ocular chemical injuries

1. Chemical injuries

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

3. Epidemiology
Chemical injuries are responsible for approximately 7% of
work-related eye injuries .
More than 60% of chemical injuries occur in workplace
accidents, 30% occur at home, and 10% are the result of an
assault.

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

5. Age
Chemical injuries can strike any population.
However, most injuries occur in patients aged 16-45 years.

6. Sex
Males are 3 times more likely to experience chemical injuries
than females.

7. Chemical agents
Alkalic
 Acidic

8. Alkali agents :
Ammonia, potassium hydroxide, magnesium hydroxide, and lime.
Ammonia (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 to
corneal tissue.
The severity of this injury is related to type, volume,
concentration, duration of exposure, and degree of
penetration of the chemical .
The mechanism of injury differs slightly between acids and
alkali.

11. Acid injury
Acids dissociate into hydrogen ions and anions in the cornea,
e.g.: HCl= H+
+Cl-
The hydrogen molecule damages the ocular surface by
altering the pH, while the anion causes protein denaturation,
precipitation, and coagulation .
Protein coagulation generally prevents deeper penetration of
acids.

12. Hydrofluoric acid is an exception
It behaves like an alkaline substance because the fluoride ion
has better penetrance through the stroma than most acids,
leading to more extensive anterior segment disruption.

13. Alkali injury
Alkaline substances dissociate into a hydroxyl ion and a
cation in the ocular surface. e.g.: NaOH= Na+
+
OH-
The hydroxyl ion saponifies cell membrane fatty acids,
while the cation interacts with stromal collagen and
glycosaminoglycans.
 This interaction facilitates deeper penetration into and
through the cornea and into the anterior segment.

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

15. Hughes 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 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?
The successes and failures reported for ocular surface
reconstruction procedures vary from centre to centre even for
the same grade of burns .
This difference is largely a reflection on the inadequacy of the
present classification system. (Roper Hall classification)

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

21. Duas 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 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.
The term “limbal involvement” is preferred over “limbal
ischaemia” because total loss of limbal epithelium (including
the stem cells) can occur despite little ischaemia but has
potentially the same consequences.

23. 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.

24. Grade 1 (duas classification)
 No limbal and
conjunctival
involvement

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

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

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

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

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

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

31. Permanent loss of corneal innervation: resulting in
neurotrophic keratitis.
IOP
hypotony d/t severe damage to cilliary body
Glaucoma d/t damage to outflow channels: TM
scarring, extensive PAS.
Symblepharon :proportional to extent of 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 remodelling, 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. Treatment
Medical therapy
Surgical 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 !!!