Ocular burns consist of burns to the sclera, conjunctiva, cornea, and eyelids. Chemical burns, particularly those involving the cornea, are considered a true ophthalmologic emergency and require prompt assessment and intervention to minimize morbidity.[1] Ocular burn injuries are classified by etiologic agents as either chemical injuries (eg, those caused by acid or alkali) or radiant energy injuries (eg, those caused by heat, electricity or ultraviolet [UV] radiation). See the image below.
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Severe chemical injury with early corneal neovascularization.
Many ocular burns can be adequately managed in the emergency department (ED). Transfer may be required for specialized ophthalmologic care; however, the emergency physician must evaluate the patient’s stability for transfer. In some situations, life-threatening conditions (eg, airway burns) must be addressed (securing of the airway) prior to transfer. For patients with thermal burns, transfer to a burn center is indicated in the presence of significant facial involvement or inhalation injury.
The severity of an ocular burn is directly correlated with the duration of exposure and the causative agent. In particular, chemical burn severity relates to the solution pH, contact duration, solution quantity, and solution penetrability.
Burns damage tissues primarily by denaturing and coagulating cellular proteins and secondarily by causing vascular ischemic damage. For both thermal and chemical burns, severity is determined by the depth and degree of epithelial damage and limbal ischemia. If the limbus is affected significantly, the cornea may develop recurrent epithelial defects, and conjunctival invasion onto the cornea may occur as a result of the loss of stem cells responsible for renewing corneal epithelium. Laser injuries from radiant energy cause injury to the retina through the transfer of light energy into heat, leading to tissue necrosis.[2]
A rare type of ocular injury comes from electrical burns.[3]
Radiant energy burns
Injury from radiant energy usually results from contact with hot liquids, hot gases, fireworks or molten metals. Cell death from thermal burns is limited to the superficial epithelium; however, thermal necrosis and penetration can occur.
With UV burns, epithelial injury results in punctate keratitis. Although the pain is often delayed, UV corneal burns are exquisitely painful. Lasers also can lead to direct retinal injury and, rarely, corneal injury.[2]
Chemical burns
Alkali substances are lipophilic and penetrate more rapidly than acids. Saponification of cell membrane fatty acids causes cell disruption and death. In addition, the hydroxyl ion hydrolyzes intracellular glycosaminoglycans and denatures collagen. The damaged tissues stimulate an inflammatory response, which damages the tissue further by the release of proteolytic enzymes. This is termed liquefactive necrosis.
Alkali substances can pass into the anterior chamber rapidly due to the inability to buffer alkali (within approximately 5-15 min), exposing the iris, ciliary body, lens, and trabecular network to further damage. Irreversible damage occurs at a pH value above 11.5.
Acid burns cause protein coagulation in the corneal epithelium, which limits further penetration. As a rule, these burns are nonprogressive and superficial. Hydrofluoric acid, however, is an exception to this rule: it is a weak acid that rapidly crosses the cell membrane as it remains nonionized. In this way, hydrofluoric acid acts as an alkali, causing liquefactive necrosis.
In addition, fluoride ions are released into the cells. Fluoride ions may inhibit glycolytic enzymes and may combine with calcium and magnesium to form insoluble complexes. The extreme local pain is believed to result from calcium immobilization, which leads to nerve stimulation by shifting potassium ions. Acute fluorosis can occur as the fluoride ions enter the systemic circulation, resulting in cardiac, respiratory, gastrointestinal, and neurologic symptoms. Severe hypocalcemia, which is resistant to large doses of calcium, can occur.
Thermal injuries can be caused by hot substances (eg, curling irons, hot curlers, cigarettes, and hot liquids). Hot liquids have been known to splash into the eye from substances that explode after removal from a microwave; steam from hot liquids is also a potential cause. Fire is a common cause of burns to the face and eyes.
UV keratitis may be caused by bright sunlight, particularly when the light is reflected from snow or cement. Skiers at high altitudes are particularly susceptible to this injury. Welders who view the arc without protective goggles are at risk for injury. Lasers used in industry, military, and medical practice also can cause ocular burns.[2]
Chemical agents
Multiple chemicals used in the home and work environment can lead to injury. Common acids causing ocular burns include sulfuric acid, sulfurous acid, hydrochloric acid, nitric acid, acetic acid, chromic acid, and hydrofluoric acid. Automobile battery explosion, which causes a sulfuric acid burn, is perhaps the most common acidic burn of the eye.
