Ultraviolet Keratitis 

Updated: Mar 14, 2019
Author: Alex Koyfman, MD; Chief Editor: Liudvikas Jagminas, MD, FACEP 

Overview

Background

Ultraviolet (UV) light is the most common cause of radiation injury to the eye. The cornea absorbs most UV radiation. UV radiation damage to the corneal epithelium is cumulative, similar to the effects with dermal epithelium (sunburn). Ozone in the atmosphere effectively filters most of the harmful UV radiation of wavelengths shorter than 290 nm; natural UV sources, such as the sun, rarely cause injury after short exposures. However, unprotected exposures to the sun or solar eclipses or exposure to the sun on highly reflective snow fields at high elevation can lead to direct corneal epithelial injury. The latter clinical scenario is known as snow blindness.

Artificial sources of UV radiation also cause corneal damage. Injury from a welder's arc commonly is known as flash burn, welder's flash, or arc eye. Other sources of UV radiation injury include sun tanning beds, carbon arcs, photographic flood lamps, lightning, electric sparks, and halogen desk lamps. Several outbreaks of ultraviolet keratitis have been observed in the United States after installation of improper lighting in school gymnasiums, resulting in high levels of UV radiation.[1]

Prolonged exposures to UV radiation can lead to chronic solar toxicity, which is associated with several ocular surface disorders (eg, pinguecula, pterygium, climatic droplet keratopathy, squamous metaplasia, carcinoma). The only ocular cancer associated with UV radiation is epidermoid carcinoma of the bulbar conjunctiva, which occurs with increased frequency in the tropics and subtropics and has been experimentally replicated in animal models using UV radiation. Rarely, retinal absorption of visible to near-infrared (400-1400 nm) radiation from welding arcs can lead to permanent, sight-threatening injury.[2]

Pathophysiology

The cornea transmits most of the visible light spectrum, including the UV spectrum, with absorption by the corneal epithelium.[3] The cornea absorbs 10%-20% of UV-A and close to 100% of UV-C.[4] UV rays irritate the superficial corneal epithelium, causing inhibition of mitosis, production of nuclear fragmentation, and loosening of the epithelial layer. Under experimental conditions in animals, phototoxic effects have been demonstrated at all levels of the cornea, including the stroma and endothelium.[5]

An inflammatory response occurs, which includes edema and congestion of the conjunctiva and a stippling of the corneal epithelium known as superficial punctate keratitis (SPK). SPK is a nonspecific corneal condition associated with multiple ocular disorders. It is characterized by small pinpoint defects in the superficial corneal epithelium, which stain with fluorescein. If SPK is severe, it may be followed by total epithelial desquamation, with conjunctival chemosis, lacrimation, and blepharospasm. Reepithelialization usually occurs within 36-72 hours, and long-term sequelae are rare. This SPK contrasts with the more severe effects frequently encountered with corneal damage caused by alkaline or strongly acidic chemicals. See the image below.

Diffuse uptake of fluorescein stain as seen in ult Diffuse uptake of fluorescein stain as seen in ultraviolet keratitis.

In general, ocular pain, photophobia, redness, and decreased visual acuity occur 6-12 hours after the injury. This lag time involves an unexplained pattern of corneal sensory loss and return and is thought to indicate a probable photochemical injury rather than a thermal injury to the cornea.

Epidemiology

Frequency

United States

UV keratitis and UV keratoconjunctivitis are the only radiant exposure conditions of the cornea that occur with any significant frequency in the United States.[6]

Mortality/Morbidity

No reported mortality occurs. Morbidity results from UV radiation damage to the superficial corneal epithelium, which usually heals spontaneously within 48-72 hours of the exposure. Long-term sequelae, which may result from superinfection, are rare.

Sex

No difference in incidence is observed between males and females.

Prognosis

The prognosis is excellent for full recovery within 24-76 hours.

Patient Education

Educate patients about proper eye precautions, such as the use of UV-filtering lenses or limiting exposure to the sun. The condition is preventable with the appropriate precautions.

