Management of ocular chemical injuries

Author& Disclosure:Dr.Afiqah Bt.Muhamed Faizal in correspondence to other student in group

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ASSIGNMENT OF OPHTHALMOLOGYBY:

DR.AFIQAH BINTI MUHAMED FAIZAL4 T H YEAR MEDICAL STUDENT OF

TANTA UNIVERSITY,EGYPT 2011 /2012THURSDAY,17 /05 /2012

Management of Chemical Injury to Eye


2Background and Introductionof Management of Chemical Injuries in the Eye:

Background & Introduction: Ocular burns constitute true ocular emergencies and both

thermal and chemical burns represent potentially blinding ocular injuries. Thermal burns result from accidents associated with firework explosions, steam, boiling water, or molten metal (commonly aluminium). Chemical burns may be caused by either alkaline or acidic agents

Chemical injuries to the eye represent one of the true ophthalmic emergencies. While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or acidic compounds. Alkali injuries are more common and can be more deleterious. Bilateral chemical exposure is especially devastating, often resulting in complete visual disability. Immediate, prolonged irrigation, followed by aggressive early management and close long-term monitoring, is essential to promote ocular surface healing and to provide the best opportunity for visual rehabilitation.


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Types of Chemical InjuriesALKALI BURNSAlkali burns are the most dangerous due to its rapid penetration through both the external structures like anterior chamber and cornea and the internal structures like the lens. They combine with cell membrane lipids causing disruption of cell and tissue necrosis. The higher the pH of chemical, the worsen the damage on eye. Common alkali substances contain:•Ammonia,NH3; a common ingredient in many household cleaning agentsAnd causing the most serious injury•Lye, NaOH; a common ingredient in drain cleaners and causing the mostSerious injury.•potassium hydroxide,KOH•magnesium hydroxide,Mg[OH]2•Lime, Ca[OH]2; the most common cause, which fortunately does notinflict as much damage as rapidly penetrating alkalies do.Common alkali substances at home that contain these chemicals include: •fertilizers•cleaning products (ammonia), •drain cleaners (lye)•oven cleaners•and plaster •cement (lime)


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Common alkali substance at home

Lye Lime

Ammonia(household cleaning agents containing ammonia)


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Types of Chemical Injuries

ACID BURNSAcid burns result from chemicals with a low pH and are usually less severe than alkali burns because they do not penetrate into the eye as readily as alkaline substances. The exception is a hydrofluoric acid burn, which is as dangerous as an alkali burn. Acids usually only cause damage on:Common acids causing eye burns include:•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 alkali substances at home that may contain these chemicals include:•glass polish (hydrofluoric acid)•vinegar•nail polish remover (acetic acid)


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Common acid substance at home

Automobile batteries

Glass polish

Vinegar

Nail polish remover

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Types of Chemical Injuries


IRRITANTSIrritants are substances that have a neutral pH and tend to cause more discomfort to the eye than actual damage.

-Most household detergents fall into this category. -Pepper spray is also an irritant. It can cause significant pain but usually does not affect vision and rarely causes any damage to the eye.

The severity of ocular injury depends on:•Surface area of contact•Depth of penetration depends on:•Concentration of chemicals•Time of contact between chemical trauma into first aid•Time of interference•Degree of limbal stem cell injury


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Severity of Burn

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 eye Internal segment of the eye Cornea Conjunctiva Lens

3-Deeper than the cornea are the most severe causing: cataracts glaucoma


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PATHOPHYSIOLOGY OF OCULAR INJURES

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

Necrosis of the conjuntival and corneal epithelium with disruption and occlusion of the limbal vasculature.

Loss of limbal stem cells may subsequently result in conjuntivalisation and vascularisatioin of the corneal surface or persistent corneal epithelial defects with sterile corneal ulceration and perforation.

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

Deeper penetration causes breakdown and precipitation of glycosaminoglycans and stromal corneal opacification.

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.

