chemical injury to eye by alkali, acids and irritants.
pathophysiology and management.
recent advances in management.
ITS A TRUE EMERGENCY IN OPHTHALMOLOGY
2. INTRODUCTION:
Chemical injury is one of the true ophthalmic
emergencies.
Chemical exposure to the external eye can result in
trauma ranging from mild irritation to severe
damage of the ocular surface and anterior segment
with permanent loss of vision.
3. EPIDEMIOLOGY
Chemical burns constitute 7.7% to 18% of all
ocular trauma.
2/3rd in young males
2/3rd by Alkali
60% of chemical injuries occur in workplace
accidents,30% occur at home, 10% are the result of
an assault.
20% of chemical injuries result in significant visual
and cosmetic disability.
Only 15% of patients with severe chemical injuries
achieve functional visual rehabilitation.
4. TYPES OF CHEMICALS
ALKALIES
• Most dangerous -
rapid penetration.
ACID
• Less severe than
alkali - do not
penetrate into the
eye as readily as
alkaline substances.
IRRITANTS
• Neutral pH
• More discomfort to
the eye than actual
damage.
5.
6. Alkali
More severe
-Penetrate rapidly.
They combine with cell membrane
lipids, mucopolysaccharides and to
collagen, resulting in disruption of cells
and necrosis of the tissues.
They Saponify cell membranes and
intercellular bridges, which facilitates
rapid penetration into the deeper layers
and into the aqueous and vitreous
compartments.
They causes Necrosis of
conjunctival blood vessel .
“Cooked fish eye” the cornea
appears chalky white and opaque.
Acid
-Less severe
Acids quickly denature
proteins in the corneal
stroma, forming precipitates
that retard additional
penetration.
Causing localized damage
due to its:
a)Coagulation effect
b)Protein precipitations at
epithelium level which form
a Physical barrier.
7. IRRITANTS:
PEPPER SPRAY
CHILLI GUARD: is a strong conc. Of chilli pepper
in an aerosol spray has 6 feet range.
When sprayed on face of the attacker, it puts
him/her out of action for atleast 30min.
HOLI COLORS:Green/bluish green holi colors
have been reported with the higher incidence
of ocular toxicity causing sever ocular
irritation with epithelial defect on exposure
due to the presence of malachite green.
8. LACRIMATOR
Chloroacetophenone in chemical mace (tear gas).
Can cause mild to moderate injury
Degree of severity is related to proximity of spray, and
quantity of chemical into the eye.
Can cause epithelial defects, severe persistent stromal
haze, edema, secondary to endothelial damage and
corneal neovascularization.
OTHER HOUSEHOLDS:
Hydrogen peroxide (oxidising agent)
Disinfectant,
Chlorine free bleaches,
Fabric stain removers,
Contact lens disinfectants,
Hair dyes.
9. PATHOPHYSIOLOGY OF CHEMICAL INJURIES:
1- Corneal Damage by severe chemical injuries
occurs as following:
Necrosis of the conjunctival and
corneal epithelium
Disruption and occlusion of the limbal
vasculature.
Loss of limbal stem cells
Conjunctivilization and vascularization
of the corneal surface
Persistent corneal epithelial defects
with sterile corneal ulceration
10. 2- Healing of the corneal epithelium
occurs with
Centripetal movement of cells from the
peripheral cornea, limbus, or conjunctiva and
is responsible for normal and posttraumatic
replacement of corneal epithelium.
Limbal stem cells are the cells most
qualified to restore the functional
competence of the corneal epithelial
surface after injury
If healing occur with conjunctival
epithelium , it can partial
transdifferentiate to corneal epithelium,
but can never fully expresses corneal
epithelial phenotypic features, leads to
delayed reepithelialization, superficial and
deep stromal vascularization.
11. 3. Healing of Damaged STROMAL COLLAGEN:
Maintenance and regeneration of the corneal
stroma is done by pluripotent cells- keratocyte.
Phagocytose collagen fibrils
Synthesis and secrete collagen
glycosaminoglycan, and collagenase inhibitors.
Modulated by cytokines released from the
damaged epithelium, inflammatory cells.