For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center. Also, see eMedicineHealth's patient education article Corneal Flash Burns.

 

Presentation

History

Document information regarding the nature and duration of the ultraviolet (UV) exposure in patients with UV keratitis.

Patients experience the onset of a foreign-body sensation, irritation, pain, photophobia, tearing, blepharospasm, and decreased visual acuity 6-12 hours after the exposure.

Obtain the pertinent history, including contact lens use, past ocular trauma or surgery, current medications, and allergies to medications. Inquire concerning the risk of foreign body.

Physical

Prior to examination or treatment, assess visual acuity, with corrective lenses if relevant. Perform a full examination of the eyes, including inspection of all external structures together with funduscopic and slit lamp examinations.

Examination of the lids and conjunctiva may reveal varying lid edema and conjunctival hyperemia. Tearing may be present.

A diffuse corneal haze may be seen in severe cases.

Perform a standard slit lamp examination with prior application of tetracaine 0.5% (Pontocaine) or proparacaine 0.5% (Alcaine, Ophthetic).

Fluorescein staining reveals superficial punctate epithelial surface irregularities, which usually cover the entire surface of the cornea. This condition is usually referred to as superficial punctate keratitis (SPK). If the patient's eyelid was partially closed during the exposure, a well-demarcated line separates normal from damaged corneal epithelium. Involvement of the lens is rare and occurs only after intense exposure.

The remainder of the ocular examination findings are usually unremarkable, including intraocular pressure.

Causes

Radiation injury to the eye may be caused by unprotected or long exposures to the sun, particularly at high altitude; exposure to UV radiation reflected off snow, ice, or water; and viewing of solar eclipses. In addition to the sun, sources of UV radiation include the following:

  • Welder's arcs
  • Carbon arcs
  • Sun tanning beds [7]
  • Photographic flood lamps
  • Lightning
  • Electric sparks
  • Halogen desk lamps

Complications

Potential complications of ultraviolet keratitis include the following:

  • Superinfection, rarely
  • Vision loss, rarely
  • Pterygium (rare, most commonly with chronic repeated exposures)
  • Corneal degeneration (rare, with repeated exposures) [10]
 

DDx

Diagnostic Considerations

The following are other diagnostic considerations:

  • Dry eye syndrome - Poor tear lake or a decreased tear break-up time
  • Blepharitis - Erythema, telangiectasias, and crusting of the eyelid margins
  • Trauma - Can occur from relatively mild trauma, such as chronic eye rubbing
  • Exposure keratopathy - Poor eyelid closure with failure to cover the entire globe
  • Topical drug toxicity - Neomycin, tobramycin, or drops with preservatives, including artificial tears
  • Contact lens–related disorder - Chemical toxicity, tight-lens syndrome, contact lens overwearing syndrome, or giant papillary conjunctivitis
  • Thygeson superficial punctate keratitis (SPK) - Bilateral, recurrent SPK without conjunctival injection
  • Foreign body under the upper eyelid - Typically linear SPK with fine scratches arranged vertically
  • Trichiasis and/or distichiasis - Eyelashes rubbing on the cornea
  • Entropion or ectropion - Superior or inferior SPK
  • Floppy lid syndrome - Extremely loose lids that pull away from the eye very easily
  • Associated retinopathy - Sun-gazer retinopathy associated with ultraviolet (UV) keratitis, seen particularly in psychiatric patients who stare directly into the sun

Differential Diagnoses

 

Workup

Procedures

Perform standard slit lamp examination with fluorescein in suspected cases of ultraviolet (UV) keratitis.[8]

Diffuse uptake of fluorescein is seen in the image below.

Diffuse uptake of fluorescein stain as seen in ult Diffuse uptake of fluorescein stain as seen in ultraviolet keratitis.
 

Treatment

Prehospital Care

If ultraviolet (UV) keratitis is suspected, flush eyes for several minutes with water or saline solution.

Emergency Department Care

Administration of a short-acting cycloplegic drop (eg, cyclopentolate 1%) may help relieve the pain of reflex ciliary spasm.

