1. Chemical injury to eye
Presenter : Dr. Chethana
Moderator :Dr. Shiva prasad
2. Chemical injuries are potentially
devastating ocular surface injuries
that can result in permanent visual
impairment.
DEFINATION
Principles and practices of ophthalmology: Albert and Jakobiee ‘s
3. INCIDENCE
Chemical burns constitute between 11% and 18% of all ocular
trauma
80% -industrial and/or occupational exposure-young adults
,accidental>homicidal
Male > female
Acid > alkali*
Lime burn(chunna) very common in India
*Cite this article: Vathulya M, Tiwari VK (2017) Epidemiological Profile of Chemical Burns from the
Largest Burn Centre in India. JSM Burns Trauma 2(1): 1013.
4. ETIOLOGY- ALKALI
Ammonia - Fertilizers, Refrigerants, cleaning agents ,
combines with water to form NH4OH,rapid penetration
Lye(NaOH)- Drain cleaners
Potassium hydroxide- Caustic potash
Magnesium Hydoxide – Sparklers
Lime-(Ca(OH)2)- Plaster, whitewash ,cement
AMMONIA,LYE - MOST SERIOUS BURNS
7. BIO CHEMICAL CHANGES-Alkali
Lipophilic and penetrate more rapidly than acids.
Rise in pH
Reacts with cellular lipids- Saponification - cell destruction.
The hydroxyl ion hydrolyzes intracellular
glycosaminoglycans and denatures collagen.
2-3 weeks later-stromal ulceration –proleolytic enzymes by
PMNL and epithelial cells
9. Alkali substances can pass into the anterior
chamber rapidly (approximately 5-15 min)
exposing the iris, ciliary body, lens, and
trabecular network to further damage.
Irreversible damage occurs at a pH value
above 11.5
11. Alkali burn. Note the severe conjunctival reaction and
stromal opacification blurring iris details inferiorly
12. BIO CHEMICAL CHANGES - Acid burns
Acid burns cause protein coagulation in the corneal
epithelium, which limits further penetration.
Thus, these burns usually are nonprogressive and
superficial.
Reacts with collagen shrinkage with IOP
Ciliary body damage with decreased aqueous acsorbate
levels
13. Key Features: Pathophysiology
The severity of a chemical injury is related to the surface area
of contact and the degree of penetration.
Limbal stem cells are the cells most qualified to restore
functional competence of the corneal epithelial surface after
injury.
Corneal repair by keratocytes consists of both synthesis and
degradation of stromal collagen.
Persistent inflammation may delay reepithelialization and
shift the net balance of corneal repair toward progressive
stromal ulceration.
14. The three major principles guiding evaluation and
management of chemical injury are based on
addressing each of the three main pathophysiologic
mechanisms contributing to the final outcome:
(1) regeneration of ocular surface epithelium and its
state of differentiation,
(2) stromal matrix remodeling, including repair and
degradation, and
(3) inflammation
15. PATHOPHYSILOGY
LEUCOCYTIC WAVE CHEMICAL BURN pH rise PED
12-24hrs(PMN+MONONUCLEAR LEUCOCYTES) KERATOCYTE DAMAGE Extensive LSC damage
PHAGOCYTIC DEG. STROMAL THINNING
TYPE I COLLAGENES mmp-8
Plasminogen activities STERILE CORNEAL ULCER
7 days inflam.cells
Vit C
Vit A
Na hyalurnote
Heparin
Tetracyclin,collagenase
inhibitor,oral antioxidents
steroids
steroids
prostaglandins
16. Immediate phase
Clinical features depend on
The extent of ocular surface involvement,
The depth of penetration, and
The relative toxicity and concentration
The depth of ocular surface penetration, and possible
limbal stem-cell damage, can be evaluated indirectly by
assessment of vascular ischemia and necrosis of limbal
and bulbar conjunctiva.
