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Photokeratitis

Photokeratitis
Author:
Deborah S Jacobs, MD
Section Editor:
Matthew F Gardiner, MD
Deputy Editor:
Han Li, MD
Literature review current through: Apr 2025. | This topic last updated: Oct 31, 2024.

INTRODUCTION — 

Photokeratitis, also known as ultraviolet (UV) keratitis, is an acute, painful condition of the cornea that occurs after exposure of the eye to UV radiation. Photokeratitis occurs with acute high intensity or prolonged UV exposure and specifically refers only to the effects of UV exposure on the cornea. It is not inclusive of other entities related to UV exposure, such as solar retinopathy.

While painful, photokeratitis is generally a self-limited condition.

The pathogenesis, clinical features, 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".)

PATHOGENESIS — 

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 [1] and results in surface epithelial cell death and desquamation.

The UV light spectrum includes electromagnetic waves with wavelength of 100 to 400 nm. Longer wavelength UV-A (320 to 400 nm) penetrates into deeper ocular structures and is associated with cataract development, whereas short wavelength UV-B and UV-C (<320 nm) are absorbed in the corneal epithelium, stroma, and endothelium [2]. The peak action spectrum implicated in photokeratitis occurs at 288 nm (the cutoff between UV-B and UV-C) [3,4].

In addition to desquamation of the corneal epithelium, epithelial nociceptor terminal axons are destroyed by the exposure. Corneal pain results from stimulation of the subepithelial nerve plexus by a variety of environmental insults, in the absence of the epithelium [5].

Regeneration of the epithelial surface and resolution of signs and symptoms begins occurring within 24 to 72 hours. Studies in animal models show 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 [6].

SOURCES OF ULTRAVIOLET EXPOSURE — 

Many recreational and occupational activities are associated with ultraviolet (UV) exposure and the potential for photokeratitis in unprotected eyes. Exposures include:

Recreational solar exposure, including skiing and snowboarding ("snow blindness"), outdoor water activities, hiking, and mountain climbing [7]

Sunlamps, including tanning beds

UV lights used for decorative and aesthetic purposes [2]

Germicidal UV lamps, such as used in laboratories or during the COVID-19 pandemic [8]

Arc flash from welding torches ("welder's arc eye") [9]

Damaged metal halide lamps, typically used in gymnasia and assembly halls [10-12]

Aquaria disinfection lamps [13]

Short circuit in a high-voltage line

CLINICAL FEATURES

Symptoms — Typical symptoms of photokeratitis include bilateral eye pain, foreign body sensation, red eye, photophobia, tearing, decreased vision, and burning sensation of the surrounding skin of the face and neck after exposure to ultraviolet (UV) radiation. Pain and foreign body sensation tend to be prominent features.  

Latency from exposure — The typical onset of symptoms ranges from minutes to several hours after exposure. In one case series of persons exposed to radiation from germicidal UV lamps, the median time of onset was 20 minutes, whereas the median time to onset in persons exposed to damaged metal halide lamps in another case series was seven hours (range, 4 to 11 hours) [8,10]. The latency of symptom onset is inversely proportional to the intensity and duration of UV radiation [14].

Examination — A focused ocular examination including visual acuity, external exam, and slit lamp or Wood's lamp exam, when available, should be performed. Administration of topical anesthetic (eg, ophthalmic proparacaine hydrochloride 0.5%) may be needed to obtain an accurate exam.

Typical findings include:

Bilateral ocular involvement.

Mildly reduced visual acuity, ranging from 20/20 to 20/40 (6/6 to 6/12 in metric Snellen units) in case series. Severe decrease in visual acuity is not present [2,8,15].

Eyelid and facial erythema and edema (sunburn).

Tearing (epiphora), as well as injection and edema (chemosis) of the bulbar conjunctiva.

Absence of purulent ocular discharge.

Punctate epithelial erosions of the cornea in a diffuse or interpalpebral distribution with fluorescein staining on slit lamp or Wood's lamp exam [8,15].

The remainder of the eye examination is typically unremarkable.

DIAGNOSIS — 

Symptoms and signs of photokeratitis may be seen in other ocular surface disease, so a specific history of acute high intensity or prolonged ultraviolet (UV) exposure, and inadequate protective eyewear, is crucial to make the diagnosis.

