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Binesh Tyagi

SFEH

Ocular Chemical Injuries

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INTRODUCTION

• One of the true ophthalmic emergencies.• Only ocular condition where history taking and examination should

be delayed.• Coordination with physician, surgeon and psychiatrist may be

required.• Bilateral chemical exposure is especially devastating, often resulting

in complete visual disability.

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• International Classification of Diseases • ICD-9-CM • 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• T26.60XA Corrosion of cornea and conjunctival sac, unspecified eye,

initial encounter.

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EPIDEMIOLOGY • 2/3rd in young males.• 2/3rd at Workplace vs home• 2/3rd by Alkali vs acid• 2/3rd are minor (gr. I & II) injuries

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Type of chemical injuries• ALKALI BURNS• Most dangerous -rapid penetration.

• ACID BURNS• Less severe than alkali - do not penetrate into the eye as readily as

alkaline substances.• The exception hydrofluoric acid burn, which is as dangerous as an alkali

burn.

• IRRITANTS• Neutral pH• More discomfort to the eye than actual damage.

–-Most household detergents–-Pepper spray

•It can cause significant pain but usually does not affect vision and rarely causes any damage to the eye.

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Alkalies AcidMore severe

-Penetrate rapidly (often in less than one minute), -They combine with cell membrane lipids, mucopolysaccharides and to collagen, resulting in disruption of cells and necrosis of the tissues.On the ocular surface, they saponify cell membranes and intercellular bridges, which facilitates rapid penetration into the deeper layers and into the aqueous and vitreous compartments-Necrosis of conjunctival blood vessel causing:“Cooked fish eye” the cornea is as white as chalk and opaque.

-Less severe

-Acids quickly denature proteins in the corneal stroma, forming precipitates that retard additional penetration.

-Causing localized damage due to its: a)Coagulation effectb)Protein precipitations at epithelium level -Leading to:  Physical barrier.

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Alkali substances:

• Ammonia,NH3; a common ingredient in many household cleaning agents• Lye, NaOH; a common ingredient in drain cleaners• Potassium hydroxide,KOH• Magnesium hydroxide,Mg[OH]2• Lime, Ca[OH]2; the most common cause

• Common substances at home : • Fertilizers• Cleaning products (ammonia), • Drain cleaners (lye)• Plaster,cement (lime)

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Common acids causing eye burns

• Sulphuric (H2SO4); the most common cause (an ingredient in automobile batteries)

• Sulfurous (H2SO3)• Hydrofluoric (HF; rapidly penetrating and causing the most serious

injuries)• Nitric acid• Acetic acid (CH3COOH)• Chromic acid (Cr2O3)• Hydrochloric acid (HCl)

• Common substances at home• Glass polish (hydrofluoric acid)• Vinegar

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1- The severity of a burn depends on:• Surface area of contact.• Depth of penetration, concentration, time of contact, time of

interference.• Degree of limbal stem cell injury.

2-Common area of damage in eye:Anterior segment of the eyeInternal segment of the eyeCorneaConjunctivaLens

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PATHOPHYSIOLOGY OF OCULAR INJURES

Necrosis of the conjunctival and corneal epithelium

Disruption and occlusion of the limbal vasculature.

Loss of limbal stem cells

Conjunctivilisation and vascularization of the corneal surface

Persistent corneal epithelial defects with sterile corneal ulceration

1- Corneal Damage by severe chemical injuries occurs in the following order:

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Other long term effects include ocular surface wetting disorders, symblepharon formation and cicatricial entropion.

Anterior chamber penetration results in iris and lens damage. Ciliary epithelial damage impairs secretion of ascorbate which is

required for collagen production and corneal repair. Hypotony and phthisis bulbi may ensue.

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PATHOPHYSIOLOGY OF OCULAR INJURES

2- Healing of the corneal epithelium and stroma as follows:

THE EPITHELIUM Centripetal movement of cells from the peripheral cornea, limbus,

or conjunctiva is responsible for normal and posttraumatic replacement of corneal epithelium.

