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The prognosis of a chemically burned eye hinges not only on the severity of the burn, but also on the insulting agent, the rate at which therapy is initiated, and how therapy is prescribed. Recovery from ocular burns depends on the extent of damage to corneal, limbal, and conjunctival tissues at the time of injury. Classification schemes help provide guidelines based on the corneal appearance and extent of limbal and conjunctival involvement, and allow the clinician to determine the severity of the injury and the prognosis for the injured eye.
The corneal epithelium plays an important role in maintaining the smoothness of the optical surface, keeping the stroma dehydrated, and regulating the metabolic activity of the stromal keratocytes.1 The main function of the keratocytes is maintaining and regenerating the corneal stroma.1,2 In moderate to severe chemical injuries, keratocyte synthesis of collagen becomes compromised due to deficient levels of ascorbate in the aqueous following anterior segment involvement of the ciliary body.2
In the perilimbal conjunctiva, ridges found perpendicular to the cornea house the limbal stem cells. Limbal stem cells are self-renewing and proliferate indefinitely.1 They act as a barrier to conjunctival epithelial cells and prevent them from migrating onto the corneal surface. Ocular burns often destroy the limbus, leading to limbal stem cell deficiency. The cornea then becomes invaded by bulbar conjunctival cells, leading to neovascularization, chronic inflammation, and stromal scarring, ultimately causing opacification and the loss of vision in a process known as conjunctivalization.1,2
ACIDS AND ALKALIS
Acids have a pH below 7, and irreversible damage becomes more and more likely the closer the offending agent’s pH is to 2.5. Fortunately, most acid burns are often superficial and nonprogressive, as corneal proteins bind to the acid and act as a barrier against further penetration.3
Chemicals that carry a pH greater than 7 are basic or alkaline and are correlated with a much higher likelihood of ocular morbidity. As the pH rises, corneal barriers are sloughed away, allowing for further penetration into the anterior segment, creating additional damage to uveal structures.1,2,4
Several classification systems exist to categorize the extent of chemical injuries. The most widely used is based on the Roper-Hall system, which divides injuries into four grades (Table; Figures 1-4), each with increasing severity based upon corneal appearance and extent of limbal ischemia.4-6
- Grade I. Limbal stem cells are not affected, and ischemia is not present. There may be a large epithelial defect, but the underlying cornea will remain clear. The prognosis for full recovery is excellent.
- Grade II. Partial limbal ischemia is present affecting less than one-third of the limbus. The cornea may be hazy, but anterior segment structures are typically visible. The prognosis is favorable, but persistent epithelial dysfunction can be present along with conjunctivalization.
- Grade III. Extensive limbal ischemia is present involving one-third to one-half of the limbus. Stromal haze will limit visualization of the iris and lens. The prognosis is guarded, and surgery may be required.
- Grade IV. Greater than one-half of the limbus is ischemic along with complete loss of the corneal epithelium. There is also loss of proximal conjunctival epithelium. The cornea will appear porcelainized, and its opaqueness will not allow for views of other anterior segment structures. The prognosis is extremely poor.
PHASES OF RECOVERY
McCulley et al divided the clinical course into several distinct phases.7 In each phase, multiple events occur as the cornea attempts to repair itself. These include epithelial regrowth and migration, collagen synthesis and degradation, and activation and migration of keratocytes.1,2,7
- Acute phase (days 0-7). Reepithelialization begins if there are sufficient limbal stem cells. Treatment efforts are directed at encouraging epithelial migration, controlling inflammation, and avoiding topical medications and bandage contact lenses that may damage the fragile epithelium. Keratocyte activation also starts during this phase, allowing the initiation of collagen synthesis with little or no collagen breakdown.