Hydrofluoric acid may be found at home in rust removers, aluminum brighteners, and heavy-duty cleaners. Certain industries use hydrofluoric acid in brick cleaning, glass etching, electropolishing, and leather tanning. Hydrofluoric acid also is used to control fermentation in breweries. Ocular hydrofluoric toxicity can occur from liquid or gaseous exposure.
Common alkali substances contain ammonium hydroxide, potassium hydroxide, sodium hydroxide, calcium hydroxide, and magnesium hydroxide. Substances that contain such compounds and can be found in a home include lye, cement, lime, and ammonia. Laundry detergent pods are also becoming a new source of exposure in the pediatric population.[4] Air bags aerosolize sodium hydroxide on inflation and may cause alkali keratitis.[5] Additionally, sparklers and flares contain magnesium hydroxide and phosphorus.
Certain chemical agents, such as mustard gas, can result in chronic and delayed-onset keratitis.[6]
Ocular burns represent 7-18% of the eye injuries seen in EDs.[7] Eye injuries account for 3-4% of all occupational injuries.[8] The vast majority (84%) are chemical burns. Thermal burns account for 16% of ocular burn cases. Approximately 15-20% of patients with facial burns exhibit ocular injury. The ratio of the relative frequencies of acids and alkalis as the causative agents of chemical injury ranges from 1:1 to 1:4, according to several studies.
International statistics
A report from a developing country found that up to 80% of ocular chemical burns were due to industrial or occupational exposure. A report from Norway indicated that fish bile was the cause of 14% of the ocular chemical burns reported in northern Norway.[9] Acid attacks on women that often include the eyes and lead to serious morbidity have been a serious problem in the developing world.[10]
Age- and sex-related demographics
Any age group may be at risk for ocular burns. One study indicated that the average age of patients with ocular burns was 36 years. There is a strong association of ocular burns with younger age groups within the occupational setting.
Ocular burns are more common in males than in females. This difference probably reflects the male predominance in the industrial occupations at highest risk for ocular injuries, such as construction and mining.
Photographs of right eye after airbag-related alkali burn at 1 week (a), 2 months (b), 4 months (c), and 6 months (d) after the initial motor vehicle ....
Prognosis depends on both prompt recognition and emergent irrigation. This is especially important in those with concurrent polytrauma in whom other injuries are often prioritized, but careful attention should be given to ocular burns that are time sensitive.[11]
The prognosis depends on the depth of the injury. Corneal burns are classified into 4 grades by the Roper Hall scale, as follows:
Grade 1 - Only corneal epithelial loss is present, and no conjunctival ischemia is found; the prognosis is very good
Grade 2 - Some corneal edema and haze are present, and the conjunctival ischemia affects less than one-third of the limbus; some permanent scarring may occur
Grade 3 - The cornea has significant haziness, and limbal ischemia is less than one half of the limbus; the prognosis is variable, and vision usually is impaired
Grade 4 - The cornea is opaque, and limbal ischemia is greater than one half of the limbus, with a possibility of globe perforation; the prognosis is poor
A newer scale by Dua et al subdivides the grade 4 of Roper Hall since they may be treated by autolimbal transplantation or amniotic sheets by corneal specialists and fare better than in the past.[12] The grading scheme then splits the limbus into 12 clock hours as follows:
Grade 1 - 0 clock hours of limbal involvement; 0% conjunctival involvement; prognosis is very good
Grade 2 - ≤3 clock hours of limbal involvement; ≤30% conjunctival involvement; prognosis is good
Grade 3 - >3-6 clock hours of limbal involvement; >30-50% conjunctival involvement; prognosis is good
Grade 4 - >6-9 clock hours of limbal involvement; >50-75% conjunctival involvement; prognosis is good to guarded
Grade 5 - >9 to < 12 clock hours of limbal involvement; >75% to < 100% conjunctival involvement; prognosis is guarded to poor
Grade 6 - Total limbal involvement; total conjunctival 100% involvement; prognosis is very poor
Gupta et al showed a clinically significant difference between outcomes in the Roper Hall and Dua classification, with the subdivision of the grade 4 Roper Hall being split into 3 categories and lead to differences in visual acuity when managed with amniotic membrane transplantation.[13, 14] Both systems may present a challenge to those with less experience in grading limb ischemia than corneal specialists.[15]
The major concerns with ocular burns are final visual acuity (ie, degree of visual impairment) and cosmetic appearance (eg, extent of scarring).