12. Degradation of the basement membrane
collagen
(initiated by MMP–9 )
Degradation of the corneal stromal matrix
(by MMP–1 and MMP–8(collagenase type 1)
Collagen type 1 synthesis peak point
(at 14-21 days)
Coincide with maximum MMP activity
Shift of equation toward collagenase activity
may show sterile corneal ulceration.
13. CLASSIFICATION OF INJURY:
The clinical findings immediately following
chemical exposure can be used to assess the
severity and prognosis of the injury.
Prognostic guideline based on:
1. Corneal appearance
2. Extent of limbal ischemia
3. Percentage of conjunctival involvement.
16. CLINICAL COURSE
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 (days 7–21), and
4. Late phase(day 21 to several months later).
17.
18. LATE PHASE (> 21 DAYS TO SEVERAL MONTHS)
Corneal re-
epithelialization
patterns divide
injured eyes into
two groups.
1st group,
epithelialization
is complete or is
nearly complete
with sparing of
limbal stem cells.
2nd group, limbal
stem cell
damage results
in corneal re-
epithelialization
from conjunctival
epithelium
19. LATE PHASE….
symblepharon formation, cicatricial
entropion, and trichiasis,
fibrovascular pannus.
vascularization and scarring, goblet
cell and mucin deficiency, and
recurrent or persistent erosions.
2nd group has the worst prognosis
with severe ocular surface damage
20. MANAGEMENT
Regardless of the underlying chemical involved,
common goals of management include the
following:
(1) Removing the offending agent,
(2) Promoting ocular surface healing,
(3) Controlling inflammation,
(4) Preventing infection,
(5) Controlling IOP.
21. IMMEDIATE MANAGEMENT (REMOVING
OFFENDING AGENT)
1. Irrigation :
most important step in the management of
chemical injuries.
Immediate copious irrigation of eye minimum for 30
minutes by sterile balanced buffered solution:
•Normal saline solution
•Ringer's lactate solution
•Diphoterine or Cederroh eye wash solution
•Normal saline with bicarbonate
•Balanced salt solution(BSS)
Even plain tap water may be used without waiting for
the ideal fluid.
22. Heavy metals like sodium, potassium and
calcium (e.g. Lime or Ca(OH)2) react violently
and explosively with water
Produce caustic hydroxide
Liberating much heat in its production
Result in combination of thermal and
chemical burn.
Immediately Brush off/pick out as many
particles of sodium or potassium as possible
Then to direct a high pressure jet of water at
the remainder.
Ignition of particles will occur, but if the flow
is great enough, the heat will be dissipated
by water.
23. EYE IRRIGATION…..
Eyelids should be immobilized with a
retractor or eye speculum, and topical
anesthetic should be instilled.
Irrigation may be accomplished using
.Handheld intravenous tubing, .Nasal
cannula connected to iv tube, .Irrigating
eyelid speculum, .Morgan medi-
FLOW Lens (a special scleral contact lens
that can be connected to IV tubing)
24. EYE IRRIGATION….
• Instill topical anesthesia
• Sweep the fornices with a moist sterile
cotton swab to remove any retained
foreign material.
Check the PH of tears for evidence of
neutrality with litmus paper inside the
lower lid.
Continue irrigation until litmus paper
shows neutrality of tears
If no litmus available urinary PH strip
can be used, if none is available irrigate
for another 20 min.
25. 2.Debridement of necrotic epithelium
3. Paracentesis
External perfusion of alkali-burned eyes may be
incapable of lowering aqueous pH by more than 1.5
units.
removing aqueous by paracentesis.
reduction in pH (another 1.5 units)
buffered phosphate solution may be used to
refill the anterior chamber,
26. RECOMMENDED TREATMENT
ACUTE PHASE:(FIRST 1-2 WEEKS)
1.Antimicrobial therapy
Prophylactic topical antibiotics are always warranted
during the initial treatment stages.
Preferably preservative free antibiotic drops and
ointments.
27. 2.Topical lubrication(TEAR SUBSTITUTE)
Topical viscoelastics( preservative free eye drop q2h)
Useful:
1. in facilitating corneal epithelial migration in grade I
and II injuries,
2. in minimizing conjunctival scarring and
symblepharon formation after grade III and IV injuries.