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

The epithelium heals by migration of epithelial cells which originate from limbal stem cells.

Damaged stromal collagen is phagocytosed by keratocytes and new collagen is synthesized.


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N.B.

- Although limbal ischaemia is usually associated with loss of limbal stem cells, this is not always the case. - Transient ischaemia, or ischaemia occurring soon after the injury but recovering in the ensuing days, may allow limbal stem cells to survive, recover or repopulate the affected sector. - Similarly, superficial “limbal involvement” can result in 360° of surface staining with deeper stem cells surviving. This situation may not become apparent until a few days after the injury. - Because it is clinically not possible to evaluate this situation at the time of injury, it is proposed that the extent of limbal involvement at the time of injury, be based on the clock hours of limbal staining observed.


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Alkalies Acid More severe than acid burns due to:-Penetrate rapidly into eye ball (often in less than one minute), through the cornea and anterior chamber.

-They combine with cell membrane lipids, mucopolysaccharides and to collagen, thereby resulting in the disruption of the 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 than alkali burns.-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. Buffering effect (Corneal tissue has an inherent buffering capacity that tends to equilibrate local pH to physiological levels, but severe chemical injuries exhaust the cellular and extracellular resources, allowing extremes of pH that are incompatible with tissue survival)


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Diagnosis

-Diagnosis is made from the history.The staging is guided by the clinical picture .

-Intraocular structures in the anterior segment ofthe eye can also be involved and can be associatedwith lens opacities and secondary glaucoma.


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Severe Chemical burn


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Severe acid burn on eye


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Acute alkali burn

Acute alkali burn of greatest severity. Perilimbal blanching, chemosis, and corneal opacification are evident.


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Severe alkali burn

Acute alkali burn of severe degree. The eye rolled upward in avoidance (Bell phenomenon), exposing the lowest aspect of the cornea to the greatest damage.


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Alkali burn(chemical burn)

Corneal opacity following lime burn.


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Alkali injury

‘cooked fish eye’ following alkali injury. The cornea is white as chalk and opaque. There’s superficial and deep corneal vascularization.


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Alkali burn

Heavily vascularized cornea with symblepharon several years after severe chemical burn. Poor prognosis is expected for penetrating keratoplasty.


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Chemical burn

Opaque vascularised cornea after severe chemical burn.


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Chemical burn

Chemical burn typically affecting cornea inferiorly.


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Chemical injury

- total destructive effect of a lye burn

Superglue Injury


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Chemical burn

Following burn from hot aluminum:conjunctivalization of the corneal surface

Alkali burn stage II


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Alkali burn stage III

Alkali burn stage III


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Complication of Chemical injury

Conjunctival adhesions following chemical injury

Symblepharon formation following a chemical injury


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Acid burn

Acid burn with corneal erosion below


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Severe Alkali Burn

Severe alkali burn. A. Two weeks after injury: pannus begins to invade the opaque cornea from above. B. Three weeks after injury: pannus grows as the

cornea begins to thin and clear. C. Seven weeks after injury: collagenolytic erosion and descemetocele in advance of the pannus. D. Eight weeks after

injury: frank perforation of the cornea.


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Acid injury

Mild acid injury Severe acid injury

Scar from acid injury


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Chemical burn on conjunctiva and cornea

Alkali injury. When no corneal reepithelization had occurred by 4 weeks.

Lime injury. Superficial and deep corneal vascularization is present, and the eye is dry due to loss of most of the goblet cells.


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•Signs:

1- Symptoms: 2- Signs:

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

- eye lid edema,- chemosis,- conjunctival injection - corneal abrasions

Clinical Pictures


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Effects of Ocular Surface Burn


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Classification of ocular surface burn


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A new 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 Clinical findings 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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Complications

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

2-Secondary complications include the following: Secondary glaucoma Secondary cataract Conjunctival scarring Corneal thinning and perforation Complete ocular surface disruption with corneal scarring and vascularization Corneal ulceration (sterile or infectious) Complete globe atrophy (phthisis bulbi): See the image below.

