eMedicine Specialties > Emergency Medicine > Ophthalmology

Burns, Ocular

Cheri N Melsaether, MD, Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center
Carlo L Rosen, MD, Assistant Professor of Medicine, Harvard Medical School; Program Director, Department of Emergency Medicine, Beth Israel Deaconess Medical Center/ Harvard Affiliated Emergency Medicine Residency program

Updated: Aug 12, 2009

Introduction

Background

Burns to the sclera, conjunctiva, cornea, and eyelid are considered ocular burns. Ocular burn injuries are classified by etiologic agents as either chemical injuries (ie, acid, alkali) or radiant energy injuries (ie, thermal, ultraviolet [UV]). Chemical burns, particularly those involving the cornea, are considered a true ophthalmologic emergency.1

Pathophysiology

Ocular burn severity correlates directly to exposure duration 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 through vascular ischemic damage. Whether thermal or chemical, the severity of burns results from 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 due to the loss of stem cells responsible for renewing corneal epithelium.

Thermal burns

Injury from radiant energy usually results from contact with hot liquids, hot gases, or molten metals. Cell death from thermal burns is limited to the superficial epithelium; however, thermal necrosis and penetration can occur.

Ultraviolet burns

Epithelial injury results in a punctate keratitis. Although the pain is often is delayed, UV corneal burns are exquisitely painful.

Alkali 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 (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

Acid burns cause protein coagulation in the corneal epithelium, which limits further penetration. Thus, these burns usually are nonprogressive and superficial. Hydrofluoric acid is an exception. It is a weak acid that rapidly crosses the cell membrane as it remains nonionized. In this way, hydrofluoric acid acts like 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 fluorinosis 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.

Frequency

United States

Ocular burns represent 7-18% of ocular traumas presenting to EDs.2 Eye injuries account for 3-4% of all occupational injuries.3 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 frequency of acids versus alkalis as the causative agents in chemical injury varies from 1:1 to 1:4, based on several studies.

International

In one report from a developing country, 80% of ocular chemical burns were due to industrial and/or occupational exposure. Interestingly, fish bile has been shown to cause 14% of ocular chemical burns in Norway.

Mortality/Morbidity

  • Ocular burns: The major concern with ocular burns is final visual acuity and cosmetic appearance.
  • Thermal burns: Thermal burns can cause significant corneal and ocular adnexal injuries. Stern et al reviewed 127 patients who sustained ocular injury secondary to thermal burns.4 These researchers found that eyelid burns were the most common complication, occurring in 52 patients. Of those 52 burn victims, approximately 60% developed eyelid contractures.4 Early surgical consultation and aggressive intervention have been recommended to protect the globe. Other thermal ocular injuries include corneal burns and/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 their eye.4 With prompt treatment and early ophthalmologic intervention, thermal burns generally have good visual outcomes.
  • Chemical burns: 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. Up to 1-2 years of corrective surgery are 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.5 In 1995, almost one third of corneal transplants were for eyes that sustained 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.

Sex

Ocular burns are more common in males than in females. This likely reflects the male predominance in industrial occupations, such as construction and mining, at highest risk for ocular injury.

Age

Any age group may be at risk of ocular burns. One study indicated that the average age of patients with ocular burns is 36 years. There is a strong association of ocular burns among younger age groups within the occupational setting.

Clinical

History

  • Thermal burns
    • 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. Patients most commonly complain of tearing, photophobia, or a foreign body sensation.
    • Burns from fire exposure may require a heightened index of suspicion because ocular burns might be overlooked in the setting of larger body burns.
    • Burns to the cornea can occur with sparing of the eyelids because individuals may keep their eyes open as they try to escape a fire.
  • Chemical burns
    • Chemical injuries usually result from a substance being sprayed or splashed in the face.6
    • Alkali injuries occur more frequently than acid burns and are likely more detrimental.
  • UV burns
    • Patients with 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. "Arc eye" presents several hours after exposure with painful, weeping eyes.
    • Excessive exposure to sunlight (eg, snow blindness, tanning booths) is another common cause.

Physical

  • In the initial physical examination, assess for other potential life-threatening injuries.
  • Initial physical examination of the eye may be limited to pH and visual acuity.
  • 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.
  • With UV injuries, a punctate keratitis may be noted.