- Intermediate phase (days 7-21). Epithelial migration continues. Grade I injuries are typically reepithelialized, but patients with grade II will most likely have persistent epithelial defects. Grades III to IV will have minimal to no reepithelialization. Keratocytes will continue to function during this phase to repair the damage to the stroma, but collagenase activity peaks and concurrently starts to break down collagen. Treatment during this phase should maximize collagen synthesis and minimize collagenase activity.
- Late repair phase (after day 21). Eyes with grade I injuries will typically have a normal corneal surface reestablished. Focal limbal stem cell loss and focal conjunctivalization may still be present in grade II. Eyes with grade III trauma typically demonstrate delayed reepithelialization, and the cornea may become repopulated with conjunctival epithelium. Eyes with grade IV injuries will continue to have a denuded cornea and subsequent corneal melt requiring surgical intervention.
TREATMENT AND MANAGEMENT
Chemical injuries have two waves of inflammation that occur after the trauma.1,2 The first wave happens within 12 to 24 hours of the injury, and little can be done to prevent it. It is brought about by blood elements from the injured conjunctiva and uvea, necrotic tissue, and chemotaxis. The second and more destructive wave of inflammation typically begins at day 7 and peaks when corneal repair and degradation are maximal, usually between days 14 to 21. Aggressive treatment of the first wave and preventative treatment of the second wave with high-dose corticosteroids and other antiinflammatories will help minimize inflammation and hopefully prevent a corneal melt. The key is to successfully maximize corticosteroids’ antiinflammatory effects during the first 7 to 10 days while the risk-benefit ratio is more favorable and then to dramatically cut back thereafter.1,2
After neutralization of pH has taken place, patients with grade I injuries should be placed on topical antibiotics four times daily. Cycloplegics should be prescribed along with nonpreserved artificial tears. Even mild injuries have significant inflammation; therefore, prednisolone acetate 1% four times a day is recommended.2 Patients with mild injuries will often complain of discomfort for months following the trauma. Treating their dry eye disease and meibomian gland dysfunction may help reestablish their ocular surface and comfort.2
The intensive use of topical corticosteroids in the acute phase cannot be overstressed in patients with grade II to IV injuries.1,2,8 Corneal melting from activation of stromal collagenases typically does not occur until 10 to 14 days after the injury.1 Therefore, the first week of treatment represents a window in which corticosteroids can be used to help suppress the intense inflammation and give the ocular surface a chance to heal. Prednisolone acetate 1% hourly while awake during the first week, followed by a dramatic taper after 7 days to twice daily is required for proper inflammation control.1,2
Autologous or umbilical cord serum should be considered during the acute phase to help promote reepithelialization. Autologous serum replaces individualized antibodies and has antiinflammatory and antiscarring properties.9 Umbilical cord serum is similar, although it includes additional growth factors.10
Topical sodium ascorbate (10%) and citrate (10%) promote collagen synthesis and should be used during the acute phase to help rebuild stromal tissue.2,8 Due to anterior segment involvement, ascorbate levels in the aqueous are diminished, and oral vitamin C will not be converted to ascorbate in the anterior chamber and is therefore of limited value.2,8
Sutureless amniotic membranes have a tremendous benefit during the acute phase and should be placed on the eye within the first week following the trauma.11 Their ease of access and powerful healing properties make them a useful adjunct when treating chemical injuries. They greatly enhance patients’ chances for reepithelialization by helping restore limbal stem cell function, and further prevent efflux of immune cells, ultimately reducing inflammation.9,11-14
Topical fluoroquinolones should be used at least four times a day, as well as long-acting cycloplegics such as atropine or homatropine. Oral narcotics for pain control are helpful, and oral tetracycline derivatives can be used to inhibit matrix metalloproteinases.1,2 In patients with a secondary increase in intraocular pressure, oral medications are preferred over topical agents while the cornea is healing.15
Topical nonsteroidal antiinflammatory drugs are not indicated due to their potential to disrupt epithelial healing and their lack of appropriate antiinflammatory effects.2 In the acute phase, the eye is typically too inflamed to tolerate a bandage contact lens, and phenylephrine and other vasoconstrictors should not be used because they may increase ischemia.2
Surgical management is needed when healing has slowed or when medical management is no longer effective. If epithelial healing falters or is absent or if progressive corneal melting occurs despite intensive medical therapy, surgical intervention may be required. Fortunately, there are many surgical maneuvers that may decrease the chances of significant ocular and visual morbidity. Surgical treatments range from simple debridement of necrotic tissue to limbal stem cell transplantation and the implantation of artificial corneas.