(phthisis bulbi=Shrinkage and atrophy of the eyeball following a severe inflammation (e.g. uveitis), absolute glaucoma or trauma.) Complete cicatrization of the corneal surface following chemical injury.


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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 ptrygium.

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


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Complications

4- Anterior chamber : turbidity & reaction.

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

6- Secondary glaucoma : Early: prostaglandin release , secondary to severe iritis shrinkage of collagen fibers of the sclera.Late: Occlusion of aqueous veins & anterior ciliary vessels by conjunctival fibrosis. Atrophia bulbi may follow severe cases.


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Representative photographs of patients with severe ocular surface burns (Grade 4 Roper Hall Classification and the equivalent Dua 4, 5, 6 ocular burn). The upper row shows the clinical pictures of the patients at presentation, and the lower row shows the corresponding slit-lamp photographs of the same patient at final follow-up visit: A–D: Grade 4 chemical burns (6–9 clock hours of limbal ischaemia); E–H: Grade 5 chemical burns (9–11 clock hours of limbal ischaemia); I–L: Grade 6 chemical burns (12 clock hours of limbal ischaemia); A, B, E, F, I, J: patients treated with standard medical therapy; C, D, G, H, K, L: patients who underwent amniotic membrane transplantation.


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Laboratory Study

The pH of the ocular surface should be periodically tested. Irrigation should be continued until the pH reaches neutrality.

No other laboratory tests are generally necessary unless other systemic injuries are concurrent


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Medical Care

Treatment of chemical injuries to the eye requires medical and surgical intervention, both acutely and in the long term, for maximal visual rehabilitation.

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, and (5) controlling IOP.


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Immediate Management of Chemical Burns


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Management of Ocular Chemical Injury

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)

However, immediate irrigation with even plain tap water is preferred without waiting for the ideal fluid. If available, the eye should be anesthetized prior to irrigation.Ideally,the eye should be irrigated with irrigation solution and must contact the ocular surface by: •special irrigating tubing (eg, Morgan lens) •lid speculum. Irrigation should be continued until the pH of the ocular surface is neutralized, usually requiring 1-2 liters of fluid.


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Eye Irrigation

2)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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Guidelines for first aid for chemical burns

Speed in irrigation is also important as certain organic solvents are quickly absorbed into the blood stream via the skin or by inhalation and cause systemic toxicity.

Irrigation should continue even during the transport to the hospital.

Never apply acid to base, or base to acid as it can cause exothermic reaction generating heat resulting in further damage.

Victims of mass casualty due to contact with the hazardous materials (Hazmat) should be removed from the zone of immediate danger and then decontaminated. Decontamination at a hospital is discouraged due to potential spread of the substance to other patients. All the areas utilised for decontaminating victims must themselves be decontaminated after use.

Water is contraindicated as a first aid measure in chemical burns caused by the heavy metals like sodium, potassium and calcium(e.g.Lime or Ca(OH)2).

They react violently and explosively with water to produce caustic hydroxide liberating much heat in its production and thus result in combination of thermal and chemical burn.

Immediate treatment in these cases is to- brush off/pick out from the skin as many

particles of sodium or potassium as possible and

- 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.

Covering the remaining particles with oil, although prevents combustion, cannot halt the tissue damage as the remaining metal particles continue to react with tissue water.


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Instrument and kit used for eye irrigation


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Eye irrigation


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Transfer

After completing initial irrigation and treatment, patients should be transferred to facilities that have ophthalmologists available to assume care for them.


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Acute Management of Chemical Burns


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Acute Management: after transfer to hospital

It’s better to place an eye speculum and topical anaethesia in the eye before irrigation.

The lower lid is pulled down and the upper lid is everted to irrigate the fornices.