Use of a bland ointment (eg, Lacrilube) may help reduce pain. Ointments may interfere with healing in severe corneal injuries.

Many practitioners administer topical antibiotic ointment or drops (eg, erythromycin or gentamicin). However, no evidence supports this practice. If an eye patch is used with an antibiotic ointment, the patient should use antibiotic drops after the eye patch has been removed.

Application of a semipressure dressing with the eye well closed underneath was once the standard of care, but today this method of treatment is controversial. While these dressings may offer good pain relief, they may also delay reepithelialization. Moreover, some patients find the loss of sight and depth perception (in the case of single-eye patching) more traumatic than the pain itself. When used, the dressing is to be left on for 24 hours. The dressing should not be replaced by the patient without professional assistance because excessive pressure can cause further damage to the eye.

UV keratitis symptoms vary from extreme pain to a minor annoyance, depending on individual patient factors and the severity of the injury. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a reasonable first-choice analgesic. Narcotic/acetaminophen combinations are useful for breakthrough pain.

Topical anesthetic may be administered only in the ED; frequent use retards epithelial healing and may lead to corneal ulcer formation. To date, the only evidence showing that topical anesthetics causing more harm in uncomplicated corneal abrasions is from experimental animal studies, case reports, and case series. Based on available evidence, it is most likely reasonable to send patients home with dilute topical anesthetics for a period of no more than 24 hours without patients having complications, but larger studies will need to occur before this recommendation can be made. The relief provided by topical anesthetics is so immediate and dramatic that patients are highly motivated to take a bottle home with them. Be careful not to allow the patient to take the bottle surreptitiously.

Topical NSAIDs are not approved for this indication but are used for many other painful and allergic eye conditions.[9] Topical NSAIDs for UV keratitis and corneal abrasions is an off-label use but has become common practice in many places.

Consultations

Ophthalmologic consultation is not usually necessary for this condition but may be obtained at the discretion of the emergency physician in the ED or if substantial healing has not occurred within 24-48 hours.

Long-Term Monitoring

Follow-up care with an ophthalmologist is not usually necessary for ultraviolet (UV) keratitis except in cases of extensive corneal damage or in patients with preexisting serious eye conditions.

 

Medication

Medication Summary

The goal of ultraviolet (UV) keratitis therapy is to treat the pain associated with damage in the corneal epithelium resulting from UV light exposure and to prevent infection while the cornea heals. Some medications include ophthalmic antibiotics, topical cycloplegics, ophthalmic anesthetics, ophthalmic and parenteral nonsteroidal anti-inflammatory drugs (NSAIDs), and other analgesics.

Ophthalmic anesthetics

Class Summary

These agents are indicated for pain relief. Local anesthetics stabilize the neuronal membrane and prevent the initiation and transmission of nerve impulses, thereby producing the local anesthetic action.

Proparacaine 0.5% (Alcaine, Ophthetic)

Has rapid onset of anesthesia that begins 13-30 sec after instillation. However, has short duration of action of about 15-20 min. Since prolonged eye anesthesia can eliminate patient's awareness of mechanical damage to the cornea, drug should not be used outside the ED. Frequent use of anesthetics may retard healing. Least irritating of all topical anesthetics. Prevents initiation and transmission of impulse at nerve cell membrane by stabilizing and decreasing ion permeability.

Tetracaine hydrochloride solution (Altacaine)

Tetracaine hydrochloride ophthalmic solution, USP 0.5% acts by decreasing the permeability of the neuronal membrane, thereby decreasing the flux of sodium, potassium, and other ions associated with propagation of the nerve impulse. The onset of anesthesia usually begins within 30 seconds and lasts a relatively short period. Transient symptoms such as stinging, burning, and conjunctival redness may occur. A rare, severe, immediate allergic corneal reaction has been reported, characterized by acute diffuse epithelial keratitis with filament formation and/or sloughing of large areas of necrotic epithelium, diffuse stromal edema, descemetitis, and iritis.

