Chemical burns are one of the true ophthalmologic emergencies. The ophthalmologist and general practitioner thus needs to be aware of the management of this type of eye injury.

1. DR CHIMOZI TEMBO
DR VRUNDA PATEL
MODERATOR: DR MOONGA

2. Outline
 Introduction
 Pathophysiology
- Acid Injury
- Alkali Injury
 Epidemiology
 Management
- Emergency
- Classification
- Medical and surgical therapy
 Late Complications
 References

3. Introduction
 Chemical injuries to the eye represent one of the true ophthalmic
emergency.
 Time is truly critical.
 Alkali injuries are more common and can be more clinically challenging,
with a significant potential for long-term morbidity.
 Bilateral chemical exposure is especially devastating, often resulting in
complete visual disability.

4. Pathophysiology
The severity of this injury is related to
 chemical composition
 pH
 volume
 concentration
 Duration of contact, and degree of penetration of the chemical.
 The mechanism of injury differs slightly between acids and alkali.

5. Acid Injury
 Acids dissociate into hydrogen ions in the cornea
 Especially at pH of less than 4.
 Hydrogen molecule damages ocular surface by altering pH
 Protein denaturation, precipitation, and coagulation.
 Protein coagulation creates a barrier- prevents deeper penetration and
ground glass appearance of corneal stroma

6.  Hydrofluoric acid is an exception
 Behaves like an alkaline substance
 Fluoride ion has better penetrance through stroma than most acids,
leading to more extensive anterior segment disruption

7. Some common acids

8. Alkali Injury
 Alkaline substances are lipophilic and can penetrate cell membranes.
 Dissociate into a hydroxyl ion (OH) and a cation in the ocular surface.
 Hydroxyl ion saponifies cell membrane fatty acids.
 Cation interacts with stromal collagen and glycosaminoglycans- destroyed
and release proteolytic enzymes
 This facilitates deeper penetration into and through cornea and into
anterior segment.

9. Some common alkali

10. Pathophysiology
 Necrosis of the conjunctival and corneal epithelium with disruption and
occlusion of the limbal vasculature.
 Loss of limbal stem cells may lead to conjunctivalization and
vascularization of the corneal surface, or persistent corneal epithelial
defects with sterile corneal ulceration and perforation.
 Longer-term effects include ocular surface wetting disorders,
symblepharon formation and cicatricial entropion.

11.  Deeper penetration causes the breakdown and precipitation of
glycosaminoglycans and stromal corneal opacification.
 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 in severe cases.

12. Healing
 Epithelium - migration of epithelial cells originating from limbal stem
cells.
 Damaged stromal collagen is phagocytosed by keratocytes and new
collagen is synthesized

13. Epidemiology
Frequency-USA
 Chemical injuries ¬ 7% of work-related eye injuries treated at US hospital
emergency departments.
 More than 60% of chemical injuries occur in workplace accidents, 30% at
home, and 10% assault.
 Safety glasses can help prevent injuries, but industrial accidents often
involve chemicals under high pressure.
 Generally, 11.5%- 22.1% of all ocular trauma

14. Mortality/Morbidity
 20% of chemical injuries result in significant visual and cosmetic
disability.
 Only 15% of patients with severe chemical injuries achieve functional
visual rehabilitation.

15. Sex
 Males are 3 times more likely to experience chemical injuries than
females.

16. Age
 Chemical injuries can strike any population
 Most injuries occur in patients aged 16-45 years

18. Emergency treatment
A chemical burn is the only eye
injury that requires emergency
treatment without formal clinical
assessment

19. Copious irrigation
 Crucial to minimize duration of contact with the chemical
 Normalize the pH in conjunctival sac as soon as possible
 If both eyes have been burned, the irrigation must be done alternatively
 If cornea be opaque and iris discoloured, AC irrigated with BSS
 Irrigation improves the prognosis even if hours have elapsed since the
injury
 Speed and efficacy of irrigation most important prognostic factor
following chemical injury.