Only partial transdifferentiation of conjunctival epithelium to corneal epithelium is possible but conjunctiva-derived epithelium never fully expresses corneal epithelial phenotypic features.

Associated with delayed reepithelialization, superficial and deep stromal vascularization, persistence of goblet cells in the corneal epithelium, and poor epithelium-basement membrane adhesion.

Limbal stem cells are the cells most qualified to restore the functional competence of the corneal epithelial surface after injury

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Damaged STROMAL COLLAGEN The maintenance and regeneration of the corneal stroma -responsibility of

the pluripotent cells- keratocyte. Keratocyte Function:

Phagocytosis of collagen fibrilsSynthesis and secretion of collagen glycosaminoglycan ground

substance, collagenase, and collagenase inhibitors.Modulated by cytokines from the epithelium, inflammatory cells, and

other keratocytes.

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Degradation of the basement membrane collagen

(initiated by MMP–9 )

Degradation of the corneal stromal matrix

(by MMP–1 and MMP–8(collagenase types)

Detected earliest at 9 hrs

Collagen type 1 synthesis peak point

(at 14-21 days)

Coincide with maximum MMP activity

Intervening period may show sterile corneal ulceration.

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Symptoms Signs

- Pain- Lacrimation- Photophobia- Blepharospasm- Diminution of vision

- Eye lid edema,- Chemosis,- Corneal abrasions

Clinical Pictures

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Effects of Ocular Surface Burn

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• Roper-Hall/ modified Hughes classification• Degree of corneal involvement• Limbal ischemia.

• Dua classification • Limbal involvement (in clock hours) • Percentage of conjunctival involvement.

In a randomized controlled trial of acute burns, the Dua classification was found to be superior to the Roper-Hall in predicting outcome in severe burns. However, both classification schemes are commonly employed in daily practice.

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

Classification

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Classification of ocular surface burn

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Dua classification of ocular surface burns

The analogue scale records accurately the limbal involvement in clock hours of affected limbus/percentage of conjunctival involvement. While calculating percentage of conjunctival involvement, only involvement of bulbar conjunctiva, up to and including the conjunctival fornices is considered.

Grade Prognosis Limbal involvement Conjunctival involvelment

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 limbal involvement

>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–<12 clock hours of limbal involvement

>75–<100% 9.1–11.9/75.1–99.9%

VI Very poor Total limbus (12 clock hours) involved

Total conjunctiva (100%) involved

12/100%

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Medical Care Regardless of the underlying chemical involved, common goals of

management include the following: (1) removing the offending agent, (2) promoting ocular surface healing, (3) controlling inflammation, (4) preventing infection, (5) controlling IOP.

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IMMEDIATE MANAGEMENT OF CHEMICAL BURNS

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1(Remove inciting chemical (irrigation)

Immediate copious irrigation of eye (every second counts) by sterile balanced buffered solution:•Normal saline solution •Ringer's lactated solution •Normal saline with bicarbonate•Balanced salt solution(BSS)

Even plain tap water may be used without waiting for the ideal fluid.Preferably, eye should be anaesthetized before irrigation.

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Eye Irrigation2)Evert the upper eyelid and irrigate, and irrigate under lower lid.• Remove all solid particles from under lids.   • After 5 to 10 minutes of irrigation and if litmus paper is

available test pH of lower inside of lid.  • Continue irrigation until pH is below or above a pH of 7.0.  • If no litmus available irrigate for 20 min 

Special irrigating tubing(Morgan’s lens):

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• Water is contraindicated• In chemical burns caused by the heavy metals like

sodium, potassium and calcium (e.g. Lime or Ca(OH)2).

React violently and explosively with water Produce caustic hydroxide Liberating much heat in its production Result in combination of thermal and chemical burn.

• Immediate treatment Brush off/pick out from the skin as many particles of

sodium or potassium as possible Then to direct a high pressure jet of water at the remainder. Ignition of particles will occur, but if the flow is great

enough, the heat will be dissipated by water.

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Eye irrigation

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History

• Time of injury• Eyes rinsed or not, if yes- duration,

solution, speed• Mechanism of injury• Type of chemical• Packaging of chemical available?• Eye protection gear used?

