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Chemical Injury in Eye
Chan Suet MeiMedical officer
HRPB
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Introduction
One of the true ophthalmic emergencies.
Serious damage results from either strongly basic (alkaline) compounds
or acidic compounds.
Alkali injuries -more common,more deleterious.
Immediate, prolonged irrigation, followed by aggressive earlymanagement and close long-term monitoring to promote ocular surface
healing and to provide best opportunity for visual rehabilitation.
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Pathophysiology
Severity : type, volume, concentration, duration of exposure, and degree
of penetration of the chemical.
Acid Injury
Acids dissociate into hydrogen ions and anions in the cornea.
The hydrogen molecule damages the ocular surface by altering the pH,while the anion causes protein denaturation, precipitation, and
coagulation.
Protein coagulation generally prevents deeper penetration of acids and is
responsible for the ground glass appearance of the corneal stroma
following acid injury. Hydrofluoric acid is an exception; it behaves like an alkaline substance
because the fluoride ion has better penetrance through the stroma than
most acids, leading to more extensive anterior segment disruption.
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Pathophysiology
Alkali Injury
Alkaline substances dissociate into a hydroxyl ion and a cation in the
ocular surface.
The hydroxyl ion saponifies cell membrane fatty acids, while the cation
interacts with stromal collagen and glycosaminoglycans. This interaction facilitates deeper penetration into and through the
cornea and into the anterior segment.
Subsequent hydration of glycosaminoglycans results in stromal haze.
Collagen hydration causes fibril distortion and shortening, leading to
trabecular meshwork alterations that can result in increased intraocularpressure (IOP).
Additionally, the inflammatory mediators released during this process
stimulate the release of prostaglandins, which can further increase IOP.
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Presentation
History
History of a liquid or a gas being splashed or sprayed into the eyes or of
particles falling into the eyes.
Specific nature of the chemical and the mechanism of injury (eg, simple
splash vs high-velocity blast)Common complaints
Pain (often extreme)
Foreign body sensation
Blurred vision
Excessive tearing
Photophobia
Red eyes
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Presentation
A thorough physical examination should be deferred until the affected eye
is irrigated copiously, and the pH of the ocular surface is neutralized.
Physical
Decreased visual acuity
Increased IOP Conjunctival inflammation
Particles in the conjunctival fornices
Perilimbal ischemia
Corneal epithelial defect
Stromal haze Corneal perforation
Anterior chamber inflammatory reaction
Adnexal damage/scarring
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Common sources of alkali Common sources of acids
Cleaning products (eg, ammonia)
Fertilizers (eg, ammonia)
Drain cleaners (eg, lye)
Cement, plaster, mortar (eg, lime)
Airbag rupture (eg, sodium
hydroxide)
Fireworks (eg, magnesium hydroxide)
Potash (eg, potassium hydroxide)
Battery acid (eg, sulfuric acid)
Bleach (eg, sulfurous acid)
Glass polish (eg, hydrofluoric;
behaves like alkali)
Vinegar (eg, acetic acid)
Chromic acid (brown discoloration of
conjunctiva)
Nitric acid (yellow discoloration ofconjunctiva)
Hydrochloric acid
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Classification of severity of
ocular surface burns by Roper-Hall
Grade Corneal appearance Limbal
Ischemia
Prognosis
Grade I Clear cornea:Corneal
epithelial damage
None Good
Grade II Corneal haze : Iris
details visible
1/2 Poor
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Severe Ocular BurnsHarold Merle,1 Max Gerard2 and Norbert Schrage3
European Ophthalmic Review, 2011;5(2):1303
The worst ocular lesions are chemical burns caused by strong bases andacids. Associated with the destruction of limbal stem cells
(LSCs).
There are repeated epithelial ulcerations, chronic stromal ulcers, deepstromal neovascularisation, conjunctival invasion and evencorneal perforations.
The initial clinical examination is difficult because the symptomatology issevere, but nevertheless it helps to classify the lesions, to establish aprognosis and to guide the therapeutic care.
The classification system used most is that implemented by Hughes andmodified by Roper-Hall.
It is now completed neatly by those proposed by Dua and Wagoner, whichare based on the importance of the deficit of LSCs.
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Management of ocular surface chemical burnsJean-Jacques Gicquel
Br J Ophthalmo Feb 2011 Vol 95 No 2
Joseph et al noticed that the clinical outcome of patients with a Grade IVof Roper-Hall who had received similar treatments was highly variable
Dua et al drew the conclusion that Roper-Hall lacked precision andproposed a new classification on an analogue scaleexpressed as thenumber of clock hours of limbal involvement and percentage of
conjunctival involvement, which could be broken down into six grades
Conjunctival involvement is of major importance.
Even if the limbus is entirely destroyed, if a sufficient amount ofconjunctiva remains, it will still be able to re-epithelialise the cornealsurface, prevent stromal perforation and secure the ocular surface forpossible secondary LSCT at a later date.
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Grade Prognosis Clinical Findings Conjunctival
involvements
Analogue scale
I Very good 0 clock hours of limbal
involvement
0% 0/0%
II Good 3 clock hours of limbal
involvement
30% 0.1-3/1-29.9%
III Good >3-6 clock hours of limbalinvolvement
>30%-50% 3.1-6/31-50%
IV Good to
guarded
>6-9 clock hours of limbal
involvement
>50%-75% 6.1-9/51-75%
V Guarded to
poor
>9-75%-
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Grade 1 ocular surface burn.
Large corneal burn following accidental exposure to ammonia.
