Acid Injury
Mechanism: Denatures and coagulates tissue proteins
Penetration: Coagulated proteins form a barrier, often limiting damage to superficial layers
Exceptions: Hydrofluoric acid and strong acids can penetrate deeply
Chemical Injury (Alkali/Acid) of the Conjunctiva and Cornea
Key Points at a Glance
Section titled “Key Points at a Glance”1. What is Chemical Injury of the Conjunctiva and Cornea?
Section titled “1. What is Chemical Injury of the Conjunctiva and Cornea?”Chemical injury of the conjunctiva and cornea (chemical burn) is a condition in which the cornea and conjunctiva are damaged by chemical substances such as acids or alkalis entering the eye. It is an ophthalmic emergency requiring immediate response.
According to large-scale diagnostic registries, new diagnoses of ocular surface burns, including chemical eye injuries, are reported at 65–78 per 100,000 people 1). The average age is 48 years, but there is a bimodal peak including those under 1 year of age 1). Alkali injuries are more common than acid injuries 1). Workplace injuries are the most frequent, and among occupational eye injuries, chemical burns are the second most common after metallic foreign bodies 1).
Causative substances include various agents such as acids, alkalis, surfactants, and organic solvents. Alkaline substances are found in cement, slaked lime, quicklime (desiccants), mold removers, and hair dyes. Acidic substances include toilet bowl cleaners (hydrochloric acid) and battery fluid (sulfuric acid).
Q
Which is more severe: alkali injury or acid injury?
A
Generally, alkali injuries are more severe. Alkalis are lipid-soluble and saponify the lipids of cell membranes, causing liquefactive necrosis and penetrating deep into tissues rapidly without forming a barrier. Ammonia, for example, penetrates the cornea quickly, and even sodium hydroxide can reach the anterior chamber in a short time 7, 8). In contrast, weak acids often cause superficial damage because protein denaturation in the superficial layers forms a barrier. However, strong acids and hydrofluoric acid have high deep-penetrating ability and can cause severe damage similar to alkalis.
2. Main Symptoms and Clinical Findings
Section titled “2. Main Symptoms and Clinical Findings”Subjective Symptoms
Section titled “Subjective Symptoms”- Eye pain: Mild cases involve a foreign body sensation; severe cases involve intense pain
- Vision loss: Due to corneal opacity or edema
- Tearing and blepharospasm: Reflex reactions to chemical irritation
Clinical Findings
Section titled “Clinical Findings”Mild cases show conjunctival injection and corneal epithelial defects. In severe cases, the entire cornea degenerates and becomes white and opaque. When accompanied by conjunctival necrosis, the conjunctiva appears white and edematous without injection. This finding may appear mild at first glance, so caution is required.
Fluorescein staining is used to evaluate corneal epithelial defects. When the corneal and conjunctival epithelium is extensively damaged, the entire area may stain uniformly and thinly, making it appear as if there are no epithelial defects.
| Assessment Item | Finding |
|---|---|
| Corneal opacity | Clear to white opacity |
| Limbus involvement | Loss of POV and extent of limbal ischemia |
| Conjunctival necrosis | White edema without injection |
Severe chemical injuries can lead to complications such as iritis, cataract, secondary glaucoma, symblepharon, and pseudopterygium.
3. Causes and Risk Factors
Section titled “3. Causes and Risk Factors”Mechanisms of Acid and Alkali Injury
Section titled “Mechanisms of Acid and Alkali Injury”Alkali Injury
Mechanism: Saponifies cell membrane lipids, causing liquefactive necrosis
Penetration: Does not form a barrier; penetrates deeply within a short time
Anterior chamber penetration: Leads to secondary iritis, cataract, and glaucoma
In severe chemical injuries, assault cases account for a certain proportion; there is a report of an ammonia assault case reaching Roper-Hall Classification Grade IV1).
4. Diagnosis and Examination Methods
Section titled “4. Diagnosis and Examination Methods”Initial Evaluation
Section titled “Initial Evaluation”Measure the pH of tears using pH test paper. If it is not neutral (pH 7–7.2), perform immediate irrigation. Recheck pH 20 minutes after irrigation and re-irrigate if necessary.
