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Photokeratitis

Photokeratitis
Literature review current through: May 2024.
This topic last updated: Sep 19, 2022.

INTRODUCTION — Photokeratitis, also known as ultraviolet (UV) keratitis, is an acute syndrome that occurs after UV irradiation of the eyes. The exposure may not be initially apparent to the patient, as there is a latent period (6 to 12 hours) between exposure and onset of symptoms. Although intensely painful, photokeratitis is generally a self-limited condition with complete resolution.

The presentation, diagnosis, treatment, and prevention of photokeratitis will be reviewed here. The general evaluation of patients with a red eye is discussed separately. (See "The red eye: Evaluation and management".)

SOURCES OF ULTRAVIOLET EXPOSURE — Many recreational and occupational activities are associated with ultraviolet (UV) exposure and the potential for photokeratitis in unprotected eyes. Welder's arc burns and snowblindness are the best known examples of photokeratitis, but other exposures include:

Other recreational solar exposure

Sunlamps

Short circuit in a high-voltage line

Laboratory or germicidal UV lamps

Damaged metal halide lamps, typically used in gymnasia and assembly halls [1-3]

Aquaria disinfection lamps [4]

PRESENTATION — The affected patient is not aware of the radiation insult until 6 to 12 hours after the exposure, when the patient develops bilateral eye pain, injection, photophobia, and inability to open the eyes. The latency is absolutely characteristic. Associated facial erythema and edema are often present and suggest radiation exposure as the source of the injury. The patient is typically distraught and pacing or rocking, due to severe pain.

PATHOGENESIS AND NATURAL HISTORY — The cornea transmits most light in the visible spectrum but absorbs light in the ultraviolet (UV) spectrum. This absorption occurs primarily in the multilayered corneal epithelium [5] and results in surface epithelial cell death and desquamation within hours.

UV-A (320 to 400 nm) falls into the part of the spectrum that is only 10 to 20 percent absorbed by the cornea, whereas the cornea absorbs nearly 100 percent of UV-C (<290 nm). The clinical findings associated with solar UV photokeratitis are related to exposures at approximately 290 nm (the cutoff between UV-B and UV-C), energy that is mostly absorbed by the corneal epithelium [6].

Epithelial nociceptor terminal axons are destroyed by the exposure. Corneal pain results from stimulation, in the absence of epithelium, of the subepithelial nerve plexus by a variety of environmental insults [7].

Regeneration of the epithelial surface and resolution of signs and symptoms occurs within 24 to 72 hours. Studies in animal models reveal that this rapid response is due to macrophage migration inhibitory factor, an integral component of the host alarm system and stress response and a contributor to wound healing [8].

DIAGNOSIS — A careful history will typically yield the antecedent exposure along with failure to use protective eyewear. The eye pain is associated with photophobia and foreign body sensation, symptoms that are characteristic of a keratitis. Photokeratitis is typically bilateral and involves most of the corneal surface, which accounts for the incapacitating nature of this condition. (See "The red eye: Evaluation and management".)

Examination — There may be erythema of the face and lids. Visual acuity is typically mildly to moderately reduced but may be difficult to obtain without administration of topical anesthetic.

Penlight examination reveals tearing as well as generalized injection and edema (chemosis) of the bulbar conjunctiva. There is no discharge or involvement of the tarsal conjunctiva, which distinguishes photokeratitis from conjunctivitis.

The cornea may appear mildly hazy. Instillation of fluorescein reveals superficial punctuate staining of the cornea in the interpalpebral fissure. The pupils may be miotic. The remainder of the eye examination is unremarkable.

TREATMENT — Treatment of photokeratitis is supportive, with acknowledgment that the pain related to this syndrome is severe (anecdotally reported as comparable to childbirth or a kidney stone). There is no evidence from clinical trials on the efficacy of various treatment options. Initial treatment with oral analgesics and lubricant antibiotic ointments can be undertaken by the primary care or emergency clinician.

