chemical injuries f eye : clinical features,classification ,pathogenesis, management.

1. Chemical injuriesChemical injuries
Dr.Prashant .P. Patel.Dr.Prashant .P. Patel.
Senior resident,Senior resident,
Aravind Eye Hospital Tirunelveli.Aravind Eye Hospital Tirunelveli.

2. Chemical injuriesChemical injuries
• One of the true ophthalmic emergencies.One of the true ophthalmic emergencies.
• Serious damage generally results fromSerious damage generally results from
either strongly basic (alkaline) compoundseither strongly basic (alkaline) compounds
or acidic compounds.or acidic compounds.
• Alkali injuries are more common and canAlkali injuries are more common and can
be more deleterious.be more deleterious.

3. EpidemiologyEpidemiology
• Chemical injuries are responsible forChemical injuries are responsible for
approximately 7% of work-related eyeapproximately 7% of work-related eye
injuries .injuries .
• More than 60% of chemical injuries occurMore than 60% of chemical injuries occur
in workplace accidents, 30% occur atin workplace accidents, 30% occur at
home, and 10% are the result of anhome, and 10% are the result of an
assault.assault.

4. Mortality/MorbidityMortality/Morbidity
• As many as 20% of chemical injuriesAs many as 20% of chemical injuries
result in significant visual and cosmeticresult in significant visual and cosmetic
disability.disability.
• Only 15% of patients with severe chemicalOnly 15% of patients with severe chemical
injuries achieve functional visualinjuries achieve functional visual
rehabilitation.rehabilitation.

5. AgeAge
• Chemical injuries can strike anyChemical injuries can strike any
population.population.
• However, most injuries occur in patientsHowever, most injuries occur in patients
aged 16-45 years.aged 16-45 years.

6. SexSex
• Males are 3 times more likely toMales are 3 times more likely to
experience chemical injuries than females.experience chemical injuries than females.

7. Chemical agentsChemical agents
• AlkalicAlkalic
• AcidicAcidic

8. Alkali agents :
• Ammonia, lye ,potassium hydroxide, magnesium
hydroxide, and lime.
• Ammonia and lye (NaOH) tend to produce the most
serious injuries.
• Magnesium hydroxide found in fireworks may
combine with thermal injury to produce a particularly
devastating injury.
• Lime(CaOH2) particularly in the form of plaster, is the
most commonly encountered alkali injury; fortunately, it
tends to cause less severe injury.

9. Acidic agents
• Sulfuric, sulfurous, hydrofluoric, nitrous,
acetic, chromic,and hydrochloric acids.
• Sulfuric acid injury is the most commonly
seen, usually after battery explosions.
• The most severe acid injuries are
associated with hydrofluoric acid.

10. Interaction of chemical agent toInteraction of chemical agent to
corneal tissue.corneal tissue.
• The severity of this injury is related toThe severity of this injury is related to
type, volume, concentration, duration oftype, volume, concentration, duration of
exposure, and degree of penetration ofexposure, and degree of penetration of
the chemical .the chemical .
• The mechanism of injury differs slightlyThe mechanism of injury differs slightly
between acids and alkali.between acids and alkali.

11. Acid injuryAcid injury
• Acids dissociate intoAcids dissociate into hydrogen ionshydrogen ions andand
anionsanions in the cornea, e.g.: HCl= Hin the cornea, e.g.: HCl= H++
+Cl-+Cl-
• TheThe hydrogen moleculehydrogen molecule damages thedamages the
ocular surface byocular surface by altering the pHaltering the pH, while the, while the
anionanion causescauses protein denaturationprotein denaturation,,
precipitation, and coagulationprecipitation, and coagulation ..
• Protein coagulation generally preventsProtein coagulation generally prevents
deeper penetration of acids.deeper penetration of acids.

12. Hydrofluoric acidHydrofluoric acid is anis an
exceptionexception
• ItIt behaves like an alkaline substancebehaves like an alkaline substance
because the fluoride ion has betterbecause the fluoride ion has better
penetrance through the stroma than mostpenetrance through the stroma than most
acids, leading to more extensive anterioracids, leading to more extensive anterior
segment disruption.segment disruption.