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If nature of chemical substance is known

If nature of chemical is unknown or not available

Strong acid

Weak alkali

Strong alkali

Weak acid

Iodine Starch solution Milk

Aniline Alcohol 10%Glycerine 10%

Lime a) Pick particles with forcepsb) Wash by:

EDTA 0.1%Neutral ammonium tartrate 10%Saturated sugar solution

Tap water

Dilute chemical substance

*for all except LIME*Milk Dilution

Buffer acid and alkaliForm superficial film which protect the underlying tissue

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1- Remove inciting chemical • Instill topical anesthesia• Sweep the fornices with a moist sterile cotton swab to remove

any retained foreign material.• Double eversion of upper lid

• especially important when particulate matter (eg, plaster) is responsible for the injury.

2- Paracentesis • External perfusion of alkali-burned animal eyes may be

incapable of lowering aqueous pH by more than 1.5 units.

• further decrease can be achieved by– removing aqueous by paracentesis.– buffered phosphate solution may be used to refill the anterior

chamber, a greater reduction in pH (another 1.5 units) is possible.

3- Early Assessment

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Recommended Treatment Graded approach depending on the severity of

injury. Mild burns (Roper-Hall grade I)

Respond well to medical treatments and lubrication.

Moderate to severe burns More intensive medical therapies and surgery.

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1- Steroids• Reduce inflammation• Neutrophil infiltration• Impair stromal healing by reducing collagen synthesis and inhibiting

fibroblast migration• Must be tailed off after 7-10 days when sterile corneal ulceration is most

likely to occur.• May be replaced by topical NSAIDS, which do not affect keratocyte

function.

2- Ascorbic acid• Reverses a localized tissue scorbutic state• Promote synthesis of mature collagen by corneal fibroblasts.

Topical sodium ascorbate 10% is given 2 -hourly in addition to a systemic dose of 2g q.i.d.

MEDIACTION

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3- Citric acid • Powerful inhibitor of neutrophil activity• Reduces the intensity of the inflammatory response• Chelation of extracellular calcium by citrate also appears to inhibit

collagenase.

Topical sodium citrate 10% given 2- hourly for about 10 days.

Aim is to eliminate the second wave of phagocytes, which normally occurs 7 days after the injury.

4- Tetracyclines• Collagenase inhibitors • Inhibit neutrophil activity• Reduce ulceration.

They are administered both topically and systemically {Doxycycline 100 mg b,d.}.

-Topical antibiotic, aggressive lubrication with eye ointments (steroid antibiotic combinations) to prevent symblepharon.

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• 5- Tear Substitutes• 6- Occlusive Therapy• 7- Bandage Soft Contact Lens• 8- Autologous Serum

– Fibronectin and epidermal growth factors• 9-Retinoic Acid

May promote goblet cell recovery and improve ocular surface function

Transdifferentiation of the conjunctival epithelium to a corneal epithelial phenotype.

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• 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, short acting cycloplegic like

cyclopentolate three times a day

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• Grade II • As for grade I• Prednisolone acetate 1% hourly while awake for the first 7-10 days.

• Tapering if the epithelium has not healed by day 10-14.• If an epithelial defect persists after day 10, consider

progestational steroids (1% medroxyprogesterone qid) • 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

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• Grade III • As for Grade II • Consider amniotic membrane transplant placement.• Ideally be performed in the first week of injury

• 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.

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MID TERM MANAGEMENT OF OCULAR CHEMICAL BURNS

Inflammation Infection prophylaxis IOP control Pain management

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Control inflammationInflammatory mediators released from the ocular surface at the time of injury causing:•Tissue necrosis•Attract further inflammatory reactants

causes: •Inhibits reepithelialization •Corneal ulceration •Perforation

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After a week, continued assessment of the risk of infection is essential. Persistent epithelial defects, necrotic corneal stroma, and corneal melting all facilitate infection and therefore necessitate the continued use of topical antibiotics.

*Prophylactic topical antibiotics are always warranted during the initial treatment stages.

-Cyanoacrylate tissue adhesive may be applied for the treatment of small corneal perforations to avoid infection.

