Eye burn: what it is and how it manifests itself

An eye burn is damage to the ocular surface and anterior segment tissue caused by chemical agents (alkalis, acids, irritants), heat/steam, or excessive ultraviolet radiation. Clinically, alkalis are considered the most severe chemical burns: they quickly penetrate the tissue, causing liquation necrosis and deep destruction. Acids more often cause coagulation necrosis and somewhat limit the depth of damage, but concentrated burns (e.g., sulfuric acid from batteries) are also dangerous. Ultraviolet radiation (welding, sun glare on snow/water, tanning beds) causes photokeratitis—a painful but usually reversible damage to the corneal epithelium within 24-72 hours. [1]

The key to the best outcome is immediate and copious irrigation of the eye until the tear film pH returns to normal (target range: 7.0-7.2) and all debris is removed from the conjunctival fornices by everting the eyelids. The choice of solution is secondary to the speed of initiation of irrigation: water, saline, or Ringer's lactate solution are acceptable; buffered solutions are ideal if immediately available. [2]

Even with seemingly mild injuries, the risk of late complications should not be underestimated: corneal scarring, limbal stem cell deficiency, neovascularization, and secondary glaucoma. For moderate and severe burns, the first few weeks are crucial, while the following months require disciplined therapy and competent reconstructive tactics. [3]

Below is a systematic analysis: ICD-10/ICD-11 codes, epidemiology, causes and risk factors, pathogenesis, symptoms, classifications (Roper-Hall, Dua), complications, “when to see a doctor”, diagnosis (step-by-step), differential diagnosis, detailed treatment (including new methods), prevention, prognosis and FAQ.

Code according to ICD-10 and ICD-11

In ICD-10, chemical and thermal eye injuries are coded in block T26, "Burns and corrosions limited to the eye and its appendages." Within this block, distinctions are made between burns of the eyelids/periocular area, burns of the cornea and conjunctival sac, destruction of the eyeball, and other specifications; for chemical injuries, the subheading "corrosion" is used. [4]

ICD-11 uses a cluster approach: the basic section NE00-NE0Z "Burns of the eye or internal organs," to which modifiers for depth, area, and causative factor (corrosive substances, etc.) are added. For rupture/destruction of the eyeball, the code from NA06 is indicated with a reference to "code chemical burn of the eye in NE00." [5]

Table 1. Coding examples

Situation	ICD-10 (example)	ICD-11 (example)
Chemical "corrosion" of cornea and conjunctival sac, unspecified eye, initial presentation	T26.60XA	NE00 + chemical burn expanders, depth/area
Thermal burn of the eyelid	T26.0	ND90 (external surface burn, face/eyelid) + degree
Destruction of the eyeball due to a chemical burn	T26.2	NA06.8 "trauma of the eyeball", code chemical burn separately in NE00

Source of codes and structure: official navigators ICD-10/ICD-11. [6]

Epidemiology

Chemical burns are among the most common occupational eye injuries; two-thirds of cases occur at work, with men suffering more frequently (ratio up to 3-8:1), and alkalis causing approximately two-thirds of severe injuries. The estimated incidence in developed countries is approximately 51-56 cases per 1,000,000 population per year, according to large studies in the US and UK. The financial burden on emergency departments reaches tens of millions of dollars per year. [7]

Population data from New Zealand over 10 years give an estimated incidence of significant chemical injuries of 9.5 ± 4.3 per 100,000 persons per year, with a male predominance and a median age of approximately 40 years. This is consistent with international estimates, indicating stability of risk across working ages.[8]

In pediatric practice, chemical injuries are most often household-related, with detergents and laundry capsules leading the way; the highest age risk is 1-2 years. Mild injuries in children usually heal quickly, but delayed rinsing and underestimation of the injury worsen the outcome. [9]

Photokeratitis (ultraviolet burn) is common in risk groups: welders, climbers/skiers, tanning salon users; symptoms appear 6-12 hours after exposure and in most cases resolve within 1-3 days with supportive care. [10]

