Lecture on Ocular Burn &Amp; Chemical Injuries For 4th Year MBBS Undergraduate Students By Prof. Dr. Hussain Ahmad Khaqan

1. Ocular Burn & Chemical Injuries
Prof. Dr. Hussain Ahmad Khaqan
 MD
 FRCS(Glasgow)
 FCPS(Ophth.)
 FCPS(Vitreo Retina)
 MHPE (KMU)
 CICO(UK)
 CMT(UOL)
 Fellowship in Medical Retina (LMU, Munich)
 Fellowship in Vitreo Retinal Surgery (LMU, Munich)
 Consultant Ophthalmologist & Retinal Surgeon
Professor of Ophthalmology
Lahore General Hospital, Lahore
Ameer Ud Din Medical College, Lahore
Post Graduate Medical Institute, Lahore
Shaukat Khanum Memorial Cancer Hospital & Research Centre ,Lahore

2. Ocular Burn Injuries

3. DEFINITION
• Thermal injury is defined as the tissue damage
caused primarily by denaturing and coagulating
cellular proteins and secondarily by causing vascular
ischemic damage

4. CAUSES
1. Heat
2. Electricity
3. Ultraviolent radiation

5. CLINICAL FEATURES CONTINUE
Keratopathy:
1. Spectrum ranges from mild punctate/confluent
defects (e.g. most cigarette ash injuries) to severe
limbitis and permanent opacification, stromal
melting or perforation (e.g. from molten metal,
which may form a complete cast between lid and
globe).

6. 2. Conjunctival injection, ischemia (the eye may be
white), chemosis, necrosis, and cataract (if severe).
3. Exposure keratopathy may occur acutely if there is
significant loss of lid tissue, or as a late complication
of lid cicatrization
CLINICAL FEATURES CONTINUE

7. Figure: Ocular thermal/burn injury.

8. • Lids
1. Superficial (1st degree) burns: commonly caused by
sunburn or short-duration flash burns. Dry burns
with oedema and no blistering; erythema and pain
are common; heals in ≤1wk, accompanied by
superficial peeling and no scar formation (although
discoloration may occur).
CLINICAL FEATURES CONTINUE

9. • Partial thickness (2nd degree) burns: causes include
longer-duration scalds and flame injury. Blisters and
weeping of the skin, intense erythema, significant
pain, and temperature sensitivity. Heals in 1–4wk,
with little scarring, but pigmentary changes common
CLINICAL FEATURES CONTINUE

10. • Full-thickness (3rd degree) burns: commonly caused
by chemical, electrical, flame, and scald injuries. Skin
appears dry, inflexible, and leathery, with little/no
pain. Heals with significant cicatrization and scarring.
CLINICAL FEATURES

11. Figure: Ocular and periocular burn

12. MANAGEMENT CONTINUE
• It is vital to first assess the extent of the burns injury.
If there is any suspicion from the history or
examination that the mouth/airways may have been
involved, immediate anaesthetic assistance is
mandatory with a view to assessing and stabilizing
the airway.

13. • Inhalational burns injuries can lead to airway
oedema and fatal airways/respiratory compromise.
1. Systemic
• Liaise with a burns specialist to optimize systemic
care and preferably for admission to a specialist
burns unit. Some general principles are included
here.
MANAGEMENT CONTINUE

14. Resuscitation with IV fluids
• Fluid resuscitation is critical within the first 24h. The
amount of fluid resuscitation can be determined
from the % BSA (body surface area) involved.
MANAGEMENT CONTINUE

15. • Estimate fluid replacement by the Parkland
Formula: Fluid for first 24h (mL) = 4 × patient's weight
in kg × % BSA (body surface area)
MANAGEMENT CONTINUE

16. • General skin care
1. Air-fluidized bed if large BSA (body surface area)
involved.
2. Reverse barrier nursing.
3. Leave intact blisters, and gently remove necrotic
skin only
MANAGEMENT CONTINUE

17. 2. Ocular
• Essentially as for chemical injuries, but limited role
for irrigation. In summary:
• Topical antibiotics: Prophylaxis
• Topical cycloplegia: For comfort / Anterior chamber
activity
MANAGEMENT CONTINUE

18. • Topical lubricants (preservative-free, e.g. carmellose
1–4-hourly + liquid paraffin).
• Consider topical steroids, especially in the presence
of significant oedema (preservative-free, e.g.
prednisolone 0.5–1% initially 4–8×/d for <10d).
MANAGEMENT CONTINUE

19. MANAGEMENT OF LID THERMAL INJURIES
continue..
• Superficial burns: cool compresses; lubrication; pain
control.
• Partial-thickness burns: topical antibiotic ointment;
copious lubrication ±occlusion dressing or moisture
chamber; trim eyelashes if singed (lash particles
cause irritation.

20. • Full-thickness burns: as for partial-thickness burns +
debride dead tissue and eschar; protect the eye with
lubrication, jelonet® and Geliperm® dressings, and
tarsorrhaphy.
MANAGEMENT OF LID THERMAL INJURIES

21. COMPLICATIONS CONITNUE
1. Loss of lid tissue: leads to corneal exposure.
2. Lid cicatrization: leads to entropion/ectropion,
trichiasis, and corneal exposure.
3. Epiphora: from damage to the punctae/lacrimal
ducts.