28. 3.Anti-inflammatory therapy
Corticosteriods:
Prednisolone acetate 1% qid to q 1 h for 7- 10 days
with rapid taper thereafter
Dexamethasone 1% q2h for 7-10 days
Reduce inflammation
Neutrophil infiltration
Impair stromal healing by reducing collagen
synthesis and 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.
29. 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.
Medroxy progesterone 1% qid.
30. 4.Ascorbate
. 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 Ascorbic acid (Vit-C)
1 -2gm PO bd.
31. 5.Collagenase Inhibitors
Tetracycline derivatives are efficacious in reducing
collaginase activity probably is due to chelation of
zinc at the active site of the collagenase
enyzme.(inhibits matrix metalloproteasase)
Doxycycline is the most potent tetracycline
collagenase inhibitor(100mg BD),
Tetracycline 250 mg QID
Minocycline 100mg BD
32. Sodium citrate (10% topical qid)
Cysteine, acetylcysteine,
Sodium ethylenediaminetetraacetic acid (EDTA),
CalciumEDTA, and penicillamine.
These impairs chemotaxis, phagocytosis and release
of lysosomal enzymes.
INVESTIGATIONAL DRUGS
1.Synthetic thiol and carboxyl–peptide collagenase
inhibitors are10 000-fold more potent collagenase
inhibitors in vitro than acetylcysteine.
2.Recombinant tissue inhibitors of
metalloproteinases (TIMP)
33. 6.Cycloplegics
Reduce cilliary spasm and pain.
Prevent posterior synechiae, Which form later, altering
the anterior segment architecture and impending
transfer of aquous fluid between the post & anterior
chamber
Atropine l % or homatropine 2% tid
7.Control of lOP
Timolol 0.5% bd
Brimonidine 0.1%-0.2% tid
Dorzolamide2%/brinzolamide1% bid
Acetazolamide 250 mg PO q 12 h-q 6 h
Methazolamide 25- 50 mg PO q 12 h,
34. 8.OCCLUSIVE THERAPY
for Management of large persistent
epithelial defect
. Hydrophilic and collagen bandage
lenses.
Useful in mild to moderate chemical injury
to protect the migrating epithelium from
the ‘windshield-wiper’ effect of the
eyelids.
. Patching
35. . Temporary tarsorrhaphy: may be beneficial for
protecting ocular surface epithelium.
.Glued – on contact lens:
Useful in chemical injury of moderate to great
severity.
Contact lens glued with butyl-2-cyanoacrylate
adhesive to de-epithelialized stroma.
36. 9.Autologous Serum
Fibronectin and epidermal growth factor benefit in
promoting reepithelialization.
Blood drawn into dry, sterile containers containing
no anticoagulants, clots and serum can be
separated & refrigerated until needed.
10.Amniotic membrane transplant for large and
persistent epithelial defect.
37. CHRONIC MANAGEMENT (3WEEKS AND
BEYOND)
1.Topical lubrication
2..Antimicrobial therapy (continue qid n discontinue
when surface epithelium is intact)
3.Anti-inflammatory therapy- NSAIDS can be used
(Ideally, corticosteroid use should be stopped or
minimized)
4. Continue intraocular pressure lowering agents.
5.Inhibitors of matrix metalloprotease/ collagenase
inhibitors
(Continue until surface epithelium is intact)
38. 6. TISSUE ADHESIVE
Effective in arresting further sterile corneal
ulceration and in maintaining the integrity of the
globe,
It is best reserved for impending or actual
perforations that are 1 mm or smaller.
May be removed or allowed to extrude
spontaneously after 6–8 weeks, when a secure
fibrovascular scar has formed and eliminated the
risk of subsequent stromal ulceration.
39. 7.Retinoic acid
May play a role in the late management of
persistent ocular surface abnormalities.
Promote goblet cell recovery and improve ocular
surface function
In grade III/IV injuries, in which reepithelialization
must come from conjunctival epithelium, retinoic
acid may promote partial, transdifferentiation of the
conjunctival epithelium to a corneal epithelial
phenotype.
40. 8. Surgical therapy
Early surgical intervention with
a) .Advancement of Tenon fascia/ conjunctiva
b). limbal stem cell transplantation when inflammation
is controlled
c). Rotational tarsoconjunctival graft for scleral necrosis
d). Amniotic membrane transplantation may be
necessary to achieve successful reepithelialization.
