chemical injury in eye

8/11/2019 Chemical Injury in Eye

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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

chemical injury in eye

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