Continue irrigation until pH reaches close to normal. Wash with available antidote if available:


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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 forceps

b) Wash by:-EDTA 0.1% (universal

antidote)-Neutral ammonium

tartarate 10%-Saturated sugar

solution

Tap water

Dilute chemical substance

*for all except LIME*Milk - Dilution

-Buffer acid and alkali-Form superficial film

which protect the underlying tissue


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Promote ocular surface healing1- Remove inciting chemical • After instilling topical anesthesia, sweep the fornices with a moist sterile cotton swab to remove any retained

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

2- Debridement Once irrigation has been initiated, an exhaustive search of the fornices is necessary to

locate and remove sequestered particles of caustic material. If allowed to remain, these particles dissolve slowly, allowing additional toxic substances to leach into surrounding tissues.

The search must include double eversion of the lids after application of 0.5% proparacaine solution and deep swabbing of the conjunctival recesses using moistened cotton-tipped applicators. Careful attention must be directed to those regions where extreme chemosis is likely to hide particulate matter in crypts and folds.

3- Paracentesis The relative importance of irrigation is diminished slightly by findings that external

perfusion of alkali-burned animal eyes, although vital in reducing surface pH, may be incapable of lowering aqueous pH by more than 1.5 units.

A further decrease in pH by 1.5 units can be achieved by removing aqueous by paracentesis, using a 25- or 27-gauge needle inserted at the limbus under slit lamp visualization. If buffered phosphate solution is then used to refill the anterior chamber, a greater reduction in pH (another 1.5 units) is possible.

4- Early Assessment During the first hour or two of emergency treatment with irrigation, debridement, and

possibly paracentesis, critical evaluation of the severity of injury dictates the nature of further therapy.


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Promote ocular surface(epithelial) healing

Promote ocular surface )epithelial) healingOnce the inciting chemical has been completely removed, epithelial healing can begin by:

Treatment Functions

-Artificial tear supplement

-Ascorbate

-Therapeutic bandage contact lens

-Amniotic membrane transplant in eyes with acute ocular burns

-as it cause poorly produce adequate tears. -improvement in corneal healing.-until the epithelium has regenerated.-promotes faster healing of epithelial.


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Med Term Management of Ocular Chemical Burns


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Control inflammation

Inflammatory mediators released from the ocular surface at the time of injury causing:•tissue necrosis•attract further inflammatory reactantsThis robust inflammatory response causing: •inhibits reepithelialization •corneal ulceration •PerforationControlling inflammation will help to break this inflammatory cycle by using:


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Control infection and cicatrization

-Topical antibiotic, aggressive lubrication with eye ointments )steroid antibiotic combinations) to prevent symblepharon. As the first week of treatment draws to a close, 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. *Long-term use of topical antibiotics, however, can lead to development of bacterial resistance or corneal toxicity from preservatives.

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

-Topical steroids should not be used if the corneal epithelium is intact.

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


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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 suppressants is advocated to reduce IOP in severe exposure and both as an initial therapy and during

the later recovery phase, if IOP is high (>30 mm Hg).


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Control Pain

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


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Improves healing

1- Steroids reduce inflammation and neutrophil infiltration. However, they also impair stromal healing by reducing collagen synthesis and inhibiting fibroblast migration. For this reason topical steroids may be used initially but must be tailed off after 7-10 days when sterile corneal ulceration is most likely to occur. They may be replaced by topical NSAIDs, which do not affect keratocyte function.

2- Ascorbic acid reverses a localized tissue scorbutic state and improves wound healing by promoting the synthesis of mature collagen by corneal fibroblasts. Topical sodium ascorbate 10% is given 2 -hourly in addition to a systemic dose of 2 gq.i.d. 3. 3- Citric acid is a powerful inhibitor of neutrophil activity and reduces the intensity of the inflammatory response. Chelation of extracellular calcium by citrate also appears to inhibit collagenase. Topical sodium citrate 10% is given 2- hourly for about 10 days. The aim is to eliminate the second wave of phagocytes, which normally occurs 7 days after the injury.