Causes

  • Thermal burns
    • Thermal injuries can be caused by hot substances (eg, curling irons, hot curlers, cigarettes, hot liquids).
    • Hot liquids have been known to splash into the eye from substances that explode after removal from a microwave.
    • Fire can cause burns to the face and eyes.
  • Chemical burns: Multiple chemicals used in the home and work environment can lead to injury.
    • Acidic chemicals
      • 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.
    • Alkali chemicals
      • 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.
      • Air bags aerosolize sodium hydroxide on inflation and may cause an alkali keratitis. Additionally, sparklers and flares contain magnesium hydroxide and phosphorus.
  • UV burns
    • Bright sun, particularly when reflected from snow or cement, may cause UV keratitis.
    • Skiers at high altitudes are particularly susceptible to this injury.
    • Welders who view the arc without protective goggles are at risk.
  • Chemical warfare: Certain agents, such as mustard gas, result in chronic and delayed-onset keratitis.7

Differential Diagnoses

Corneal Ulceration and Ulcerative Keratitis
Ultraviolet Keratitis

Workup

Laboratory Studies

  • 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.

Treatment

Prehospital Care

  • Irrigation
    • With chemical injury, immediate initiation of copious irrigation has the greatest impact on prognosis.8 Irrigation also helps to clear any residual particulate matter from the eye.
    • In ideal situations, 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 for 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 facilitates cooperation. A wire lid speculum can also be used to assist in eyelid retraction.

Emergency Department Care

When a patient presents to the ED with an ocular burn, assessing the potential for coexisting life-threatening injuries is important. These may need to be addressed prior to or simultaneously with treatment of the eye. In particular, a fire victim sustaining ocular thermal burns must first have the airway and breathing evaluated. Alkali injuries to the face also may cause tracheal or esophageal burns.

  • All ocular burns require topical antibiotics, pain relief, and tetanus immunization.
  • Thermal burns: The 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, which may require lid eversion to remove debris. Irrigation also aids in debris removal as well as to cool the surface.
    • Treat intraocular inflammation.
    • Patch the eye to establish a conducive environment for reepithelialization.
    • When the lids are burned, cool saline compresses are needed, and adequate lubrications for the globe are important. The burned eyelashes and eschar may need to be removed.
  • Chemical burns
    • The most important treatment of chemical burns is extensive immediate irrigation. Sterile higher osmotic solutions such as amphoteric solution (Diphoterine) or buffered solutions (BSS or lactated Ringer) are ideal. If 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 due to the cornea's higher osmotic gradient (420 mOs/L).
    • The duration and amount of irrigation is determined by the eye pH. Continue irrigation until the pH remains at 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, lid speculum, or bent paperclip. The end of intravenous 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.
    • Following 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.
    • More severe burns, particularly alkali burns, require hospitalization. The patient requires topical ophthalmic antibiotics, pain medication, cycloplegics, and mydriatics. If secondary glaucoma develops, the patient requires ocular pressure–lowering medication.

Consultations

  • Patients with minor thermal and UV burns can be discharged from the ED to follow-up care with an ophthalmologist within 24 hours.
  • 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.

Medication

The goal of therapy is to reduce inflammation, pain, and risk of infection. If secondary glaucoma develops, administer ocular pressure–lowering medications.

In addition to the medications described below, ascorbic acid may promote collagen production. Following alkali burns, the level of ascorbic acid decreases. Some researchers have demonstrated that the topical administration of 10% ascorbic acid may reduce corneal perforation. However, this treatment is being used only experimentally.

In the treatment 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 from 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.

Additionally, subconjunctival injections of calcium gluconate and calcium chloride have not been found to be beneficial.

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). Some authors recommend the use of topical steroids in some patients, particularly those with alkali and hydrofluoric acid burns. The advocates believe steroids may limit intraocular inflammation and decrease the formation of fibroblasts on the cornea. Others argue the risks of potential infection and ulceration outweigh the possible benefits.

Consider each patient on an individual basis with a consulting ophthalmologist.

Cycloplegic mydriatics

Aid in the prevention of ciliary spasm. Additionally, these agents are believed to stabilize the permeability of blood vessels, thus reducing inflammation. Homatropine 5% often is recommended because of its medium duration of 12-24 h, a time within which the patient should have a follow-up examination by an ophthalmologist. Longer acting cycloplegics, such as scopolamine and atropine, are used less commonly.


Homatropine (Isopto-homatropine)

Blocks responses of sphincter muscle, iris, and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).
Induces mydriasis in 10-30 min and cycloplegia in 30-90 min. These effects last up to 48 h.

Dosing

Adult

Solution (2%): 1-2 gtt; repeat q15-20min prn
Solution (5%): 1 gtt; repeat q15-20min prn
For prolonged cycloplegia: 1-2 gtt at intervals of up to q3-4h

Pediatric

Administer as in adults, but only use 2% solution

Interactions

None reported

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly patients in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur but are rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorption


Atropine (Isopto-atropine)

Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine; effects produce mydriasis and cycloplegia.