17. Signs & Symptoms
Pain
Redness
Irritation
Tearing
Inability to keep the eye open
Sensation of something in the eye
Swelling of the eyelids
Blurred vision
18. Hughe’s classification
Mild
Moderately severe
Very Severe
depending on amount of corneal edema and
conjunctival blanching
19. Classification of severity of ocular surface
Burns by Roper-Hall
Grade Prognosis Cornea Epi/Conjun limbus
1 Good Yes No limbal ischaemia
2 Good Yes <1/3
Corneal haze,
iris details visible
3 Guarded Yes >1/3 -1/2
Iris details obscured
4 poor Yes >1⁄2 limbal ischaemia
Cornea opaque,
iris and pupil obscured
Br J Ophthalmol. 2004 October; 88(10): 1353–1355
corneal haze as an important prognostic variable. Rapidly changes
20.
21. Modification in GRADING
Dua et al, limbal fluroscein staining as a marker of
limbal stem cell damage.
Fornices & mucocutaneous junction of the conjunctiva
are important for conjunctival regeneration
Limbal involvement prefered over limbal
ischemia(Transient)
22. New classification of ocular surface
burns. DUA et al
Grade Prognosis Clinical findings Conj.invol.
I Very good 0 clock hours 0%
II Good <3 clock hours. <30%
III Good >3–6 clock hours. >30–50%
IV Guard >6–9 clock hours >50–75%
V poor >9–<12 clock hours >75–<100%
VI Very poor Total limbus 100%
26. Mc. CULLEY CLINICAL COURSE OF CHEMICAL INJURY
Immediate phase
Acute up to 1 week
Early Repair 1-3weeks
Late repair >3wks
(Balance between collagen synthesis & collagen degradation)
27. Acute stage
Mild burns – epi defect with limbal vessels sparing
Severe burns- epi damage with limbal ischemia
pH will reduce aqueous glucose and ascorbate ,
which further aggravates ischemia
Inflammation is active / Bimodal rise in iop
Haling and re-epithelisation starts
28. Grade I injuries - heal
Grade II injuries - There is slow but progressive
reepithelialization , although the sector of limbal stem-
cell loss may show little or no reepithelialization.
Grade III and IV injuries - show no reepithelialization.
there is little or no collagenolytic activity during this
phase. IOP rise, infiltration of the peripheral cornea with
polymorphonuclear leukocytes and other inflammatory
cells begins.
29. Early repair- 7 to 21days
Grade 1or 2 burns,
Epithelium
regeneration
Corneal
neovascularisation
Clearing of stroma
Synthesis of GAG’s
Laying down of new
collagen
Peaks at 14th
day
Grade 3 0r 4
Epi reg may not start
and progress
Stomal haze reduces
ulceration by
proteolytic
enzymes/collagenase
activity
3rd
week
30. Late repair -> 3 weeks
Grade 1 to 2 –heal with good prognosis
Grade 3 to 4 –complications,scarring,xerophthalmia,
symblepharon, ankyloblepharon, glaucoma, uveitis,
cataract, lagophthalmos, cicatrial entropion or
ectropion, trichiasis, dry eye etc,
Conjunctva – goblet cells – keratinisation
Cornea – if breakdown of collagen is more –thinning
descmetacoele and perforeation
31. If synthesis is more than breakdown – corneal opacity
Which in turn influenced by corneal vascularisation
Nutrients and inhibitors of collagenase are brought to the
cornea leading to ulceration
If limbal epi cells are intact – smooth and rapid re-
epithelisation , otherwise conjunctivalisation
Lids and adnexa – affect the tear film
32. (a) Type I healing pattern: normal epithelial recovery. After a grade I injury with no limbal stem-cell loss, complete
reepithelialization with a normal corneal phenotype is complete within 1 week. (b) Type II healing pattern: delayed
differentiation. After a grade II injury with limbal stem-cell loss from the 7– to 9–o'clock position, there is delayed
reepithelialization through the late repair phase, with development of superficial vascular pannus and impaired corneal
epithelial differentiation in the affected quadrant. (c) Type III healing pattern: fibrovascular pannus. After a grade III
injury with complete limbal stem-cell loss, progressive corneal epithelialization with conjunctivally derived epithelium over
a 4–month period results in fibrovascular pannus covering the entire cornea. (d) Type IV healing pattern: sterile corneal
ulceration. After a grade IV injury with complete limbal stem-cell loss, as well as loss of conjunctival epithelium and
vascularity in the entire nasal quadrant, there is no corneal reepithelialization. Sterile corneal ulceration of the nasal and
inferior corneal stroma begins 3 months after injury∼ .