There is no limbal or conjunctival involvement.
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(A) Grade 3 (4.5/30%) ocularsurface burn.
(B) and (C) the surviving limbalepithelium demonstratescircumferential migration oftongue-shaped projectionsapproaching limbal epithelial
cover to denuded limbus. (D) The entire limbus has healed
with limbal epithelium and thecorneal surface too is almostcompletely healed with corneal
(limbal derived) epithelium. Theconjunctival defect is closingwith conjunctival epithelium.Fluorescein stained diffuse viewof the cornea.
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Grade 3 (5/35%) ocular surface burnfollowing an accident involving an industrialalkaline chemical.
Five clock hours of the limbus and 35% of theconjunctiva were involved.
(A) Diffuse view with patient looking straightillustrating the extent of limbal involvement.
(B) Diffuse view with patient looking up and
out and (C) looking up and in to show the extent ofconjunctival involvement.
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Treatment
Medical Care
Common goals of management include the following:
Removing the offending agent - Ideally, the irrigation solution should be balanced saltsolution or Ringers lactate solution. In alkali burns, some authors recommend the useof an amphoteric
solution such as diphoterine.
Promoting ocular surface healing - non-preserved tear substitutes (promoting the re-epithelialisation in a context in which the tear film is abnormal due to the destruction of goblet cells)
Topical mucomimetic agents such as sodium hyaluronate should be used in order to increase the
wetability of the surface and the tear-film stability. This also reduces conjunctival fibrosis.
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Controlling inflammation- Topical steroids instilled on an hourly basis in order to prevent a secondary destruction of the surrounding
tissues.
- They will limit the inflammatory processes by diminishing chemotaxis of inflammatory cells and bystabilising cellular and lysosomal membranes of polymorphonuclear leucocytes.
- For a long time, steroids were considered to be a contraindication for fear of provoking cornealperforations by countering the action of tissue inhibitors of metalloproteases.
- Recent studies have contradicted this dogma.- After the acute phase, teroids may slow down the re-epithelialisation
process as well as healing of the collagen matrix.
- They should be stopped after 7-10 days but can be reintroduced 6 weeks after the burn, in order toreduce chronic ocular surface inflammation.
Preventing infection
Controlling IOP Control pain- paracetamol, Soft CL bandage, AMT
*The amniotic membrane (AM) is avascular and acellular. It will facilitate epithelial healingacting as a basement membrane (it sharescommons collagen isoforms with theconjunctivalbasement membrane)
http://www.sarawakeyecare.com/caseoftheweek/fig23amt.jpg -
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Medical Care
Topical antibiotics
Erythromycin opthalmic
Macrolide broad-spectrum antibioticCiloxanFluoroquinolone broad-spectrum bacteriocidal antibioticVigamox
Carbonic anhydrase inhibitors
Methazolamide (Neptazane)Acetazolamide (Diamox)
Cycloplegic mydriatics
Homatropine
Scopolamine ophthalmic
* Relieve pain and minimise risk of iris lens synaechiae.
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Medical CareB- adrenergic blockers
Timolol maleate 0.25%, 0.5% (Betimol, Istalol, Timoptic, Timoptic XE)Levobunolol hydrochloride 0.25%, 0.5% (Betagan)
Betaxolol ophthalmic (Betoptic S)
Topical corticosteroids
Prednisolone acetate 1% (Pred Forte, Econopred)Fluorometholone acetate 0.1% (FML, FML Forte, Flarex)
Rimexolone 1% (Vexol)
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Medical Care
Ascorbate Critical cofactor necessary for collagen fibril synthesis.
The antioxidant properties of vitamin C eye-drops limit the effects of free radicalsreleased after an ocular surface chemical burn. Endogenous vitamin C being
secreted physiologically in the aqueous humour by the ciliary body and quickly
depleted after a severe chemical burn).
Its use is recommended for the treatment of Grade II burns and over.
Systemic vitamin C does not have a proven efficacy.
*The combined effect of citrate/ascorbate treatment in alkali-injured rabbit eyes.
Pubmed. Cornea.1991 Mar;10(2):100-4. Pfister RR, Haddox JL, Yuille-Barr D.
Source:Eye Research Laboratories, AMI/Brookwood Medical Center, Birmingham,AL 35209.
The average depth of ulceration was significantly less for the citrate/ascorbate
group
http://www.ncbi.nlm.nih.gov/pubmed?term=Pfister%20RR%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Haddox%20JL%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Yuille-Barr%20D%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Yuille-Barr%20D%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Yuille-Barr%20D%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Yuille-Barr%20D%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Haddox%20JL%5BAuthor%5D&cauthor=true&cauthor_uid=2019118http://www.ncbi.nlm.nih.gov/pubmed?term=Pfister%20RR%5BAuthor%5D&cauthor=true&cauthor_uid=2019118 -
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Treatment
Surgical care
Remove inciting chemical
Promote ocular surface healing
Debride necrotic conjunctival/corneal tissue
Temporary amniotic membrane patching
Limbal stem cell transplant Cultivated corneal epithelial stem cell sheet transplantation
Lysis of conjunctival symblepharon.
Prevent infection: Cyanoacrylate tissue adhesive may be applied forthe treatment of small corneal perforations.
Visual rehabilitation Penetrating keratoplasty with or without cataract extraction
Keratoprosthesis
Control IOP: Glaucoma filtering surgery or aqueous tube shunt placementmay be used for cases of increased IOP refractory to medical management.
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Thank you