Radiant energy burns
Thermal burns can cause significant corneal and ocular adnexal injuries. Stern et al, reviewing 127 patients who sustained ocular injury secondary to thermal burns, found that eyelid burns were the most common complication, occurring in 52 patients.[16] . Of those 52 burn victims, approximately 60% developed eyelid contractures.
Early surgical consultation and aggressive intervention have been recommended to protect the globe. Other thermal ocular injuries include corneal burns or abrasions, conjunctivitis, cataracts, and corneal perforation. Fortunately, the need for enucleation is rare; only 2 of the 127 burn victims in the study by Stern et al lost the injured eye.[16] With prompt treatment and early ophthalmologic intervention, thermal burns generally have good visual outcomes. Laser injuries typically affect the retina, with corneal sparing, although there are cases of corneal damage. They often heal over time without intervention, but they require specialized referral.[2]
Chemical burns
See the images below.
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Stromal haze with opacification of the cornea.
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Complete cicatrization of the corneal surface.
Chemical burns are often bilateral and frequently result in devastating vision loss. Ocular complications of severe burns include glaucoma, corneal perforation, cataracts, scarring of the cornea, conjunctival cul-de-sac, conjunctiva and eyelid complications, retinal detachment, and corneal ulcerations.
As much as to 1-2 years of corrective surgery may be needed to correct damage from more severe burns. A study by Kuckelkorn et al reported that one-third of 131 patients with ocular burns were considered disabled; approximately 15% were considered blind.[17] In 1995, almost one-third of corneal transplants were for eyes that sustained a chemical injury. Unfortunately, the success rate for transplants for this condition is less than 50%. Some patients require 4-5 transplants before success is achieved.
Primary prevention and patient counseling on proper eye protection is essential because more than 90% of injuries can be avoided with the use of eye protection.[18]
Welders must be informed of the importance of keeping on safety goggles while working. People who spend significant amounts of time outdoors must be made aware of the danger of UV keratitis, particularly at high altitudes. In addition, workers in laboratories and other industrial fields are at risk. In the United States, the Occupational Safety and Health Administration (OSHA) mandates that eye-wash stations are readily available in work environments with injurious corrosive materials.[19]
An estimated 90% of chemical eye injuries are avoidable. It is essential to emphasize the importance of wearing safety glasses when working with hazardous materials or in hazardous situations. Children sustain chemical burns most often when they are unsupervised. It is therefore critical to keep all hazardous home products in an area that is difficult for a child to access.
For patient education resources, see the Burns Center, as well as Eye Injuries, Chemical Eye Burns, Thermal (Heat or Fire) Burns, and How to Instill Your Eyedrops.
Thermal injuries most often result from direct contact with a hot object (eg, curling iron, cigarette). Although these burns can affect a large ocular surface area, they are usually superficial. Patients with superficial burns often complain of symptoms similar to a corneal abrasion. Common complaints include tearing, photophobia, or a foreign body sensation.
A heightened index of suspicion may be required in the case of burns from fire exposure, in that ocular burns might be overlooked in the setting of larger body burns. Burns to the cornea may occur with sparing of the eyelids because individuals may keep their eyes open as they try to escape a fire. A review of a single burn center's retrospective data showed that 5% of patients had concomitant ocular thermal ocular burns.[20]
Patients with ultraviolet (UV) burns usually have an obvious history, although it may not be readily apparent to the patient. The most common form of radiation burn is due to unprotected welding. Patients with so-called arc eye present several hours after exposure with painful, weeping eyes. Also common is a history of excessive exposure to sunlight (as with snow blindness or prolonged or frequent use of tanning booths).
Chemical burns
Chemical injuries usually result from a substance being sprayed or splashed in the face.[21] Alkali injuries occur more frequently than acid burns and are more detrimental.
In the initial physical examination, assess for other potentially life-threatening injuries. The initial physical examination of the eye may be limited to the determination of pH level and evaluation of visual acuity. Topical ocular anesthetics may be used to facilitate the initial examination but should not delay irrigation.