• Late surgical intervention:
Penetrating keratoplasty may be necessary for visual
rehabilitation.
42. CONJUNCTIVAL AND TENON’S
ADVANCEMENT (TENOPLASTY)
Its use 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.
43. AMNIOTIC MEMBRANE TRANSPLANTATION:
Amniotic membrane is semitransparent innermost
layer of the fetal membrane.
It consists of an avascular stromal matrix, a thick
basement membrane, and an epithelial monolayer.
The tissue may be transplanted to the corneal
surface with the basement membrane oriented
downwards or upwards. (‘onlay’ or ‘inlay’ grafts)
44. AMT…
Promoting epithelialization.(Release epidermal
growth factor)
“Onlay” patch Invariably dissolves in a few weeks
“Inlay” patch becomes incorporated into the
substratum, persists for months. Then replaced by
new fibrotic stromal tissue that partially conserves
the corneal thickness.
45. 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.
In unilateral/ asymmetrical cases of chemical injury
conjunctival limbal autograft transplantation (CLAU)
is usually performed by harvesting contralateral
limbal stem cells from the uninjured or less injured
fellow eye and transferring them to the injured or
more injured eye.
46. Lr-CLAG
(Living-related conjunctival limbal allograft
transplantation)
In severe bilateral injuries,
from a living relative.
CLAG from cadaveric donor, technically the same
procedure as Lr-CLAG.
The risk of allograft rejection is higher.
47. KLAT (KERATOLIMBAL ALLOGRAFT TRANSPLANTATION)
is a technique for transferring limbal stem cells from a
donor cadaver to treat severe bilateral injuries.
48. There is a significant risk of graft rejection,but
successful preservation of limbal stem-cell function
and corneal clarity has been reported with
prolonged, aggressive topical and systemic
immunosuppression.
49. Ex vivo expansion of limbal stem cells is
currently being investigated as an improvement of
existing limbal stem-cell transplantation techniques.
50. MUCOSAL MEMBRANE TRANSPLANTATION:
For the Mechanical abnormalities of the bulbar and
palpebral conjunctiva related to progressive
scarring.
Can be harvested from oral and nasal mucosa
Used to reconstruct the fornix and restore normal
lid–globe relations.
Although such grafts do not restore the corneal
epithelial functions provided by limbal stem-cell
transplantation,
They improves impaired goblet cell function of the
conjunctiva.
51. LAMELLAR KERATOPLASTY:
Progression of stromal ulceration to the
descemetocele stage may chance to perforate the
cornea.
Lamellar keratoplasty may be the procedure of
choice to re-establish the architectural integrity of
the eye.
52. PENETRATING KERATOPLASTY-
Once perforation has occurred a lamellar transplant
is difficult to perform and is less likely to seal the
perforation.
A full thickness blow out patch can be cut from
corneal donor material.
A standard trephine can be used to excise a circular
button for penetrating keratoplasty.
53. Healing occurs with scarring but the primary goal is
the restore the anterior chamber and preserve the
eye.
Optical penetrating keratoplasty may be necessary
for visual rehabilitation, but this should only be
performed after appropriate rehabilitation of the
ocular surface has been achieved.
54. Kerato prosthesis –
May be useful in severe chemical injury in which
the prognosis is hopeless for penetrating
keratoplasty because of irreparable damage to the
ocular surface.
The greatest limiting factor has been collagenolytic
erosion of the interfaces at which corneal tissue
adjoins prosthetic material
59. COMPLICATIONS…
7. Iritis, endophthalmitis, and panophthalmitis.
8. Secondary glaucoma :
Early: prostaglandin release , secondary to severe
iritis leads to shrinkage of collagen fibers of the
sclera.
Late: Occlusion of aqueous veins & anterior ciliary
vessels by conjunctival fibrosis.
9.Atrophic bulbi may follow severe cases.
61. REFERENCES:
Jackobiec’s principles n practice of ophthalmology
Krachmer’s fundamentals, disease and
mamanagent (Cornea)
Yanoff n Duker ophthalmology
Postgraduate ophthalmology, Zia choudhary,
Vanathi.
American academy of ophthalmology.
Internet resources.