Presence of sunburn on the surrounding eyelids and face can also be helpful in ruling in the diagnosis, as it is generally absent in other considered diagnoses.

DIFFERENTIAL DIAGNOSIS — 

The differential diagnosis of patients presenting with eye pain, foreign body sensation, tearing, conjunctival injection, and mildly decreased visual acuity, as seen in photokeratitis, includes other ocular surface disease such as conjunctivitis, dry eye syndrome, exposure keratopathy, corneal abrasion, and infectious keratitis.

Conjunctivitis is often diagnosed in patients presenting with a red eye. Conjunctivitis is commonly viral, bacterial, or allergic in etiology. Distinguishing features more suggestive of conjunctivitis include history of a preceding viral prodrome in the case of viral conjunctivitis, purulent discharge in the case of bacterial conjunctivitis, or pruritus in the case of allergic conjunctivitis. Pain is typically a less prominent feature of conjunctivitis. (See "Infectious conjunctivitis".)  

Dry eye syndrome can present with similar symptoms and examination findings as photokeratitis, including foreign body sensation and mild impairment in visual acuity. The chronicity of symptoms related to dry eye, and absence of a history of ultraviolet (UV) exposure aids in differentiating the conditions. (See "Dry eye disease", section on 'Symptoms'.)

Exposure keratopathy is characterized by corneal damage due to abnormal exposure of the ocular surface to the outside environment from incomplete eyelid closure (lagophthalmos) and disruption of the tear film. Lagophthalmos can occur in neurologic conditions such as seventh nerve (Bell) palsy, as well as in ventilated or critically ill patients or those undergoing surgeries under general anesthesia. Patients with a history of sedative or illicit drug use may also be predisposed to exposure keratopathy. In contrast to photokeratitis, exposure keratopathy ends to cause punctate epithelial erosions in the inferior one-third of the cornea [16].

Corneal abrasion can also cause acute symptoms of significant pain, foreign body sensation, and tearing. In contrast to photokeratitis, corneal abrasions are typically unilateral and mechanical in etiology. (See "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

Infectious keratitis should also be considered. Infectious keratitis may be due to viral, bacterial, or fungal organisms, and can be vision-threatening. In contrast to photokeratitis, infectious keratitis is typically unilateral and visual acuity may be severely reduced. Contact lens use is the biggest risk factor for bacterial keratitis [17]. A history of contact lens use, and duration of wear, should be elicited. Referral to ophthalmology is recommended if symptoms are severe or visual acuity is significantly decreased, particularly in those with contact lens use. (See "Complications of contact lenses", section on 'Infectious keratitis'.)

MANAGEMENT — 

Treatment of photokeratitis is primarily supportive and is similar to the treatment of uncomplicated corneal abrasions. We suggest initial treatment with lubricant eye drops, antibiotic ointments, avoidance of contact lens use, and oral analgesics. There is no evidence from clinical trials on the efficacy of various treatment options.

Recommended therapies

Lubricant eye drops, gel, or ointment – Topical lubricant eye drops, gel, or ointment may be prescribed or obtained over the counter.  

Antibiotic ointments – Topical antibiotic ointments can improve comfort and may provide prophylaxis against the theoretical risk of superinfection. These can be used as an alternative to lubricants [18]. We suggest treating patients with an antibiotic ointment (eg, ophthalmic erythromycin, bacitracin, or polymyxin-bacitracin), prescribed three to four times daily for two to three days.

Avoidance of contact lens use – As with most acute ocular surface conditions, contact lens use should be avoided until symptoms have resolved.

Oral analgesics – Patients with mild to moderate ocular pain may be treated with oral nonsteroidal anti-inflammatory drugs (NSAIDs). For severe pain, low dose oral opioids may be considered for adequate pain relief. We suggest hydrocodone 5 mg every four to six hours as needed for the first 24 to 48 hours. Pain control permits sleep and helps recovery.

Re-examination – Patients should be reexamined in two to three days for improvement of signs and symptoms. Worsening visual acuity or pain could suggest an alternate or concurrent ocular condition, and should prompt referral to an ophthalmologist.