After copious irrigation, a full ophthalmologic examination is required. This may reveal tearing, conjunctival injection, scleral injection, scleral blanching, corneal defects, corneal opacification, uveitis, glaucoma, or globe perforation. Decreased visual acuity may be noted. Fluorescein evaluation is needed to determine the extent of the injury. Repeat pH testing should be performed until normalization with copious irrigation. If pH fails to normalize, troubleshooting of pH paper should be attempted with pH testing of the examiner’s eye. With UV injuries, punctate keratitis may be noted. Lid eversion is necessary to evaluate for the presence of retained solid substances.
Evaluating airway and breathing in patients who have sustained ocular thermal burns during a fire is essential.
Ocular pH measurement is essential in the evaluation of a chemical burn. No additional laboratory studies are warranted in cases of isolated ocular injury; additional studies should be considered if warranted by coexisting injuries.
Evaluate all patients with alkali injuries to the face for tracheal and esophageal burns, which are potentially life-threatening. Hydrofluoric acid burns can cause significant hypocalcemia. Consider checking the calcium level for burns that are not limited to the eye.
Many ocular burns can be adequately managed in the emergency department (ED). The emergency physician should consider at least a telephone consultation with an ophthalmologist for any patient with significant chemical eye exposure. Any serious thermal burn, any alkali chemical globe exposure, or any vision-threatening injury most likely warrants emergent ophthalmologic consultation.
Transfer may be required for specialized ophthalmologic care; however, the emergency physician must evaluate the patient’s stability for transfer. In some situations, life-threatening conditions (eg, airway burns) must be stabilized prior to transfer. For patients with thermal burns, transfer to a burn center is indicated in the presence of significant facial involvement or inhalation injury. Tetanus status should be checked and updated, if necessary.
With a chemical injury, immediate initiation of copious irrigation has the greatest impact on prognosis.[22] Irrigation also helps to clear any residual particulate matter from the eye. Delayed treatment may result in significant morbidity.[11]
Ideally, the affected eye should be irrigated as soon as possible in an eyewash or shower station with sterile saline solution. Sterile physiologically balanced solutions reduce the chances of further damage to the eye. If sterile saline is not available, cold tap water allows dilution of the agent.
The patient must try to open the eyelids as wide as possible to obtain the best irrigation. Topical anesthetic prior to irrigation or insertion of a lid speculum, such as the Morgan lens, facilitates cooperation. A wire lid speculum can also be used to assist in eyelid retraction.
When a patient presents to the ED with an ocular burn, it is important to assess the potential for coexisting life-threatening injuries. These may have to be addressed before or simultaneously with treatment of the eye. In particular, fire victims who have sustained ocular thermal burns must first have their airway and breathing evaluated. Alkali injuries to the face also may cause tracheal or esophageal burns.
Topical antibiotics, pain relief, and tetanus immunization are required for all ocular burns. Some chemical and thermal burns may require nonpreserved lubricants. Adequate lubrication helps to prevent the formation of symblepharon (ie, adhesions of the eyelid to the eyeball).[23]
Some authors advocate using topical steroids in selected patients (eg, those with alkali and hydrofluoric acid burns), arguing that this may limit intraocular inflammation and decrease the formation of fibroblasts on the cornea. Others argue that the risks of potential infection and ulceration outweigh the possible benefits. In general, steroid preparations should not be used unless recommended by an ophthalmologist, because they can slow healing and predispose the eye to infection. An acute rise in intraocular pressure is less of a risk with short-term use.
Radiant energy burns
Treatment of isolated thermal corneal burns usually can be considered virtually identical to the treatment of corneal abrasions. In addition to a discussion of appropriate follow-up care, ED treatment includes the following:
Remove the offending agents, if necessary everting the lid to remove debris; irrigation also aids in debris removal besides cooling the surface
Treat intraocular inflammation
Patch the eye to establish an environment conducive to reepithelialization
If the lids are burned, apply cool saline compresses are needed and use adequate lubrication for the globe; the burned eyelashes and eschar may have to be removed
Patients with minor thermal and ultraviolet (UV) burns can be discharged from the ED to follow-up care with an ophthalmologist within 24 hours.