13. Alkali injuryAlkali injury
• Alkaline substances dissociate into aAlkaline substances dissociate into a hydroxylhydroxyl
ionion and aand a cationcation in the ocular surface.in the ocular surface.
e.g.: NaOH= Nae.g.: NaOH= Na++
+ OH-+ OH-
• TheThe hydroxyl ion saponifies cell membrane fattyhydroxyl ion saponifies cell membrane fatty
acidsacids, while the, while the cationcation interacts with stromalinteracts with stromal
collagen and glycosaminoglycans.collagen and glycosaminoglycans.
• This interaction facilitatesThis interaction facilitates deeper penetrationdeeper penetration
into and through the cornea and into the anteriorinto and through the cornea and into the anterior
segment.segment.

14. Classification of chemical injuriesClassification of chemical injuries
• Hughes classification.Hughes classification.
• Modified Hughes classification.Modified Hughes classification.
• Roper Hall classification.Roper Hall classification.
• Duas clasification.Duas clasification.

15. Hughes classificationHughes classification
MildMild Erosion of corneal epithelium, faint hazinessErosion of corneal epithelium, faint haziness
of cornea, no ischemic necrosis ofof cornea, no ischemic necrosis of
conjunctiva or sclera.conjunctiva or sclera.
Moderat-Moderat-
-ely-ely
severesevere
Corneal opacity blurs iris details, mildCorneal opacity blurs iris details, mild
ischemic necrosis of conjunctiva or sclera.ischemic necrosis of conjunctiva or sclera.
VeryVery
severesevere
Blurring of pupillary outline, significantBlurring of pupillary outline, significant
ischemic necrosis of conjunctiva or sclera.ischemic necrosis of conjunctiva or sclera.

16. The Modified Hughes classification
• A grade I injury involves little or no loss of
limbal stem cells and presents with little or
no evidence of ischemia.
• A grade II injury involves subtotal loss of
limbal stemcells and presents with
ischemia of less than one-half of the
limbus.

17. The Modified Hughes classification
• A grade III injury involves loss of>1/2 to
total limbal stem cells with preservation of
the proximal conjunctival epithelium.
• A grade IV injury involves total limbal
stem-cell loss as well as loss of the
proximal conjunctival epithelium and
presents with extensive damage to the
entire anterior segment.

18. Roper hall classificationRoper hall classification
GradeGrade PrognosisPrognosis LimbalLimbal
ischemiaischemia
CornealCorneal
involvementinvolvement
11 GoodGood NoneNone EpithelialEpithelial
damage.damage.
22 GoodGood <1/3<1/3 Haze but irisHaze but iris
details aredetails are
visible.visible.
33 GuardedGuarded 1/3-1/21/3-1/2 Total epithelialTotal epithelial
loss with hazeloss with haze
that obscuresthat obscures
iris details.iris details.
44 PoorPoor >1/2>1/2 Cornea opaqueCornea opaque
with iris pupilwith iris pupil

19. Why new classification?Why new classification?
• The successes and failures reported forThe successes and failures reported for
ocular surface reconstruction proceduresocular surface reconstruction procedures
varyvary from centre to centrefrom centre to centre even for theeven for the
same grade of burns .same grade of burns .
• This difference is largely aThis difference is largely a reflection onreflection on
the inadequacythe inadequacy of the presentof the present
classification system. (Roper Hallclassification system. (Roper Hall
classification)classification)

20. • Suppose for grade IV burns, In the Roper-HallSuppose for grade IV burns, In the Roper-Hall
classification grade IV implies betweenclassification grade IV implies between 50%–50%–
100% limbal ischaemia100% limbal ischaemia and is equated with aand is equated with a
poor prognosispoor prognosis..
• However, with present management strategies,However, with present management strategies,
an eye withan eye with 50% or even 75% limbal ischaemia50% or even 75% limbal ischaemia
can expect a good to fair outcomecan expect a good to fair outcome, whereas an, whereas an
eye witheye with 100% ischaemia100% ischaemia is very likely to have ais very likely to have a
poor outcome.poor outcome.