Severity Classification
Section titled “Severity Classification”Severity is assessed after irrigation. Check for corneal and conjunctival epithelial defects, limbal ischemia, and conjunctival necrosis. Also record corneal opacity, anterior chamber inflammation, and intraocular pressure. Initial classification is used to determine treatment intensity and timing of reconstruction.
| Classification | Main Evaluation Axis | Clinical Use |
|---|---|---|
| Kinoshita Classification | POV remaining and conjunctival necrosis | Estimates corneal epithelial regeneration ability and prognosis |
| Roper-Hall Classification | Corneal opacity and limbal ischemia | Used for severity comparison in international literature |
| Dua classification | Clock hours of limbal involvement and percentage of conjunctival involvement | To further stratify the most severe cases |
Kinoshita classification
Section titled “Kinoshita classification”The Kinoshita classification focuses on how much of the palisades of Vogt (POV) remain. POV are the niche for corneal epithelial stem cells. Fluorescein staining is performed after irrigation. Corneal and conjunctival epithelial defects, limbal whitening, and conjunctival necrosis are assessed. The difference between Grade 3a and 3b is important. Both involve total corneal epithelial defects. The difference is whether POV partially remain or are completely lost.
| Grade | Main findings | Interpretation |
|---|---|---|
| Grade 1 | Conjunctival injection only. No corneal epithelial defect | Limbal stem cells are preserved. Prognosis is good |
| Grade 2 | Conjunctival injection. Partial corneal epithelial defect | Epithelial defect is confined to the cornea. Re-epithelialization is likely with conservative treatment |
| Grade 3a | Partial conjunctival necrosis. Total corneal epithelial defect. POV partially remain | Limbal function is partially preserved. Re-epithelialization is delayed but corneal epithelial regeneration can be expected |
| Grade 3b | Partial conjunctival necrosis. Total corneal epithelial defect. POV completely disappears. | Limbus function is lost. Watch for conjunctival invasion, persistent epithelial defect, and corneal melting. |
| Grade 4 | Limbus and conjunctival necrosis extending more than half the circumference. Total corneal epithelial defect. POV completely disappears. | Most severe. High likelihood of severe LSCD, symblepharon, corneal perforation, and need for ocular surface reconstruction. |
In Grades 1 and 2, limbal stem cells are preserved. Prognosis is good. In Grade 3a, POV remains. Even with total corneal epithelial defect, regeneration can be expected. In Grades 3b and 4, limbal epithelium also disappears. Regeneration as transparent corneal epithelium is difficult. Conjunctival epithelium with blood vessels covers the cornea. During the cicatricial phase, consider limbal transplantation or cultured epithelial cell sheets.
Roper-Hall Classification and Dua Classification
Section titled “Roper-Hall Classification and Dua Classification”| Grade | Roper-Hall Classification Findings | Prognosis |
|---|---|---|
| I | Corneal epithelial defect. No limbal ischemia. | Good |
| II | Mild corneal opacity with visible iris details. Limbal ischemia less than one-third. | Good |
| III | Total corneal epithelial defect and stromal opacity. Iris details unclear. Limbal ischemia 1/3 to 1/2 | Caution |
| IV | Severe corneal opacification. Iris and pupil not visible. Limbal ischemia >1/2 | Poor |
The Dua classification evaluates limbal involvement in clock hours. Conjunctival involvement is assessed by area percentage.
| Dua Grade | Limbal involvement | Conjunctival involvement |
|---|---|---|
| I | None | None |
| II | ≤3 clock hours | ≤30% |
| III | >3 to ≤6 clock hours | >30% to ≤50% |
| IV | >6 to ≤9 clock hours | >50% to ≤75% |
| V | >9 to <12 clock hours | >75% to <100% |
| VI | 12 clock hours (total) | 100% |
Grade IV in the Roper-Hall classification is subdivided into IV to VI. This is suitable for stratifying severe cases2, 3).
AS-OCTA is useful for evaluating limbal ischemia. AS-OCTA is anterior segment optical coherence tomography angiography. Clinical evaluation alone may underestimate limbal ischemia. AS-OCTA enables more objective assessment4).
Q
What are the differences in severity classifications for chemical injuries?
A
The Kinoshita classification focuses on the residual POV. It facilitates prediction of corneal epithelial regenerative capacity. The Roper-Hall classification assesses corneal opacity and limbal ischemia. The Dua classification quantifies limbal and conjunctival damage. It is particularly suitable for prognostic evaluation of severe cases 2, 3).