4- Tetracyclines are collagenase inhibitors and also inhibit neutrophil activity and reduce ulceration. They are administered both topically and systemic-ally {e.g. doxycycline 100 mg b,d.}.


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1- CORRECTION OF LID DEFORMITY2-CONJUNCTIVAL OR MUCOUS MEMBRANE

GRAFT3-AMNIOTIC MEMBRANE

TRANSPLANTATION4-LIMBAL STEM CELL TRANSPLANTATION

5-PENETRATING KERATOPLASTY6-KERATOPROSTHESIS

Delayed Management of Chemical Burn

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Conjunctival or mucous membrane graftDivision of symblephara may be followed by a mucosal graft from the upper conjunctival fornix of an unaffected fellow eye or from buccal mucosa. The graft should be secured deep in the fornix by double-armed mattress sutures that first engage the periosteum of the orbital margin and then pass through the lid to be tied over a square of 0.005-inch silicone rubber sheet.An interim prosthesis, such as an acrylic shell or ring, must be used to separate the lids from the globe, or symblephara rapidly recurs. If there is bilateral injury or if it is not possible to use a mucosal graft, larger sheets of the very flexible 0.005-inch silicone rubber can be fashioned to line the exposed subconjunctival tissue in the deepened fornix . It is possible to use similarly a microthin polyvinyl plastic film of the type used for food wrap in the kitchen; this is easy to obtain and readily sterilizable with heat. These prosthetic sheets must be sutured securely to the periosteum of the orbital margin, after which a scleral shell is inserted. Although conjunctiva grows over these dissected surfaces, preservation of the deepened fornices remains a major challenge because regrowth of symblephara is almost the rule. As the cicatricial bands form once again, retention of a scleral shell or silicone rubber sheets becomes increasingly difficult. In an attempt to inhibit reformation of lysed symblephara, beta-irradiation has been applied after excision of the scar tissue.

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Reconstruction of contracted fornices several months after severe alkali burn. After lysis of symblephara, sheets of silicone rubber were sutured deep into the fornices. A scleral shell was inserted as a conformer


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Amniotic membrane transplantationSchematic 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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Amniotic membrane transplantation(AMT)

Amniotic membrane is obtained under sterile conditions after elective caesarean delivery from a seronegative donor.1) AMT promoted healing of the ocular surface in all patients, as

complete epithelialisation was achieved in all cases. It helps in corneal and conjunctival differentiation and regeneration.

2) This action of amniotic membrane is by virtue of the epithelial basement membrane layer providing a mechanical support and acting as an internal splint.

3) beneficial biological properties such as secretion of cytokines, growth factors and protease inhibitors which decrease surface inflammation and prevent fibrosis and symblepharon formation.

4) AMT stabilises the ocular surface and provides a conducive surface for further procedures such as auto-limbal and allo-limbal transplantation, lamellar or penetrating keratoplasty.

5) AMT can be considered as a useful surgical option in moderate chemical burns with non-healing epithelial defects. It may also be used judiciously in severe cases where close monitoring and follow-up are not possible, and compliance with medication is not satisfactory

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Limbal stem cell transplantation

Surgical procedure for conjuctival limbal autograft (CLAU). The conjunctivalized pannus is removed from the corneal surface by peritomy followed by superficial keratectomy with blunt dissection in the recipient eye (A). The cicatrix was removed from the subconjunctival space (B). This invariably results in the recession of the conjunctival edge to 3 to 5 mm from the limbus from the superior and inferior limbal regions (C). Two strips of limbal conjunctival free grafts, each spanning 6 to 7 mm limbal arc length, are removed by superficial lamellar keratectomy at 1 mm within the limbus (D) and by including 5 mm of adjacent conjunctiva. These two free grafts are transferred and secured to the recipient eye at the corresponding anatomic sites by interrupted 10-0 nylon sutures to the limbus and 8-0 vicryl sutures to the sclera.


