All you need to know at Post-Graduate Level about Chemical Injuries.

1. Dr. Karan Bhatia
MBBS, DOMS, DNB, FCPRS
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2. Introduction
• True ophthalmic emergency
• Only ocular condition where history
taking and examination should be
delayed
B/L Chemical
Exposure
Devastating
effect
Complete
visual disability
2

3. Types of chemicals
Alkalies
Most dangerous
Rapid Penetration
Acid
Less severe than alkali
Do not penetrate into eye as
readily as alkaline substances
Exception  HFL acid burn
 ‘As dangerous as an alkali
burn’
Irritants
Neutral pH
More discomfort to eye rather
than actual damage
Most household detergents,
pepper spray
Can cause significant pain, but
usually does not affect vision
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4. Alkalies
Penetrate rapidly
(often in less than one minute)
Disruption of cells & Necrosis of tissue
Combine with cell membrane lipids,
mucopolysaccharides and to collagen
On Ocular Surface
Facilitates rapid penetration Deeper layers,
aqueous, vitreous
Saponify cell membranes & intercellular
bridges
Necrosis of conjunctival blood vessels  “Cooked fish eye” (Cornea – as white as chalk & opaque

5. Acids
Quickly denature proteins
in the corneal stroma
Form precipitates
Retard additional
penetration
• Coagulation effect
• Protein
precipitations at
epithelium level
Localized
damage
Physical
barrier
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6. Chemical Example
Sulfuric Acid Battery Acid, Industrial Cleaner
Acetic Acid Vinegar, Glacial Acetic Acid
Hydrochloric Acid Chemical Laboratories
Sulfurous Acid Bleach, Refrigerant, fruit and vegetable preservative
Hydrofluoric Acid Glass polishing, gasoline alkylation, silicone production
Ammonia Fertilizers, refrigerants
Lye Drain cleaner
Lime Plastic, mortar, cement, white wash
Potassium hydroxide Caustic potash
Magnesium hydroxide Sparklers, incendiary devices
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7. Severity of burn
Surface area
of contact
Depth of
penetration
Concentration
of substance
Time of
contact
Time of
interference
Degree of
limbal stem
cell injury
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8. Phase Day Recovery
Initial 0 • Clinical findings relate to severity of injury
• Graded according to degree of limbal, corneal and conjunctival involvement
Acute 0-7 • Epithelial regrowth begins to occur (if there is sufficient amount of undamaged limbal
stem cells)
• Rx – directed at encouraging growth while quelling inflammation
Early Repair 7-21 • Corneal/ conjunctival epithelium & keratocytes proliferate
• Mild injuries  complete re-epithelialization
• Severe injuries  persistent epithelial defects
• Activity of collagenase peaks by day 14-21, while collagen synthesis continues
• Rx – should attempt to maximize collagen synthesis while minimizing collagenase
activity
Late Repair >21 • Mild injuries (limbal stem population intact) Repair is completed
• Grade II injuries (focal stem cell loss)  Focal conjunctivalization of cornea
• More Severe injuries  Delayed re-epithelization of cornea  Repopulation by
conjunctival epithelium/ stromal ulceration  Permanent scarring
• Severe limbal damage (despite optimal management) – Eye cannot be salvaged
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9. Pathophysiology – Damage
Necrosis of the conjunctival & corneal epithelium
Disruption & occlusion of the limbal vasculature
Loss of limbal stem cells
Conjunctivalisation & vascularization of the corneal surface
Persistent corneal epithelial defects with sterile corneal
ulceration
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10. Other long term effects
• Ocular surface wetting disorders
• Symblepharon formation
• Cicatricial entropion
Anterior chamber penetration
• Iris damage
• Lens damage
Ciliary epithelial damage
• Impairs secretion of ascorbate 
Required for collagen production &
corneal repair
Hypotony & phthisis bulbi
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11. Pathophysiology
Centripetal movement of cells from the peripheral cornea, limbus, or conjunctiva  Responsible
for normal & posttraumatic replacement of corneal epithelium
Only partial trans-differentiation of conjunctival epithelium to corneal epithelium – possible
• But conjunctiva-derived epithelium never fully expresses corneal epithelial phenotypic features
Associated with delayed re-epithelialization, superficial & deep stromal vascularization, persistence
of goblet cells in the corneal epithelium & poor epithelium-basement membrane adhesion
Limbal stem cells  cells most qualified to restore the functional competence of the corneal
epithelial surface after injury
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Healing of corneal epithelium and stroma

12. Healing of damaged stromal collagen
Keratocytes
• Pluripotent cells
• Responsible for maintenance & regeneration of corneal stroma
• Phagocytosis of collagen fibrils
• Synthesis & secretion of collagen GAG ground substance, collagenase & collagenase inhibitors
• Modulated by cytokines from epithelium, inflammatory cells, & other keratocytes
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13. Degradation of the basement membrane
collagen
(initiated by MMP–9 )
Degradation of the corneal stromal matrix
(by MMP–1 and MMP–8(collagenase types)
Detected earliest at 9 hrs
Collagen type 1 synthesis peak point
(at 14-21 days)
Coincide with maximum MMP activity
Intervening period may show sterile corneal
ulceration
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14. Clinical Picture
Symptoms
• Pain
• Lacrimation
• Photophobia
• Blepharospasm
• Diminution of vision
Signs
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15. Effects of Ocular Surface Burn
Structure Immediate effect Delayed effect
Lid
Edema Cicatrical entropion
Dermatitis Cicatrical ectropion
Ulcer
Conjunctiva
Conjunctival injection Symblepharon
Ulcer Xerosis
Chemosis Pseudopterygium
Cornea
Edema Vascularized opacities
Ulcer Xerosis
Perforation
Uvea
Anterior Uveitis Iridocyclitis
Atrophic bulbi
IOP May increase Increased (conjunctival fibrosis)
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16. Classifications
Roper-Hall/ modified
Hughes
Degree of
corneal
involvement
Limbal
ischemia
Dua
Limbal
involvement
(in clock hours)
Percentage of
conjunctival
involvement
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In a randomized controlled trial of acute burns, Dua classification  superior to the Roper-Hall in predicting
outcome in severe burns
However, both classification schemes  commonly employed in daily practice

