Chemical eye burns: first aid and treatment

A chemical eye burn is an emergency in which acids, alkalis, or irritants damage the epithelium, corneal stromal structures, conjunctiva, and limbal area. Alkali burns are the worst-case scenario: they rapidly penetrate the tissue, causing corneal "melting" and limbal ischemia. Acids often form a coagulation scab and partially limit penetration, but concentrated burns (such as sulfuric acid from batteries) also cause severe morbidity. The first minute and continuous irrigation are crucial. [1]

The key to saving vision is immediate irrigation with any available safe solution (water, saline, Ringer's lactate solution) to a pH of 7.0-7.2, with mandatory eversion of the eyelids and removal of particles from the conjunctival fornices. The key isn't the "perfect" solution, but the speed at which irrigation begins—every minute counts. The volume can reach 2-10 liters or more, and the duration should be at least 20-30 minutes, with a repeat pH check 5-10 minutes after stopping. [2]

Even seemingly "minor" injuries are fraught with late complications: limbal stem cell deficiency, neovascularization, persistent corneal opacity, and secondary glaucoma. Therefore, the treatment algorithm includes not only irrigation but also a pharmacological "window of opportunity" (ascorbate/citrate/doxycycline), surface protection (lens-bandage, amniotic membrane), and proper rehabilitation. [3]

This article systematically covers ICD-10/ICD-11 codes, epidemiology, causes and risk factors, pathogenesis, symptoms, classifications (Roper-Hall, Dua), complications, diagnostic and treatment algorithms (including modern methods), prevention, prognosis and FAQ - based on AAO/EyeWiki, StatPearls, current reviews and national guides. [4]

Code according to ICD-10 and ICD-11

In ICD-10, chemical and thermal eye injuries are classified under block T26, "Burn and corrosion limited to the eye and its appendages," with subcategories for eyelid, cornea/conjunctival sac, destruction of the eyeball, and others. The suffix "corrosion" is used for the chemical nature (acid/alkali). For external causes and circumstances, appropriate factor codes are added. [5]

ICD-11 uses a cluster approach: the basic section NE00-NE0Z "Burns of the eye or internal organs", to which modifiers for depth, area, causative factor (for example, "corrosive substances"), as well as anatomical clarifications (limbal zone, etc.) are added "post-coordination". This allows for more accurate coding of the clinical presentation of severe chemical burns. [6]

Table 1. Code examples

Situation	ICD-10 (example)	Note	ICD-11 (example)	Note
Corneal and conjunctival sac corrosion	T26.6	"Corrosion" = chemical burn	NE00 + expanders	Chemical burn, depth/area
Burn of the eyelid/periocular area	T26.0	Thermal/chemical	ND90+ degree	"Outer surface, face/eyelid"
Destruction of the eyeball due to a burn	T26.2	Severe injury	NA06 + link to NE00	Eyeball trauma + eye burn

Source: official navigators ICD-10/ICD-11 (WHO/ICD). [7]

Epidemiology

Chemical eye burns are a common occupational injury and a common household problem. In developed countries, the estimated incidence is approximately 51-56 cases per 1,000,000 population per year; men are more frequently affected (ratio up to 3-8:1) due to occupational factors. Up to ≈2/3 of severe cases are caused by alkalis. [8]

Children are a distinct risk group: the peak incidence occurs between 1 and 2 years of age, with detergents and laundry capsules leading the way. In children, mild lesions typically heal quickly, but delayed rinsing significantly worsens outcomes. [9]

New retrospective series (2024) confirm that standardized protocols (frequent preservative-free lubrication, antibiotic coating, early inflammation control) are associated with better outcomes, but the severity of the entry injury remains a key predictor. [10]

Photokeratitis (ultraviolet "burn") occurs in welders, skiers/mountaineers, and tanning bed users; it is usually reversible, but repeated episodes without protection increase the risk of chronic ocular surface problems.[11]

