eMedicine Specialties > Emergency Medicine > Ophthalmology

Burns, Ocular

Author: Cheri N Melsaether, MD, Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center
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
Contributor Information and Disclosures

Updated: Nov 1, 2007

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.

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. Eye injuries account for 3-4% of all occupational injuries. 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.¹ 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.¹ 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.¹ 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.² 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.
  • 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.

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