21. Duas clasificationDuas clasification
GradeGrade PrognosisPrognosis Clinical findingsClinical findings
limbal involvementlimbal involvement
ConjunctivalConjunctival
involvementinvolvement
AnalogueAnalogue
scalescale
11 V. goodV. good 0 clock hours of0 clock hours of
limbal involvementlimbal involvement
0%0% 0/0%0/0%
22 GoodGood 3 clock hours of3 clock hours of
limbal involvementlimbal involvement
30%30% 0.1–3/0.1–3/
1–29.9%1–29.9%
33 GoodGood >3–6 clock hours>3–6 clock hours
of limbalof limbal
involvementinvolvement
>30–50%>30–50% 3.1–6/3.1–6/
31–50%31–50%
44 Good to guardedGood to guarded >6–9 clock hours>6–9 clock hours
of limbalof limbal
involvementinvolvement
>50–75%>50–75% 6.1–9/6.1–9/
51–75%51–75%
55 Guarded to poorGuarded to poor >9–<12 clock>9–<12 clock
hours of limbalhours of limbal
involvementinvolvement
>75–<100%>75–<100% 9.1–11.9/9.1–11.9/
75.1–99.9%75.1–99.9%
66 Very poorVery poor Total limbus (12Total limbus (12
clock hours)clock hours)
Total conjunctivaTotal conjunctiva
(100%) involved(100%) involved
12/12/
100%100%

22. • The analogue scale records accurately theThe analogue scale records accurately the
limbal involvement in clock hours of affectedlimbal involvement in clock hours of affected
limbus/percentage of conjunctival involvement.limbus/percentage of conjunctival involvement.
• While calculating percentage of conjunctivalWhile calculating percentage of conjunctival
involvement,involvement, only involvement of bulbaronly involvement of bulbar
conjunctivaconjunctiva, up to and including the conjunctival, up to and including the conjunctival
fornices is considered.fornices is considered.
• The termThe term “limbal involvement“limbal involvement” is preferred over” is preferred over
“limbal ischaemia“limbal ischaemia” because” because ttotal loss of limbalotal loss of limbal
epithelium (including the stem cells) can occurepithelium (including the stem cells) can occur
despite little ischaemia but has potentially thedespite little ischaemia but has potentially the
same consequences.same consequences.

23. • Although limbal ischaemia is usuallyAlthough limbal ischaemia is usually
associated with loss of limbal stem cells,associated with loss of limbal stem cells,
this is not always the casethis is not always the case ..
• Transient ischaemia, or ischaemiaTransient ischaemia, or ischaemia
occurring soon after the injury butoccurring soon after the injury but
recovering in the ensuing days, may allowrecovering in the ensuing days, may allow
limbal stem cells to survive, recover orlimbal stem cells to survive, recover or
repopulate the affected sector.repopulate the affected sector.

24. Grade 1 (duas classification)Grade 1 (duas classification)
• No limbal andNo limbal and
conjunctivalconjunctival
involvementinvolvement

25. Grade 3 (4.5/30%) ocular surfaceGrade 3 (4.5/30%) ocular surface
burn .burn .
Four and a half clock hours ofFour and a half clock hours of
limbus involvementlimbus involvement
with 30%with 30% conjunctivalconjunctival
involvement .involvement .

26. Grade 6 (12/100%) ocular surfaceGrade 6 (12/100%) ocular surface
burn .burn .
 The entire limbus and theThe entire limbus and the
entire conjunctiva are involved.entire conjunctiva are involved.

27. PathophysilogyPathophysilogy
• Acute stage (immidiate to 1 week)Acute stage (immidiate to 1 week) ::
depending on degree of chemical penetration,depending on degree of chemical penetration,
corneal and conjunctival epithelium, keratocytes,corneal and conjunctival epithelium, keratocytes,
corneal nerves, endothelium, iris ,ciliary body,corneal nerves, endothelium, iris ,ciliary body,
lens epithelium suffer losses to some degree.lens epithelium suffer losses to some degree.
• IOP elevationIOP elevation : bimodal: bimodal
Initial peakInitial peak: compression of globe d/t shortening: compression of globe d/t shortening
of collgen fibers.of collgen fibers.
Second peak:Second peak: increased EVP, TM damage, TMincreased EVP, TM damage, TM
obstruction by inflammatory cells.obstruction by inflammatory cells.

28. • Corneal cloudingCorneal clouding: d/t stromal oedema and: d/t stromal oedema and
changes in proteoglycans.changes in proteoglycans.
• InfiltrationInfiltration of ocular structures by PMNs,of ocular structures by PMNs,
monocytes, etc.monocytes, etc.