The goals of treatment in a patient with a chemical injury are restoring the normal ocular surface anatomy, controlling inflammation, and improving corneal clarity. With today’s understanding of chemical injuries and new treatment modalities, it is possible to maintain and restore vision in all but the most severely burned eyes.
Nicholas Colatrella, OD, FAAO, Dipl ABO, ABCMO, is adjunct professor of optometry at Illinois College of Optometry & University of Missouri, St Louis, and medical director of PineCone Vision Center in Sartell, Minnesota. He acknowledged no financial interest in the products mentioned herein. Dr. Colatrella may be reached at (320) 258-3915; email@example.com.
Jeffrey R. Varanelli OD, FAAO, is an optometrist at Simone Eye Center in Warren, Michigan. He acknowledged no financial interest in the products mentioned herein. Dr. Varanelli may be reached at (586) 558-2981; firstname.lastname@example.org.
- Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol. 1997;41:275-313.
- Colby K. Chemical Injuries of the Cornea. In: Stern GA, ed. Focal Points: Clinical Modules for Ophthalmologists. San Francisco, CA: American Academy of Ophthalmology. 2010;28:1-14.
- Friedenwald JS, Hughes WF, Hermann H. Acid burns of the eye. Arch Ophthalmol. 1946;35:98-108.
- Ralph R. Chemical Burns of the Eye. In: Tasman W, Jaeger E, eds. Duanes Clin Ophthalmol. Philadelphia: Lippincott-Raven;1990;28:1-21.
- Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc UK. 1965;85:631-653.
- Dua H, King A, Joseph A. A new classification of ocular surface burns. Br J Ophthalmol. 2001;85:1379-1383.
- McCulley JP. Chemical injuries. In: Smolin G, Thoft RA, eds. The Cornea: Scientific Foundation and Clinical Practice. Boston: Little, Brown and Co;1987:527-542.
- Brodovsky SC, McCarty CA, Snibson G, et al. Management of alkali burns: an 11-year retrospective review. Ophthalmology. 2000;107:1829-1835.
- Shahriari H, Tokhmehchi F, Reza M, et al. Comparison of the effect of amniotic membrane suspension and autologous serum on alkaline corneal epithelial wound healing in the rabbit model. Cornea. 2008;27:1148-1150.
- Sharma N, Goel M, Velpandian T, et al. Evaluation of umbilical cord serum therapy in acute ocular chemical burns. Invest Ophthalmol Vis Sci. 2011;52:1087-1092.
- Kheirkhah A, Johnson D, Paranjpe D, et al. Temporary sutureless amniotic membrane patch for acute alkaline burns. Arch Ophthalmol. 2008;126:1059-1066.
- Tseng S, Prabhasawat P, Barton K, et al. Amniotic membrane transplantation with or without limbal allografts for corneal surface reconstruction in patients with limbal stem cell deficiency. Arch Ophthalmol. 1998;116:431-441.
- Fish R, Davidson R. Management of ocular thermal and chemical injuries. Including amniotic membrane therapy. Curr Opin Ophthalmol. 2010;21:317-321.
- Tejwani S, Kolari R, Sangwan S, et al. Role of amniotic membrane graft for ocular chemical and thermal injuries. Cornea. 2007;26:21-26.
- Gicquel J. Management of ocular surface chemical burns. Br J Ophthalmol. 2011;95:159-161.