1) Chemical injuries to the eye are common, ranging from mild irritation to complete destruction of ocular tissues. Alkali agents are more damaging than acids due to their ability to penetrate tissues. 2) Treatment depends on severity but generally involves immediate irrigation, antibiotics, steroids, and artificial tears. More severe injuries may require amniotic membrane transplantation or limbal stem cell transplant. 3) Even with treatment, complications can include dry eye, glaucoma, eyelid scarring, and vision loss. Patients require long-term follow up due to risk of these complications.

1. CHEMICAL INJURY By Dr. Ibrahim Khalil El-
Nakhal

2. Chemical trauma to the
external eye is a common
problem that can range in
severity from mild irritation
to complete destruction of
the ocular surface
epithelium, corneal
opacification, loss of vision,

3. EPIDEMIOLOGY

4. Chemical injuries to the eye
represent between 11.5%-22.1% of
ocular traumas. About two thirds of
these injuries occur in young men.
The majority occur in the workplace
as a result of industrial accidents. A
minority of injuries occur in the home
or secondary to assault. Alkali
materials are found more commonly
in building materials and cleaning
agents and occur more frequently

5. ETIOLOGY

6. The chemical may be in the form of a solid,
liquid, powder, mist, or vapor. And may result of
acid, alkali, or neutral agents. Chemical injuries
can occur in the home, most commonly from
detergents, disinfectants, solvents, cosmetics,
cleaners, ammonia, bleach, and other common
household alkaline agents.
Fertilizers and pesticides are common offending
agents in agricultural chemical injuries.
In the workplace, plaster and cement products
are frequent causes of alkali burns due to
calcium hydroxide. Chemical injuries occurring in
industry are usually caused by caustic chemicals

8. Some of the worst ocular chemical
injuries result from strong alkalis or
acids. Whenever possible, the
offending chemical agent should be
identified, because the severity of a
chemical injury depends on the pH,
the volume and duration of contact,
and the toxicity of the chemical

9. PATHOPHYSIOLOGY

10. ALKALI BURNS
Alkali agents are lipophilic and therefore penetrate
tissues more rapidly than acids. They saponify the fatty
acids of cell membranes, penetrate the corneal stroma
and destroy proteoglycan ground substance and
collagen bundles. The damaged tissues then secrete
proteolytic enzymes, which lead to further damage.
Strong alkaline substances may also penetrate the
anterior chamber, producing severe tissue damage and
intense inflammation. The visual prognosis is often
determined by the extent of ocular surface injury The
most unfavorable visual prognosis is associated with
extensive limbal epithelial damage and intraocular
chemical penetration. Severe damage to the limbal area
can leading to ischemia to the limbus .

11. ACID BURNS
Acids are generally less harmful than alkali
substances. They cause damage by
denaturing and precipitating proteins in the
tissues they contact. The coagulated
proteins act as a barrier to prevent further
penetration (unlike alkali injuries). The one
exception to this is hydrofluoric acid, where
the fluoride ion rapidly penetrates the
thickness of the cornea and causes
significant anterior segment destruction.

12. SYMPTOMS

13. The most common symptoms are
•Severe pain.
•Epiphora.
•Blepharospasm.
•Reduced visual acuity.

14. Two major classification for corneal
burns are the Roper-Hall (modified
Hughes) classification and the Dua
classification. The Roper-Hall
classification is based on the degree
of corneal involvement and limbal
ischemia. The Dua classification is
based on an estimate of limbal
involvement (in clock hours) and the
percentage of conjunctival

16. PRIMARY
PREVENTION

17. Since the majority of injuries
occur at work, protective eye
shields are mandatory when
handling potentially corrosive
substances. However, even
protective are no match for
chemicals under high pressure.

18. MANAGEMENT

19. IRRIGATION

20. Early irrigation is critical in limiting the
duration of chemical exposure. The goal of
irrigation is to remove the offending
substance and restore the physiologic pH. It
may be necessary to irrigate as much as 20
liters to achieve this.
irrigating solutions :
Normal Saline (NS), Normal Saline with
Bicarbonate (NS + Bicarb), Lactated Ringer’s
solution (LR), Balanced Saline Solution and
water

21. MEDICAL THERAPY
The aims of medical treatment are to enhance recovery of the corneal
epithelium and augment collagen synthesis, while also minimizing
collagen breakdown and controlling inflammation.
•Antibiotics: a topical antibiotic ointment like erythromycin
ointment four times daily can be used to provide ocular lubrication
and prevent superinfection. Stronger antibiotics (e.g. a
topical fluoroquinolone) are employed for more severe injuries (e.g.
Grade II and above).
•Steroid drops: In the first week following injury, topical steroids can
help calm inflammation and prevent further corneal breakdown
In mild injuries, topical prednisolone (Predforte) can be employed
four times daily. In more severe injuries, prednisolone can be used
every hour. After about one week of intensive steroid use, the
steroids should be tapered because the balance of collagen synthesis
vs. collagen breakdown may tip unfavorably toward collagen