29. Early repair phase (1 to 3 weeks)Early repair phase (1 to 3 weeks)
• InflammationInflammation parallels the epithelial regeneration.parallels the epithelial regeneration.
• Conjunctival and corneal epitheliumConjunctival and corneal epithelium begins tobegins to
regenerate.regenerate.
• Corneal opacities begin to clearCorneal opacities begin to clear, they clear completely, they clear completely
during this period in mild to moderate injuries.during this period in mild to moderate injuries.
• Invasion of fibroblasts andInvasion of fibroblasts and synthesis of new collagen ,synthesis of new collagen ,
GAGGAG reach a peak by 14 days after injury.reach a peak by 14 days after injury.
• It is during this stage thatIt is during this stage that corneal ulcerationcorneal ulceration tends totends to
occur.occur.

30. Late repair phaseLate repair phase
• Corneal vascularizationCorneal vascularization in more severein more severe
corneal injuries.corneal injuries.
• Tear film abnormalityTear film abnormality::
1)aqueous deficiency1)aqueous deficiency :d/t damage to:d/t damage to
accessory lacrimal glands and scarring ofaccessory lacrimal glands and scarring of
ductule opening of major lacrimal gland.ductule opening of major lacrimal gland.
2)Mucin deficiency2)Mucin deficiency: d/t damge to goblet: d/t damge to goblet
cells.cells.

31. • Permanent loss of corneal innervationPermanent loss of corneal innervation: resulting: resulting
in neurotrophic keratitis.in neurotrophic keratitis.
• IOPIOP
• hypotonyhypotony d/t severe damage to cilliary bodyd/t severe damage to cilliary body
• GlaucomaGlaucoma d/t damage to outflow channels: TMd/t damage to outflow channels: TM
scarring, extensive PAS.scarring, extensive PAS.
• SymblepharonSymblepharon :proportional to extent of:proportional to extent of
conjunctival necrosis.conjunctival necrosis.

32. • Three main pathophysiologic mechanisms
are target for treatment.
• (1) Regeneration of ocular surface
epithelium and its state of differentiation.
(2) Stromal matrix remodeling,including
repair and degradation.
(3) Inflammation.

33. EPITHELIAL INJURY, REPAIR,
AND
DIFFERENTIATION
• Both conjunctival epithelium and limbal stem-
cell populations may resurface the chemically
injured corneal epithelium.
• Conjunctiva-derived epithelium never fully
expresses corneal epithelial phenotypic features.
• Reestablishment of a phenotypically normal
corneal epithelial surface with limbal stem cell-
derived cell populations is the first major
principle in the therapeutic management.

34. CORNEAL STROMAL MATRIX
INJURY,
REPAIR, AND ULCERATION
• Matrix metalloproteinases (MMP), are responsible for the
initial rate-limiting cleavage of collagen molecules.
• Excessive degradation of the matrix by MMP–1 and
MMP–8, relative to type I collagen synthesis, may result
in enzymatic degradation of the corneal stroma, a
process referred to as sterile corneal ulceration.
• Exploitation of known pharmacologic intervention,which
helps shift the balance toward repair, rather than
ulceration, is the second major principle in the
management of severe chemical injuries.

35. INFLAMMATION
• The association of inflammatory cell infiltration
(especially with polymorphonuclear leukocytes)
into the corneal stroma with sterile corneal
ulceration is well documented.
• Persistent inflammation may delay
reepithelialization and perpetuate continued
recruitment of additional inflammatory cells.
• Rigorous control of inflammation is the third
major principle in the therapeutic management
of severe chemical injuries.

36. CLINCAL COURSE AND
EVALUATION
• McCulley has divided the clinical course of
chemical injuries into four distinct
pathophysiologic and clinical phases.
• 1.Immediate
2.Acute (days 0–7)
3.Early repair (days 7–21)
4.Late repair (day 21 to several months
later) phases.

37. IMMEDIATE PHASE
• The extent of surface involvement can be
determined by the size of the corneal and
conjunctival epithelial defects.

38. • The depth of corneal and intraocular
penetration can be estimated by
evaluating corneal clarity, intraocular
inflammation, intraocular pressure,and
lens clarity.

