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

1 good Corneal epithelial No limbal ischaemia

damage

2 good Corneal haze, iris <1/3 limbal ischaemia

details seen

3 guarded Total epithelial 1/3-1/2 limbal

loss,stromal ischaemia
haze,iris details
obscured
4 poor Cornea opaque,iris >1/2 limbal ischaemia
and pupil obscured
Grade Prognosis Clinical Conjunctival Analogue
findings involvement scale

1 Very good 0 clock hours of 0% 0/0%

limbal
involvement
2 good <3 clock hours <30% 0.1-3/1-29.9%
of limbal
involvement
3 good >3-6 clock hours >30-50% 3.1-6/31-50%
of limbal
involvement

4 Good to >6-9 clock hours >50-75% 6.1-9/51-75%

guarded of limbal
involvement

5 Guarded to poor > 9-<12 clock >75-<100% 9.1-11.9/75.1-

hours of limbal 99.9%
involvement

6 Very poor Total limbus (12 Total 12/100%

clock )involved conjunctiva
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)