Chemical burns
The most important treatment of chemical burns is extensive immediate irrigation. Sterile higher-osmotic solutions, such as amphoteric solution (Diphoterine; Prevor, Valmondois, France) or buffered solutions (eg, BSS Plus [Alcon, Fort Worth, TX] or lactated Ringer solution), are ideal. If these are not available, sterile isotonic saline is an appropriate irrigant. Hypotonic solutions, such as water, result in deeper penetration of corrosive material into the corneal structures as a result of the cornea’s higher osmotic gradient (420 mOsm/L).
The duration and amount of irrigation are determined by the ocular pH. Continue irrigation until the pH remains at a normal level for 30 minutes. Use of a Morgan lens or other eye irrigation system can minimize interference from blepharospasm, which can often be severe. If these are unavailable, the lid can be retracted manually with a Desmarres retractor, a lid speculum, or even a bent paperclip.
The end of intravenous (IV) tubing can direct the stream of sterile fluid across the eye. In addition, use a cotton swab to remove any particulate matter that may be retained in the fornices. Soak the swab in ethylenediaminetetraacetic acid (EDTA) 1% if the causative agent contained calcium oxide.
After irrigation, a thorough ophthalmologic examination is mandatory. If the injury is minor, the patient may be discharged with topical ophthalmic antibiotics, oral analgesics, and an eye patch. Follow-up evaluation should occur within 24 hours.
In the case of hydrofluoric acid burns, optimum care has not been established. Some studies have used 1% calcium gluconate as an irrigant or as eyedrops to treat these burns. Magnesium compounds also have been used anecdotally for hydrofluoric acid burns; however, little research supports their effectiveness. Irrigation with magnesium chloride has been found to be nontoxic to the eye. Benefits of this treatment have been reported anecdotally even 24 hours after injury, when other treatments had been unsuccessful.
Some authors recommend drops every 2-3 hours because irrigation may be irritating and may lead to corneal ulceration. Do not undertake subconjunctival injection.
Ascorbic acid may promote collagen production. After alkali burns, the level of ascorbic acid decreases. Some researchers have demonstrated that topical administration of 10% ascorbic acid may reduce corneal perforation. At present, however, this treatment is being used only experimentally and may be recommended by ophthalmologists. Oxygen therapy was studied and showed faster corneal epithelial defect healing and quicker vascularization of ischemic areas, although vision outcomes were not reported.[24]
Follow-up care
Follow-up care should occur within 24 hours after patient discharge. Topical antibiotics and possibly cycloplegics are usually required when the patient is discharged. Patients should not be discharged with ophthalmologic topical anesthetics, because these agents can cause corneal endothelial toxicity, corneal ulceration, and scarring.
For more severe burns, particularly alkali burns, hospitalization is necessary. The patient will require topical ophthalmic antibiotics, pain medication, cycloplegics, and mydriatics. If secondary glaucoma develops, the patient will require ocular pressure–lowering medication. Inpatient treatment in a burn center is required for patients with more severe burns or alkali burns.
Active surgical intervention to remove necrotic tissue can optimize the outcome by reducing continued inflammation. In selected cases, amniotic membrane patching may also be considered.[25, 26, 27] Tissue engineering for conjunctival reconstruction is a developing field that may offer new therapies as well.[28, 29, 30] In one study, subconjunctival application of autologous regenerative factor-rich plasma (RFRP) was effective in treating ocular alkali burns.[31]
The goal of therapy is to reduce inflammation, pain, and risk of infection. If secondary glaucoma develops, administer ocular pressure–lowering medications. Agents that are commonly used in patients with ocular burns include cycloplegic mydriatics, ophthalmic antibiotics, analgesics, and toxoids.
Several proprietary products are now on the market to be used in the industrial setting for chemical ocular exposures.[32]
Clinical Context:
Homatropine blocks the responses of the sphincter muscle of the iris and the muscle of the ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia). It induces mydriasis in 10-30 minutes and cycloplegia in 30-90 minutes; these effects last up to 48 hours.
Clinical Context:
Atropine ophthalmic acts at parasympathetic sites in smooth muscle to block the response of the sphincter muscle of the iris and the muscle of the ciliary body to acetylcholine; its effects produce mydriasis and cycloplegia.
Clinical Context:
Scopolamine ophthalmic blocks the action of acetylcholine at parasympathetic sites in smooth muscle, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).
The goal of therapy is to reduce inflammation, pain, and risk of infection. If secondary glaucoma develops, administer ocular pressure–lowering medications. Agents that are commonly used in patients with ocular burns include cycloplegic mydriatics, ophthalmic antibiotics, analgesics, and toxoids.