20.  Tap water to avoid any delay
 Sterile balanced buffered solution
- normal saline or Ringer lactate
until pH neutral.
 Polyvalent, hypertonic,
amphoteric compound, such as
Diphoterine
 -effective against acids, alkali, and
agents with oxidative or redox
activity.
 Giving set, nasal cannula, Morgan
lens

21.  Explain to the patient
 Use topical anaesthetics
 Separate eyelids +/- lid speculum
 Remove all particles with a cotton-
tipped applicator or forceps.
 Gently rinse cornea and fornices
using an infusion line
 Bottle should be 30−80 cm above
eye level.
 Proceed with irrigation even if the
injury is open globe. Closure with
sutures should follow, not precede,
rinsing.

22.  Double-eversion of the upper
eyelid
 Rinse palpebral conjunctiva and
fornices
 Any retained particulate matter
trapped in fornices is identified and
removed.
 Debridement
 Necrotic areas of corneal epithelium
at the slit lamp to promote re-
epithelialization and remove
associated chemical residue.

23. History
 What happened?
 When did it happen?
 Name of agent that caused injury?
 What characteristics (e.g., pH, concentration) does this agent have and how
much got onto the eye?
 Work-related injury? If yes, was a witness present? Was a report filed?
 Was injury self-inflicted?
 Was the eye irrigated after the injury? If yes, with what and for how long?
 What therapy has been employed so far?
 How much pain is there now?
 How has vision been effected?

24. Post irrigation
 Measure pH of ocular surface
 Slit lamp examination
 Fluorescein staining
 Take visual acuity and IOP
 Grade the injury.

25. Grading systems
 Plan appropriate subsequent treatment and afford an indication of likely ultimate
prognosis
 Two major classification schemes
 Roper-Hall classification
- degree of corneal involvement and limbal ischemia
 Dua classification
- estimate of limbal involvement (in clock hours) and the percentage of conjunctival
involvement
 Randomized controlled trial of acute burns, Dua classification was found to be superior
to Roper-Hall in predicting outcome in severe burns.

26. Roper-Hall classification
 For prognosis assessment
 Corneal clarity and severity of limbal ischaemia.
 Limbal ischaemia - assessed by observing patency of deep and superficial
vessels at limbus.
 Four grades

27. GRADE 1
 Clear cornea with epithelial
damage only and no limbal
ischaemia
 Excellent prognosis

28. GRADE 2
 Corneal haze but visible iris detail
 Less than one-third of the limbus
being ischaemic.
 Good prognosis.

29. GRADE 3 total loss of corneal epithelium
 stromal haze obscuring iris detail
 Between one-third and half limbal
ischaemia
 Guarded prognosis

30. GRADE 4
 Opaque cornea
 more than 50% of the limbus
showing ischaemia.
 Poor prognosis.

31. Roper Hall summary table

32. Dua classification

34. Medical treatment
 Aims:
- enhance recovery of the corneal epithelium
- controlling inflammation
- augment collagen synthesis
- minimizing collagen breakdown
 Grade I and II often treated successfully with medical treatment alone.
 Admission for severe injuries (grade IV +/- III) to ensure adequate eye
drop instillation.
 Preferably preservative-free drops

35. Promote epithelial wound healing and
differentiation
Tear Substitutes
 Facilitate corneal epithelial migration in grade I and II injuries
 Minimizing conjunctival scarring and symblepharon formation after
grade III and IV injuries
 Use with ointments at bedtime for persistent keratopathy and recurrent
epithelial erosions.
Platelet rich plasma eye drops
 Rich in growth factors -can lead to faster epithelialization for certain
classes of burns

36. Control inflammation
Corticosteroids
 Mainstay of therapy for reduction of tissue injury related to acute
inflammation
 Decrease inflammatory cell infiltration, also address anterior uveitis
 Interfere with stromal repair by impairing both keratocyte migration and
collagen synthesis.
 ‘window of opportunity’ is first 7–10 days

37. Progestational steroids and non steroidal anti inflammatory drugs
(NSAIDs).
 Taper corticosteroids by substituting
 Medroxyprogesterone 1% to inhibit collagenase and reduce ulceration
 NSAIDs as additive and/0r substitute later

38. Augment collagen synthesis and minimizing
collagen breakdown-Ascorbic Acid & Citrate
Ascorbic acid
 Reverses a localized tissue scorbutic state and
 Is a cofactor in rate limiting step in collagen synthesis
 Promotes synthesis of mature collagen by corneal fibroblasts.
 Topical sodium ascorbate 10% and systemic dose of 1–2 g vitamin C (L-
ascorbic acid)
 Not in patients with renal disease

39. Citric acid
 Chelation of extracellular calcium by citrate also appears to inhibit
collagenase
 Calcium chelator - impaired chemotaxis, phagocytosis, and release of
lysosomal enzymes of polymorphonuclear leukocytes.
 Aim to eliminate second wave of phagocytes, about 7 days after injury
 Ascorbate and citrate can be tapered as the epithelium heals

40. Tetracyclines
 Effective collagenase inhibitors and also inhibit neutrophil activity and
reduce ulceration.
 Topically (tetracycline ointment) and systemic (doxycycline)
Acetylcysteine 10%
 Alternative anticollagenase agent given topically.

