chemical injury to eye...acute emergency

1. CHEMICAL INJURIES
SIVATEJA CHALLA

2. • INTRODUCTION
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOGENESIS
• CLASSIFICATION/GRADING
• CLINICAL COURSE
• CLINICAL FEATURES
• MANAGEMENT

3. CHEMICAL INJURIES
• One of the true ophthalmic emergencies
• Often result in significant ocular morbidity and generally
strike young adults in the prime of life.
• Alkali injuries are more common and can be more
deleterious

4. EPIDEMIOLOGY
• 2/3rd in young males.
• 2/3rd at Workplace vs home
• 2/3rd by Alkali vs acid
• 2/3rd are minor (gr. I & II) injuries
• In India common d/t fire cracker injuries,lime or after
accidental injury with holi colours

5. ETIOLOGY
• Alkalic agents
• Acidic agents

6. COMMON ALKALI SUBSTANCE
at homeCompound
Common
sources
Comments
Ammonia [NH3] Fertilizers NH4OH fumes
Refrigerants Very rapid penetration
Cleaning agents (7%
solution)
Lye [NaOH] Drain cleaners
Penetrates almost as rapidly
as ammonia
Potassium
hydroxide [KOH]
Caustic potash Severity similar to that of lye
Magnesium
hydroxide
[Mg(OH)2]
Sparklers
Produces combined thermal
and alkali injury
Lime [Ca(OH)2] Plaster
Most common cause in
workplace
Mortar Poor penetration
Cement
Toxicity increased by retained
particulate matter
Whitewash

7. COMMON ACID SUBSTANCE
home
Acid Strength Use
Sulfuric (H2SO4) Strong
Car batteries, fertilizer, making other
acids, explosives, dyes, refining
petroleum
Nitric (HNO3) Strong
Fertilizers, explosives, rocket
propellant, production of nylon
Chromic
(H2CrO4)
Strong
An intermediate in electroplating,
ceramic glazes, wood preservation
Hydrofluoric
(HF)
Weak, but
most reactive
anion
Etching glass, semiconductor
production, rust remover

8. PATHOPHYSIOLOGY
• 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.

9. 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.

10. 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

11. CLASSIFICATION OF CHEMICAL
INJURIES
• Hughes classification.
• Modified Hughes/Roper Hall classification.
• Duas clasification.

12. Hughes classification
• Mild
– Erosion of corneal epithelium.
– Faint haziness of cornea.
– No ischemic necrosis of conjunctiva or sclera
• Moderately severe.
– Corneal opacity blurring iris details.
– Minimal ischemic necrosis of conjunctiva and
sclera
• Very severe
– Blurring of pupillary outline
– Blanching of conjunctival and scleral vessels
Hughes WF Jr: Alkali burns of the eye. I. Review of the literature and summary of present
knowledge. Arch Ophthalmol 35:423, 1946
Hughes WF Jr: Alkali burns of the eye. II. Clinical and pathological course. Arch Ophthalmol 36:189,
1946

13. • Roper-Hall/ modified Hughes classification
• Degree of corneal involvement
• Limbal ischemia.
• Dua classification
• Limbal involvement (in clock hours)
• Percentage of conjunctival involvement.
• In a randomized controlled trial of acute burns, the Dua
classification was found to be superior to the Roper-Hall
in predicting outcome in severe burns. However, both
classification schemes are commonly employed in daily
practice.

14. Roper Hall classification.
Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc UK,
1965;85:631–53.

15. DUAS CLASSIFICATIONburns
Gr Prognosis Clinical findings(clock
hrs of limbal involvement
Conjunctival
involvelment
Analogue
scale
I Very good 0 clock hours 0% 0.0%
II Good ⩽3 clock hours ⩽30% 0.1-3/1-30%
III Good >3–6 clock hours >30–50% 3.1-6/31-50%
IV Good to guarded >6–9 clock hours >50–75% 6.1-9/51-755
V Guarded to poor >9–<12 Clock hours >75–<100% 9.1-11.9/75.1-
99.9%
VI Very poor 12 clock hours involved Total conjunctiva
(100%) involved
12/100%
A new classification of ocular surface burns: Harminder S Dua, Anthony J King,
Annie Joseph, Br J Ophthalmol 2001;85:1379–1383.

