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Chemical (Alkali and Acid) Injury of the

Conjunctiva and Cornea
Original article contributed by:
All contributors:
Assigned editor:
Review:

Danielle Trief, MD, James Chodosh MD, Kathryn Colby MD

Danielle Trief, MD and Maria A. Woodward, MD
Maria A. Woodward, MD
Not reviewed

Chemical (alkali and acid) injury of the conjunctiva and cornea is a true ocular emergency and
requires immediate intervention. Chemical injuries to the eye can produce extensive damage to
the ocular surface and anterior segment leading to visual impairment and disfigurement. Early
recognition and treatment ensures the best possible outcome for this potentially
blinding condition.

Contents

1 Disease Entity
o 1.1 International Classification of Diseases
o 1.2 Epidemiology
o 1.3 Etiology
o 1.4 Pathophysiology

1.4.1 Alkali

1.4.2 Acids

o 1.5 Primary prevention

2 Diagnosis
o 2.1 History
o 2.2 Physical examination
o 2.3 Symptoms

3 Management
o 3.1 Irrigation
o 3.2 Medical therapy

3.2.1 Standard Treatments

3.2.2 Other Treatments:

o 3.3 Surgical Treatments

o 3.4 Recommended Treatment

3.4.1 Grade I

3.4.2 Grade II

3.4.3 Grade III

3.4.4 Grade IV

o 3.5 Stages of Ocular Recovery

o 3.6 Follow up
o 3.7 Other long term complications

3.7.1 Glaucoma

3.7.2 Dry eye

3.7.3 Damage to the eyelids or palpebral conjunctiva

4 Additional Resources

5 References

Disease Entity
International Classification of Diseases
ICD-9-CM 940.2 alkaline chemical burn to cornea and conjunctiva, 940.3 acid chemical burn to
the cornea and conjunctiva, 372.06 chemical conjunctivitis
ICD-10-CM T26.60XA Corrosion of cornea and conjunctival sac, unspecified eye, initial
encounter.

Epidemiology
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
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
Alkali
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 destroy
proteoglycan ground substance and collagen bundles. The damaged tissues then secrete
proteolytic enzymes, which lead to further damage.[4][5]

Acids
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]

Primary prevention
Since the majority of injuries occur at work, protective eye shields are mandatory when handling
potentially corrosive substances (OSHA regulation, 1910.133). However, even protective
goggles are no match for chemicals under high pressure.

Diagnosis
History
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 1 800-2221222.

Physical examination
Prior to a full ophthalmic exam, the pH of both eyes should be checked. If the pH is not in
physiologic range, then the eye must be irrigated to bring the pH to an appropriate range
(between 7 and 7.2). It is recommended to wait at least five minutes after irrigation before
checking the pH to ensure that the pH does not rise or fall secondary to retained particulate
matter.
The physical exam should be used to assess the extent and depth of injury (see classification
schemes below). Specifically, the degree of corneal, conjunctival and limbal involvement 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 fluorescein under 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

The most common symptoms are severe pain, epiphora, blepharospasm, and reduced visual
acuity.

Management
Irrigation

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]

Medical therapy

Patients with mild to moderate injury (Grade I and II) have a good prognosis and can often be
treated successfully with medical treatment alone. 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.[3]

Standard Treatments
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).
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.
Steroid drops- In the first week following injury, topical steroids can help calm inflammation
and prevent further corneal breakdown.[14] 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 breakdown.[16]

Other Treatments:
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). In one study, severe alkali burns in rabbit eyes were associated with
reduced ascorbic acid levels in the aqueous humor. This reduction correlated with corneal
stromal ulceration and perforation. Systemic administration of Vitamin C helped promote
collagen synthesis and reduce the level of ulceration.[17]Care must be taken in patients with
compromised renal function because high levels of Vitamin C are potentially toxic to the
kidneys.[18]
Doxycycline- acts independently of its antimicrobial properties to reduce the effects of matrix
metalloproteinases (MMPs), which can degrade type I collagen. The tetracycline class inhibits
MMPs by restriction of the gene expression of neutrophil collagenase and epithelial gelatinase,
suppression of alpha 1 antitrypsin degradation and scavenging reactive oxygen species, thereby
reducing ocular surface inflammation.[19][20]
Citrate drops- histological sections of cornea from alkali burns reveal an intense
polymorphonuclear infiltrate (PMN).[21] 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 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]