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If no significant epithelialization has taken place over a denuded cornea by the third to sixth week after a severe chemical injury, eventual conjunctivalization with vascularization will probably occur unless the eye also has suffered profound loss of conjunctiva.

The various characteristics of conjunctival tissue, including its vasculature and goblet cells, are slowly lost as the conjunctivalized cornea undergoes transdifferentiation to a metabolically-imperfect corneal epithelium.

Because of its instability and its tendency to vascularize after minor trauma, this new epithelial covering derived from conjunctiva is less desirable than true corneal epithelium.

To re-establish corneal epithelium over the exposed stroma after a severe chemical injury, it may be necessary to consider a limbal stem cell autograft or homograft.

A patient with a monocular chemical burn is a candidate for an autograft, but homologous tissue must be used if both eyes have sustained significant damage.

The clarity, degree of adherence, and stability of the epithelial layer that results from limbal stem cell transplantation cannot be matched by any other current method of re-establishing tissue protection over denuded stroma.

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Surgical procedure of keratolimbal allograft (KLAL). In the host eye the fibrovascular pannus is completely removed leaving in most of the limbal stem cell deficiency (LSCD) cases a clear residual corneal stromal bed. One layer of amniotic membrane with basal membrane up is place over the cornea as a graft and secure with interrupted 8-0 vicryl to residual conjunctiva and scleral tissue around the limbus. The donor central corneal button is removed by trephine and the residual limbal ring is trimmed off and the underlying stroma is thinned to create a smooth and thin corneal–scleral limbal ring. The limbal tissue is then lay around cornea and secure with interrupted 10-0 nylon suture. In order to promote corneal epithelial healing another amniotic membrane is placed over the cornea as a patch and secure to the scleral with running 10-0 nylon for 1 or 2 weeks (figure not shown). If amniotic membrane is dissolved before 2 weeks, exposure and/or severe inflammation should be suspected and addressed.

(Reprinted from Tsubota K, Satake Y, Kaido M, et al: Treatment of severe ocular surface disorders with corneal epithelial stem-cell transplantation. N Engl J Med 340:1697, 1999, with permission)


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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. (Courtesy of Alan Carlson, MD)


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Penetrating keratoplasty (PK)

- Penetrating keratoplasty (PK) is one of the most common forms of tissue transplantation currently performed. It can be an extremely successful procedure, with dramatic visual improvement for the patient.- can also be one of the most challenging and frustrating procedures for a patient to

endure, with a prolonged convalescence, delayed visual improvement, and many postoperative challenges.

- The technique of keratoplasty, or corneal grafting, involves removing the dysfunctional elements of the cornea and replacing those elements with healthy tissue. Full thickness keratoplasty is termed penetrating keratoplasty, and partial-thickness keratoplasty is termed lamellar keratoplasty.

- the current number of procedures performed on an annual basis is decreasing slightly due to:

* reflects improved cataract removal technique and technology, such as phacoemulsification and posterior chamber intraocular lens placement.* Many other complications can occur in the late postoperative period, some of which are peculiar to corneal transplant surgery and others of which may be seen after any intraocular surgery. * Chronic progressive nonspecific endothelial decompensation manifests as a gradual onset of graft edema secondary to endothelial dysfunction not associated with prior rejection, uveitis, or glaucoma. *Recurrence of host disease in the graft may be seen in several situations.


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Cultures plus Keratoplasty


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Keratoprosthesis

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Keratoprosthesis in chemical injury. Collagenolytic lysis occurs around the central optical post.

Keratoprosthesis for corneal reconstruction after chemical injury has been largely unsatisfactory. The greatest limiting factor has been collagenolytic erosion of the interfaces at which corneal tissue adjoins prosthetic material


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Keratoprosthesis in a grossly scarred cornea


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Summary of Suggested Action During the 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.

Penetrating keratoplasty, with exquisite attention to the small details favoring success, may be performed.