Dosing

Adult

Solution (1%): 1-2 gtt qid; compress lacrimal sac by digital pressure for 1-3 min after instillation
Ointment: Apply 0.5-inch ribbon in conjunctival sac tid; compress lacrimal sac by digital pressure for 1-3 min after instillation

Pediatric

Solution (0.5%): 1-2 gtt into eye(s) bid/tid
Ointment: Not established

Interactions

Coadministration with other anticholinergics has additive effects

Contraindications

Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid use in Down syndrome and in children with brain damage (patients may demonstrate hyperreactive response to topical atropine)


Scopolamine (Isopto-hyoscine)

Blocks action of acetylcholine at parasympathetic sites in smooth muscle, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Dosing

Adult

1-2 gtt qid

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; primary glaucoma or initial stages of disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid excessive systemic absorption by compressing lacrimal sac, using digital pressure for 1-3 min after instillation; may produce drowsiness, blurred vision, or sensitivity to light (due to dilated pupils); observe caution while driving or performing other tasks requiring alertness, coordination, or physical dexterity

Antibiotics (ophthalmic)

Patients with burns to the cornea, conjunctiva, and sclera usually are administered prophylactic, broad-spectrum, topical ophthalmic antibiotic drops or ointment (eg, tobramycin, gentamicin, ciprofloxacin, norfloxacin, bacitracin). Neomycin and sulfa drugs are used less frequently because of a high incidence of sensitivity. Patients with burns to the skin (eg, eyelids) rarely are administered prophylactic antibiotics.


Tobramycin (Tobrex, AKTob)

Interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits, resulting in defective bacterial cell membrane.
Available as solution and as ointment.

Dosing

Adult

Solution: 1-2 gtt q4h during waking hours; less frequently at night
Severe infections: 2 gtt q30-60min initially; followed by less frequent intervals of administration
Ointment: Apply 0.5-inch ribbon in conjunctival sac bid/tid
Severe infections: Apply q3-4h

Pediatric

<2 years: Not established
>2 years: Administer as in adults

Interactions

Effects are decreased when used concurrently with gentamicin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use in deep-seated ocular infections or in those that may become systemic; prolonged use of antibiotics may result in bacterial or fungal overgrowth of nonsusceptible organisms


Gentamicin (Genoptic)

Aminoglycoside antibiotic used for gram-negative bacterial coverage. Commonly used in combination with an agent against gram-positive organisms.

Dosing

Adult

Ointment: Apply 0.5-inch (0.04-cm) ribbon in conjunctival sac bid/tid
Solution: 1-2 gtt q2-4h
Severe infections: 2 gtt qh

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; mycobacterial, viral, and fungal infections of eye; avoid using with steroid combinations after uncomplicated removal of foreign body from cornea

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to secondary infections


Ciprofloxacin (Ciloxan)

Bactericidal antibiotic that inhibits bacterial DNA synthesis and consequently growth by inhibiting DNA-gyrase in susceptible organisms.
Indicated for pseudomonal infections and those due to multidrug-resistant gram-negative organisms.

Dosing

Adult

1-2 gtt q2h while awake for 2 d; followed by 1-2 gtt q4h while awake for another 5 d

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, mycobacterial, and fungal eye infections; avoid coadministration with steroid combinations after uncomplicated removal of a foreign body from cornea

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

A white crystalline precipitate located in superficial portion of corneal defect may occur (onset starts in 1-7 d); precipitate usually is cleared within 2 wk and does not adversely affect clinical course or outcome; do not use in ocular infections that may become systemic; superinfections may occur with prolonged or repeated antibiotic therapy

Analgesics

Some ophthalmologists are advocating 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.


Diclofenac (Voltaren)

Has analgesic properties. Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which in turn results in decreased formation of prostaglandin precursors.
Also facilitates outflow of aqueous humor and decreases vascular permeability.

Dosing

Adult

1 gtt qid for up to 2 wk

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Corneal thinning may occur

Toxoids

Used to induce active immunity.


Tetanus toxoid

Used to induce active immunity against tetanus in selected patients. Immunizing agents of choice for most adults and children >7 y are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.
Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product.
In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is mid thigh laterally.

Dosing

Adult

Primary immunization: 0.5 mL IM; administer 2 injections 4-8 wk apart and a third dose 6-12 mo after second injection
Booster dose: 0.5 mL q10y

Pediatric

Administer as in adults

Interactions

Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization due to poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens; avoid concurrent use of medication with systemic chloramphenicol since it may impair amnestic response to tetanus toxoid; concurrent use of tetanus immune globulin may delay development of active immunity by several days (interaction is nevertheless clinically insignificant and does not preclude concurrent use)

