Updated: Aug 12, 2009
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
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.
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.
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.
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.
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.
Corneal Ulceration and Ulcerative
Keratitis
Ultraviolet Keratitis
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.
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.
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.
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.
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
Administer as in adults, but only use 2% solution
None reported
Documented hypersensitivity; narrow-angle glaucoma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
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
Solution (0.5%): 1-2 gtt into eye(s) bid/tid
Ointment: Not established
Coadministration with other anticholinergics has additive effects
Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid use in Down syndrome and in children with brain damage (patients may demonstrate hyperreactive response to topical atropine)
Blocks action of acetylcholine at parasympathetic sites in smooth muscle, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).
1-2 gtt qid
Not established
None reported
Documented hypersensitivity; primary glaucoma or initial stages of disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
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.
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
<2 years: Not established
>2 years: Administer as in adults
Effects are decreased when used concurrently with gentamicin
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
Aminoglycoside antibiotic used for gram-negative bacterial coverage. Commonly used in combination with an agent against gram-positive organisms.
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
Apply as in adults
None reported
Documented hypersensitivity; mycobacterial, viral, and fungal infections of eye; avoid using with steroid combinations after uncomplicated removal of foreign body from cornea
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
1-2 gtt q2h while awake for 2 d; followed by 1-2 gtt q4h while awake for another 5 d
Not established
None reported
Documented hypersensitivity; viral, mycobacterial, and fungal eye infections; avoid coadministration with steroid combinations after uncomplicated removal of a foreign body from cornea
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
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.
1 gtt qid for up to 2 wk
<12 years: Not established
>12 years: Administer as in adults
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Corneal thinning may occur
Used to induce active immunity.
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.
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
Administer as in adults
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)
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
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
See 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
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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
Cheri N Melsaether, MD, Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center
Disclosure: beth israel deaconess medical center Honoraria Other
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.
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, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
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.
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.
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.
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.
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Burns, Chemical (from Dermatology)
Hydrofluoric Acid Burns (from Emergency Medicine)
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