Supportive care includes:

Oral analgesics – The pain from photokeratitis is typically severe, especially at the onset. Mild oral opioids are usually necessary for adequate pain relief. We suggest that patients are given oxycodone 5 to 10 mg every 4 to 6 hours as needed for the first 24 to 48 hours. Pain control permits sleep and helps recovery.

Lubricant antibiotic ointments – Topical antibiotic ointments can improve comfort and may provide prophylaxis against superinfection [9]. We suggest treating patients with an antibiotic ointment (eg, erythromycin, bacitracin, or polymyxin-bacitracin), prescribed three to four times daily for two to three days.

Patients should be reexamined in one to two days for resolution of signs and symptoms. They should be referred to an ophthalmologist for any new or persistent signs or symptoms.

Photophobia can be relieved with cycloplegic drops (cyclopentolate 1% or homatropine 2 to 5%). However, these agents can result in pupil dilation lasting days, which may be distressing to the patient. We suggest that patients not be treated with cycloplegics. Pressure patching of the worse eye may offer some relief. However, it has not been proven to speed healing after corneal abrasion [10] and is unlikely to improve healing after ultraviolet (UV) irradiation. We suggest that patients not be treated with eye patching.

We recommend that topical anesthetics not be dispensed or prescribed, although they may be used during the initial examination [11]. Continued use can lead to dependency, corneal toxicity, persistent corneal epithelial defects, corneal ulceration, and loss of the eye [11]. Corneal anesthesia, whether pathologic or pharmacologic, can lead to neurotrophic ulceration related to the absence of neural input that generates protective reflexes, including tearing and blinking. Neurotrophic keratitis is analogous to foot ulcers seen in diabetic neuropathy.

SEQUELAE — Conventional teaching is that the cornea heals without sequelae after an episode of photokeratitis. However, this has never been studied systematically or with regard to the particular spectra of differing ultraviolet (UV) sources.

Long-term effects of chronic solar UV exposure to the cornea include pterygium and a rare corneal degeneration (climatic droplet keratopathy) [12]. However, an association of these syndromes with prior acute episodes of photokeratitis has never been shown.

A disproportionate number of radiation-associated eye conditions occur in welders [13], but again, association with prior acute episodes has not been shown. UV radiation can cause damage to the corneal endothelium [14]. However, one study that compared welders with office workers found no evidence of increased endothelial damage among the welders [15].

Adverse health effects of UV radiation, other than photokeratitis, include erythema, pterygium, some types of cataract, non-melanocytic skin cancer, and cutaneous malignant melanoma [16].

PREVENTION — Photokeratitis is preventable. Those with recreational exposure should use well-fitting sunglasses that block most ultraviolet (UV)-A and UV-B radiation and meet the American National Standards Institute (ANSI) standards for nonprescription and prescription sunglasses [17] or equivalent standards outside the United States.

UV-blocking glasses or contact lenses should not be used when occupational exposures require UV-blocking safety goggles [16]. Those with potential face and occupational exposures should use protectors meeting ANSI standards for eye and face protectors and for occupational and educational personal eye and face protection devices. These measures are considered to provide adequate protection for most workers exposed to solar and artificial solar UV sources [16]. Facilities using metal halide and mercury vapor lamps should adhere to US Food and Drug Administration (FDA) radiologic health program recommendations [18] or equivalent international standards.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Photokeratitis (arc eye) (The Basics)")

SUMMARY AND RECOMMENDATIONS

Photokeratitis (ultraviolet [UV] keratitis) is an acute syndrome causing severe eye pain that begins 6 to 12 hours after exposure to UV light. (See 'Presentation' above.)

The surface layer of the corneal epithelium is desquamated, exposing subepithelial nerve endings; the surface regenerates with resolution of symptoms in 24 to 72 hours. (See 'Pathogenesis and natural history' above.)