Therapies we do not recommend

We recommend that topical anesthetics not be dispensed or prescribed, although they may be used during the initial examination [19]. Continued use can lead to dependency, corneal toxicity, persistent corneal epithelial defects, corneal ulceration, and loss of the eye. Corneal anesthesia, whether pathologic or pharmacologic, can lead to neurotrophic keratitis and 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.

We do not routinely use cycloplegics in the treatment of photokeratitis, unless photophobia is severe and functionally limiting. While photophobia can be relieved with cycloplegic drops (cyclopentolate 1% or homatropine 2 to 5%), cycloplegic agents can result in prolonged loss of visual accommodation resulting in inability to do near work, which may be bothersome to the patient.

Pressure patching of the worse eye may offer some relief. However, it has not been proven to speed healing after corneal abrasion [20] and is unlikely to improve healing after ultraviolet (UV) irradiation. We suggest that patients not be treated with eye patching.

PROGNOSIS — 

Case series describe full recovery from photokeratitis with conservative management within three to seven days [2,8,15]. There are no well-described long-term sequalae of acute, intense exposure to UV radiation.    

Long-term effects of chronic solar UV exposure to the eye include pterygium, some types of cataracts, ocular surface squamous neoplasia, and rarely, corneal degeneration (climatic droplet keratopathy) [21].

Adverse non-ocular health effects of UV radiation include sunburn, non-melanocytic skin cancer, and cutaneous malignant melanoma [22].

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 [23] or equivalent standards outside the United States.

When occupational exposures require UV-blocking safety goggles, UV blocking glasses or contact lenses should not be substituted [22]. Those with potential face and occupational exposures should use protectors meeting ANSI standards for eye and face protectors. These measures are considered to provide adequate protection for most workers exposed to solar and artificial solar UV sources [22]. Facilities using metal halide and mercury vapor lamps should adhere to US Food and Drug Administration (FDA) radiologic health program recommendations [24] 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

Definition – Photokeratitis (ultraviolet [UV] keratitis), is an acute, painful condition of the cornea that occurs after exposure of the eye to UV radiation. (See 'Introduction' above.)

Pathogenesis – Exposure to acute high intensity or prolonged UV radiation causes desquamation of the surface layer of the corneal epithelium, exposing subepithelial nerve endings, causing pain and other symptoms. (See 'Sources of ultraviolet exposure' above and 'Pathogenesis' above.)

Clinical features – Typical symptoms of photokeratitis include bilateral eye pain, foreign body sensation, red eye, photophobia, tearing, decreased vision, and burning sensation of the surrounding skin of the face and neck. Symptoms occur in minutes to hours from the exposure to UV radiation.

Examination shows mildly reduced visual acuity, eyelid and facial erythema, tearing, conjunctival injection, and chemosis. Fluorescein staining may reveal punctate epithelial erosions of the cornea. Severe decrease in visual acuity and purulent ocular discharge should not be present. (See 'Clinical Features' above.)

Management – We suggest patients with photokeratitis be treated supportively with eye lubricant drops, gel, or ointment or antibiotic ointment (Grade 2C).

Patients with mild to moderate ocular pain may be treated with oral nonsteroidal anti-inflammatory drugs (NSAIDs). For severe pain, we suggest low doses of an oral opioid such as hydrocodone (Grade 2C). A reasonable dose is 5 mg every four to six hours as needed for the first 24 to 48 hours. Pain control permits sleep and helps recovery.

We recommend that topical anesthetics not be dispensed or prescribed, although they may be used during the initial examination (Grade 1C). Continued use can lead to dependency, corneal toxicity, persistent corneal epithelial defects, corneal ulceration, and loss of the eye.

In addition, we suggest patients not be treated with cycloplegics (Grade 2C). (See 'Management' above.)

Prognosis – Full recovery from photokeratitis with conservative management is expected within three to seven days. (See 'Prognosis' above.)

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

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  2. Chan JYY, Chow VWS, Chan CKM, et al. Photokeratitis in Outdoor Event Participants Exposed to UV Radiation Display. JAMA Ophthalmol 2024; 142:568.
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  16. American Academy of Ophthalmology. 2016-2017 Basic and Clinical Science Course Section 8: External Disease and Cornea, 2016. p.66.
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  23. American National Standards Institute. Available at: https://www.ansi.org/ (Accessed on October 10, 2011).
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