39. • The depth of ocular surface penetration,
and possible limbal stem-cell damage, can
be evaluated indirectly by assessment of
vascular ischemia and necrosis of limbal
and bulbar conjunctiva.

40. ACUTE PHASE
• During the first week, important parameters that
should be monitored include evidence of
reepithelialization ,intraocular pressure, and
progressive ocular inflammation.
• Grade I injuries tend to heal.
• Slow but progressive reepithelialization in grade
II injuries.
• Grade III and IV injuries show no
reepithelialization.

41. EARLY REPAIR PHASE
• During the early repair phase, epithelial
migration continues in less severe injury
(grade II) but remains delayed in more
severe injuries (grades III and IV).
• In severe chemical injuries, a second
wave of inflammatory cell infiltration
begins after 7 days and continues to
progress over the next several weeks.

42. LATE REPAIR PHASE
• Corneal inflammation,collagen synthesis,
and collagenase activity are peaking.
• A type I healing pattern (normal epithelial
recovery)corresponds to a grade I limbal
stem-cell injury in that restoration of an
intact and phenotypically normal corneal
epithelial surface has occurred by this
stage.

43. • A type II healing pattern (delayed
differentiation) corresponds to a grade II
limbal stem-cell injury. Sectorial corneal
epithelial defect in the quadrant
corresponding to limbal stem-cell loss.

44. • A type III healing pattern (fibrovascular
pannus) corresponds to a grade IIIinjury:
conjunctivalization of the ocular surface,
and the ultimate outcome is a tectonically
stable but scarred and vascularized
cornea.

45. • A type IVhealing pattern (sterile corneal
ulceration) corresponds to a grade IV
injury in which there has been complete
loss of limbal stem cells and proximal
conjunctival epithelium with ischemic
necrosis.
• Sterile corneal ulceration

46. TreatmentTreatment
• Medical therapyMedical therapy
• Surgical therapySurgical therapy

47. MEDICAL THERAPY
• Management of the severely chemically injured
eye must be directed toward:
• Promoting ocular surface epithelial recovery
with proper phenotypic transdifferentiation,
• Augmenting corneal repair by supporting
keratocyte collagen productionand minimizing
ulceration related to collagenase activity, and
• Controlling inflammation.

48. Irrigation
• Early attempts at irrigation by the patient and
coworkers usually are inadequate, permitting
significant penetration of the chemical agent.
• Copious irrigation with any nontoxic irrigating
solution must be immediately initiated on
presentation, irrespective of the prior history of
irrigation.
• Irrigation for a minimum of 30 min and checking
the pH of tears for evidence of neutrality is
recommended.

49. • Failure to achieve neutrality often is
evidence of a retained reservoir of
chemical in the eye.
• This is particularly true in plaster injuries,
in which particles embedded in the upper
tarsal conjunctiva can provide continued
slow release of alkali into the tear film.
• Using topical anesthesia, all particles
should be removed with fine forceps or by
scraping with a disposable scalpel (e.g.,
Bard–Parker No. 15 blade).

50. Débridement
• Débridement of necrotic corneal epithelium is
necessary to allow proper reepithelialization,
irrespective of the severity of the injury.
• It is important to débride necrotic conjunctival
tissue because this tissue has been shown to be
a nidus of continued inflammation from retained
caustic materials.

51. PROMOTE EPITHELIAL WOUND
HEALING
AND DIFFERENTIATION
• The recovery of an intact and
phenotypically normal corneal epithelium
is the rate-limiting determinant of
prognosis of a chemical injury.
• Initially, aggressive medical therapy is
indicated to facilitate reepithelialization.

52. Tear Substitutes
• The use of topical Tear Substitutes may be
useful in facilitating corneal epithelial migration
ingrade I and II injuries and in minimizing
conjunctival scarring and symblepharon
formation after grade III and IV injuries.
• After reepithelialization, frequent administration
of unpreserved tear substitutes and
administration of ointments at bedtimemay be
necessary to benefit persistent keratopathy and
recurrent epithelial erosions.

53. Occlusive therapy
• Although there is a theoretical advantage to
protecting the migrating epithelium from the
‘windshield-wiper’ effect of the eyelids, occlusive
therapy (patching, taping) is of little use in the
acute care of the chemically injured eye.
• If epithelial defects persist into the early and late
repair phases, the cause usually is persistent
inflammation or limbal stem-cell deficiency, both
of which are unresponsive to occlusive therapy.