Table 2. Key epidemiological landmarks

Indicator	Meaning
Incidence of chemical burns	≈51-56 per 1,000,000/year
The proportion of alkalis among heavy ones	≈2/3
Sex ratio	Men more often (up to 3-8:1)
Peak in children	1-2 years
Trend	The outcome determines the severity and speed of the onset of assistance [12]

Reasons

The main agents are alkalis (sodium/potassium hydroxides, ammonia, lime), acids (sulfuric, hydrochloric, acetic), and irritants (peroxide, alcohols). Alkalis are lipophilic and quickly penetrate the epithelium, causing "liquation" necrosis; acids coagulate proteins and partially "block" penetration. The exception is hydrofluoric acid, which behaves aggressively, like an alkali. [13]

Household scenarios: spraying cleaning products, kitchen chemicals, laundry detergent capsules, battery acid. Industrial: construction, agricultural chemicals, car batteries, laboratories. Wearing contact lenses during exposure aggravates the course of the disease. [14]

Classic mistakes: attempting to “neutralize” acid with alkali (or vice versa), late initiation of irrigation, failure to evert the eyelids and remove particles (e.g. lime) from the conjunctival fornices. [15]

Ultraviolet injuries (welding, snow/water, solariums) are a separate category, usually mild/moderate in severity, but requiring the same principles of early pain relief and surface protection. [16]

Risk factors

Severity is determined by: the type of agent (alkali > acid), concentration/volume, time before irrigation, the presence of particles in the conjunctival fornices (cement, lime), and previous surface pathologies (dry eye, surgery). Even minutes of delay increase the depth of the lesion. [17]

Occupational hazards: cleaning, construction, battery manufacturing, dry cleaning. PPE and the presence of emergency eyewashes are critical here. [18]

Household risks: storing chemicals within reach of children, lack of labeling, aerosolization in poorly ventilated areas, mixing up bottles. [19]

Behavioral factors: neglect of protective glasses when welding/grinding, sports without a UV filter, attempts at self-medication with “neutralization”. [20]

Table 3. What makes a chemical eye burn worse?

Factor	Why is it dangerous?
Alkali (pH > 11.5)	Rapidly destroys lipids and collagen
Delayed flushing	Increases depth and area
Particles in the vaults (lime)	Long-term "feeding" of the burn
High concentration/volume	More reaction substrate
Lack of PPE/fountains	Late start of assistance [21]

Pathogenesis

Alkalis saponify membranes, break down glycosaminoglycans, and activate collagenases and metalloproteinases, causing "liquation" necrosis that extends deep into the stroma and all the way to the anterior chamber. This is accompanied by limbal ischemia and loss of limbal stem cells, which disrupts corneal epithelial regeneration. [22]

Acids cause coagulative necrosis with the formation of a scab that partially limits diffusion, but highly concentrated agents (sulfuric acid, HF) attack deeply and rapidly. [23]

During the first 24 hours, a deficiency of ascorbate in the anterior chamber fluid and excessive metalloproteinase activity are critical, increasing the risk of stromal "melting" and perforation. Anticollagenolytic strategies (ascorbate/citrate/tetracyclines) are warranted here. [24]

Ultraviolet radiation induces epithelial apoptosis with peak symptoms occurring within 6-12 hours; in most cases, the defect closes within 24-72 hours with supportive therapy.[25]

Table 4. Pathogenesis targets and therapeutic points

Target	What's happening	How do we influence
Metalloproteinases	Collagen breakdown	Doxycycline citrate
Ascorbate deficiency	Collagen synthesis disorder	Ascorbate (topical)
Limbic ischemia	Stem cell loss	Tenonplasty/reconstruction
Inflammation	Scarring, neovascularization	Short course of steroids under control [26]

Symptoms

Acute: sharp pain, "sand," blepharospasm, lacrimation, photophobia, blurred vision. In severe alkali burns - stromal opacity, limbal ischemia, decreased/loss of vision, increased intraocular pressure. [27]