22. 4. Conjunctival burns: cicatricial changes,
symblepharon, and severe dry eye (through damage
to goblet cells, accessory lacrimal and meibomian
glands (MGs)).
5. Significant limbal ischemia: conjunctivalization,
vascularization, and opacification of the cornea.
COMPLICATIONS

23. Figure: Conjunctivalization of the cornea

24. CHEMICAL INJURY

25. DEFINITION
• A chemical burn occurs when any type of chemical
enters the eye.

26. CAUSES CONTINUE
1. Acids:
• Hydrofluoric acid
• Sulphuric acids

27. Figure: Acid (HCL) burn

28. 2. Alkalis:
• Ammonia,
• Sodium
• Hydroxide
• Lime
CAUSES

29. Figure: Alkali burn

30. PROGNOSTIC FACTORS
The severity of a chemical corneal injury is determined
by the following:
• pH
• Duration of contact
• Corneal involvement
• Limbal involvement
• Conjunctival involvement

31. CLINICAL FEATURES
1. Conjunctival injection or ischemia
2. Perilimbal ischemia/limits
3. Anterior chamber activity and fibrin
4. Scleral necrosis, vitritis, necrotic retinopathy

32. CLASSIFICATION OF SEVERITY
Classification of severity of ocular surface burns
Grade Comeal appearance Limbal ischemia Prognosis
I Clear cornea Nil Good
II Hazy cornea ; iris details visible <1/3 Good
III Opaque cornea; iris detail 1/3 to ½ guarded
IV Opaque cornea; iris detail obscured >1/2 Poor

33. Alternative Classification of severity of ocular surface
burns, highlighting limbal involvement
Grade Limbal involvement (clock
hours)
Conjunctival
involvement (%)
Prognosis
I 0 0 Very Good
II ≤3 ≤30 Good
III >3-6 >30-50 Good
IV >6-9 >50-75 Good to guarded
V >9-12 >75-<100 Guarded to poor
VI 12 (total) 100 (total) Very poor

34. COMPLICATIONS CONTINUE
• Conjunctival burns: cicatrization (scarring),
symblepharon formation, loss of goblet cells,
keratinization.
• Significant limbal ischemia: conjunctivalization,
vascularization, and opacification of the cornea.

35. • Full-thickness burns: scleritis, vitritis, retinitis,
glaucomatous optic neuropathy or hypotony, iris,
ciliary, and lenticular damage.
• Periorbital burns: first-/second-/third-degree
chemical burns of periorbital tissues.
COMPLICATIONS

36. Figure: Symblephron formation following chemical injury.

37. Figure: Limbal ischemia (inferonasally quadrant)
following alkali burn

38. Figure: Periorbital burn

39. WORK-UP CONTINUE
• History: Time of injury? Specific type of chemical?
Time between exposures until irrigation was started?
Duration/amount of and type of irrigation? Eye
protection?

40. • Slit lamp examination with fluorescein staining.
Eyelid eversion to search for foreign bodies. Evaluate
for conjunctival or corneal ulcerations or defects.
Check the intraocular pressure (IOP).
WORK-UP CONTINUE

41. • In the presence of a distorted cornea, IOP may be
most accurately measured with a Tono-Pen,
pneumotonometry, or care. Gentle palpation may be
used if necessary.
WORK-UP

42. TREATMENT CONTINUE
• Treatment should be instituted IMMEDIATELY, even
before testing vision, unless an open globe is
suspected
Immediate irrigation
• Neutralization of pH (7.0-7.4) by irrigation before full
history and examination.

43. • Test pH with litmus paper, then instil topical
anaesthetic; insert a speculum, and irrigate with
water, normal saline, Ringer lactate solution, or
Hartmann’s solution through IV (intravenous) tubing,
and deliver a minimum of 2L or until normal pH is
restored.
TREATMENT CONTINUE

44. Acute: all injuries
• Admit: if severe or any other concerns.
• Topical antibiotics
• Topical cycloplegia
• Topical lubricants
• Oral analgesia (e.g. paracetamol ± codeine).
TREATMENT CONTINUE

45. Acute: injuries with IOP (intraocular pressure)
• Acetazolamide 250mg 4×/d ± topical β-blocker
(e.g. preservative-free timolol 0.5% 2×/d).
• Alpha-agonists should be avoided because of
their vasoconstrictive properties, especially if
limbal ischemia is present.
TREATMENT CONTINUE

46. Long-term: Complicated Cases
• Poor corneal healing
• Medical treatment for persistent epithelial defects.
Surgical treatment includes techniques to assist
epithelial migration (amniotic membrane (AM)
transplantation) and re-epithelialization of the cornea
(limbal stem cell transplantation)
TREATMENT CONTINUE

47. Corneal opacification
• Consider limbal epithelial stem cell transplantation
followed by penetrating keratoplasty (PK) if adequate
tear film. In bilateral cases, Keratoprosthesis remains
a surgical option in severely damaged eyes.
TREATMENT

48. THANK YOU