54. Hydrophilic Contact Lens
• May facilitate corneal epithelial
regeneration and prevents symblepheron
formation.
• Lens with greatest oxygen permeability
should be preferred.

55. SUPPORT REPAIR AND MINIMIZE
ULCERATION
• Ascorbate
• It is a cofactor in the rate-limiting step of collagen formation.
• Damage to the cilliary body epithelium by intraocular chemical
injury results in decreased secretion of ascorbate and a reduction in
its concentration in the anterior chamber.
• Both topical and systemic ascorbate have been shown to decrease
the incidence of sterile corneal ulceration after chemical injury.
• Topical application is superior to systemic supplementation.

56. Collagenase Inhibitors
• Tetracycline derivatives are efficacious in
reducing collagenase activity.
• It is due to chelation of zinc at the active
site of the collagenase enyzme.
• Doxycycline is the most potent tetracycline
collagenase inhibitor.

57. CONTROL
INFLAMMATION
• Corticosteroids:
• Corticosteroids traditionally have been the
mainstay of therapy for the reduction of tissue
injury related to acute inflammation.
• Corticosteroids have no adverse effect on the
rate of epithelial wound healing.( in the setting of
acute inflammation)
• By decreasing inflammatory cell infiltration, they
may facilitate migration indirectly by partially
ameliorating inflammation-induced delays in
corneal epithelial migration.

58. • Corticosteroids do interfere with stromal repair
by impairing both keratocyte migration and
collagen synthesis.
• Fortunately, the deleterious effects of
corticosteroids do not become apparent until the
early repair phase.
• The key to successful corticosteroid use is to
maximize the antiinflammatory effect during the
‘window of opportunity’ in the first 7–10 days,
when there is little risk associated with
corticosteroid use.

59. • Late repair phase corticosteroid-related
complications are more likely to occur.
• Therapy can be modified by tapering
corticosteroids by substituting
progestational steroids nonsteroidal
antiinflammatory drugs (NSAIDs).

60. Progestational Steroids
• Progestational steroids have less
antiinflammatory potency than do
corticosteroids but have only a minimal
effect on stromal repair and collagen
synthesis.
• Medroxyprogesterone 1% to inhibit
collagenase and reduce ulceration after
chemical injury.

61. • Progestational steroids may be substituted
for corticosteroids after 10–14 days, when
suppression of inflammation still is
required but interference with stromal
repair is undesirable.

62. NSAIDs
• NSAIDs may prove to be an effective
additive for corticosteroids in the first week
and a substitute or additive for
progestational steroids after the first week.

63. Citrate
• Citrate is a calcium chelator that
decreases the membrane and intracellular
levels of calcium, resulting in impaired
chemotaxis, phagocytosis, and release of
lysosomal enzymes of polymorphonuclear
leukocytes.
• It significantly reduces the incidence of
corneal ulceration.

64. SURGICAL THERAPY
• CONJUNCTIVAL AND TENON’S
ADVANCEMENT (TENOPLASTY)
• The use of conjunctival and Tenon’s
advancement, or tenoplasty, is based on the
principle of using vital connective tissue within
the orbit to reestablish limbal vascularity and to
facilitate corneal reepithelialization with
conjunctival epithelium.
• This technique is recommended to facilitate
initial stabilization of a grade IV injury.

65. AMNIOTIC MEMBRANE
TRANSPLANTATION
• AM Action Mechanisms
• Provides a new basement membrane
• Provides a new stroma that exerts
Antiinflammatory action
Antiscarring action
Antiangiogenic action

66. • It consists of an avascular stromal matrix, a thick
basement membrane, and an epithelial
monolayer.
• When used with the basement membrane
oriented downward, the amniotic membrane acts
like a biologic bandage contact lens or an ‘onlay’
(patch) graft, promoting epithelialization beneath
the membrane.

67. • When used with basement membrane
oriented upward it acts like an ‘inlay’ graft,
which promotes epithelialization over its
surface.
• Irrespective of the transplantation
technique, amniotic tissue facilitate
reepithelialization if complete or partial
limbalstem-cell function is present.