Infection prophylaxis

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Cyanoacrylate tissue adhesive

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Control IOP (increase secondary to chemical injuries)

Control IOP (increase secondary to chemical injuries)• Oral acetozolamide(Diamox) or topical beta-blockers or aqueous• Always in initial therapy and during • the later recovery phase, if IOP is high (>30 mm Hg).

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Control Pain

Control pain• Severe chemical burns can be extremely painful. • Cycloplegic agents for ciliary spasm• Oral pain medication initially to control pain.

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Complications

1-Primary complications:• Conjunctival inflammation• Corneal abrasions• Corneal haze and edema• Acute rise in IOP• Corneal melting and perforations

2-Secondary complications:• Secondary glaucoma• Secondary cataract• Conjunctival scarring• Corneal thinning and perforation• Corneal scarring and

vascularization• Corneal ulceration (sterile or

infectious)• Complete globe atrophy (phthisis

bulbi)

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Complications

1- Eye lid:

- Trichiasis, madarosis, symblepharon, ankyloblepharon.

2- Conjunctiva:

-Scarring, destruction of goblet cells & accessory lacrimal glands.

- Severe dryness.

- Symblepharon.

- Pseudo pterygium.

3- Cornea:- Destruction of limbal stem cells- chronic limbal deficiency or failure. - Ulceration, recurrent corneal erosions, opacification, vascularization

thinning & perforation.

Complications

4- Anterior chamber : turbidity & reaction.

5- Iris : iritis, endophthalmitis, panophthalmitis in corneal perforations.

6- Secondary glaucoma :

Early: prostaglandin release , secondary to severe iritis leads to shrinkage of collagen fibers of the sclera.

Late: Occlusion of aqueous veins & anterior ciliary vessels by conjunctival fibrosis.

Atrophic bulbi may follow severe cases.

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1- Correction of lid deformity

2- Conjunctival or mucous membrane graft

3- Amniotic membrane transplantation

4- Limbal stem cell transplantation

5- Penetrating keratoplasty

6- Keratoprosthesis

DELAYED MANAGEMENT OF CHEMICAL BURN

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Amniotic membrane transplantation

Schematic diagram

(above) showing double armed 4-0 silk fornix retaining sutures tied over bolsters, and 10-0 monofilament nylon sutures anchoring the amniotic membrane to the lid margins;

(below) sagittal view showing amniotic membrane lining the entire ocular surface.

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Limbal stem cell transplantation

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Penetrating Keratoplasty

Removing the affected corneal button measuring 7mm in

diameter .

After removal of the corneal button. An intraocular lens can be seen centrally.

Interrupted corneal sutures (10/0 nylon) were used to suture the donor cornea to the recipient's.

Clear graft after penetrating keratoplasty utilizing and showing a continuous (running) 24-bite suture.

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Keratoprosthesis

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Keratoprosthesis in a grossly scarred cornea

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Others in Late(Chronic) Period

• The tear film should be augmented when necessary with preservative-free artificial tears.

• Lysis of symblephara and reconstruction of the fornices, possibly with mucosal grafts, may be performed.

• Silicone rubber sheets and an acrylic conformer are useful.

• Correction of cicatricial entropion and trichiasis is necessary if keratoplasty is anticipated.

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Further inpatient care

In patients with severe chemical injuries, short hospitalization may be warranted to closely monitor: •IOP•Corneal integrity•Medication use•Pain control

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Prognosis

• According to Roper Hall classification

• Grade 1 – Excellent prognosis• Grade 2 – Good prognosis• Grade 3 – Guarded prognosis• Grade 4 – Very poor prognosis• Higher-grade injuries are more susceptible to secondary complications

leading to poor prognosis.

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Deterrence/Prevention

• Education and training regarding the prevention of chemical exposures in the workplace.

• Persons who may be exposed to chemicals in the workplace are advised to wear safety goggles.

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• A common, mostly avoidable ocular emergency.• Immediate and intense irrigation is of utmost importance.• Continuous assessment and planning is very important as early

picture may be misleading.

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