Chemical (Alkali and Acid) Injury of the Conjunctiva and CorneaOriginal article contributed by:

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

All contributors: Danielle Trief, MDAssigned editor:Review: 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

 [hide] 

1 Disease Entityo 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 Acidso 1.5 Primary prevention

2 Diagnosiso 2.1 History

o 2.2 Physical examination

o 2.3 Symptoms

3 Managemento 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 IVo 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[edit source]

International Classification of Diseases[edit source]

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[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]

Primary prevention[edit source]

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[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.

Physical examination[edit source]

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 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 Ringer’s 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[edit source]

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[edit source]

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:[edit source]

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 tetracyclineclass 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[edit source]

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/Tenon’s 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 Tenon’s 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 patient’s

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[edit source]

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[edit source]

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[edit source]

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[edit source]

As for Grade II

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

first week of injury

Grade IV[edit source]

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[edit source]

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[edit source]

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[edit source]

Glaucoma[edit source]

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[edit source]

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[edit source]

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[edit source]

American Academy of Ophthalmology: http://www.aao.org

American Association of Poison Control Centers: http://www.aapcc.org (1-800-222-1222)

Iowa State University’s 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/

References[edit source]

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