Table 2. Key epidemiological landmarks

Indicator	Meaning
Incidence of chemical eye burns	~51-56 per 1,000,000/year (USA/UK)
The share of alkalis among severe burns	≈ 2/3
Gender	Men more often (up to 3-8:1)
Peak in children	1-2 years (household cleaning products)
Time to symptoms in photokeratitis	6-12 hours

Reasons

The main chemical agents are alkalis (ammonia, sodium/potassium hydroxides, lime), acids (sulfuric, hydrochloric, acetic), and irritants (alcohols, peroxide). Alkalis are lipophilic, quickly penetrate the epithelium, and cause stromal tissue damage; acids coagulate proteins and partially "block" further penetration, but concentrated solutions and high-energy scenarios (battery explosion) cause severe injuries. An exception is hydrofluoric acid, which "behaves" like an alkali. [11]

Thermal burns occur when exposed to steam, hot liquids, red-hot objects, or flashes; they are often combined with chemical burns (e.g., acid vapor). Ultraviolet burns occur during welding, intense sun with snow/water, and in solariums. [12]

Classic household mistakes: failure to immediately rinse, attempts to "neutralize" the injury with chemicals, delays in everting the eyelids and removing particles, and wearing contact lenses during the injury. At work, there is a shortage of eye protection and emergency water fountains. [13]

Risk factors

Severity is determined by: 1) the nature of the agent (alkali is heavier than acid), 2) concentration/volume, 3) time before irrigation, 4) presence of particles in the conjunctival fornices (calcium), 5) local conditions (dry eye, previous surgery). A delay of minutes increases the depth of the lesion. [14]

Occupational hazards: construction, dry cleaning, cleaning, battery, agricultural, and laboratory processes. Safety glasses and training significantly reduce injuries. [15]

For photokeratitis, consider welding without a shield, mountain/water sports without UV-filtered goggles, and tanning beds. For children, consider access to household chemicals and laundry capsules. [16]

Table 3. What makes a burn worse

Factor	Why is it dangerous?
Alkaline, pH > 11.5	Rapid penetration, "spreading" necrosis
Delayed irrigation	Increase in depth and area of damage
Particles in the vaults	Long-term "feeding" of the burn
High volume/concentration	More substrate for reaction
Lack of PPE	Higher risk and severity of injury

Pathogenesis

Alkalis destroy lipid membranes (saponification), hydrolyze glycosaminoglycans and collagen, causing "liquation" necrosis; the damage extends deep into the anterior chamber. Acids denature and coagulate proteins, forming a scab that partially limits penetration (with the exception of hydrofluoric acid). [17]

Over the course of hours to days, inflammation, activation of metalloproteinases, ascorbate deficiency in the aqueous humor, limbal ischemia, and loss of limbal stem cells—the primary "reservoir" for corneal epithelial regeneration—develop. This increases the risk of persistent defects, ulcers, melting, and perforation. [18]

In photokeratitis, ultraviolet light induces apoptosis of the corneal surface epithelium; symptoms manifest with a delay of 6-12 hours and usually regress as the corneal epithelium re-thematizes within 24-72 hours. [19]

Symptoms

Acute: sharp pain, lacrimation, photophobia, blepharospasm, "sand in the eyes," blurred vision. In severe chemical burns - corneal opacity, limbal ischemia, decreased/loss of vision, increased intraocular pressure. [20]

Photokeratitis is characterized by severe pain and photophobia 6-12 hours after bright ultraviolet exposure; bilaterality is typical. Symptoms usually resolve within 1-3 days. [21]

Increasing pain after “improvement,” decreased vision, “dark veil,” appearance of purulent discharge, increased redness, nausea/headache (with a sharp increase in IOP) are alarming signs and a reason for immediate examination. [22]

Table 4. Picture by burn type

Type	Characteristic manifestations	Gravity landmarks
Alkaline	Rapid increase in pain, corneal opacity, limbal ischemia	Limb ischemia rate, stromal transparency
Acid	Burning, redness, pain; with concentrates - scab	Depth of necrosis, “visibility” of the iris
Ultraviolet	Pain after 6-12 hours, photophobia, bilateral	The epithelium is restored within 24-72 hours

