Photokeratitis is an acute corneal epithelial disorder that occurs after exposure to ultraviolet (UV) radiation without protective equipment1. It corresponds to a “sunburn” of the eye and is also called ultraviolet keratitis2.
Ultraviolet radiation is classified into the following three types by wavelength:
Photokeratitis is broadly divided into two types based on the light source:
ICD-10 codes: H16.131 (right eye), H16.132 (left eye), H16.133 (both eyes), H16.139 (unspecified).
The type of ultraviolet radiation causing them differs. Electric ophthalmia is caused by UVC (short-wavelength ultraviolet) from artificial sources such as welding or germicidal lamps, and is highly damaging. Snow blindness is caused by UVB (medium-wavelength ultraviolet) from sunlight, and symptoms are generally mild with a slightly longer incubation period. For details, see “Pathophysiology and Detailed Mechanism” section.
Symptoms appear after an incubation period of 30 minutes to 24 hours following UV exposure 1. A typical pattern is performing welding work or skiing during the day, then developing symptoms at night and visiting the emergency room 4.
Usually bilateral. May be accompanied by erythema of the face and eyelids (sunburn from UV radiation).
Ultraviolet radiation induces apoptosis (programmed cell death) in corneal epithelial cells. Because there is a time lag between cell shedding and exposure of the subepithelial nerves, symptoms appear 30 minutes to 24 hours after exposure, not immediately. For details, see the “Pathophysiology and Detailed Mechanism” section.
Arc Eye (Electric Ophthalmia)
Arc welding: The most common cause. It occurs when working without a protective face shield or from nearby exposure.
Germicidal lamps and mercury vapor lamps: Emit short-wavelength UVC. Accidental exposure occurs in laboratories and medical facilities.
Acetylene welding: One of the artificial light sources that emit UVC.
Snow Blindness
Ski slopes: High reflectivity of snow leads to exposure to large amounts of UVB3.
High-altitude mountaineering: The atmosphere is thinner, reducing UV scattering. The albedo (reflectivity) of fresh snow can reach up to 90%1. UV exposure increases by approximately 4% for every 300 m increase in altitude3.
Tanning salons and sunlamps: Exposure to artificial UVB/UVA light sources.
Other sources of exposure include damaged metal halide lamps (used in gymnasiums, etc.) and bursting halogen lamps.
Spending more than 1.5 to 2 hours at a ski resort on a sunny day without protective glasses or goggles increases the risk of developing the condition. In fact, a study of climbers and outdoor workers reported that about 87% of UV keratitis cases occurred in those not wearing protective eyewear, and the remaining cases wore sunglasses lacking side shields 3.
Without protection, exposure exceeding about 1.5 to 2 hours at a sunny ski resort is considered a threshold for onset. However, with artificial light sources containing UVC, such as welding arcs, even very short exposure can cause the condition.
History taking is most important. The history of UV exposure and the latency period until symptom onset are key to diagnosis.
It is necessary to differentiate from other diseases that present with bilateral hyperemia, pain, and photophobia.
| Disease | Key differentiating points |
|---|---|
| Viral conjunctivitis | Unilateral onset, hyperemia also in the palpebral conjunctiva |
| Contact lens overwear | History of contact lens use |
| Dry eye | Short tear break-up time, no UV exposure history |
| Drug toxicity | History of eye drop use |
| Chemical exposure | History of contact with chemical substances |
| Upper eyelid foreign body | Unilateral, vertical linear abrasion |
Photokeratitis is a self-limiting disease. The corneal epithelium typically regenerates within 24 to 72 hours 1. Treatment is mainly supportive 1,4.
Contact lens wearers should discontinue use until the cornea heals.
Re-evaluate within 1–2 days after the initial visit to confirm improvement in symptoms and findings. If new pain or worsening occurs, reassess promptly.
Topical anesthetics interfere with corneal epithelial repair and worsen damage, so prescribing them to patients is contraindicated. They should only be used temporarily during examinations; for home use, oral analgesics are recommended.
The cornea is transparent and transmits visible light (400–700 nm) while absorbing ultraviolet light (10–400 nm). Although the corneal epithelium accounts for only about 10% of the total corneal thickness, it contains a high density of nucleic acids and proteins, thus absorbing most of the UV radiation1.
Ultraviolet light is absorbed by nucleic acids and aromatic amino acids in living tissues, causing cell damage by denaturing genes and proteins. Among these, cyclobutane pyrimidine dimers (CPDs) induced by UVB irradiation are the most frequent DNA lesions, leading to apoptosis if repair is insufficient6.
The effects of different UV wavelengths on the cornea are shown below.
| UV Type | Wavelength | Main Mechanism of Action |
|---|---|---|
| UVC | 10–280 nm | Directly absorbed by the epithelium. Most damaging. |
| UVB | 280–320 nm | Direct DNA damage |
| UVA | 320–400 nm | Oxidative stress (indirect) |
When corneal epithelial cells absorb ultraviolet light, apoptosis (programmed cell death) is induced2. In animal experiments, apoptosis has been observed in all three layers of the cornea within 5 hours after UV irradiation at 300 nm2. Damaged epithelial cells are shed over time, exposing the subepithelial corneal nerve plexus. This nerve exposure is the cause of severe pain1.
The latency period from exposure to symptom onset (30 minutes to 24 hours) reflects the time required for apoptosis and shedding of epithelial cells1.
Electric ophthalmia is caused by short-wavelength ultraviolet light including UVC, and tends to be more damaging with a shorter latency period. On the other hand, snow blindness is mainly caused by UVB from sunlight, and because the wavelength is relatively longer, symptoms are milder and the time to onset tends to be longer.
Animal experiments have shown that with massive ultraviolet exposure, damage can extend beyond the epithelium to the corneal stroma and endothelium.
Cumulative lifetime exposure to ultraviolet radiation is a risk factor for pterygium, ultraviolet-related corneal degeneration, malignant melanoma, and non-melanoma skin cancer 2. Chronic UV exposure also causes oxidative stress to corneal endothelial cells and the lens, contributing to corneal endothelial damage and cataracts 2,6.
以下はいずれも PubMed/PMC で実在を確認した peer-reviewed の文献である。