Contraindications

Documented hypersensitivity; history of any type of neurologic symptoms or signs following administration; FDA recommends that elective tetanus immunization be deferred during any outbreak of poliomyelitis because tetanus toxoid injections are an important cause of provocative poliomyelitis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use to treat actual tetanus infections or for immediate prophylaxis of nonimmunized individuals (use instead tetanus antitoxin, preferably human tetanus immune globulin); diminished antibody response to active immunization may be observed in patients receiving immunosuppressive therapy; better to defer primary diphtheria immunization until immunosuppressive therapy discontinued; routine immunization of symptomatic and asymptomatic HIV-infected persons is recommended

Follow-up

Further Inpatient Care

  • Inpatient treatment in a burn center is required for patients with more severe burns and/or alkali burns.
  • Active surgical intervention to remove necrotic tissue can optimize the outcome by reducing continued inflammation. In selected cases, amniotic membrane patching might also be considered.9,10

Further Outpatient Care

  • Follow-up care should occur within 24 hours after patient discharge. Topical antibiotics and possibly cycloplegics usually are required when the patient is discharged.

Transfer

  • 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) may prevent a transfer.
  • For patients with thermal burns, transfer to a burn center is indicated in the presence of significant facial involvement or inhalation injury.

Deterrence/Prevention

See Patient Education.

Complications

  • Visual impairment
  • Scarring

Prognosis

  • The prognosis depends on the depth of the injury. Corneal burns are classified into 4 grades, as follows:
    • Grade 1: Only corneal epithelial loss is present. No conjunctival ischemia is found. The prognosis is very good.
    • Grade 2: Some corneal edema and haze are present. The conjunctival ischemia affects less than one third of the limbus. Some permanent scarring may occur.
    • Grade 3: Cornea has significant haziness. Limbal ischemia is less than one half of the limbus. Prognosis is variable, and vision usually is impaired.
    • Grade 4: Cornea is opaque, and the limbal ischemia is greater than one half of the limbus. Globe perforation is possible. The prognosis is poor.

Patient Education

Primary prevention and patient counseling on proper eye protection is essential because over 90% of injuries can be avoided with the use of eye protection.11

  • Chemical burns
    • An estimated 90% of chemical eye injuries are avoidable. 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. Keeping all hazardous home products in an area that is difficult for a child to access is critical.
  • Ultraviolet burns
    • Inform welders of the importance of keeping on safety goggles while working.
    • People who spend significant amounts of time outdoors must be aware of the danger of UV keratitis, particularly at high altitudes.
  • For excellent patient education resources, visit eMedicine's Eye and Vision Center and Burns Center. Also, see eMedicine's patient education articles Eye Injuries, Chemical Eye Burns, Thermal (Heat or Fire) Burns, and How to Instill Your Eyedrops.

Miscellaneous

Medicolegal Pitfalls

  • Evaluate all patients with alkali injuries to the face for tracheal and esophageal burns, since these may be life-threatening injuries.
  • Evaluating airway and breathing in patients who have sustained ocular thermal burns during a fire is essential.
  • Hydrofluoric acid burns can cause significant hypocalcemia. Consider checking the calcium level for burns that are not limited to the eye.
  • Lid eversion is necessary to evaluate for the presence of retained solid substances.
  • Patients should not be discharged with ophthalmologic topical anesthetics, as this can cause corneal endothelial toxicity, corneal ulceration, and scarring.
  • Only administer steroid preparations if recommended by an ophthalmologist because these medications can slow healing and predispose the eye to infection. Acute rise in intraocular pressure is less of a risk in short-term use.

References

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Keywords

eye burns, ocular burns, sclera burns, conjunctiva burns, cornea burns, eyelid burns, conjunctival burns, scleral burns, corneal burns, chemical burns to the eye, ocular injury

Contributor Information and Disclosures

Author

Cheri N Melsaether, MD, Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center
Disclosure: beth israel deaconess medical center Honoraria Other

Coauthor(s)

Carlo L Rosen, MD, Assistant Professor of Medicine, Harvard Medical School; Program Director, Department of Emergency Medicine, Beth Israel Deaconess Medical Center/ Harvard Affiliated Emergency Medicine Residency program
Carlo L Rosen, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Douglas Lavenburg, MD, Clinical Professor, Department of Emergency Medicine, Christiana Care Health Systems
Douglas Lavenburg, MD is a member of the following medical societies: American Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Anna I Cheh, MD, Wende R Reenstra, MD, PhD, and Loice Swisher, MD, to the development and writing of this article.

Further Reading

Related eMedicine topics 
  
Burns, Chemical (from Ophthalmology)
Burns, Chemical (from Emergency Medicine)
Facial Burns (from Otolaryngology and Facial Plastic Surgery)
Burns, Chemical (from Dermatology)
Hydrofluoric Acid Burns (from Emergency Medicine)  

Guidelines  

Management of Burns and Scalds in Primary Care  

Eye

Clinical studies  

The Role of Amniotic Membrane Transplantation in Ocular Chemical Burns

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