Management of ocular chemical injuries

Management of Chemical
Injury to Eye

ASSIGNMENT OF OPHTHALMOLOGY
BY:
DR.AFIQAH BINTI MUHAMED FAIZAL
4 TH Y E A R M E D I C A L S T U D E N T O F
TANTA UNIVERSITY,EGYPT 2011/2012
THURSDAY,17/05/2012
Author& Disclosure:Dr.Afiqah Bt.Muhamed Faizal in
correspondence to other student in group

Background and Introduction
of 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.


Types of Chemical Injuries
ALKALI BURNS
Alkali 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 agents
And causing the most serious injury
•Lye, NaOH; a common ingredient in drain cleaners and causing the most
Serious injury.
•potassium hydroxide,KOH
•magnesium hydroxide,Mg[OH]2
•Lime, Ca[OH]2; the most common cause, which fortunately does not
inflict 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)

Common alkali substance at home

 Lye  Lime

 Ammonia(household
cleaning agents
containing ammonia)


ACID BURNS
Acid 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)

Common acid substance at home

 Automobile batteries  Vinegar

 Glass polish  Nail polish remover


IRRITANTS
Irritants 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


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


PATHOPHYSIOLOGY OF OCULAR INJURES
1-Damage by severe chemical injuries occurs  Anterior chamber penetration results in
in the following order: iris and lens damage.
 Necrosis of the conjuntival and  Ciliary epithelial damage impairs
corneal epithelium with disruption and secretion of ascorbate which is required
occlusion of the limbal vasculature. for collagen production and corneal
 Loss of limbal stem cells may repair.
subsequently result in  Hypotony and phthisis bulbi may
conjuntivalisation and ensue.
vascularisatioin of the corneal 2- Healing of the corneal epithelium and
surface or persistent corneal stroma as follows:
epithelial defects with sterile  The epithelium heals by migration of
corneal ulceration and perforation. epithelial cells which originate from
 Other long_term effects include ocular limbal stem cells.
surface wetting  Damaged stromal collagen is
disorders, symblepharon formation phagocytosed by keratocytes and new
and cicatricial entropion. collagen is synthesized.
 Deeper penetration causes breakdown and
precipitation of glycosaminoglycans and
stromal corneal opacification.


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

Alkalies Acid
More severe than acid burns due to: -Less severe than alkali burns.
-Penetrate rapidly into eye ball (often in less than one -Acids quickly denature proteins in the corneal
minute), through the cornea and anterior chamber. stroma, forming precipitates that retard additional
penetration.
-They combine with cell membrane lipids,
-Causing localized damage due to its:
mucopolysaccharides and to collagen, thereby resulting a)Coagulation effect
in the disruption of the cells and necrosis of the tissues. b)Protein precipitations at epithelium level
On the ocular surface, they saponify cell membranes and
intercellular bridges, which facilitates rapid penetration -Leading to:
into the deeper layers and into the aqueous and vitreous Physical barrier.
compartments Buffering effect (Corneal tissue has an inherent
buffering capacity that tends to equilibrate local pH
to physiological levels, but severe chemical injuries
-Necrosis of conjunctival blood vessel causing: exhaust the cellular and extracellular resources,
“Cooked fish eye” the cornea is as white as chalk and allowing extremes of pH that are incompatible with
opaque. tissue survival)


Diagnosis

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

- Intraocular structures in the anterior segment of
the eye can also be involved and can be associated
with lens opacities and secondary glaucoma.


Severe Chemical burn


Severe acid burn on eye


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


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.


Alkali burn(chemical burn)

Corneal opacity following lime burn.


Alkali injury

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


Alkali burn

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


Chemical burn

Opaque vascularised cornea after severe chemical
burn.


Chemical burn

Chemical burn typically affecting cornea inferiorly.


Chemical injury

- total destructive effect of  Superglue Injury
a lye burn


Chemical burn

 Following burn from hot  Alkali burn stage II
aluminum:conjunctivaliza
tion of the corneal surface


Alkali burn stage III

 Alkali burn stage III


Complication of Chemical injury

Conjunctival adhesions  Symblepharon formation
following chemical injury following a chemical
injury


Acid burn

 Acid burn with corneal erosion below


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.