41. In addition
Cycloplegia
 May improve comfort.
Topical antibiotic
 Used for prophylaxis of bacterial infection

42. IOP
 Should be monitored, with treatment if necessary;
 Oral acetazolamide recommended
Symblepharon
 prevented by lysis of developing adhesions with a sterile glass rod or damp
cotton bud.

43. Surgical therapy
 Early surgery to
- promote revascularization of limbus
- restore the limbal cell population
- re-establish the fornices.

44. Tenoplasty
 Advancement of Tenon capsule with suturing to limbus
 Re-establishing limbal vascularity to help prevent corneal ulceration
Limbal stem cell transplantation
 From patient’s other eye (autograft) or from donor (allograft)
 Aimed at restoring normal corneal epithelium

45. Amniotic membrane grafting
 Rapidly restore conjunctival surface
 Suppress fibrosis
 Physically-improve patient comfort by reduction of eyelid friction; prevent
symblepharon formation.
 Biological role in wound healing and anti-inflammatory
 Gluing or keratoplasty may be needed for actual or impending perforation

46. Treatment summary
 Grade I
i. Topical antibiotic four times /day
ii. Prednisolone acetate 1% four times /day
iii. Preservative free artificial tears as needed
iv. +/- short acting cycloplegic like cyclopentolate three times /day

47.  Grade II
i. Topical antibiotic drop- fluoroquinolone four times daily
ii. Prednisolone acetate 1% or dexamethasone 4 times/day to hourly first 7-
10 days. Taper +/- 1% medroxyprogesterone four times daily
iii. Long acting cycloplegic like atropine
iv. Sodium ascorbate drops (10%) 1-2 hourly while awake
v. Oral Vitamin C, 2 grams four times daily
vi. Doxycycline, 100 mg twice daily and taper(avoid in children); TEO
vii. Sodium citrate 10% 2 hourly about 10 days
viii. Preservative free artificial tears as needed
ix. Debridement of necrotic epithelium and application of tissue adhesive
as needed

48.  Grade III
 As for Grade II
 Consider amniotic membrane transplant in 1st week of injury. Cover
palpebral conjunctiva by suturing to the lids in OT

49.  Grade IV
 As for Grade II/III
 Early surgery usually necessary.
 For significant necrosis, Tenoplasty; amniotic membrane transplant

50. Complications
Late sequelae of chemical injury.
 Conjunctival band
 Symblepharon
 Cicatricial entropion of the upper eyelid
 Dry eye
 Corneal scarring
 Glaucoma

51. Late surgery may involve: division of
Conjuctival bands and symblephara
Conjuctival bands Symblephara

52. Late Surgery
 Correction of eyelid deformities
such as cicatricial entropion

53. Keratoplasty for Cornea scarring
 Complete cicatrization of corneal
surface following chemical injury.
 Keratoplasty should be delayed for
at least 6 months
 allows maximal resolution of
inflammation.

54. Keratoprosthesis
 may be required in a very severely
damaged eye.

55. References
 Bowling B, (2016), Kanski’s Clinical ophthalmology, A Systematic
Approach, 8th edition, Elsevier limited, UK.
 http://emedicine.medscape.com/article/1215950-overview#a6
 http://eyewiki.aao.org/Chemical_(Alkali_and_Acid)_Injury_of_the_Conj
unctiva_and_Cornea
 http://es.slideshare.net/drsafaa1/chemical-eye-trauma-by-dr-safaa-refaat-
47458210
 http://www.slideshare.net/saanvi2011/ocular-chemical-injury
 Kuhn F, (2008), Ocular traumatology, Springer-Verlag Berlin Heidelberg,
New York, USA

56. MERRY CHRISTMAS AND A PROSPEROUS NEW YEAR