Classification, forms and stages

In practice, two scales are used: Roper-Hall (corneal transparency and limbal ischemia) and Dua (percentage of limbal and conjunctival damage). Both correlate with prognosis and treatment plan. [23]

The stages of the process are: acute period (0-7 days), early reparative (7-21 days), late reparative (>21 days). In severe cases, a deficiency of limbal stem cells with corneal conjunctivalization develops. [24]

Forms: chemical (alkaline/acid/irritants), thermal (steam, flame, hot object), ultraviolet (welding, sun, solarium). Combined injuries are possible. [25]

Table 5. Roper-Hall scale

Degree	Forecast	Cornea	Limbic ischemia
I	Favorable	The epithelium is damaged	No
II	Favorable	Clouding, pupil visible	< 1/3
III	Doubtful	Stromal fog, pupil not visible	1/3-1/2
IV	Adverse	Opaque	> 1/2

Complications and consequences

Early: persistent epithelial defects, ulcers and “melting” of the cornea, secondary infection, ↑intraocular pressure, synechiae. [26]

Late: corneal neovascularization and scarring, limbal stem cell deficiency, symblepharon, ectropion/entropion, dry eye, secondary glaucoma and permanent vision loss.[27]

Severe consequences of photokeratitis are rare, but repeated episodes and lack of protection increase the risk of chronic ocular surface problems.[28]

When to see a doctor

Immediately (today): any chemical burns, exposure to an unknown substance, no improvement after 20-30 minutes of rinsing, blurred vision, presence of particles (lime, cement), pain that prevents opening the eye. [29]

Urgently in the first 24 hours: thermal burn, photokeratitis with significant pain, inability to put on/remove contact lenses due to pain, symptoms of ↑IOP (pain, nausea, “rainbow circles”). [30]

Consult an ophthalmologist immediately after irrigation: if the pH does not stabilize in the range of 7.0-7.2, if corneal opacity obscures details of the iris, if there are areas of limbal ischemia. [31]

Table 6. "Home care" or "emergency care"?

Scenario	Tactics
Chemical burn of any caliber	Rinse + emergency examination
Thermal burn, severe pain	Same day inspection
Mild photokeratitis, improvement within 24 hours	Follow-up examination according to indications
Any "red flags"	See an ophthalmologist immediately

Diagnostics

Step 1. Irrigate immediately. Begin irrigation with any available non-caustic fluid (water/saline/Ringer's lactate) without delay. Have a doctor administer anesthetic drops to ensure tolerability; aim for a pH of 7.0-7.2 and monitor it every 5-10 minutes, continuing irrigation until stable normalization is achieved. [32]

Step 2. Mechanical decontamination. Double eversion of the upper eyelid, eversion of the lower eyelid, and combing the fornices with cotton swabs to remove particles (especially lime). Check and revise the pH within 1 hour after stopping irrigation. [33]

Step 3. Basic examination. Visual acuity, pH, fluorescein biomicroscopy (epithelial defects), assessment of limbal ischemia, measurement of intraocular pressure. Roper-Hall/Dua classification. [34]

Step 4. Additionally, as indicated. Photographic documentation, anterior segment OCT, if perforation is suspected - careful examination, without an irrigating contact lens; decision on hospitalization and early surgical control. [35]

Table 7. Mini-diagnostic algorithm

Stage	What are we doing?	For what
Irrigation	Up to pH≈7.0-7.2; liters of solution if necessary	Reducing the depth of the burn
Eversion of the eyelids and cleaning of the fornices	Removal of particles (lime, cement)	Elimination of "secondary ignition"
Fluorescein examination	Epithelial defect/ulcer	Treatment plan
IOP measurement	Identification of complications	Antiglaucoma therapy tactics

Differential diagnosis

We differentiate chemical burns from purely irritating instillations (alcohols, perfume aerosols): with a chemical burn, the pain and clouding are greater, and there is often limbal ischemia and epithelial defect. [36]

