CHEMICAL BURNS

PRESENTER -DR RAHUL

MODERATOR -DR SANGIT

OCULAR BURNS
Ocular burns constitute true ocular

emergencies
Both thermal and chemical burns represent

potentially blinding ocular injuries

Thermal burns result from accidents

associated with
-firework explosions
- steam
- boiling water
-molten metal (commonly aluminium)

Chemical burns
Chemical burns may be caused by either

alkaline or acidic agents

Alkali more frequently used in household

cleaning agents and many building materials

So Alkali injuries occurs more frequently than

acid injuries

Causes
Common sources of alkali are as follows:
Cleaning products (eg .ammonia) most
serious injury
Fertilizers (eg, ammonia)
Cement, plaster, (eg, lime)most common

injury
Fireworks (eg, magnesium hydroxide)

Pathophysiology
Alkaline agents have both hydrophilic and

lipophilic properties
which allow them to rapidly penetrate cell

membranes and enter the anterior chamber

Alkali damage results from interaction of the

hydroxyl ions

Pathophysiology
It causes saponification of cell membranes

and cell death along with disruption of the

extracellular matrix
Cations react with carboxyl group of stromal

collagen
And Glycosaminoglycans (GAGS)
Hydration of Gagas result in loss of clarity of

stroma

Increased IOP:
collagen deformation and
shortening
distorts trabecular
meshwork
An immediate rise in IOP

Pathophysiology
Penetration into AC may be almost

immediately after ammonia

Within 3-5 min after sodium hydroxide injury

Penetration into AC
Damage to ciliary body
epithelium

Decreased secretion of
ascorbate

Concentration in AC
decreases

stromal repair and

collagen synthesis
decreases

Acid injury
Common sources of acids are as follows:
Battery acid (eg, sulfuric acid)
Bleach (eg, sulfurous acid)
Glass polish (eg, hydrofluoric; )

Pathophysiology
Acids tend to cause less damage than alkalis
corneal proteins bind acid and act as a

chemical buffer.
coagulated tissue acts as a barrier to further

penetration of acid.
Acid binds to collagen and causes fibril

shrinkage which can cause symblepharon

formation

Classification
There is no ideal classification or grading

system for
ocular alkali burns
The principal weakness of grading system is

that injuries to the cornea are not uniformly

associated with injuries to the surrounding
tissues

Classification of severity of ocular

surface burns by Roper-Hall
Grade

prognosis

cornea

limbus

good

Corneal epithelial No limbal

damage
ischaemia

good

Corneal haze, iris <1/3 limbal

details seen
ischaemia

guarded

Total epithelial
loss,stromal
haze,iris details
obscured

1/3-1/2 limbal
ischaemia

poor

Cornea
opaque,iris and
pupil obscured

>1/2 limbal
ischaemia

Grade

Prognosis

Clinical
findings

Conjunctival
involvement

Analogue
scale

Very good

0 clock hours
of limbal
involvement

0%

0/0%

good

<3 clock
hours of
limbal
involvement

<30%

0.1-3/1-29.9%

good

>3-6 clock
hours of
limbal
involvement

>30-50%

3.1-6/31-50%

>50-75%

6.1-9/51-75%

Good to
guarded

>6-9 clock
hours of
limbal
involvement

Guarded to
poor

> 9-<12 clock >75-<100%

hours of
limbal
involvement

9.1-11.9/75.199.9%

Very poor

Total limbus

12/100%

Total

Clinical stages
The clinical course can be divided into three

distinct stages
I )Acute stage (immediate to 1 week)
II) Early repair stage (1-3week)
III) Late repair stage and sequel ( 3 weeks and
longer )

I )Acute stage (immediate to 1

week)
In mild burns the corneal and conjunctival

epithelium
have defects with sparing of limbal blood
vessels
in severe burns the epithelium is destroyed

and there is immediate limbal ischaemia due

to damage to blood vessels.

intraocular pressure
Rise in intraocular pressure in a bimodal

manner
An initial peak is due to compression of the

globe as a result of hydration and longitudinal

shortening of collagen fibrils.
The second peak due to impedence of

aqueous humor outflow

II Early repair stage (1-3week):

This stage is characterized by replacement of

destroyed cells and extracellular matrix.

In grade I and II chemical burns

- regeneration of epithelium
-neovascularization of cornea
-clearing of stroma
-beginning of synthesis of collagen
glycosaminoglycans

In grade III and IV

regeneration of epithelium may not start and

progress
stroma remains hazy
endothelium replaced by a retrocorneal

membrane.

Cont..
In this stage, corneal ulceration tends to

occur.
Stromal ulceration is due to action of

digestive enzymes such as

collagenase,metalloprotinase
released from regenerating corneal epithelium

and polymorphonuclear leukocytes.

III Late repair stage and sequele

( 3 weeks and longer )
This stage is characterized by completion of

healing
with a good prognosis (grade I and II )
complication in those with a guarded visual

prognosis
(grade III and IV)
Complications are primary and secondary

Complications
Primary complications
Conjunctival inflammation
Corneal abrasions
Corneal haze and edema
Acute rise in IOP
Corneal melting and perforations

Secondary complications
Secondary glaucoma
Secondary cataract
Conjunctival scarring
Corneal thinning and perforation
Complete ocular surface disruption with

corneal scarring and vascularization

Corneal ulceration(sterile or infectious)
Complete globe atrophy (phthisis bulbi):

Clinical case
4 yr boy presented to LEI with h/o plaster

falling into eyes while playing at construction

site
Eye wash given

History
Most often, the patient gives a history of a

liquid or a gas being splashed or sprayed into

the eyes or of particles falling into the eyes.
we have to ask the patient regarding the

specific nature of the chemical and the

mechanism of injury (eg, simple splash vs
high-velocity blast).

