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Contents
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1 Disease Entity
1.2 Epidemiology
1.3 Etiology
1.4 Pathophysiology
1.4.1 Alkali
1.4.2 Acids
1.5 Primary prevention
2 Diagnosis
2.1 History
2.3 Symptoms
3 Management
3.1 Irrigation
3.4.1 Grade I
3.4.2 Grade II
3.4.4 Grade IV
3.6 Follow up
3.7.1 Glaucoma
4 Additional Resources
5 References
Epidemiology[edit source]
Chemical injuries to the eye represent between 11.5%-22.1% of ocular traumas. [1]About two thirds of
these injuries occur in young men. The vast 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 than acid
injuries.[2]
Etiology[edit source]
Chemical injuries occur as a result of acid, alkali, or neurtral agents. Common causes of alkali and
acid injuries are listed below.[2][3]
Pathophysiology[edit source]
Alkali[edit source]
Alkali agents are lipophilic and therefore penetrate tissues more rapidly than acids.
They saponify the fatty acids of cell cell membranes, penetrate the corneal stroma and
destroyproteoglycan ground substance and collagen bundles. The damaged tissues then
secrete proteolytic enzymes, which lead to further damage.[4][5]
Acids[edit source]
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). [5] 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.[6]
Diagnosis
[edit source]
History[edit source]
The severity of ocular injury depends on four factors: the toxicity of the chemical, how long the
chemical is in contact with the eye, the depth of penetration, and the area of involvement. It is
therefore critical to take a careful history to document these factors. The patient should be asked
when the injury occurred, whether they rinsed their eyes afterwards and for how long, the
mechanism of injury (was the chemical under high pressure?), the type of chemical that splashed in
the eye, and whether or not they were wearing eye protection. If available, it is helpful to obtain the
packaging of the chemical. There is often product information on this packaging including chemical
composition. If this information is not immediately available, chemical information can be found by
contacting the local poison control center at aapcc or 1 800-222-1222.
schemes below). Specifically, the degree of corneal, conjunctival and limbalinvolvement should be
documented, as it can be used to predict ultimate visual outcome.[7]
The palpebral fissures should be checked and the fornices should be swept during the initial exam.
Both the palpebral and bulbar conjunctiva should be examined with fluoresceinunder a cobalt blue
light. As above, retained particulate matter can cause persistent damage, despite irrigation.
The intraocular pressure should also be documented, as alkali injuries have been found to both
acutely and chronically cause an elevation of IOP.[8]
Two major classification schemes for corneal burns are the Roper-Hall (modified Hughes)
classification[9][10] and the Dua classification.[11] 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 involvement. In a randomized
controlled trial of acute burns, the Dua classification was found to be superior to the Roper-Hall in
predicting outcome in severe burns.[7] However, both classification schemes are commonly employed
in daily practice.
Symptoms[edit source]
The most common symptoms are severe pain, epiphora, blepharospasm, and reduced visual acuity.
Management
[edit source]
Irrigation[edit source]
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. To optimize patient comfort and ensure effective delivery of the
irrigating solution, a topical anesthetic is generally administered. An eyelid speculum or Morgan
Lens (MorTan, Missoula MT) can be used to keep the eye open, while the irrigating solution is
delivered through IV tubing. There has been some debate on the most effective irrigating solutions. A
study by Herr et al. compared Normal Saline (NS), Normal Saline with Bicarbonate (NS +
Bicarb),Lactated Ringers solution (LR), and Balanced Saline Solution Plus (BSS Plus, Alcon
Laboratories, Fort Worth, TX) irrigating solutions to investigate which solution optimized patient
comfort. They found that patients tolerated and preferred BSS irrigation compared to NS, NS +
Bicarb, and LR.[12] In experiments in rabbit eyes following sodium hydroxide injury, a borate buffer
solution called Cedderroth eye wash(Cedderroth Industrial Products, Upplands Vaasby Sweden) and
a Diphthorine and Previn solution (Prevor, Cologne Germany) more efficiently normalized the pH
compared to saline and phosphate buffer solutions.[13] Of course, early irrigation is paramount to
limiting the duration of chemical exposure. If clean water is available at the site of injury and a
standard irrigating solution is not, then the eyes should immediately be washed out with water. [14][15]
proteolytic enzymes. Citrate is a potent chelator and can therefore decrease proteolytic activity.