Acid injury

Mild acid injury Severe acid injury

Scar from acid injury


Chemical burn on conjunctiva and cornea
 Alkali injury. When no corneal  Lime injury. Superficial and
reepithelization had occurred deep corneal vascularization is
by 4 weeks. present, and the eye is dry due
to loss of most of the goblet
cells.


Signs:•

Clinical Pictures

1- Symptoms: 2- Signs:

- Pain - eye lid edema,
- Lacrimation - chemosis,
- Photophobia
- conjunctival injection
- Blepharospasm
- Diminution of vision - corneal abrasions


Effects of Ocular Surface Burn


Classification of ocular surface burn


A new classification of ocular surface burns
Grade Prognosis Clinical findings Conjunctival Analogue
involvelment scale
I Very good 0 clock hours of 0% 0/0%
limbal involvement
II Good ⩽3 clock hours of ⩽30% 0.1–3/1–29.9%
limbal involvement
III Good >3–6 clock hours of >30–50% 3.1–6/31–50%
limbal involvement
IV Good to guarded >6–9 clock hours of >50–75% 6.1–9/51–75%
limbal involvement
V Guarded to poor >9–<12 clock hours >75–<100% 9.1–11.9/75.1–
of limbal 99.9%
involvement
VI Very poor Total limbus (12 Total 12/100%
clock hours) conjunctiva
involved (100%) involved
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 includingFaizal
Author& Disclosure:Dr.Afiqah Bt.Muhamed the conjunctival fornices is considered.

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.

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.

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.


 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.

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


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.


Immediate Management of
Chemical Burns


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.

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):


Guidelines for first aid for chemical burns

 Water is contraindicated as a first aid  Speed in irrigation is also important as
measure in chemical burns caused by the certain organic solvents are quickly absorbed
heavy metals like sodium, potassium and
calcium(e.g.Lime or Ca(OH)2). into the blood stream via the skin or by
 They react violently and explosively with inhalation and cause systemic toxicity.
water to produce caustic hydroxide  Irrigation should continue even during the
liberating much heat in its production and transport to the hospital.
thus result in combination of thermal and
chemical burn.  Never apply acid to base, or base to acid as it
 Immediate treatment in these cases is to can cause exothermic reaction generating
- brush off/pick out from the skin as many heat resulting in further damage.
particles of sodium or potassium as possible  Victims of mass casualty due to contact with
and
the hazardous materials (Hazmat) should be
- then to direct a high pressure jet of water at
the remainder. removed from the zone of immediate danger
- Ignition of particles will occur, but if the and then decontaminated. Decontamination
flow is great enough, the heat will be at a hospital is discouraged due to potential
dissipated by water. spread of the substance to other patients. All
 Covering the remaining particles with oil, the areas utilised for decontaminating
although prevents combustion, cannot halt victims must themselves be decontaminated
the tissue damage as the remaining metal
particles continue to react with tissue water. after use.


 Instrument and kit used
for eye irrigation


Eye irrigation


Transfer

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


Acute Management of Chemical
Burns


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:


If nature of chemical If nature of chemical is
substance is known unknown or not available

Strong Weak alkali
acid Tap Dilute chemical
Strong Weak acid water substance
alkali *for all except LIME*
Iodine Starch solution Milk Dilution
Milk Buffer acid and alkali
Aniline Alcohol 10% Form superficial film
Glycerine 10% which protect the
Lime a) Pick particles with underlying tissue
forceps
b) Wash by:
EDTA 0.1% (universal
antidote)
Neutral ammonium
tartarate 10%
Saturated sugar
solution

Promote ocular surface healing
1- 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.

Promote ocular surface(epithelial) healing

Promote ocular surface (epithelial) healing
Once the inciting chemical has been completely removed,
epithelial healing can begin by:
Treatment Functions
-Artificial tear supplement -as it cause poorly produce
adequate tears.
-Ascorbate -improvement in corneal
healing.
-Therapeutic bandage contact lens -until the epithelium has
regenerated.
-Amniotic membrane transplant in -promotes faster healing of
eyes with acute ocular burns epithelial.


Med Term Management of
Ocular Chemical Burns


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


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.


Cyanoacrylate tissue adhesive


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).


Control Pain

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


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.}.