16. Dua’s classification

17. CLINICAL COURSE
Mc Culley four phases
• Immediate (day 0)
• Acute( day 0-day 7 )
• Early repair (day 7 – day 21)
• Late repair ( after 21 days )

18. Multiple events
• Epithelial regrowth and migration
• Collagen synthesis and degradation
• Activation and migration of keratocytes

19. PATHOPHYSIOLOGY OF OCULAR INJURES
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 19
1.Corneal Damage by severe chemical injuries occurs in the following order:

20. 20
2- Healing of the corneal epithelium and stroma as follows:
 THE EPITHELIUM
 Centripetal movement of cells from the peripheral cornea, limbus,
or conjunctiva is responsible for normal and posttraumatic
replacement of corneal epithelium.
 Only partial transdifferentiation of conjunctival epithelium to
corneal epithelium is possible but conjunctiva-derived epithelium
never fully expresses corneal epithelial phenotypic features.
 Limbal stem cells are the cells most qualified to restore the
functional competence of the corneal epithelial surface after injury

21. Damaged STROMAL COLLAGEN
 The maintenance and regeneration of the corneal stroma -
responsibility of the pluripotent cells- keratocyte.
 Keratocyte Function:
Phagocytosis of collagen fibrils
Synthesis and secretion of collagen glycosaminoglycan
ground substance, collagenase, and collagenase inhibitors.
Modulated by cytokines from the epithelium, inflammatory cells,
and other keratocytes.
21

22. ACUTE STAGE (IMMEDIATE TO 1 WEEK)
• In mild burns the corneal and conjunctival epithelium
have defects with sparing of limbal blood vessels
• In severe burns the epithelium is destroyed and there is
immediate limbal ischaemia due to damage to blood
vessels.

23. • Rise in intraocular pressure in a bimodal manner
• An initial peak is due to compression of the
globe as a result of hydration and longitudinal
shortening of collagen fibrils.
• The second peak due to impedence of aqueous
humor outflow

24. EARLY REPAIR STAGE (1-3WEEK)
• This stage is characterized by replacement of
destroyed cells and extracellular matrix.
GRADE 1 AND GRADE 2 BURNS GRADE 3 AND GRADE 4 BURNS
regeneration of epithelium regeneration of epithelium may not
start and progress
neovascularization of cornea limited
clearing of stroma stroma remains hazy
beginning of synthesis of collagen
glycosaminoglycans
endothelium replaced by a
retrocorneal membrane
In stage 3 and 4, corneal ulceration tends to occur.
Stromal ulceration is due to action of digestive
enzymes such as collagenase, metalloprotinase

25. LATE REPAIR STAGE AND SEQUELE
( 3 WEEKS AND LONGER )
• This stage is characterized by completion of
healing
• Corneal inflammation,collagen synthesis, and
collagenase activity are peaking.

26. TYPE
TYPE 1  Corresponds to gr 1 injury
 COMPLETE RE EPITHELIALIZATION occurs
 Corneal phenotypically normal
TYPE 2  Gr 2 injury
 Sectorial corneal epithelial defect in the quadrant
corresponding to LSCD
 Delayed epithelialization
 SUPERFICIAL VASCULAR PANNUS
HEALING PATTRENS

27. TYPE
TYPE 3  gr 3 injury
 No re epithelialisation,FIBROVASCULAR PANNUS formed
 Conjunctivalization of cornea occurs
 ultimate outcome is a tectonically stable but scarred and
vascularized cornea
TYPE 4  Gr 4 injurySTERILE ULCERATION
 No conj and corneal epithelium d/t complete limbal ischemia
and conj necrosis
 Sterile ulceration,AS necrosis, PAS, cataract, glaucoma,
hypotony and pthisis bulbi
HEALING PATTRENS

28. CLINICAL FEATURES
SYMPTOMS
- Pain
- Lacrimation
- Photophobia
- Blepharospasm
- Diminution of vision
SIGNS
- Eye lid edema,
- Chemosis,
- Corneal abrasions

29. Effects of Ocular Surface Burn

30. MANAGEMENT
 Treatment of chemical injuries to the eye requires medical and
surgical intervention, both acutely and in the long term, for maximal
visual rehabilitation.
 Common goals of management include the
following:
 Removing the offending agent
 Promoting ocular surface healing
 Controlling inflammation
 Support of reparative processes
 Prevention of complications

