This document summarizes the pathophysiology and management of chemical eye injuries. It discusses that chemical injuries can cause significant damage through alkali or acid exposure. Treatment involves immediate irrigation, debridement if needed, and aggressive medical therapy including corticosteroids, ascorbate, antibiotics and citrate to promote reepithelialization during the acute and early repair phases. More severe injuries may require surgical interventions like limbal stem cell transplantation or amniotic membrane transplantation depending on the degree of limbal involvement and prognosis.

1. Dr.Deepti Mujumdar
MBBS,MS Ophthalmology

2.  One of the true ophthalmic emergencies.
 Serious damage generally results from either strongly
basic (alkaline) compounds or acidic compounds.

3.  Chemical injuries are responsible for approximately 7%
of work-related eye injuries.
 > 60% -workplace accidents
 30% -occur at home
 10% are the result of an assault.
 MORBIDITY- Severe chemical injuries result in
significant visual and cosmetic disability.

4.  Chemical injuries can strike any population.
 However, most injuries occur in patients aged 16-45
years.
 Males are 3 times more likely to experience chemical
injuries than females.

5.  Ammonia, lye,potassium hydroxide, magnesium hydroxide,
and lime.
 Ammonia and lye (NaOH) tend to produce the most serious
injuries.
 Magnesium hydroxide found in fireworks.
 Lime(CaOH2) particularly in the form of plaster, is the most
commonly encountered alkali injury.

6.  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.

7.  The severity of the injury is related to
i. Type
ii. Volume
iii. Concentration
iv. Duration of exposure
v. Degree of penetration of the chemical .
 The mechanism of injury differs slightly between acids
and alkali.

8.  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.

9.  Alkaline substances dissociate into a
hydroxyl ion and a cation in the ocular
surface. eg.: 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 the cornea and into the
anterior segment.
 Necrosis of conjunctival blood vessel
causing:
 cornea appear as white as chalk and
opaque.

10.  Necrosis of the conjunctival and corneal epithelium
 Disruption and occlusion of the limbal vasculature.
 Loss of limbal stem cells
 Conjunctivilisation and vascularization of the
corneal surface
 Persistent corneal epithelial defects with sterile
corneal ulceration
 Perforation

11.  IOP elevation : bimodal
Initial peak: compression of globe due to shortening of collgen
fibres.
Second peak: TM damage, TM obstruction by inflammatory
cells.
 Corneal clouding: due to stromal oedema and changes in
proteoglycans.
 Other long term effects include ocular surface wetting
disorders, symblepharon formation and cicatricial entropion.
 Anterior chamber penetration results in iris and lens damage.
 Ciliary epithelial damage impairs secretion of ascorbate which
is required for collagen production and corneal repair.
 Hypotony and phthisis bulbi may ensue.
 Permanent loss of corneal innervation: resulting in
neurotrophic keratitis.

12. THE EPITHELIUM
 Centripetal movement of cells from the peripheral cornea, limbus, or
conjunctiva is responsible for normal and post-traumatic replacement of
corneal epithelium.
 Associated with delayed re-epithelialization, superficial and deep stromal
vascularization and poor epithelium-basement membrane adhesion.
 Limbal stem cells are the cells most qualified to restore the functional
competence of the corneal epithelial surface after injury.
STROMAL COLLAGEN
 The maintenance and regeneration of the corneal stroma -responsibility of
the pluripotent cells- keratocyte.
 Phagocytosis of collagen fibrils.
 Synthesis and secretion of collagen glycosaminoglycan ground
 substance, collagenase, and collagenase inhibitors.

13.  Degradation of the basement membrane collagen(initiated by
MMP–9 )
 Degradation of the corneal stromal matrix (by MMP–1 and
MMP–8
 Collagen type 1 synthesis peak point(at 14-21 days)
 Intervening period may show sterile corneal ulceration.

14.  Symptoms
 - Pain
 - Lacrimation
 - Photophobia
 - Blepharospasm
 - Diminution of vision
 Signs
 - Eye lid edema
 - Chemosis
 - Corneal abrasions

15.  Hughes classification.
 Modified Hughes classification.
 Roper Hall classification.
 Duas clasification.

16. Mild Erosion of corneal epithelium, faint haziness of
cornea, no ischemic necrosis of conjunctiva or
sclera.
Moderately
severe
Corneal opacity blurs iris details, mild ischemic
necrosis of conjunctiva or sclera.
Very severe Blurring of pupillary outline, significant ischemic
necrosis of conjunctiva or sclera.