22. •Cycloplegic agents: such as atropine or cyclopentolate can help with
comfort.
•Artificial tears: and other lubricating eye drops, preferably preservative
free, should be used generously for comfort.
•Ascorbic acid: is a cofactor in collagen synthesis and may be depleted
following chemical injury. Ascorbic acid can be used as a topical drop
(10% every hour) or orally (two grams, four times daily in adults).
•Doxycycline: acts independently of its antimicrobial properties to reduce
the effects of matrix metalloproteinases (MMPs), which can degrade type I
collagen thereby reducing ocular surface inflammation
•Citrate drops: histological sections of cornea from alkali burns reveal an
intense polymorphonuclear infiltrate (PMN). PMNs provide a major source
of proteolytic enzymes, which can dissolve the corneal stromal collagen.
Deficiency in calcium inhibits the PMNs from granulating and releasing
proteolytic enzymes. Citrate is potent chelator and can therefore
decrease proteolytic activity.
•Platelet rich plasma eye drops: have been found to be rich in growth

23. SURGICAL TREATMENTS
•Debridement of necrotic epithelium: should be performed
as early as possible because necrotic tissue serves as a
source of inflammation and can inhibit epithelialization.
•Conjunctival/Tenon’s transposition (Tenonplasty): in
Grade IV burns Tenon’s transposition can be employed to
reestablish limbal vascularity and facilitate re-
epithelialization.

24. •Amniotic membrane transplantation (AMT): the
purpose of AMT is to rapidly restore the conjunctival
surface and to reduce limbal and stromal
inflammation. The benefits are thought to be two fold:
physical and biological
Physically, AMT has been shown to improve patient
comfort by reduction of eyelid friction. and may also
prevent symblepharon formation.
biologically It expresses TGFB1 and epidermal growth
factor, which have roles in wound healing. It has also
been found to have antiinflammatory properties.
Taken together, these biological effects may dampen
inflammation, promote epithelial growth, prevent
scarring and prevent neovascularization.

25. •Limbal stem cell transplant
Much of the damage following chemical injuries results from
limbal ischemia and the subsequent loss of stem cells capable
of repopulating the corneal epithelium.Limbal stem cell
transplants have been employed to replace this critical group
of cells. Limbal autografts can be used from the healthy
contralateral eye if only one eye is injured in a chemical burn
•Cultivated oral mucosal epithelial transplantation (COMET)-
can also be used to promote re-epithelialization and reduce
inflammation in corneal burns. The cells are harvested from
the patient’s own buccal mucosa
•Boston Keratoprosthesis In cases with severe inflammation,
limbal stem cell transplants and corneal transplants do not
survive. In these most difficult cases, the Boston

26. RECOMMENDED TREATMENT
Patients with mild to moderate injury (Grade I and II) have a good
prognosis and can often be treated successfully with medical
treatment alone.
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, consider a short acting cycloplegic like
cyclopentolate three times a day

27. Grade II
•Topical antibiotic drop like fluoroquinolone four times daily
•Prednisolone acetate 1% hourly while awake for the first 7-10
days.
•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

28. Grade III
As for Grade II
Consider amniotic membrane transplant. This should ideally be
performed in the first week of injury
Grade IV
As for Grade II/III
Early surgery is usually necessary. For significant necrosis, a
Tenonplasty can help re-establish limbal vascularity. An
amniotic membrane transplant is often necessary due to the
severity of the ocular surface damage.

29. FOLLOW UP

30. With severe chemical burns, patients
should initially be followed daily. If
there is concern for compliance with
medication or if the patient is a child,
one should consider inpatient
admission. Once the health of the
ocular surface has been restored,
follow up can be spread apart.
However, even in the healthiest
appearing eyes, patients need long

31. COMPLICATIONS

32. •Glaucoma
ranging in frequency from 15%-55% in patients with severe
burns. The mechanism of glaucoma is multifactorial and
includes contraction of the anterior structures of the globe
secondary to chemical and inflammatory damage, inflammatory
debris in the trabecular meshwork, and damage to the
trabecular meshwork itself. Glaucoma medications should be
prescribed as necessary to maintain normal intraocular
pressure
•Dry eye
Chemical injury can destroy conjunctival goblet cells, leading to
a reduction or even absence of mucus in the tear film
•Damage to the eyelids or palpebral conjunctiva
•Direct chemical damage to the conjunctiva can lead to scarring,
forniceal shortening, symblepharon formation and

33. THANK YOU