For thermal burns - depending on the circumstances (steam/flame/oil) and combination with eyelid skin burns. For photokeratitis - depending on the delay of symptoms of 6-12 hours and bilaterality without contact with the chemical. [37]

We exclude penetrating trauma, infectious keratitis, acute attack of closed-angle glaucoma (pain, nausea, “rainbow circles”, high IOP). [38]

Treatment

The first line is irrigation: begin immediately, without delay. Water, saline, or Ringer's lactate are suitable; a buffered solution is ideal if it is readily available. The goal is a tear film pH of approximately 7.0-7.2; monitor the pH every 5-10 minutes and re-irrigate if it deviates. Volumes easily reach 1-2 liters or more; for severe alkali burns, "liters to neutralize" may be required. [39]

Irrigation technique and particle removal. Double eversion of the upper eyelid, eversion of the lower eyelid, and thorough sanitization of the fornices with cotton swabs. If pain is a concern, local anesthetics are administered in the doctor's office, after which irrigation is continued. For continuous, hands-free irrigation, an irrigation lens (Morgan type) may be used by trained personnel; this speeds up the process in cases of severe blepharospasm. [40]

Basic medication regimen for mild to moderate burns. Frequent use of preservative-free artificial tears, antibiotic ointment (e.g., erythromycin) at night, cycloplegic (cyclopentolate/atropine) for pain and spasm prevention, cautious short-term use of topical steroids as prescribed by an ophthalmologist for the first 3-7 days to control inflammation (with gradual withdrawal). For photokeratitis, supportive therapy: oral analgesics, artificial tears, antibiotic ointment at night; as a rule, epithelial restoration occurs within 24-72 hours. [41]

Extended antidissection therapy for moderate to severe burns. Frequent instillations of 10% ascorbate drops and 10% citrate drops to prevent stromal melting (inhibition of collagenolysis), plus oral doxycycline (or other tetracyclines) as a matrix metalloproteinase inhibitor. Ascorbate is preferable for topical administration (it penetrates the anterior segment better than systemic administration); citrate has been associated with better outcomes in severe burns in a number of studies. [42]

Pain and intraocular pressure control. Non-narcotic analgesics; if IOP increases, topical antiglaucoma agents (preservative-free, if possible), selected by an ophthalmologist. Antiglaucoma prostaglandins are generally avoided in the acute period due to their inflammatory profile; β-blockers and carbonic anhydrase inhibitors are preferred. [43]

Surface protection and epithelialization. A soft bandage lens (sterile, under antibiotic cover) reduces pain and accelerates epithelialization; for extensive defects, a temporary amniotic membrane (including a cryopreserved ring system) is used for protection and inflammation modulation. The effectiveness of the membrane in the acute period depends on the severity; the decision is made by the specialized team. [44]

Limbal and fornix management. Symblepharon prevention (rings, active fornix stretching, frequent instillation), early tenoplasty in case of limbal ischemia. In the late phase, with limbal stem cell deficiency – SLET/CLET/KLAL (simple or cultured limbal transplant, allogeneic options) with immunosuppression if necessary. [45]

Antimicrobial and anti-inflammatory strategy. Antibiotics are administered topically as a prophylactic measure for epithelial defects; systemic antibiotics are used as clinically indicated. Topical steroids are effective in suppressing "sterile" inflammation and preventing scarring, but should be prescribed and titrated by an ophthalmologist; in mild burns, their benefit versus the risk of delayed epithelialization is debated and requires caution. [46]

Special cases. Hydrofluoric acid: at least 30 minutes of irrigation with water/saline; topical calcium gluconate is discussed, but the evidence base is limited. If perforation is suspected, avoid irrigating lenses, perform a gentle examination, and conduct surgical tactics as indicated. [47]