Cycloplegics

Class Summary

These agents relax ciliary muscle spasm that can cause a deep aching pain and photophobia. Cycloplegics are used to facilitate eye examination and provide relief of symptoms in patients with moderate-to-severe eye injury. Cycloplegic agents also are mydriatics, thus before using them it is important to ensure that the patient does not have glaucoma. This medication could provoke an acute angle-closure glaucoma attack in a susceptible patient.

Cyclopentolate 0.5-1% (Cyclogyl)

Prevents muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation. Induces mydriasis in 30-60 min and cycloplegia in 25-75 min.

Antibiotics, ophthalmic

Class Summary

The routine use of topical antibiotics remains controversial. Many emergency physicians have stopped its use for minor injuries, although others continue routine treatment with a broad-spectrum antibiotic ointment for lubrication and infection prophylaxis. This treatment persists despite its unproven efficacy, discomfort, and evidence that ointments may retard corneal epithelial healing.

Erythromycin ophthalmic (Ilotycin, AK-Mycin)

Indicated for treatment of infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.

Gentamicin (Genoptic, Garamycin)

Aminoglycoside antibiotic used for gram-negative bacterial coverage.

Analgesics

Class Summary

Although most NSAIDs are used primarily for their anti-inflammatory effects, they are effective analgesics and are useful for the relief of mild to moderate pain. Pain control is essential to quality patient care. Although oral narcotics may be sedating, they should be prescribed and are nearly always needed to gain adequate pain control. Prescribing adequate pain medications on the first visit is essential to prevent a revisit solely for pain control. Only a small quantity is needed since this is a self-limited problem with short duration.

Ibuprofen (Motrin, Advil, Nuprin, Rufen)

Usually the DOC for mild to moderate pain, if no contraindications exist; inhibits inflammatory reactions and pain, probably by decreasing cyclooxygenase activity, which results in the inhibition of prostaglandin synthesis

Oxycodone and acetaminophen (Percocet, Tylox, Roxicet)

Drug combination indicated for the relief of moderate to severe pain.

Ophthalmic analgesic

Class Summary

Some ophthalmologists are advocating that diclofenac (Voltaren) or ketorolac (Acular) drops be used despite lack of official indications. These topical agents have been shown to relieve pain in multiple situations including corneal abrasions, allergies, and postsurgical pain.

Ketorolac tromethamine 0.5% (Acular)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation.

Diclofenac ophthalmic (Voltaren)

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors.

 

Questions & Answers

Overview

What is ultraviolet keratitis?

What is the pathophysiology of ultraviolet keratitis?

What is the prevalence of ultraviolet keratitis in the US?

What is the mortality and morbidity associated with ultraviolet keratitis?

What are the sexual predilections of ultraviolet keratitis?

What is the prognosis of ultraviolet keratitis?

What is included in patient education about ultraviolet keratitis?

Presentation

What is the focus of clinical history to evaluate ultraviolet keratitis?

What is included in the physical exam to evaluate ultraviolet keratitis?

What causes ultraviolet keratitis?

What are the possible complications of ultraviolet keratitis?

DDX

Which conditions should be included in the differential diagnoses of ultraviolet keratitis?

What are the differential diagnoses for Ultraviolet Keratitis?

Workup

How is ultraviolet keratitis diagnosed?

Treatment

What is included in prehospital care of ultraviolet keratitis?

What is included in emergency department (ED) care of ultraviolet keratitis?

Which specialist consultations are beneficial to patients with ultraviolet keratitis?

What is included in long-term monitoring of ultraviolet keratitis?

Medications

What is the role of medications in the treatment of ultraviolet keratitis?

Which medications in the drug class Ophthalmic analgesic are used in the treatment of Ultraviolet Keratitis?

Which medications in the drug class Analgesics are used in the treatment of Ultraviolet Keratitis?

Which medications in the drug class Antibiotics, ophthalmic are used in the treatment of Ultraviolet Keratitis?

Which medications in the drug class Cycloplegics are used in the treatment of Ultraviolet Keratitis?

Which medications in the drug class Ophthalmic anesthetics are used in the treatment of Ultraviolet Keratitis?