A second peak of pain and worsening symptoms may occur after a few hours due to progression of necrosis and inflammation. Lack of improvement after 20-30 minutes of irrigation is a warning sign requiring continued irrigation and urgent examination. [28]

Photokeratitis is characterized by a delay of 6-12 hours before the manifestation of pain and photophobia, often bilaterally; epithelialization is usually completed in 1-3 days with proper care. [29]

Red flags: Increasing pain/redness, milky cornea, areas of pale, bloodless limbus (ischemia), decreased vision, nausea/headache (possible increase in pressure). [30]

Table 5. Picture by agent type

Type	Signs	Expected dynamics
Alkali	Rapid clouding, limbal ischemia	Often severe, long lasting
Acid	Pain, scab, limited penetration	Varies in concentration
Irritants	Burning, hyperemia	Usually reversible
Ultraviolet	Pain after 6-12 hours, bilaterally	Epithelialization 24-72 h [31]

Classification, forms and stages

In practice, the Roper-Hall (corneal transparency + limbal ischemia) and Dua (percentage of limbal and conjunctival damage) are used – both correlate with prognosis and management. The Dua scale clarifies severe cases, "cutting" the category with significant ischemia into sublevels. [32]

Staging: immediate stage (minutes-hours), acute (up to 7 days), early reparative (7-21 days), late reparative (>21 days). Each stage has its own goals: decontamination, inflammation control, stimulation of epithelialization, prevention of scarring/symblepharon, rehabilitation. [33]

Forms: chemical (alkaline/acid/irritant), thermal (steam, flame, molten metal) and ultraviolet (welding, snow/water, solarium). Combined injuries are possible. [34]

Table 6. Classifications in "one picture"

Scale	Key criteria	What does it predict?
Roper-Hall	Corneal transparency, limbal ischemia rate	Risk of perforation/loss of vision
Dua	% of limbus and conjunctiva damage (more precisely, severe)	Need for reconstruction/grafts [35]

Complications and consequences

Early: persistent epithelial defects, ulcers, stromal "melting", secondary infection, increased intraocular pressure, adhesions. These events require intensive anti-inflammatory and anticollagenolytic therapy. [36]

Late: corneal neovascularization/scarring, limbal stem cell deficiency with conjunctivalization, symblepharon, entropion/ectropion, chronic dry eye, secondary glaucoma. Reconstructive interventions are often indicated. [37]

UV injuries usually resolve with complete recovery, but with frequent episodes without protection, chronic surface problems and photosensitivity may occur.[38]

Table 7. Red flags and what to do

Sign	Tactics
Limbal ischemia, "milky" cornea	Emergency ophthalmologist, intensive care
Pain that prevents you from opening your eye	Continue irrigation, anesthesia by a doctor
pH outside 7.0-7.2 after 30 min	Continue rinsing, checking every 5-10 minutes
Decreased vision, ↑IOP	Urgent examination, antiglaucoma measures [39]

When to see a doctor

Immediately today: any chemical burns, exposure to an unknown substance, failure to stabilize pH after 20-30 minutes of irrigation, presence of particles (lime), deterioration of vision, severe pain. Begin irrigation before any transport. [40]

Urgently in the first 24 hours: thermal burn, severe photokeratitis, inability to remove/insert lenses due to pain, symptoms of increased intraocular pressure (pain, rainbow circles, nausea). [41]

Children with any chemical exposure require a low threshold for examination by an ophthalmologist; laundry detergents cause severe conjunctival-corneal lesions.[42]

Diagnostics

Step 1 - Irrigation and pH. Begin irrigation immediately (water/NaCl/Ringer's lactate), aiming for a pH of 7.0-7.2; monitor pH every 5-10 minutes, repeating until stable normalization is achieved. Aim for 2-10 liters and ≥30 minutes, depending on severity. [43]