Rehabilitation and "long-distance." Ocular surface stabilization (preservative-free tear substitutes, cyclosporine/lifitegrast as indicated), IOP control, dry eye treatment. In the late phase after stabilization, keratoplasty (penetrating or lamellar) is used for persistent opacification; for visual rehabilitation, scleral prosthetic lenses (PROSE) are used. Patient education is critical for adherence (ascorbate/citrate often cause "pinching," leading patients to discontinue treatment). [48]

Table 8. What helps and what is harmful

Action	Not really	Comment
Immediate irrigation to pH 7.0-7.2	Yes	The deciding factor in the outcome
Double eversion of the eyelids and cleaning of the fornices	Yes	Removal of particles (lime)
Ascorbate 10%, citrate 10%, doxycycline	Yes	Prevention of "melting"
Neutralization of acids/alkalis	No	Increases damage/heat generation
Long-term home anesthesia of the eyes	No	Risk of epithelial toxicity

Prevention

At work: safety glasses/shields with side protection, emergency eyewashes, training in the "IRRIGATE, IRRIGATE, IRRIGATE" algorithm, and labeling and storage of reagents. This reduces the frequency and severity of injuries. [49]

At home: Keep household chemicals out of the reach of children, especially laundry detergent capsules; work with acids/alkalis with ventilation turned on; avoid aerosolization. When welding or using a tanning bed, wear glasses with certified UV protection. [50]

In sports and in the mountains - glasses with ultraviolet filters and side protection; on water and snow - increased vigilance due to ultraviolet reflection. [51]

Table 9. Prevention by scenarios

Scenario	Measure
Manufacturing/construction	Eye protection + emergency fountain
House cleaning	Gloves/goggles, keep out of reach of children
Welding	Shield/mask training
Mountain/water sports	Glasses with UV filter

Forecast

Mild chemical and ultraviolet burns with early irrigation usually heal completely: epithelialization within 1 week, restoration of vision is rapid. [52]

Moderate and severe chemical burns are determined by the degree of limbal ischemia and corneal transparency at initial examination: the higher the Roper-Hall/Dua grade, the higher the risk of ulceration, neovascularization, limbal deficit, and visual impairment. Early and aggressive management reduces the need for surgery and improves outcomes. [53]

Rehabilitation after severe burns involves months of therapy and possible reconstructive surgery (amniotic membrane, limbal grafts, and then keratoplasty). Adherence to treatment is critical: up to 33% of patients discontinue the "stinging" ascorbate/citrate drops, which worsens the results. [54]

FAQ

How long should you flush an eye after a chemical burn? Until the pH reaches 7.0-7.2 and remains neutral; this usually takes 20-30 minutes and 1-2 liters of solution, but alkaline solutions may require more. The key is to start immediately. [55]

What solution should I use for irrigation? Whatever is immediately available and safe: water, saline, Ringer's lactate; ideally, a buffered solution, if it's immediately available. Speed is more important than choice. [56]

Is it possible to "quench" an acid with an alkali, or vice versa? No. "Neutralization" generates heat and can worsen the burn. Mechanical rinsing is the only solution. [57]

When are steroids beneficial and when are they harmful? In the first days of moderate to severe burns, they suppress sterile inflammation and reduce scarring, but are prescribed and discontinued only by an ophthalmologist; for mild burns, their benefit is questionable due to the risk of delayed epithelialization. [58]

What to do for "eye sunburn" (photokeratitis)? Rest, cold compresses on closed eyelids, preservative-free artificial tears, antibiotic ointment at night, and oral analgesics; the condition usually resolves within 1-3 days. Home use of anesthetics is contraindicated. [59]

Table 10. Initial therapy “package” by severity

Heaviness	What is required	What to consider
Light (RH I-II)	Irrigation to pH 7.0-7.2; artificial tears; antibiotic ointment; cycloplegic	A short course of steroids under supervision
Moderate	+ frequent preservative-free tear substitutes; IOP control	Ascorbate 10%/citrate 10%; doxycycline orally; bandage lens
Severe (RH III-IV)	All of the above + antiglaucoma drops; prevention of symblepharon	Amniotic membrane; tenoplasty; early consultation for SLET/CLET/KLAL