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.[3]
Conjunctival/Tenons transposition (Tenonplasty)- in Grade IV burns, anterior segment necrosis
can result from loss of limbal vascular blood supply. In severe limbal ischemia, a sterile corneal
ulceration can ensue. After removal of necrotic tissue, a tenonplasty (advancement of the
conjunctiva and Tenons to the limbus) can be employed to reestablish limbal vascularity and
facilitate re-epithelialization.[26]

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
re-epithelialization 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]

Recommended Treatment
While there is variability in treatment strategies of chemical burns, most authors recommended a
graded approach depending on the severity of injury. Mild burns (Roper-Hall grade I) respond
well to medical treatments and lubrication, while more severe burns necessitate more intensive
medical therapies and surgery. Below is a paradigm for the initial treatment of chemical injury
based on the Roper-Hall grade of injury.[3][45]

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

Grade II

Topical antibiotic drop like fluoroquinolone four times daily

Prednisolone acetate 1% hourly while awake for the first 7-10 days. Consider tapering the
steroid if the epithelium has not healed by day 10-14. If an epithelial defect persists after
day 10, consider progestational steroids (1% medroxyprogesterone four times daily)

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 adhesive as needed

Grade III

As for Grade II

Consider amniotic membrane transplant/Prokera placement. This should ideally be

performed in the first week of injury. Experienced surgeons have emphasized placement
of the amniotic membrane to cover the palpebral conjunctiva by suturing to the lids in the
operating room, not just covering the cornea and bulbar conjunctiva.

Grade IV

As for Grade II/III

Early surgery is usually necessary. For significant necrosis, a Tenonplasty can help
reestablish limbal vascularity. An amniotic membrane transplant is often necessary due to
the severity of the ocular surface damage.

Stages of Ocular Recovery

Stages of ocular recovery following chemical injury- [3][6]

Figure E

Figure F

*Images courtesy of Dr. Kathryn Colby (Massachusetts Eye and Ear Infirmary)

Follow up
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 term monitoring for glaucoma and dry
eye as below.

Other long term complications

Glaucoma
Glaucoma is quite common following ocular injury, ranging in frequency from 15%-55% in
patients with severe burns.[8] 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.[46] More severe burns (Roper-Hall Grade III or IV) have been found to have
significantly higher intraocular pressure at presentation and were more likely to require long
term glaucoma medication and undergo glaucoma surgery than grade I or II injuries.[8] 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, and compromising the proper dispersion of the precorneal tear film. This
mucus deficiency results in keratoconjunctivitis sicca (dry eye).[47] Even in well-healed eyes,
chronic dry eye can cause significant morbidity because of discomfort, visual disturbance, and
potential for damage of the ocular surface.

Damage to the eyelids or palpebral conjunctiva

Direct chemical damage to the conjunctiva can lead to scarring, forniceal shortening,
symblepharon formation and ciccatricial entropion or ectropion. These entities are encountered
weeks to months after injury and can be treated by suppressing inflammation and with early
amniotic membrane transplantation or oral mucosal graft.[3][48][49]

Additional Resources
American Academy of Ophthalmology: http://www.aao.org
American Association of Poison Control Centers: http://www.aapcc.org (1-800-222-1222)
Iowa State Universitys Chemistry Material Safety Data Sheets:
http://avogadro.chem.iastate.edu/MSDS/
Occupational Safety and Health Administration requirement for eye protection at work:
http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=9778
Amniograft & Prokera: http://www.biotissue.com/

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