Citrate also appears to inhibit collagenases.[22][23]
1% Medroxyprogesterone- is a progestational steroid and has less anti-inflammatory potency than
corticosteroids, but has a minimum effect on stromal repair.Medroxyprogesterone can therefore be
substituted for cortical steroids after 10-14 days of steroid treatment. [2][24]
Platelet rich plasma eye drops- have been found to be rich in growth factors and platelet rich
plasma eye drops can lead to faster epithelialization for certain classes of burns.[25]
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. Numerous studies have found a reduction in pain following AMT for
moderate to severe burns.[27][28] Through its physical actions, AMT may also
prevent symblepharon formation. Amniotic membrane is also felt to have biologic effects. [29] It
expresses TGFB1 and epidermal growth factor, which have roles in wound healing.[30][31] It has also
been found to have anti-inflammatory properties.[32][33][34] Taken together, these biological effects may
dampen inflammation, promote epithelial growth, prevent scarring and prevent neovascularization.
New delivery devices like ProKera (Bio-Tissue, Miami, Florida), which consists of a piece
of cryopreserved amniotic membrane clipped into a dual ring system, like a symblepharon ring,
allows rapid and sutureless placement of amniotic membrane.[35] A recent Cochrane review found
only one randomized controlled trial of amniotic membrane for treatment of chemical ocular burn in
the first seven days following injury.[1]Patients with moderate burns were found to have a significantly
better visual acuity following AMT compared to medical therapy alone.[36] However, this was an
unmasked trial and there were uneven baseline characteristics of the control and treatment eyes.
[1]
While case series and reviews show great promise of AMT in the treatment of chemical burns,
conclusive evidence is still lacking.
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 stem cells are located at the base of the limbal epithelium and are responsible for
repopulation of cells in the corneal epithelium and inhibition of conjunctival growth over the cornea.
[37]
Limbal autografts can be used from the healthy contralateral eye if only one eye is injured in a
chemical burn.[38] When both eyes are injured, transplants have been attempted from living related
donors. In a recent study from China, a portion of the limbus of HLA matched living related
donors (allograft) was transplanted following chemical injury. Patients experienced a reduction in
vascularity, improved corneal opacity and corneal epithelialization without the need for systemic
immunosuppression.[37] Another option is to use cadaveric donors. This requires systemic
immunosuppression.[39] When possible, limbal stem cell transplantation should be delayed until ocular
surface inflammation has quieted.[40][41]
Cultivated oral mucosal epithelial transplantation (COMET)- can also be used to promote reepithelialization and reduce inflammation in corneal burns. The cells are harvested from the patients
own buccal mucosa so that systemic immunosuppression is not necessary.[42][43]
Boston Keratoprosthesis- Severe chemical injury leads to chronic inflammation and scarring,
making visual recovery challenging. In cases with severe inflammation, limbal stem cell transplants
and corneal transplants do not survive. In these most difficult cases, the Boston
Keratoprosthesis can be used. Because it is independent of stem cell function, it does not require
systemic immunosuppression.[44]
If there is pain, consider a short acting cycloplegic like cyclopentolate three times a day
As for Grade II
Consider amniotic membrane transplant/Prokera placement. This should ideally be
performed in the first week of injury
Figure E
Figure F
*Images courtesy of Dr. Kathryn Colby (Massachusetts Eye and Ear Infirmary)
even in the healthiest appearing eyes, patients need long term monitoring for glaucoma and dry
eye as below.
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