17. Roper Hall Classification
Grade Prognosis Limbal Ischaemia Corneal Involvement
I Good None Epithelial Damage
II Good <1/3 Haze
But Iris details visible
III Gaurded 1/3-1/2 Total Epithelial Loss
With haze that obscures Iris details
IV Poor >1/2 Cornea opaque
With Iris and pupil obscured
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18. Dua’s Classification
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Grade Prognosis Limbal involvement Conjunctival involvement Analogue scale
I Very good 0 CH 0% 0/0%
II Good ⩽3 CH ⩽30% 0.1–3/1–29.9%
III Good >3–6 CH >30–50% 3.1–6/31–50%
IV Good to guarded >6–9 CH >50–75% 6.1–9/51–75%
V Guarded to poor >9–<12 CH >75–<100% 9.1–11.9/75.1–99.9%
VI Very poor Total limbus (12 CH) involved Total conjunctiva (100%)
involved
12/100%

19. Management
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20. Goals of management
Removing Offending agent
Promoting ocular surface healing
Controlling inflammation
Preventing infection
Controlling IOP
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21. Immediate Management
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22. Immediate Management
Immediate copious irrigation of eye (every second counts) with
• Normal saline solution
• Ringer's lactate solution
• Normal saline with bicarbonate
• Balanced salt solution(BSS)
• Ideal solution not available  Plain Tap Water
Evert UL, LL  Irrigate
• Remove all solid particles from under lids
• After 5 to 10 minutes of irrigation , If litmus paper  available  Test pH of lower inside of
lid  Continue irrigation until pH is below or above a pH of 7.0.
• Litmus paper unavailable  irrigate for 20 min
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23. Morgans Lens
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24. History
Time of injury
Eyes rinsed or not, if yes- duration, solution, speed
Mechanism of injury
Type of chemical
Packaging of chemical available?
Eye protection used?
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25. Medical Management
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26. 1) Steroids
Reduce inflammation
Neutrophil infiltration
Impair stromal healing by reducing collagen synthesis & inhibiting fibroblast
migration
Must be tailed off after 7-10 days when sterile corneal ulceration is most likely to
occur
May be replaced by topical NSAIDS, which do not affect keratocyte function
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27. 2) Ascorbic Acid
Reverses a localized tissue scorbutic state
Promote synthesis of mature collagen by corneal
fibroblasts
Topical sodium ascorbate 10% is given 2 -hourly in
addition to a systemic dose of 2g QID
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28. 3) Citric Acid
Powerful inhibitor of neutrophil activity
Reduces the intensity of the inflammatory response
Chelation of extracellular calcium by citrate also appears to inhibit collagenase.
Topical sodium citrate 10% given 2 hourly for about 10 days.
Aim is to eliminate the second wave of phagocytes, which normally occurs 7 days after
the injury
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29. 4) Tetracyclines
Collagenase inhibitors
Inhibit neutrophil activity
Reduce ulceration
Tab. Doxycycline 100 mg BD
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30. Tear Substitutes
Topical antibiotics
Bandage Soft Contact Lens
Autologous Serum
• Fibronectin and epidermal growth factors
Retinoic Acid
• May promote goblet cell recovery and improve ocular surface function
• Transdifferentiation of the conjunctival epithelium to a corneal epithelial
phenotype.
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31. Grade I
Topical antibiotic ointment QID
Prednisolone acetate 1% QID
Preservative free artificial tears as needed
Cycloplegics
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32. Grade II
As for grade I
Prednisolone acetate 1%
• 1 hourly while awake for the first 7-10 days
• Tapering if the epithelium has not healed by day 10-14
• Epithelial defect persists after day 10  consider progestational steroids (1% medroxyprogesterone QID)
Long acting cycloplegics
• Atropine
Oral Vitamin C
• 2 grams four times a day
Doxycycline
• 100 mg BD (avoid in children)
Sodium ascorbate drops (10%) hourly while awake
Preservative free artificial tears as needed
Debridement of necrotic epithelium & application of tissue adhesive as needed
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33. Grade III
As for Grade II
Consider AMT
•Ideally be performed in the first week of injury
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Grade IV
As for Grade II/III
Early surgery  usually necessary
For significant necrosis  Tenonplasty  can help reestablish limbal vascularity
AMT – often necessary

34. Cyanoacrylate tissue adhesive
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35. IOP Control
• Oral Acetazolamide or Beta-
Blockers
• Initial therapy
• Late Recovery Phase – if IOP >30
mm of Hg
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36. Delayed Management
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
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37. 37

38. 38

39. Limbal stem cell transplantation
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40. 40
Penetrating Keratoplasty

41. Keratoprosthesis
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42. Prevention
• Education & training regarding prevention of chemical exposures
workplace
• Persons who may be exposed to chemicals in workplace  advised to
wear safety goggles
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43. • Thankyou
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