5. Standard Treatment
Section titled “5. Standard Treatment”Initial Management: Eye Irrigation
Section titled “Initial Management: Eye Irrigation”Regardless of the type of chemical, immediate eye irrigation is the most important step. The time to irrigation and the volume of irrigant determine the prognosis 6, 7).
At the scene, irrigate with running tap water for at least 20 minutes. At the ophthalmology clinic, after topical anesthesia, irrigate the conjunctival sac with normal saline or lactated Ringer’s solution. Continue until the pH is neutralized; in severe alkali injuries, this may require 30 minutes or more. Tap water is hypotonic and increases fluid influx into the corneal stroma, so isotonic solutions are preferred in medical settings.
During or after irrigation, evert the upper eyelid. Remove any solid material remaining in the conjunctival sac or fornix. Residual lime or cement particles can cause persistent damage. Recheck the pH 20 minutes after irrigation.
Conservative Treatment
Section titled “Conservative Treatment”Acute Phase Pharmacotherapy
Anti-inflammatory: Topical and systemic corticosteroids to suppress secondary tissue damage
Infection prophylaxis: Topical antibiotics
Mydriasis: Atropine sulfate eye drops to prevent iritis and reduce pain
Epithelial regeneration promotion: Sodium hyaluronate eye drops, therapeutic contact lenses, autologous serum eye drops
Corneal melting suppression: In severe cases, ascorbic acid, doxycycline, and citrate may be used adjunctively
Medications to Note
NSAID eye drops: Generally avoided as they may delay epithelial healing
Preserved eye drops: Preservative-free is preferable as preservatives inhibit epithelial regeneration.
Long-term steroid use: While suppressing inflammation, it may delay epithelialization and worsen corneal melting.
Secondary glaucoma: Intraocular pressure is managed with beta-blockers or acetazolamide.
The strength of evidence varies by treatment. Irrigation is the most consistently recommended. Acute-phase steroids are useful for controlling inflammation. However, in severe cases or those with persistent epithelial defects, tapering should be considered after 1–2 weeks7, 8). Ascorbic acid, citrate, and doxycycline are adjunctive therapies aimed at inhibiting corneal melting. Evidence is primarily from animal studies, case series, and reviews, and does not replace standard treatment7, 8).
Surgical Treatment
Section titled “Surgical Treatment”Surgical intervention is likely necessary for Roper-Hall classification grade III or higher, or Kinoshita classification grade 3b or higher.
Acute-phase surgical treatment: Necrotic tissue removal, amniotic membrane transplantation, and tenonplasty are performed. Amniotic membrane transplantation aims to promote epithelialization and control inflammation, but a 2022 Cochrane review found uncertain benefits in moderate cases and no clear benefit in severe cases9). Therefore, decisions should be individualized based on severity, conjunctival necrosis, limbal ischemia, and institutional experience. Tenonplasty is a procedure that advances Tenon’s capsule to the limbus to restore vascular supply in cases of limbal and scleral ischemia, and is useful for globe salvage in severe chemical trauma5). Postoperative re-epithelialization rates are high, but symblepharon is the most common complication5).
Scar-phase surgical treatment: Ocular surface reconstruction is performed using limbal stem cell transplantation (autologous or allogeneic), amniotic membrane transplantation, and penetrating keratoplasty. In severe bilateral cases, femtosecond laser-assisted large-diameter lamellar keratolimbal transplantation allows simultaneous transplantation of limbal stem cells and corneal stroma, with reported good visual improvement10).
Q
In what cases is tenonplasty indicated?
A
The main indication for tenonplasty is limbal and scleral ischemia associated with severe chemical trauma5). By advancing Tenon’s capsule from the orbital side to the limbus and fixing it, vascular supply to the ischemic area is restored and conjunctival epithelial migration is promoted. It is performed when established ischemia is observed in severe cases. However, in the most severe cases with 360-degree circumferential limbal and scleral ischemia, Tenon’s capsule itself may also be ischemic, limiting its effectiveness5).
6. Pathophysiology and Detailed Mechanism
Section titled “6. Pathophysiology and Detailed Mechanism”The extent of damage in chemical trauma is determined by the type of agent, pH, concentration, contact time, and area of injury.