17.  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 stem cells and
presents with ischemia of less than one-half of the limbus.
 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. Grade Prognosis Limbal ischemia Corneal involvement
1 Good None Epithelial damage.
2 Good <1/3 Haze but iris details are
visible.
3 Guarded 1/3-1/2 Total epithelial loss with
haze that obscures iris
details.
4 Poor >1/2 Cornea opaque with iris
pupil details obscured

19. Grade Prognosis Clinical findings
limbal involvement
Conjunctival
involvement
Analogue
scale
1 Very good 0 clock hours of
limbal involvement
0% 0/0%
2 Good 3 clock hours of
limbal involvement
30% 0.1–3/
1–29.9%
3 Good >3–6 clock hours of
limbal involvement
>30–50% 3.1–6/
31–50%
4 Good to guarded >6–9 clock hours of
limbal involvement
>50–75% 6.1–9/
51–75%
5 Guarded to poor >9–<12 clock hours
of limbal involvement
>75–<100% 9.1–11.9/
75.1–99.9%
6 Very poor Total limbus (12
clock hours) involved
Total conjunctiva
(100%) involved
12/
100%

20.  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.

21. Three main pathophysiologic mechanisms are target for
treatment.
 Regeneration of ocular surface epithelium and its state
of differentiation.
 Stromal matrix remodeling including repair and
degradation.
 Inflammation.

22.  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.

23.  The extent of surface involvement can
be determined by the size of the corneal
and conjunctival epithelial defects.
 The depth of corneal and intraocular
penetration can be estimated by
evaluating corneal clarity, intraocular
inflammation, intraocular pressure,and
lens clarity.
 possible limbal stem-cell damage, can be
evaluated indirectly by assessment of
vascular ischemia and necrosis of limbal
and bulbar conjunctiva.

24.  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.

25.  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, inflammatory cell infiltration
continues to progress over the next several weeks.

26.  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.
 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.

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

28.  Medical therapy
 Surgical therapy

29.  Copious irrigation with any nontoxic
irrigating solution must be immediately
initiated on presentation.
 Irrigation for a minimum of 30 min and
checking the pH of tears for evidence of
neutrality is recommended.
Debridement
 Of necrotic corneal epithelium is necessary
to allow proper reepithelialization,
irrespective of the severity of the injury.
Paracentesis

30.  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.

31.  The use of topical Tear Substitutes
(unpreserved) may be useful in facilitating
corneal epithelial migration minimizing
conjunctival scarring and symblepharon
formation.
 Administration of ointments at bed time
Topical antibiotics
Cycloplegics

32.  May facilitate corneal epithelial regeneration and prevents
symblepheron formation.
 Lens with greatest oxygen permeability should be preferred.

33. 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.
 Topical application is superior to systemic supplementation.
 Topical sodium ascorbate 10% is given 2 -hourly in addition to
a systemic dose of 2g q.i.d.

34.  Tetracycline derivatives are efficacious in reducing collagenase
activity.
Doxycycline 100mg bd
Tetracycline ointment QID
 Acetylcysteine 10% 6 times

35.  Corticosteroids:
 mainstay of therapy for the reduction of tissue injury related to acute
inflammation.
 Interfere with stromal repair by impairing both keratocyte migration
and collagen synthesis.
 maximize the anti-inflammatory effect during the ‘window of
opportunity’ in the first 7–10 days, when there is little risk associated
with corticosteroid use.
 Therapy can be modified by tapering corticosteroids & replaced by
nonsteroidal anti-inflammatory drugs (NSAIDs).
 Progestational Steroids - Medroxyprogesterone 1%

36.  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.
 Topical sodium citrate 10% given 2- hourly for about 10 days.
Control of IOP

37.  CONJUNCTIVAL AND TENON’S ADVANCEMENT (TENOPLASTY):
to re-establish limbal vascularity and to facilitate corneal re-
epithelialization
 LIMBAL STEM-CELL TRANSPLANTATION: Conjunctival limbal
autograft transplantation (CLAU)
 AMNIOTIC MEMBRANE TRANSPLANTATION
 MUCOSAL MEMBRANE TRANSPLANTATION
 PENETRATING KERATOPLASTY
 KERATOPROSTHESIS : osteo- odonto keratoprosthesis

38.  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)

39.  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.

40.  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.