includes contraction of the anterior
structures of the globe secondary to chemical and inflammatory damage, inflammatory debris in the
trabecular meshwork (http://en.wikipedia.org/wiki/Trabecular_meshwork), and damage to the trabecular
meshwork itself.[46] More severe burns (Roper-Hall Grade III or IV) have been found to have significantly
higher intraocular pressure at presentation and were more likely to require long term glaucoma
medication and undergo glaucoma surgery than grade I or II injuries.[8] Glaucoma medications should be
prescribed as necessary to maintain normal intraocular pressure
Dry eye
Chemical injury can destroy conjunctival goblet cells (http://en.wikipedia.org/wiki/Goblet_cell), leading to a

reduction or even absence of mucus in the tear film, and compromising the proper dispersion of the
precorneal tear film. This mucus deficiency results in keratoconjunctivitis sicca (dry eye).[47] Even in well-
healed eyes, chronic dry eye can cause significant morbidity because of discomfort, visual disturbance,
and potential for damage of the ocular surface.
Damage to the eyelids or palpebral conjunctiva

Direct chemical damage to the conjunctiva can lead to scarring, forniceal shortening, symblepharon
formation and ciccatricial entropion (http://en.wikipedia.org/wiki/Entropion) or ectropion
(http://eyewiki.aao.org/Ectropion). These entities are encountered weeks to months after injury and can
be treated by suppressing inflammation and with early amniotic membrane transplantation or oral
mucosal graft.[3][48][49]
Additional Resources
American Association of Poison Control Centers: http://www.aapcc.org (http://www.aapcc.org) (1-
800-222-1222)
Iowa State University’s Chemistry Material Safety Data Sheets:
http://avogadro.chem.iastate.edu/MSDS/ (http://avogadro.chem.iastate.edu/MSDS/)
Occupational Safety and Health Administration requirement for eye protection at work:
http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=9778
(http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=9778)
Amniograft & Prokera: http://www.biotissue.com/ (http://www.biotissue.com/)
American Academy of Ophthalmology. Cornea/External Disease: Chemical (alkali and acid) injury of
the conjunctiva and cornea Practicing Ophthalmologists Learning System, 2017 - 2019
(http://store.aao.org/practicing-ophthalmologists-learning-system-2017-2019.html) San Francisco:
American Academy of Ophthalmology, 2017.
References
1. Clare, G., et al., Amniotic membrane transplantation for acute ocular burns. Cochrane database of
systematic reviews, 2012. 9: p. CD009379.
2. Wagoner, M.D., Chemical injuries of the eye: current concepts in pathophysiology and therapy.
Survey of ophthalmology, 1997. 41(4): p. 275-313.
3. Colby, K., Chemical injuries of the Cornea. Focal Points in American Academy of
Ophthalmology.2010. 28(1): p. 1-14.
4. Fish, R. and R.S. Davidson, Management of ocular thermal and chemical injuries, including amniotic
membrane therapy. Current opinion in ophthalmology, 2010. 21(4): p. 317-21.
5. Barouch F, Colby KA. Evaluation and initial management of patients with ocular and adnexal trauma.
In: Miller JW, Azar DT, Blodi B eds. Albert and Jakobiec's Principles and Practice of Ophthalmology,
3rd ed. Philadelphia: WB Saunders Elsevier: 2008: 5071-5092.
6. McCulley, J., Chemical Injuries. 2 ed. The Cornea: Scientific Foundation and Clinical Practice, ed.
S.G.a.T. RA1987, Boston: Little, Brown and Co.
7. Gupta, N., M. Kalaivani, and R. Tandon, Comparison of prognostic value of Roper Hall and Dua
classification systems in acute ocular burns. The British journal of ophthalmology, 2011. 95(2): p. 194-
8
8. Lin, M.P., et al., Glaucoma in patients with ocular chemical burns. American journal of ophthalmology,
2012. 154(3): p. 481-485 e1.
9. Hughes, W., Alkali burns of the eye. I. Review of the literature and summary of present knowledge.
Archives of ophthalmology, 1946. 35: p. 423.
10. Roper-Hall, M.J., Thermal and chemical burns. Transactions of the ophthalmological societies of the
United Kingdom, 1965. 85: p. 631-53.
11. Dua, H.S., A.J. King, and A. Joseph, A new classification of ocular surface burns. The British journal
of ophthalmology, 2001. 85(11): p. 1379-83.
12. Herr, R.D., et al., Clinical comparison of ocular irrigation fluids following chemical injury. The
American journal of emergency medicine, 1991. 9(3): p. 228-31.
13. Rihawi, S., M. Frentz, and N.F. Schrage, Emergency treatment of eye burns: which rinsing solution
should we choose? Graefe's archive for clinical and experimental ophthalmology = Albrecht von
Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2006. 244(7): p. 845-54.
14. Dohlman, C.H., F. Cade, and R. Pfister, Chemical burns to the eye: paradigm shifts in treatment.
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Chemical (Alkali and Acid) Injury of the

Danielle Trief, MD MSc (/User%3ADanielle.trief), James Chodosh MD

cal (Alkali and Acid) Injury of the Conjunctiva and Cornea

Chemical (alkali (http://en.wikipedia.org/wiki/Alkali) and acid (http://en.wikipedia.org/wiki/Acid)) injury of

ICD-9-CM (http://en.wikipedia.org/wiki/ICD-9#ICD-9) 940.2 alkaline chemical burn to cornea and

The most common symptoms are severe pain, epiphora

Antibiotics- A topical antibiotic ointment like erythromycin ointment

Debridement of necrotic epithelium- should be performed as early as possible because necrotic

(http://en.wikipedia.org/wiki/TGF_beta_1) and epidermal (/File%3AStage_IV_chemical_burn_with_tex

Stages of Ocular Recovery

Other long term complications

Chemical injury can destroy conjunctival goblet cells (http://en.wikipedia.org/wiki/Goblet_cell), leading to a

Damage to the eyelids or palpebral conjunctiva

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