Clinical Context:
Tobramycin ophthalmic interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits, resulting in a defective bacterial cell membrane. It is available as a solution and as an ointment.
Clinical Context:
Gentamicin is an aminoglycoside antibiotic used for gram-negative bacterial coverage. It is commonly used in combination with an agent against gram-positive organisms.
Clinical Context:
Ciprofloxacin ophthalmic is a bactericidal antibiotic that inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA-gyrase in susceptible organisms. It is indicated for pseudomonal infections and those due to multidrug-resistant gram-negative organisms.
Patients with burns to the cornea, conjunctiva, and sclera are usually treated with prophylactic topical administration of broad-spectrum ophthalmic antibiotic drops or ointment (eg, tobramycin, gentamicin, ciprofloxacin, norfloxacin, or bacitracin). Neomycin and sulfa drugs are used less frequently, because of the high incidence of sensitivity. Patients with burns to the skin (eg, eyelids) are rarely given prophylactic antibiotics.
Clinical Context:
Diclofenac ophthalmic has analgesic properties. It inhibits prostaglandin synthesis by decreasing the activity of cyclooxygenase, which in turn results in decreased formation of prostaglandin precursors. It also facilitates the outflow of aqueous humor and decreases vascular permeability.
Some ophthalmologists are advocating the application of diclofenac drops. This therapy may prove to be an effective alternative to patching in patients with insults to the cornea, permitting the patient to maintain binocular vision during treatment.
Clinical Context:
Tetanus toxoid is used to induce active immunity against tetanus in selected patients. Tetanus and diphtheria toxoids are the immunizing agents of choice for most adults and children older than 7 years. Booster doses must be administered to maintain tetanus immunity throughout life. Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product.
In children and adults, tetanus toxoid may be administered into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the midthigh laterally.
Joshua J Solano, MD, Assistant Professor of Integrated Medical Science, Core Faculty of Emergency Medicine Residency, Director of Quality Improvement and Patient Safety, Florida Atlantic University
Disclosure: Nothing to disclose.
Coauthor(s)
Carlo L Rosen, MD, Associate Professor of Medicine, Harvard Medical School; Program Director, Vice Chair for Education, Associate Director of Medical Education, Harvard Affiliated Emergency Medicine Residency Program, Department of Emergency Medicine, Beth Israel Deaconess Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Gregory Sugalski, MD, Associate Professor, Vice-Chair of Clinical Operations, Department of Emergency Medicine, Rutgers New Jersey Medical School; Associate Chief of Service, Department of Emergency Medicine, University Hospital
Disclosure: Nothing to disclose.
Additional Contributors
Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Disclosure: Nothing to disclose.
Acknowledgements
Debra Slapper, MD Consulting Staff, Department of Emergency Medicine, St Anthony's Hospital
Debra Slapper, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Cheri N M Weaver, MD Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center
Avon Global Center for Women and Justice at Cornell Law School and the New York City Bar Association, 2011. Combating Acid Violence in Bangladesh, India, and Cambodia. Available at http://www.acidviolence.org/uploads/files/Virtue_Foundation_Combating-Acid-Violence-Report-2011.pdf. Accessed: June 8, 2013.
Occupational Safety and Health Standards. OSHA. June 18, 1998. Available at http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_id=9806&p_table=STANDARDS
Severe chemical injury with early corneal neovascularization.
Photographs of right eye after airbag-related alkali burn at 1 week (a), 2 months (b), 4 months (c), and 6 months (d) after the initial motor vehicle accident with airbag deployment. Note severe limbal ischemia at 1 week (a) leading to severe conjunctivalization of the cornea at later time points. Courtesy of Shawn S Barnes, MSIV, University of Hawaii, John A Burns School of Medicine.
Stromal haze with opacification of the cornea.
Complete cicatrization of the corneal surface.
Severe chemical injury with early corneal neovascularization.
Photographs of right eye after airbag-related alkali burn at 1 week (a), 2 months (b), 4 months (c), and 6 months (d) after the initial motor vehicle accident with airbag deployment. Note severe limbal ischemia at 1 week (a) leading to severe conjunctivalization of the cornea at later time points. Courtesy of Shawn S Barnes, MSIV, University of Hawaii, John A Burns School of Medicine.
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