2. INTRODUCTION
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One of the true ophthalmic emergencies.
Only ocular condition where history taking and examination should
be delayed.
Coordination with physician, surgeon and psychiatrist may be
required.
Bilateral chemical exposure is especially devastating, often resulting
in complete visual disability.
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International Classification of Diseases
ICD-9-CM
940.2 alkaline chemical burn to cornea and conjunctiva,
940.3 acid chemical burn to the cornea and conjunctiva,
372.06 chemical conjunctivitis
ICD-10-CM
T26.60XA Corrosion of cornea and conjunctival sac, unspecified
eye, initial encounter.
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5. Type of chemical injuries
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ALKALI BURNS
Most dangerous -rapid penetration.
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ACID BURNS
Less severe than alkali - do not penetrate into the eye as readily as
alkaline substances.
The exception hydrofluoric acid burn, which is as dangerous as an alkali
burn.
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IRRITANTS
Neutral pH
More discomfort to the eye than actual damage.
–-Most household detergents
–-Pepper spray
•It can cause significant pain but usually does not affect vision and
rarely causes any damage to the eye.
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6. Alkalies
Acid
More severe
-Less severe
-Penetrate rapidly (often in less than one minute),
-They combine with cell membrane lipids,
mucopolysaccharides and to collagen, resulting in disruption
of cells and necrosis of the tissues.
On the ocular surface, they saponify cell membranes and
intercellular bridges, which facilitates rapid penetration into
the deeper layers and into the aqueous and vitreous
compartments
-Necrosis of conjunctival blood vessel causing:
“Cooked fish eye” the cornea is as white as chalk and opaque.
-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
-Leading to:
Physical barrier.
7. Alkali substances:
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Ammonia,NH3; a common ingredient in many household cleaning agents
Lye, NaOH; a common ingredient in drain cleaners
Potassium hydroxide,KOH
Magnesium hydroxide,Mg[OH]2
Lime, Ca[OH]2; the most common cause
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Common substances at home :
Fertilizers
Cleaning products (ammonia),
Drain cleaners (lye)
Plaster,cement (lime)
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8. Common acids causing eye burns
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Sulphuric (H2SO4); the most common cause (an ingredient in
automobile batteries)
Sulfurous (H2SO3)
Hydrofluoric (HF; rapidly penetrating and causing the most serious
injuries)
Nitric acid
Acetic acid (CH3COOH)
Chromic acid (Cr2O3)
Hydrochloric acid (HCl)
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Common substances at home
Glass polish (hydrofluoric acid)
Vinegar
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9. 1- The severity of a burn depends on:
•Surface area of contact.
•Depth of penetration, concentration, time of contact, time of interference.
•Degree of limbal stem cell injury.
2-Common area of damage in eye:
Anterior segment of the eye
Internal segment of the eye
Cornea
Conjunctiva
Lens
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10. PATHOPHYSIOLOGY OF OCULAR INJURES
1- Corneal Damage by severe chemical injuries occurs in the
following order:
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
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11. 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.
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12. PATHOPHYSIOLOGY OF OCULAR INJURES
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.
Associated with delayed reepithelialization, superficial and deep
stromal vascularization, persistence of goblet cells in the corneal
epithelium, 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
13. 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.
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14. 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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17. Classification
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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.
Gupta, N., M. Kalaivani, and R. Tandon, Comparison of prognostic value of Roper Hall and Dua
classification systems in acute ocular burns. The British journal of ophthalmology, 2011. 95(2): p. 194-8
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19. Dua classification of ocular
surface burns
Grade
Prognosis
Limbal involvement
Conjunctival
involvelment
Analogue scale
I
Very good
0 clock hours of
limbal involvement
0%
0/0%
II
Good
⩽3 clock hours of
limbal involvement
⩽30%
0.1–3/1–29.9%
III
Good
>3–6 clock hours of
limbal involvement
>30–50%
3.1–6/31–50%
IV
Good to guarded
>6–9 clock hours of
limbal involvement
>50–75%
6.1–9/51–75%
V
Guarded to poor
>9–<12 clock hours of >75–<100%
limbal involvement
9.1–11.9/75.1–
99.9%
VI
Very poor
Total limbus (12 clock Total conjunctiva
hours) involved
(100%) involved
12/100%
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.
20. Medical Care
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.
22. 1)Remove inciting chemical (irrigation)
Immediate copious irrigation of eye (every second counts) by
sterile balanced buffered solution:
•Normal saline solution
•Ringer's lactated solution
•Normal saline with bicarbonate
•Balanced salt solution(BSS)
Even plain tap water may be used without waiting for the ideal
fluid.
Preferably, eye should be anaesthetized before irrigation.
23. Eye Irrigation
2)Evert the upper eyelid and irrigate, and irrigate under lower
lid.
• Remove all solid particles from under lids.
• After 5 to 10 minutes of irrigation and if litmus paper is
available test pH of lower inside of lid.
• Continue irrigation until pH is below or above a pH of 7.0.
• If no litmus available irrigate for 20 min
Special irrigating tubing(Morgan’s lens):
24. • Water is contraindicated
• In chemical burns caused by the 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.
• Immediate treatment
Brush off/pick out from the skin 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.
26. 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 gear used?
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27. If nature of chemical
substance is known
Strong Weak alkali
acid
Strong Weak acid
alkali
Iodine Starch solution
Milk
Aniline Alcohol 10%
Glycerine 10%
Lime
a) Pick particles with
forceps
b) Wash by:
EDTA 0.1%
Neutral ammonium
tartrate 10%
Saturated sugar solution
If nature of chemical is
unknown or not available
Tap
water
Milk
Dilute chemical
substance
*for all except LIME*
Dilution
Buffer acid and alkali
Form superficial film
which protect the
underlying tissue
28. 1- Remove inciting chemical
• Instill topical anesthesia
• Sweep the fornices with a moist sterile cotton swab to remove
any retained foreign material.