31. IMMEDIATE MANAGEMENT

32. ACUTE MANAGEMENT
MEDICAL MANAGEMENT
1.Copious irrigation with isotonic saline/clean liquid
2.Remove chemical completely from conjunctival surface,cornea and fornices
3.Topical corticosteroids prednisolone 1% 4-6 times in gr1-2
2nd hrly in gr3-4,hrly in gr 5-6
taper when epithelial healing occurs
stop if corneal thinning or melting seen
4.Topical citrate 10% 2nd hrly
5.Topical ascorbate 2nd hrly
6.Tab doxy 100mg bd for 2 wks
7.Moxifloxacin e/d qid
8.AGM if required
9.Cycloplegics –homatropine 2%qid
SURGICAL THERAPY
1.Debridement
2.Amniotic membrane transplantation
3.Tissue adhesives,tectonic keratoplasty

33. IRRIGATION
Copious irrigation should begin
immediately at the scene of the accident
with any non-toxic liquid which is
continued during rapid transport to a
medical care facility
These solutions, with their
varying osmolarities are:
>Normal saline solution
>Ringer's lactated solution
>any clean fluid
>water
90 minutes of external irrigation
shows 1.5 unit reduction of the
elevated pH.

34. • Irrigation for a minimum of 30 min and checking the pH
of tears for evidence neutrality is recommended.
• Initial PH testing should involve both eyes even if pt says
uniocular pain, C/L eye should not be neglected
• 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.

35. MEDICAL THERAPY
1.Control inflammation
Corticosteroids mainstay for infl control in
initial period
Corticosteroids have no adverse effect on
the rate of epithelial wound healing
interfere with stromal repair by impairing
both keratocyte migration and collagen
synthesis.
 the deleterious do not become apparent
until the early repair phase
The key to successful 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.

36. Progestational steroids
• If there is no ep healing and early signs of stromal
melting noted stop 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.
• 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.

37. 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.

38. 2.Promotion of epithelialization
 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.
 Role of fibronectin,epidermal growth factor,retinoic
acid,sodium hyaluronate needs to be established

39. 3. SUPPORT REPAIR AND MINIMIZE ULCERATION
Ascorbate
• It is a cofactor in the RLS 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.

40. Tetracyclins
• 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
• Can be given 100mg bd for 2 wks

41. 4.Adjuvant therapy
a.broad spectrum antibiotic drops like moxy QID
b.If glaucoma,give tab acetazolamide BD
c.Cycloplegics like homatropine 2% QID

42. SURGICAL THERAPY
Debridement
• 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.
• The end point in removal of dead or necrotic tissue is
induction of bleeding especially in gr4-6 injuries

43. AMNIOTIC MEMBRANE TRANSPLANTATION
AM Action Mechanisms
• Provides a new basement membrane
• Provides a new stroma that exerts
Anti inflammatory action
Antiscarring action
Antiangiogenic action
It consists of an avascular stromal matrix
a thick basement memb
an epithelial monolayer.

44. • 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.
• 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.

45. 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.

46. TISSUE ADHESIVES
Can be done in cases of impending or frank perforation <
1mm in size
STEPS OF APPLICATION OF CYANOACRYLATE GLUE
1. Area surrounding the perforation is cleaned,any mucous necrotic
tissue surrounding 1-2 mm of epithelium is removed
2. Corneal surface is kept dry
3. If AC flat/iris prolapse,paracentesis Done and BSS is injected in to AC
4. cyano acrylate glue drawn in to 1ml syringe attached to 30g needle
5. Small amount glue placed directly on perforation site
6. Site of perforation is inspected for leak
7. BCL placed over the cornea,topical antibiotics instilled at the end
Can be left in place until it loosens spontaneously and reepitheliasiation
occurs

48. Tectonic keratoplasty
 Size of perforation large
 Difficult d/t corneal thinning,passage of sutures becomes
worse
 But helps in visual rehabilitation in later stages

49. CHRONIC CHEMICAL BURNS
MANAGEMENT
1.Surface stabilisation
2.Ocular surface transplantation
3.Keratoplasty

50. 1.SURFACE STABILISATION
A. Surgery of the lids to address entropion,ectropion,trichiasis
B. Management of persistent epithelial defect
1.frequent use of preservative free lubricants
2.use of preservative free antibiotics
3.Over night patching
4.autologous serum may be given 2nd hrly.umbilical cord serum has
better results
5.tarsorrhaphy if PED not healing on medical therapy
C.Symblepharon release with amniotic membrane
transplantation in some cases