68. • In cases of incomplete limbal stem-cell loss, it
may be effective in the treatment of persistent
epithelial defects, recurrent epithelial erosions,
and persistent epitheliopathy, and in the
reduction of chronic inflammation.
• In cases of complete limbal stem-cell function, it
may be used in conjunction with limbal stem-cell
transplantation.

69. LIMBAL STEM-CELL
TRANSPLANTATION
• This technique is the best method of
reestablishing a phenotypically correct corneal
epithelial surface early in the clinical course of a
grade III or IV injury.
• Conjunctival limbal autograft transplantation
(CLAU):
• In unilateral cases of chemical injury or
asymmetric chemical injuries.
• Is usually performed by harvesting contralateral
limbal stem cells from the uninjured or less
injured fellow eye.

70. • In severe bilateral injuries, limbal allograft
transplantation from a living relative or a
cadaver donor are the only viable options.
• Living-related conjunctival limbal allograft
transplantation (lr-CLAG):the limbal stem
cells are harvested from a close relative
and transferred to the injured eye.

71. • Keratolimbal allograft transplantation (KLAT)
• It is a technique for transferring limbal stem cells
from a donor cadaver to treat severe bilateral
injuries.
• Ex vivo expansion of limbal stem cells:
• This procedure involves the dissection of a small
piece of donor limbal tissue, growth and
expansion of viable limbal stem cells in culture,
and transplantation of the epithelial sheet to the
recipient eye.

73. MUCOSAL MEMBRANE
TRANSPLANTATION
• Mechanical abnormalities of the bulbar
and palpebral conjunctiva related to
progressive scarring include restriction of
extraocular movement, fornix
foreshortening and obliteration,
symblepharon formation, incomplete lid
closure, cicatricial entropion, trichiasis,
and lid margin keratinization.

74. • In bilateral cases, mucosal membrane
grafts are used to reconstruct the fornix
and restore normal lid–globe relations.
• Such grafts do not restore the corneal
epithelial functions.
• Harvesting of mucosal grafts from nasal
mucosa may improve impaired goblet cell
function of the conjunctiva.

75. PENETRATING
KERATOPLASTY
• An optical penetrating keratoplasty may be
attempted after appropriate rehabilitation of the
ocular surface has been achieved.
• Performing limbal stem-cell transplantation prior
to penetrating keratoplasty or doing the
procedures simultaneously in order to facilitate
more rapid visual rehabilitation.

76. KERATOPROSTHESIS
• Keratoprosthesis may be useful in
bilateral, severe chemical injury in which
the prognosis is hopeless for penetrating
keratoplasty because of irreparable
damage to the ocular surface.
• Improved keratoprosthesis design and
better postoperative management now
offer an improved prognosis.

78. SPECIFIC THERAPY
• Acute Phase
1. Topical corticosteroids every 1–2 h.
2. Topical sodium ascorbate 10% every 2 h.
3. Topical sodium citrate 10% every 2 h.
4. Topical tetracycline 1% ointment four times a day.
5. Topical cycloplegics as needed.
6. Topical antiglaucoma medications as needed.
7. Systemic sodium ascorbate 2 g orally four times a day.
8. Systemic doxycycline 100 mg orally twice a day.
9. Consider amniotic membrane transplantation. (grade II
and III)
10. Consider conjunctival and Tenon’s advancement.
(grade IV)

79. • Early Repair Phase
1. Discontinue or taper (with close observation)
topical corticosteroids.
2. Begin progestational steroids (Provera 1%),
NSAIDs, or both, topically every 1-2 hr.
3.Continue topical and systemic sodium ascorbate.
4. Continue topical sodium citrate.
5. Continue topical tetracycline and systemic
doxycycline.

80. • Late Repair Phase
1. Taper medical therapy after reepithelialization is
complete(grade I or II).
2. Limbal stem-cell transplantation +/– amniotic
membrane transplantation (for grade III or IV
injuries).
3. Tectonic procedures (tissue adhesive, small- or
largediameter keratoplasty), if necessary.

81. Late Rehabilitation
1. Ocular surface reconstruction (amniotic
membrane transplantation, conjunctival
transplantation, mucous membrane
transplantation).
2. Limbal stem-cell transplantation.
3. Penetrating keratoplasty.
4. Keratoprosthesis.

82. BEWARE OF !!!BEWARE OF !!!