Step 2: Mechanical decontamination. Double eversion of the upper eyelid, eversion of the lower eyelid, "combing" the fornices with cotton applicators, removing particles. If severe pain occurs, local anesthetics should be administered by a physician without interrupting irrigation. [44]

Step 3 - Basic examination. Visual acuity, fluorescein biomicroscopy (epithelial defects), assessment of limbal ischemia, intraocular pressure. Classify according to Roper-Hall/Dua, take photographs for dynamics. [45]

Step 4 - additionally as indicated. OCT of the anterior segment, exclusion of perforation; hospitalization for moderate/severe burns, development of a plan for early reconstruction (amniotic membrane, tenoplasty) and prevention of symblepharon. [46]

Table 8. Mini-diagnostic algorithm

Stage	What are we doing?	For what
Irrigation to pH 7.0-7.2	Liters of solution, ≥20-30 minutes	Reduce the depth of damage
Decontamination of vaults	Particle removal	Eliminate secondary combustion
Examination + IOP	Fluorescein, limbus, pressure	Classification, plan
Documents	Photo, control plan	Forecast, commitment [47]

Differential diagnosis

Chemical burns are distinguished from irritating instillations (alcohols, perfumes) by more pronounced pain/cloudiness, the presence of limbal ischemia and epithelial defects. [48]

Thermal burns - based on history (steam/oil/flame), often with eyelid skin burns. Photokeratitis - based on a 6-12 hour delay and bilaterality without contact with the chemical. [49]

Penetrating trauma, acute attack of angle-closure glaucoma (pain, rainbow circles, ↑IOP) and infectious keratitis are excluded. [50]

Treatment

First and foremost, irrigate without delay. Any readily available, safe solution (water, 0.9% NaCl, Ringer's lactate) will do; buffer solutions are acceptable if readily available, but time-consuming irrigation is unavoidable. Aim for a pH of 7.0-7.2; check every 5-10 minutes and continue if the pH "slips" toward the acidic/alkaline side. Severe alkaline burns require up to 10 liters or more. [51]

Technique and anesthesia. Double eversion of the upper eyelid, eversion of the lower eyelid, thorough sanitization of the fornices with cotton applicators; if pain is felt by the physician, 1-2 drops of local anesthetic are administered to ensure tolerability of irrigation. For hands-free irrigation, trained personnel may use an irrigation lens; do not use if perforation is suspected. [52]

Basic regimen for mild to moderate burns. Frequent use of preservative-free artificial tears, antibiotic ointment (eg, erythromycin) at night to cover defects, a cycloplegic (cyclopentolate/atropine) for pain and spasm, a short course of topical steroids as prescribed by an ophthalmologist for the first 3-7 days with gradual withdrawal. For photokeratitis, supportive care (artificial tears, ointment at night, oral analgesics); epithelialization usually occurs within 24-72 hours. [53]

Anticollagenolytic therapy for moderate/severe burns. Frequent instillations of 10% ascorbate and 10% citrate (inhibition of collagenolysis and neutrophil activity), plus oral doxycycline as a matrix metalloproteinase inhibitor. These measures reduce the risk of stromal "melting" and perforation. Ascorbate is preferably administered topically to achieve therapeutic intraocular levels. [54]

Pain and pressure control. Non-narcotic analgesics orally; if intraocular pressure increases, topical antiglaucoma agents (beta-blocker, carbonic anhydrase inhibitor), avoiding prostaglandins in acute inflammation. IOP monitoring is mandatory for moderate/severe burns. [55]

Surface protection and stimulation of epithelialization. A soft bandage lens (sterile, under antibiotic cover) reduces pain and accelerates epithelialization. For large defects or the risk of melting, an amniotic membrane (including ring systems) mechanically protects the cornea and modulates inflammation; effectiveness is higher with early application in severe cases. [56]

Limbal and fornix management. Symblepharon prevention (rings, "stretch marks," frequent lubricant instillations), early tenoplasty in case of limbal ischemia. In the late phase, with limbal stem cell deficiency – SLET/CLET/KLAL (autologous/allogeneic limbal transplants) with immunosuppression as indicated. [57]