51. 2.Ocular surface trasplantation
 Corneal transplantation alone is not sufficient as
functional epithelial stem cells cannot be supplemented
by corneal transplant alone
 Hence some form of stem cell transpalntation is required
to stabilise ocular surface

52. Proposed classification

53. Management of LSCD

54. CONJUNCTIVAL LIMBAL GRAFT
• Auto limbal transplantation
– donor fellow eye
– Unilateral LSD
• Allo limbal transplantation
– Live related donor
– Cadaveric donor
– Bilateral LSD

55. Autolimbal transplantation
• Partial removal of the limbus from the fellow eye
• Unilateral LSCD
• Less than four to six clock hours of limbal tissue and a
moderate amount of conjunctiva
• > 6 clock hours – Donor eye LSCD

56. Technique
DONOR EYE
• Conjunctival corneal
specimens
• Two explants – each 2
clock hrs
• Superior and inferior
• 150 micron thick
• 2 mm of conjunctiva
+1mm of limbus + 2mm
peripheral cornea
RECIPIENT EYE
• Recepient bed
• Same demention
• 100 micron depth
• Same clock hours
• Sutured with 10 nylon

57. Technique

58. Advantages
o Fresh tissue-more viable cells
o Technically easier
o No antigenic load
o No rejection
Disadvantages
o Risk of iatrogenic LSD in fellow eye

59. Allo limbal transplants
• Bilateral total ocular surface disease
• Living relatives are potential donors
• Cadaver donor - "fresh" eyes
• HLA-matched tissue is preferred
• High rate of immune reactions – rejection
• Immuno suppressants for 12 months

60. Keratolimbal allograft

61. • Cadaveric donor
• Technique is not routinely used
• Bilateral cases, unilateral cases unwilling
• Advantages
Readily available
360 coverage possible
Normal eye spared
• Disadvantages
Fresh tissue
Immediate sx preferred
Rejection more,immunosuppressives post op
Technically difficult

62. Cultured limbal stem cell transplantation
• Promising technique in limbal transplantation
• Procedure of Choice
• Stem cells cultured using a small amount of tissue
• Minimizes the damage to donor tissue
• Avoids risk donor eye LSD

63. • Incidence of rejection reduced
• Donor tissue - other healthy eye (autograft)
• donor material – live related individual (allograft)
• Ex-vivo expansion of limbal epithelial cells on amniotic
membrane

64. 1. 2*2 mm piece of conj epithelium with
1mm in to clear corneal stroma at limbus
dissected and excised
2. Transported to lab in HCE(human corneal
epithelium) medium
3. In lab donor limbal tissue shreded in to
small bits
4. 3*4 aminiotic membrane sheet is
deepithelialized and bits of limbal tissue
explanted over it with BM side up
5. Incubated at 37’ with 5% co2 and 95%
air
6. Culture completes when monolayer of
cells growing from small bits merge will
take 10-14 days

65. Simple limbal epithelial transpalntation

66. Cultivated oral mucosa epithelium
transplantation (COMET)
• In bilateral cases, mucosal membrane grafts are used
to reconstruct the fornix and restore normal lid–globe
relations.
• Since autologous no immunological rxn
• Disadvantage is they maintain original phenotype ,invite
vascularisation and provide poor visual outcome

67. CONCLUSIONS
• Unilateral cases – autologous cultured stem cell
transplantation good option
• Bilateral cases cultured limbal stemcells from live related
HLA matched donors better than Keratolimbal graft
• Limbal stem cell transplantation followed by PK/LKP
better than combined surgery

68. 3.keratoplasty
• Penetrating/lamellar
• Can be done simultaneously with LSCT
• Or 2 staged procedure,6 wks following
limbal transplant

69. Penetrating Keratoplasty
69
Removing the
affected
corneal button
measuring
7mm in
diameter.
After removal of
the corneal button.
An intraocular lens
can be seen
centrally.
Interrupted
corneal sutures
(10/0 nylon)
were used to
suture the donor
cornea to the
recipient's.
Clear graft after penetrating keratoplasty
utilizing and showing a continuous
(running) 24-bite suture.

70. KERATOPROSTHESIS

72. 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)

73. 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.

74. 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.

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

76. BEWARE OF !!!