Patients often have a foreign body sensation; fluorescein staining may show punctate corneal staining. There is generalized eye injection and edema, and some patients have facial and lid erythema. Eye discharge should not be present. (See 'Examination' above.)

We suggest patients with photokeratitis be treated supportively with antibiotic ointment and oral analgesics (Grade 2C). We recommend that topical anesthetics should not be dispensed or prescribed, although they may be used during the initial examination (Grade 1C). We suggest patients not be treated with cycloplegics or eye patching (Grade 2C). (See 'Treatment' above.)

Photokeratitis is preventable. Protective eyewear should be worn for occupational or recreational exposure. (See 'Prevention' above.)

  1. Kirschke DL, Jones TF, Smith NM, Schaffner W. Photokeratitis and UV-radiation burns associated with damaged metal halide lamps. Arch Pediatr Adolesc Med 2004; 158:372.
  2. Banerjee S, Patwardhan A, Savant VV. Mass photokeratitis following exposure to unprotected ultraviolet light. J Public Health Med 2003; 25:160.
  3. Finn LE, Gutowski J, Alles S, et al. Photokeratitis Linked to Metal Halide Bulbs in Two Gymnasiums - Philadelphia, Pennsylvania, 2011 and 2013. MMWR Morb Mortal Wkly Rep 2016; 65:282.
  4. Verma AS, Dwarika D, Bhola RM, Emamali S. Photokeratitis following the manipulation of aquaria disinfection lamps. Emerg Med J 2007; 24:232.
  5. Podskochy A. Protective role of corneal epithelium against ultraviolet radiation damage. Acta Ophthalmol Scand 2004; 82:714.
  6. Parrish CM, Chandler JW. Corneal trauma. In: The Cornea, Kaufman HE, Barron BA, McDonald MB, Waltman SR (Eds), Churchill Livingstone, 1988.
  7. Bergmanson JP. Corneal damage in photokeratitis--why is it so painful? Optom Vis Sci 1990; 67:407.
  8. Kitaichi N, Shimizu T, Yoshida K, et al. Macrophage migration inhibitory factor ameliorates UV-induced photokeratitis in mice. Exp Eye Res 2008; 86:929.
  9. Upadhyay MP, Karmacharya PC, Koirala S, et al. The Bhaktapur eye study: ocular trauma and antibiotic prophylaxis for the prevention of corneal ulceration in Nepal. Br J Ophthalmol 2001; 85:388.
  10. Turner A, Rabiu M. Patching for corneal abrasion. Cochrane Database Syst Rev 2006; :CD004764.
  11. McGee HT, Fraunfelder FW. Toxicities of topical ophthalmic anesthetics. Expert Opin Drug Saf 2007; 6:637.
  12. Cullen AP. Photokeratitis and other phototoxic effects on the cornea and conjunctiva. Int J Toxicol 2002; 21:455.
  13. Tenkate TD. Optical radiation hazards of welding arcs. Rev Environ Health 1998; 13:131.
  14. Karai I, Matsumura S, Takise S, et al. Morphological change in the corneal endothelium due to ultraviolet radiation in welders. Br J Ophthalmol 1984; 68:544.
  15. Oblak E, Doughty MJ. Chronic exposure to the ultraviolet radiation levels from arc welding does not result in obvious damage to the human corneal endothelium. Photochem Photobiol Sci 2002; 1:857.
  16. Tenkate TD. Occupational exposure to ultraviolet radiation: a health risk assessment. Rev Environ Health 1999; 14:187.
  17. American National Standards Institute. Available at: https://www.ansi.org/ (Accessed on October 10, 2011).
  18. US Food and Drug Administration. Ultraviolet radiation burns from high-intensity metal halide and mercury vapor lighting remain a public health concern. Available at: https://www.fda.gov/radiation-emitting-products/alerts-and-notices/ultraviolet-radiation-burns-high-intensity-metal-halide-and-mercury-vapor-lighting-remain-public (Accessed on October 10, 2011).
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