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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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Inpatient & Outpatient Medications


Prednisolone acetate 1% (1 gtt qid)Erythromycin ophthalmic ointment (4-8

times/d)Homatropine 5% or scopolamine 0.25% (1 gtt

tid)Ascorbate (500 mg PO qid)Levobunolol hydrochloride 0.5% (1 gtt bid) or

acetazolamide (500 mg PO bid) - Pressure lowering agents, such as levobunolol and acetazolamide, are only indicated if IOP is increased (>30 mm Hg).

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Deterrence/Prevention


Education and training regarding the prevention of chemical exposures in the workplace can help prevent chemical injuries to the eye.

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

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Consultations


In most instances, patients present to nonophthalmologists for their immediate care.

At a minimum, patients with mild chemical injuries should have follow-up care arranged with an ophthalmologist.

Any patient with a moderate-to-serious injury should be immediately evaluated and followed accordingly by an ophthalmologist.

Other medical personnel may be needed as determined by the extent of the extraocular injuries sustained.


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Prognosis

In general, the prognosis of ocular chemical injuries is directly correlated with the severity of insult to the eye and adnexal structures.

Many classification systems and revisions thereof have been aimed at classifying ocular burns in relation to their prognosis, including the following systems: Hughes, Roper-Hall, and Pfister.[9] In essence, all systems aim to quantify the degree of corneal epithelial involvement, the degree of limbal stem cell loss, and the degree of conjunctival involvement.[16]

Injuries can be graded from 0-5, as follows:

• Grade 0 - Minimal epithelial defect, clear corneal stroma, no limbal ischemia

• Grade 1 - Partial-complete epithelial defect, clear corneal stroma, no limbal ischemia

• Grade 2 - Partial-complete epithelial defect, mild stromal haze, none or only mild limbal ischemia

• Grade 3 - Complete epithelial defect, moderate stromal haze, less than one third of the limbus is ischemic

• Grade 4 - Complete epithelial defect, stromal haze blurring iris details, one third to two thirds of the limbus is ischemic

• Grade 5 - Complete epithelial defect, stromal opacification, greater than two thirds of the limbus is ischemic

Grades 0-2 can be expected to heal well with proper care and follow-up examinations.

The course for grades 3-5 is more tenuous and may require surgical intervention, either limbal stem cell transplantation or penetrating keratoplasty, to regenerate the corneal surface.

Higher-grade injuries are more susceptible to secondary complications.

78

Evaluation


Visual acuityExtensive history:

When the injury occurred Chemical involved in exposure Duration of exposure Duration of irrigation How long after exposure the chemical irrigation was

begun.

79

Differential Diagnosis


Differentials Diagnosis:• Conjunctivitis, Acute Hemorrhagic• Conjunctivitis, Allergic• Corneal Abrasion• Corneal Erosion, Recurrent• Corneal Foreign Body• Keratoconjunctivitis, Atopic• Keratoconjunctivitis, Epidemic• Keratoconjunctivitis, Sicca• Ulcer, Corneal

References


80

http://journals.lww.com/coophthalmology/Abstract/2010/07000/Management_of_ocular_thermal_and_chemical.15.aspx

http://bjo.bmj.com/content/95/2/194.full http://www.medscape.com/viewarticle/739100 http://

www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/SickCall/Eye/BurnsoftheEye.htm

http://www.medscape.com/viewarticle/739099 http://www.medscape.com/viewarticle/739957 Ophthalmology for Undergraduate Medical Students (Tanta University

textbook) Kanski Clinical Ophthalmology

http://journals.lww.com/co-ophthalmology/Abstract/2010/07000/Management_of_ocular_thermal_and_chemical.15.aspx




http://bjo.bmj.com/content/95/2/194.full



http://www.medscape.com/viewarticle/739100



http://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/SickCall/Eye/BurnsoftheEye.htm






81

Thank You



82

FINISH

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