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 are prescribed by an ophthalmologist and require strict tapering due to the risk of delayed epithelialization. [58]

Special cases and new approaches. Hydrofluoric acid requires prolonged irrigation; topical calcium gluconate is discussed (the evidence base is limited). In severe cases with melting - adjuvant collagen protection, "glue"/conjunctival grafting; in later stages - lamellar/penetrating keratoplasty and rehabilitation with prosthetic scleral lenses (PROSE). [59]

Education and adherence. Patients are informed in advance that ascorbate/citrate are a "pinch" but critical to outcome; missed doses worsen the prognosis. Follow-up after 24-48 hours is mandatory, and then follow-up is based on progress. Documentation with photos helps maintain therapy and promptly escalate treatment. [60]

Table 9. What helps and what is harmful

Action	Not really	Comment
Immediate irrigation to pH 7.0-7.2	Yes	Speed is more important than a “perfect” solution
Double eversion of the eyelids, cleaning of the fornices	Yes	Removal of particles (lime/cement)
Ascorbate 10%, citrate 10%, doxycycline	Yes	Prevention of melting
"Neutralization" of chemicals at home	No	Heat generation, increased damage
Home anesthesia with drops	No	Epithelial toxicity, delayed epithelialization [61]

Prevention

Work: protective goggles/shields with side protection, emergency eyewashes and showers, training in the "IRRIGATE NOW" rule, and clear labeling of reagents. This significantly reduces the frequency and severity of injuries. [62]

Home: keep chemicals out of reach of children, do not pour into food containers, work in ventilated areas, receive first aid instructions (do not “extinguish,” but rinse with water). [63]

Sports and leisure: welding - only with a shield; mountain/water sports - goggles with a UV filter and side protection; solariums - protective goggles with complete UV blocking. [64]

Table 10. Prevention by scenarios

Scenario	Key measure
Manufacturing/construction	Eye protection + emergency fountain
House cleaning	Glasses, gloves, ventilation
Welding	Shield/mask training
Mountains/water/solarium	Glasses with UV filter

Forecast

In mild to moderate burns, if irrigation is started in the first minutes and brought to a pH of 7.0-7.2, epithelialization is usually completed within 1 week and vision is fully restored. [65]

In moderate and severe burns, outcome is predicted by the Roper-Hall/Dua grade, the proportion of limbal ischemia, and the speed of initiation of therapy. Adequate anticollagenolytic therapy and surface protection reduce the risk of perforation and the extent of reconstruction. [66]

Late rehabilitation often requires staged interventions (limbal grafts, then keratoplasty) and specialized optical devices (scleral lenses). Adherence to treatment is critical for functional recovery. [67]

Table 11. Prognostic factors

Factor	Influence
Time before irrigation starts	The faster, the higher the chance of full recovery.
Proportion of limbal ischemia	Directly linked to the risk of stem cell deficiency
Transparency of the stroma at the start	Reflects the depth of damage
Adherence (ascorbate/citrate/care)	Reduces melting, accelerates epithelialization

FAQ

How long should you flush? Until the pH reaches 7.0-7.2 and remains neutral; aim for ≥20-30 minutes and 2-10 liters; more if alkaline. Start immediately. [68]

Which solution is best? The one that is immediately available and safe: water, saline, Ringer's lactate. Speed is more important than choice. [69]

Can you "quench" acid with alkali? No. This will only increase thermal and chemical damage. Only mechanical leaching is possible. [70]

Does everyone need steroids? No. They are helpful in the first few days of moderate to severe inflammation, but should only be prescribed and discontinued by an ophthalmologist; for mild lesions, their benefit is questionable. [71]

Why ascorbate/citrate/doxycycline? This "anticollagenolytic" trio reduces stromal melting and the risk of perforation. Yes, they may sting, but it's an investment in corneal preservation. [72]