• Double eversion of upper lid
• especially important when particulate matter (eg, plaster) is
responsible for the injury.
2- Paracentesis
• External perfusion of alkali-burned animal eyes may be
incapable of lowering aqueous pH by more than 1.5 units.
• further decrease can be achieved by
– removing aqueous by paracentesis.
– buffered phosphate solution may be used to refill the anterior
chamber, a greater reduction in pH (another 1.5 units) is possible.
3- Early Assessment
29. Recommended Treatment
Graded approach depending on the severity of
injury.
Mild burns (Roper-Hall grade I)
Respond well to medical treatments and lubrication.
Moderate to severe burns
More intensive medical therapies and surgery.
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30. MEDIACTION
1- Steroids
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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.
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 q.i.d.
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31. 3- Citric acid
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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.
4- Tetracyclines
• Collagenase inhibitors
• Inhibit neutrophil activity
• Reduce ulceration.
They are administered both topically and systemically {Doxycycline 100
mg b,d.}.
-Topical antibiotic, aggressive lubrication with eye ointments (steroid
antibiotic combinations) to prevent symblepharon.
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32. • 5- Tear Substitutes
• 6- Occlusive Therapy
• 7- Bandage Soft Contact Lens
• 8- Autologous Serum
– Fibronectin and epidermal growth factors
• 9-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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33. • Grade I
• Topical antibiotic ointment (erythromycin ointment
or similar) four times a day
• Prednisolone acetate 1% four times a day
• Preservative free artificial tears as needed
• If there is pain, short acting cycloplegic like
cyclopentolate three times a day
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Grade II
As for grade I
Prednisolone acetate 1% hourly while awake for the first 7-10 days.
• Tapering if the epithelium has not healed by day 10-14.
• If an epithelial defect persists after day 10, consider
progestational steroids (1% medroxyprogesterone qid)
Long acting cycloplegic like atropine
Oral Vitamin C, 2 grams four times a day
Doxycycline, 100 mg twice a day (avoid in children)
Sodium ascorbate drops (10%) hourly while awake
Preservative free artificial tears as needed
Debridement of necrotic epithelium and application of tissue adhesive
as needed
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Grade III
As for Grade II
Consider amniotic membrane transplant placement.
Ideally be performed in the first week of injury
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Grade IV
As for Grade II/III
Early surgery is usually necessary.
For significant necrosis, a Tenonplasty can help reestablish
limbal vascularity.
• An amniotic membrane transplant is often necessary.
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36. MID TERM MANAGEMENT OF
OCULAR CHEMICAL BURNS
Inflammation
Infection prophylaxis
IOP control
Pain management
37. Control inflammation
Inflammatory mediators released from the ocular surface at the time of
injury causing:
•Tissue necrosis
•Attract further inflammatory reactants
causes:
•Inhibits reepithelialization
•Corneal ulceration
•Perforation
38. Infection prophylaxis
After a week, continued assessment of the risk of infection is essential.
Persistent epithelial defects, necrotic corneal stroma, and corneal
melting all facilitate infection and therefore necessitate the continued use
of topical antibiotics.
*Prophylactic topical antibiotics are always warranted during the
initial treatment stages.
-Cyanoacrylate tissue adhesive may be applied for the treatment of
small corneal perforations to avoid infection.
40. Control IOP (increase secondary to
chemical injuries)
Control IOP (increase secondary to chemical injuries)
• Oral acetozolamide(Diamox) or topical beta-blockers or aqueous
• Always in initial therapy and during
• the later recovery phase, if IOP is high (>30 mm Hg).
41. Control Pain
Control pain
• Severe chemical burns can be extremely painful.
• Cycloplegic agents for ciliary spasm
• Oral pain medication initially to control pain.
42. Complications
1-Primary complications:
• Conjunctival inflammation
• Corneal abrasions
• Corneal haze and edema
• Acute rise in IOP
• Corneal melting and perforations
2-Secondary complications:
• Secondary glaucoma
• Secondary cataract
• Conjunctival scarring
• Corneal thinning and perforation
• Corneal scarring and
vascularization
• Corneal ulceration (sterile or
infectious)
• Complete globe atrophy (phthisis
bulbi)
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48. Penetrating Keratoplasty
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.
51. Others in Late(Chronic) Period
• The tear film should be augmented when necessary with
preservative-free artificial tears.
• Lysis of symblephara and reconstruction of the
fornices, possibly with mucosal grafts, may be performed.
• Silicone rubber sheets and an acrylic conformer are useful.
• Correction of cicatricial entropion and trichiasis is necessary if
keratoplasty is anticipated.
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52. Further inpatient care
In patients with severe chemical injuries, short hospitalization may be
warranted to closely monitor:
•IOP
•Corneal integrity
•Medication use
•Pain control
53. Prognosis
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According to Roper Hall classification
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Grade 1 – Excellent prognosis
Grade 2 – Good prognosis
Grade 3 – Guarded prognosis
Grade 4 – Very poor prognosis
Higher-grade injuries are more susceptible to secondary complications
leading to poor prognosis.
54. Deterrence/Prevention
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Education and training regarding the prevention of chemical
exposures in the workplace.
Persons who may be exposed to chemicals in the workplace are
advised to wear safety goggles.
55. • A common, mostly avoidable ocular emergency.
• Immediate and intense irrigation is of utmost importance.
• Continuous assessment and planning is very important as early
picture may be misleading.
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