Alkaline substances saponify the lipids of cell membranes via hydroxyl ions, causing cell lysis and necrosis. Due to their lipophilic nature, they easily penetrate the epithelial layer and rapidly infiltrate deep into the stroma. Alkali that penetrates the anterior chamber can cause iritis, cataracts, and glaucoma.
Acid substances denature and coagulate tissue proteins, forming insoluble proteins. This coagulated protein acts as a barrier, so damage is often limited to the superficial layers. However, hydrofluoric acid is highly penetrative and can cause severe anterior segment destruction.
The course after chemical injury is classified into acute, early reparative, and late reparative phases. In the acute phase, damage to the corneal and conjunctival epithelium and inflammation occur. If the corneal epithelial stem cells located in the limbal corneoscleral junction are damaged, regeneration as transparent corneal epithelium becomes difficult, and conjunctival epithelium invades the cornea (conjunctivalization). Limbal ischemia increases the risk of developing limbal stem cell deficiency (LSCD), leading to corneal scarring and permanent visual impairment 1). Damage to goblet cells and decreased mucin cause tear film instability, symblepharon, and conjunctival sac shortening, further worsening the ocular surface environment.
7. Latest Research and Future Perspectives
Section titled “7. Latest Research and Future Perspectives”AS-OCTA enables objective quantification of limbal ischemia in the acute phase of chemical injury, providing more accurate severity assessment and prognosis prediction than clinical evaluation. The results of AS-OCTA correlate well with final visual outcomes, and integration into existing classification systems is expected 4).
Femtosecond laser-assisted large-diameter lamellar corneal limbal transplantation allows simultaneous transplantation of corneal stroma and limbal stem cells as a one-stage surgery for severe bilateral chemical injuries. Compared to conventional manual dissection, it enables uniform lamellar dissection, and good visual improvement has been reported 10).
The application of femtosecond lasers is limited in the number of cases, and further research is needed to establish long-term efficacy 10). Standardization of AS-OCTA and its incorporation into classification systems remain future challenges 4).
8. References
Section titled “8. References”- Hu JCW, Trief D. A narrative review of limbal stem cell deficiency & severe ocular surface disease. Ann Eye Sci. 2023;8:13. doi:10.21037/aes-22-35.
- Dua HS, King AJ, Joseph A. A new classification of ocular surface burns. Br J Ophthalmol. 2001;85:1379-83. doi:10.1136/bjo.85.11.1379.
- Gupta N, Kalaivani M, Tandon R. Comparison of prognostic value of Roper Hall and Dua classification systems in acute ocular burns. Br J Ophthalmol. 2011;95:194-8. doi:10.1136/bjo.2009.173724.
- Fung SSM, Stewart RMK, Dhallu SK, et al. Anterior Segment Optical Coherence Tomographic Angiography Assessment of Acute Chemical Injury. Am J Ophthalmol. 2019;205:165-74. doi:10.1016/j.ajo.2019.04.021.
- Sharma S, Kate A, Donthineni PR, Basu S, Shanbhag SS. The role of Tenonplasty in the management of limbal and scleral ischemia due to acute ocular chemical burns. Indian J Ophthalmol. 2022;70:3203-12. doi:10.4103/ijo.IJO_3148_21.
- Ikeda N, Hayasaka S, Hayasaka Y, Watanabe K. Alkali burns of the eye: effect of immediate copious irrigation with tap water on their severity. Ophthalmologica. 2006;220:225-8. doi:10.1159/000093075.
- Sharma N, Kaur M, Agarwal T, Sangwan VS, Vajpayee RB. Treatment of acute ocular chemical burns. Surv Ophthalmol. 2018;63:214-35. doi:10.1016/j.survophthal.2017.09.005.
- Baradaran-Rafii A, Eslani M, Haq Z, et al. Current and upcoming therapies for ocular surface chemical injuries. Ocul Surf. 2017;15:48-64. doi:10.1016/j.jtos.2016.09.002.
- Clare G, Bunce C, Tuft S. Amniotic membrane transplantation for acute ocular burns. Cochrane Database Syst Rev. 2022;9:CD009379. doi:10.1002/14651858.CD009379.pub3.
- Lin L, Xu Y, Ou Z, et al. Femtosecond laser-assisted large-diameter lamellar corneal-limbal keratoplasty in ocular chemical burns. Am J Ophthalmol Case Rep. 2025;37:102246. doi:10.1016/j.ajoc.2024.102246.