Physical examination
A thorough physical examination should be

deferred until the affected eye is irrigated

copiously
The pH of the ocular surface is neutralized.
Topical anesthetic drops may be used to aid

in patient comfort and cooperation.

Cont..
After irrigation, a thorough eye examination is

performed
special attention given to

- clarity and integrity of the cornea

-degree of limbal ischemia
- IOP.

Physical manifestations
Decreased visual acuity:

It can be decreased because of

-corneal epithelial defects,
-haze,
-increased lacrimation or discomfort.

Particles in the conjunctival

fornices
- This finding is more common with particulate
injuries, such as plaster.
- If not removed the residual particles can
serve as a reservoir for continued chemical
release and injury.
-These particles must be removed before ocular
surface healing can begin

Perilimbal ischemia:

-The degree of limbal ischemia (blanching)is the

most significant prognostic indicator for future
corneal healing
-The limbal stem cells are responsible for
repopulating the corneal epithelium.
-The greater the extent of blanching, the worse
the prognosis.

Cont..
But, the presence of intact perilimbal stem

cells does not guarantee normal epithelial

healing.
The extent of blanching should be

documented in terms of clock hours involved

Corneal epithelial defect

It can range from mild diffuse punctate

epithelial keratitis (PEK) to a complete

epithelial defect.
A complete epithelial defect may not take up

fluorescein dye rapidly , so, it may be missed.

Cont..
If an epithelial defect is suspected but not

found on the initial evaluation, the eye should

be reexamined after several minutes.
The size of the defect should be recorded so

as to document response to treatment on

subsequent visits

Stromal haze:

Haze can range from a clear cornea (grade 0)

to a complete opacification (grade 5) with no
view into the anterior chamber.
Corneal perforation:
A very rare finding at presentation
it is more likely to occur after the initial
presentation (from days to weeks) in severely
injured eyes that have poor healing capacity.

A. c inflammatory reaction

This can vary from trace cell and flare to a

vigorous fibrinoid anterior chamber reaction.

Generally, this finding is more common with

alkaline injuries because of the greater depth

of penetration

Adnexal damage/scarring:

Similar to chemical injuries on other skin

areas, it can lead to severe exposure

problems
eyelid scarring prevents proper closure,

exposing an already damaged ocular surface

Medical Care

Regardless of the underlying chemical

involved, common goals of management

include
(1)removing the offending agent,
(2) promoting ocular surface healing
(3) controlling inflammation,
(4) preventing infection,
(5) controlling IOP.

Immediate therapy
Immediate copious irrigation remains the

single most important therapy for treating

chemical injuries.
Ideally, the eye should be irrigated with a sterile

balanced buffered solution, such as normal saline

solution or Ringer's lactate solution.
However, immediate irrigation with even plain

tap water is preferred without waiting for the

ideal fluid.

The irrigation solution must contact the ocular

surface.
This is best achieved with a special irrigating

tubing (eg, Morgan lens) or a lid speculum.

Irrigation should be continued until the pH of

the ocular surface is neutralized, usually

requiring 1-2 liters of fluid.

 artificial tear supplements play an important

role in healing.
Ascorbate plays a fundamental role in

collagen remodeling, leading to an

improvement in corneal healing.
Placement of a therapeutic bandage contact

lens helpful in some patients.

Control inflammation
Inflammatory mediators released from the ocular

surface at the time of injury cause tissue necrosis

This inflammatory response not only inhibits

reepithelialization but also increases the risk of

corneal ulceration and perforation.
Controlling inflammation with topical steroids can

help break this inflammatory cycle.

.

Citrate both promotes corneal wound healing

and inhibits PMNs via calcium chelation.

Acetylcysteine (10% or 20%) can inhibit

collagenase to reduce corneal ulceration

Prevent infection
When the corneal epithelium is absent, the

eye is susceptible to infection.

Prophylactic topical antibiotics are warranted

during the initial treatment stages.

Control IOP
The use of aqueous suppressants is

advocated to reduce IOP secondary to

chemical injuries
both as an initial therapy and during the later
recovery phase, if IOP is high (>30 mm Hg)
Carbonic anhydrase inhibitors
Topical beta-blockers

Control pain
Severe chemical burns can be extremely

painful.
Ciliary spasm can be managed with the use of

cycloplegic agents
however, oral pain medication may be

necessary initially to control pain

Cycloplegic mydriatics

Surgical therapy
A)Promote Reepithelialization
B)Support repair and minimize ulceration
C)Late rehabilitation

A)Promote Reepithelialization
1)Conjunctival /tenons advancement
(tenoplasty)
2)Limbal stem cell transplantation
3)Conjunctival transplantaion
4)keratoepithelioplasty

B)Support repair and minimize

ulceration
1)Tenoplasty
2)Limbal stem cell transplantation
3)Large diameter therapeutic pk
4)Tissue adhesive

C)Late rehabilitation
1)Late stem cell transplantation
2)Conjunctival transplantation
3)Mucosal membrane grafts
4)PK

Prevention
Education and training regarding the

prevention of chemical exposures in the

workplace can help prevent chemical injuries
to the eye.
Persons who may be exposed to chemicals in

the workplace are advised to wear safety

goggles.

Patient Education
If the injury resulted from a preventable

accident, proper safety instruction should be

provided.
If a patient is left functionally monocular from

an injury, the patient should be instructed in

the use of safety eyewear (eg, polycarbonate
lens)