Delayed Management of
Chemical Burn

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


Conjunctival or
mucous membrane
graft  Reconstruction of contracted fornices several
Division of symblephara may be followed by a
mucosal graft from the upper conjunctival fornix of
months after severe alkali burn. After lysis of
an unaffected fellow eye or from buccal mucosa. The symblephara, sheets of silicone rubber were
graft should be secured deep in the fornix by
double-armed mattress sutures that first engage the sutured deep into the fornices. A scleral shell
periosteum of the orbital margin and then pass
through the lid to be tied over a square of 0.005-
was inserted as a conformer
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.

.

Amniotic membrane
Schematic diagram transplantation
(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.


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

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
Limbal stem cell transplantation
sutures to the sclera.

Limbal stem cell transplantation
 If no significant epithelialization has  To re-establish corneal
taken place over a denuded cornea by epithelium over the exposed
the third to sixth week after a severe stroma after a severe chemical
chemical injury, eventual injury, it may be necessary to consider
conjunctivalization with vascularization a limbal stem cell autograft or
will probably occur unless the eye also homograft.
has suffered profound loss of  A patient with a monocular
conjunctiva. chemical burn is a candidate for
 The various characteristics of an autograft, but homologous
conjunctival tissue, including its tissue must be used if both eyes
vasculature and goblet cells, are slowly have sustained significant
lost as the conjunctivalized cornea damage.
undergoes transdifferentiation to a  The clarity, degree of adherence, and
metabolically-imperfect corneal stability of the epithelial layer that
epithelium. results from limbal stem cell
 Because of its instability and its transplantation cannot be matched
tendency to vascularize after by any other current method of
minor trauma, this new epithelial re-establishing tissue protection
covering derived from conjunctiva is over denuded stroma.
less desirable than true corneal
epithelium.


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 Limbal stem cell transplantation
stem-cell transplantation. N Engl J Med
340:1697, 1999, with permission)

Penetrating Keratoplasty

Removing the Interrupted
affected After removal of the corneal sutures
corneal button corneal button. An (10/0 nylon)
intraocular lens were used to
measuring suture the donor
7mm in can be seen cornea to the
diameter. centrally. recipient's.

Clear graft after penetrating keratoplasty
utilizing and showing a continuous
(running) 24-bite suture. (Courtesy of Alan
Carlson, MD)

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 inFaizal graft may be seen in several situations.
Author& Disclosure:Dr.Afiqah Bt.Muhamed the

Cultures plus Keratoplasty


Keratoprosthesis


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

Keratoprosthesis in a grossly scarred cornea


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.


Further inpatient care

In patients with severe chemical injuries, short hospitalization
may be warranted to closely monitor:
•IOP
•corneal integrity
•medication use
•pain control


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).


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.


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.


Prognosis
 In general, the prognosis of ocular • Grade 1 - Partial-complete epithelial
chemical injuries is directly correlated defect, clear corneal stroma, no limbal
with the severity of insult to the eye and ischemia
adnexal structures. • Grade 2 - Partial-complete epithelial
defect, mild stromal haze, none or only mild
 Many classification systems and limbal ischemia
revisions thereof have been aimed at • Grade 3 - Complete epithelial
classifying ocular burns in relation to defect, moderate stromal haze, less than one
their prognosis, including the following third of the limbus is ischemic
systems: Hughes, Roper-Hall, and • Grade 4 - Complete epithelial
Pfister.[9] In essence, all systems aim defect, stromal haze blurring iris details, one
third to two thirds of the limbus is ischemic
to quantify the degree of corneal
• Grade 5 - Complete epithelial
epithelial involvement, the degree of defect, stromal opacification, greater than
limbal stem cell loss, and the degree of two thirds of the limbus is ischemic
conjunctival involvement.[16]  Grades 0-2 can be expected to heal well with
 Injuries can be graded from 0-5, as proper care and follow-up examinations.
follows:  The course for grades 3-5 is more tenuous
and may require surgical
• Grade 0 - Minimal epithelial intervention, either limbal stem cell
defect, clear corneal stroma, no limbal transplantation or penetrating
ischemia keratoplasty, to regenerate the corneal
surface.
 Higher-grade injuries are more susceptible
to secondary complications.

Evaluation

 Visual acuity
 Extensive history:
 When the injury occurred

 Chemical involved in exposure

 Duration of exposure

 Duration of irrigation

 How long after exposure the chemical irrigation was begun.


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

 Ophthalmology for Undergraduate Medical Students (Tanta University textbook)
 Kanski Clinical Ophthalmology


FINISH

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

Management of ocular chemical injuries

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