Chemical Injuries of the Eye

advertisement
CHEMICAL INJURIES OF
THE EYE
Ayesha S Abdullah
07.04.2015
Learning outcomes
By the end of this lecture the students would be able to
 Describe the epidemiology of chemical ocular injuries
 Correlate the pathophysiology of chemical injury with
acids and alkali to the clinical presentation &
complications
 explain the first aid measure and later management of a
case with chemical injury.
 Identify the complications of chemical injury and correlate
it with the underlying pathology, suggest ways for the
primary, secondary and tertiary prevention of such injuries
Case







Gul Nawaz aged 35 years presented to emergency
deparment with injury to the right eye while working in a
cement factory. He had severe ocular irritation with
watering, pain and photophobia.
The eye was extensively washed till the normal pH was
restored
On examination VA OD=CF 1 m, OS=6/5
He had red eye with corneal haze
There was limbal ischemia affecting less than 1/3rd of the
limbus (3 clock hours)
The IOP was 24 mmHg OD, 11 mmHg OS
Examine the given photograph
Questions









What kind of injury is this?
Acidic/ alkaline- would it make any difference?
Why was the eye washed first?
What is limbal ischemia and what is its significance in
this patient?
Why was the IOP raised?
Why such an extensive damage?
What would be the prognosis of this kind of injury?
What complications can happen?
How can chemical injuries be prevented?
Epidemiology






Why should you know this?
About 2/3rd of the chemical injuries happen at
workplace the rest at home
Almost any chemical can cause ocular irritation
Serious damage however happen with acids and
alkalis
Alkali injuries are more common because they are
used more frequently
Bilateral chemical exposure could be extremely
damaging resulting in blindness and disfigurement


Calcium hydroxide is the most common cause of
alkali ocular burns, ammonia tends to cause the
most serious burns
Sulfuric acid is the most common acidic caustic agent
but hydrofluoric acid causes the most devastating
injury
Sources

Common sources of alkali are
Cleaning products (eg, ammonia)
 Fertilizers (eg, ammonia)
 Drain cleaners (e.g, lye)
 Cement, plaster, mortar (e.g, lime)
 Airbag (automobile) rupture (e.g, sodium hydroxide)
 Fireworks (eg, magnesium hydroxide)
 Potash (eg, potassium hydroxide)


Commonest alkalis causing chemical injury are
ammonia, sodium hydroxide & lime
Sources

Common sources of acids are as follows:
Battery acid (eg, sulfuric acid)
 Bleach (eg, sulfurous acid)
 Glass polish (eg, hydrofluoric; behaves like an alkali)
 Vinegar (eg, acetic acid)
 Chromic acid (brown discoloration of conjunctiva)
 Nitric acid (yellow discoloration of conjunctiva)
 Hydrochloric acid


Commonest acids are sulphuric, sulphurous, hydrofluoric,
acetic , chromic and hydrochloric acid.
Pathophysiology

Severity depends upon
 The
nature/ properties & concentration of the chemical
 Area of the affected surface
 Length of exposure
 Associated damage e.g. thermal /electrical/ explosive
Pathophysiology



Alakli burns are more damaging than acid burns
because it penetrates deeper1
Necrosis and shedding of the corneal and conjunctival
epithelium
Damage to the limbal vasculature
Limbal ischemia
 Persistent corneal epithelial defects
 Conjunctivaliztion & vascularization of the cornea
 Corneal ulceration and perforation
 Conjunctival and adnexal scarring

Corneal healing



Loss of epithelium
Migration of cell derived from the limbal stem cells
Phagocytosis of the necrosed collagen by the
keratocytes and new collagen is laid down
Clinical presentation

History
 Ascertain

the nature of the chemical and mode of injury
Complaints are
 Pain
(often extreme)
 Foreign body sensation
 Blurred vision
 Excessive tearing
 Photophobia
 Red eye(s)
Physical examination



Physical examination: General and Ocular
A thorough physical examination should be deferred
until the affected eye is irrigated copiously, and the pH
of the ocular surface is neutralized.
After irrigation, a thorough eye examination is
performed focusing on
1. clarity and integrity of the cornea
2. degree of limbal ischemia
3. Anterior chamber reaction
4. Signs of deeper penetration of the chemical
5. IOP.
Signs



Conjunctival inflammation:
Particles in the conjunctival fornices.
Perilimbal ischemia (LI-blanching) The most significant
prognostic indicator for corneal healing. Greater the
extent of blanching, the worse the prognosis. LI is
documented as number of clock hours
Signs



Corneal epithelial defect: Corneal epithelial
damage can range from mild diffuse punctate
epithelial keratitis (PEK) to a complete epithelial
defect. 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 0-5) to a complete opacification
Increased IOP
Signs



Corneal perforation
Anterior chamber inflammatory reaction: more
common with alkali injury
Adnexal damage/scarring: Similar to chemical
injuries on other skin areas, this can lead to severe
exposure problems if eyelid scarring prevents
proper closure, thereby exposing an already
damaged ocular surface.
Grading of the extent of injury & prognosis
Goals of management


Treat Systemic injury
Goals for ocular involvement
 removing
the offending agent
 controlling inflammation
 promoting ocular surface healing
 preventing infection
 controlling IOP
Remove the chemical (irrigation)



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.
Irrigation should be continued until the pH of the ocular
surface is neutralized, usually requiring 1-2 liters of
fluid.
Promote ocular surface (epithelial)
healing





Artificial tears
Bandage contact lens
Ascorbate plays a fundamental role in collagen
remodeling, leading to an improvement in corneal
healing.
Amniotic membrane transplant
topical Sodium Ascorabte 10% given 2 hourly and
1-2 g of vitamin C given orally ( not recommended
in renal disease)
Control inflammation




Inflammatory mediators
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.
Prevent infection


When the corneal epithelium is absent, the eye is
susceptible to infection.
Prophylactic topical antibiotics during the initial
treatment stages
Control IOP
• Oral acetazolamide and topical medications
Control pain



Severe chemical burns can be extremely painful.
Oral NSAIDS
Ciliary spasm can be managed with the use of
cycloplegic agents
Surgical Care

Early





Debridement
Temporary amniotic membrane
Limbal stem cell transplant
Lysis of conjunctival symblepharon
Late





Surgery for conjunctival adhesions
Keratoplasty
Cataract extraction
Keratoprosthesis
Glaucoma surgery
Follow up



In patients with severe chemical injuries, short
hospitalization in an ophthalmic care unit to closely
monitor
In general, the prognosis of ocular chemical injuries
is directly correlated with the severity of insult to
the eye and adnexal structures.
Roper-Hall grading system
Complications

Primary complications include the following:
 Conjunctival
inflammation
 Corneal abrasions
 Corneal haze and edema
 Acute rise in IOP
 Corneal melting and perforations
Complications

Secondary complications include the following:
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)
 Blindness

Management summary




Immediate, prolonged irrigation
Followed by referral to ophthalmologist for
aggressive early management
Close long-term monitoring
Are essential to promote ocular surface healing and
to provide the best opportunity for visual
rehabilitation
Download