Acid burn is a condition in which the cornea and conjunctiva are damaged by acidic chemicals entering the eye. It is an ophthalmic emergency requiring immediate response.
The incidence of ocular chemical trauma is estimated at 65 to 78 cases per 100,000 population 1). The average age is 48 years. Alkali injuries are more common than acid injuries, but acid burns also occur as occupational injuries 1).
The most common causative agents are hydrochloric acid (toilet cleaner, industrial chemicals), sulfuric acid (battery fluid), and nitric acid (industrial chemicals). They occur in a wide range of settings, from household accidents (misuse of toilet cleaner) to occupational exposure in factories and research facilities.
Acidic agents have low tissue permeability, so damage often remains superficial. In contrast, alkalis dissolve proteins and reach deep into the cornea, causing deep damage in a short time, leading to severe stromal opacity, endothelial damage, cataract, iritis, glaucoma, and other complications.
| Causative agent | Main uses/exposure situations | Characteristics |
|---|---|---|
| Hydrochloric acid | Toilet cleaner, industrial chemicals | Volatile |
| Sulfuric acid | Battery acid, industrial chemicals | Strong acid, risk of severe injury |
| Nitric acid | Industrial chemicals, research facilities | Oxidizing |
| Hydrofluoric acid | Glass etching, semiconductors | Highly penetrating, particularly severe |
Generally, acid burns tend to remain more superficial than alkali burns and often have a better prognosis. This is because acids coagulate proteins, forming a self-protective barrier that limits penetration. However, strong acids such as sulfuric acid and hydrofluoric acid can penetrate deeply, causing severe damage similar to alkalis. Severity depends on the type of substance, pH, concentration, and contact time.
Characteristic findings of acid burns include white deposits from coagulation necrosis and relatively preserved conjunctival injection. In alkali injuries, liquefactive necrosis leads to ischemia, often resulting in white edema without injection.
Acid Burns
Injection pattern: conjunctival injection is often preserved due to coagulation necrosis
Depth of injury: a self-protective barrier forms from protein coagulation, often limiting damage to superficial layers
Exceptions with strong acids: sulfuric acid and hydrofluoric acid can penetrate deeply
Alkali Injuries
Injection pattern: saponification → liquefactive necrosis → ischemia leads to white edema without injection
Depth of injury: no barrier forms; rapid penetration into deep corneal stroma and anterior chamber
Complications: prone to iritis, cataract, and secondary glaucoma
Fluorescein staining is used to identify corneal epithelial defects. Note that when the corneal and conjunctival epithelium is extensively damaged, the entire area may stain uniformly and faintly, making it appear as if there is no epithelial defect.
Severe acid burns can also cause iritis, secondary glaucoma, and symblepharon.
Acid coagulates tissue proteins (coagulative necrosis), so ischemia that occludes blood vessels is relatively less likely to occur, and conjunctival hyperemia tends to be preserved. In contrast, alkali saponifies and liquefies cell membrane lipids, causing widespread destruction of tissues including blood vessels, resulting in white edema lacking hyperemia due to ischemia. However, strong acids can also cause extensive tissue necrosis and ischemia.
The severity of acid burns is determined by the following factors:
Hydrofluoric acid has particularly high penetrance and causes extensive destruction of the cornea, sclera, and anterior segment. Caution is needed for exposure in industrial settings (glass etching, semiconductor manufacturing).
Occupational exposure (factories, chemical research facilities) is most common, but it also occurs in household accidents (toilet bowl cleaners containing hydrochloric acid, battery acid).
Immediately after injury, measure the pH of tears using pH test paper. In acid burns, the pH is low (acidic). Perform irrigation immediately until neutral (pH 7–7.2).
In acid burns, the pH tends to normalize quickly after irrigation (faster than alkali burns). However, residual acid in the tissue may be released, so it is important to recheck the pH 20 minutes after irrigation.
The Kinoshita classification evaluates severity based on the remaining extent of the palisades of Vogt (POV), where limbal epithelial stem cells reside, and is useful for prognosis.
| Kinoshita Classification | Findings | Prognosis |
|---|---|---|
| Grade 1 | Conjunctival hyperemia, no corneal epithelial defect | Good |
| Grade 2 | Conjunctival hyperemia, partial corneal epithelial defect | Good |
| Grade 3a | Partial conjunctival necrosis, total corneal epithelial defect, partial POV remaining | Relatively good |
| Grade 3b | Partial conjunctival necrosis, total corneal epithelial defect, complete loss of POV | Poor |
| Grade 4 | Limbal conjunctival necrosis over half the circumference, total corneal epithelial defect, complete loss of POV | Poor |
The Roper-Hall classification is a 4-grade system based on the degree of corneal opacity and the extent of limbal ischemia. The Dua classification further subdivides Roper-Hall Grade IV into three stages according to the proportion of limbal and conjunctival involvement, allowing more precise prognostic assessment 1).
AS-OCTA (anterior segment optical coherence tomography angiography) is useful for evaluating limbal ischemia, as clinical assessment alone tends to underestimate the extent of limbal ischemia 2).
The examination flow is as follows:
The main difference is the rate of pH change. In acid burns, the pH tends to neutralize quickly after irrigation, so clinically it may appear mild. However, residual acid in the tissue can be released and cause the pH to drop again, so pH should be rechecked 20 minutes after irrigation. The severity classification and examination flow are the same as for alkali injuries.
Regardless of the type of chemical, starting irrigation as soon as possible is most important. The time to irrigation and the amount of irrigation are the greatest factors determining prognosis. Irrigation should be performed for at least 20 minutes, and continued as long as possible.
At the scene, start irrigation immediately with running tap water. At the ophthalmology visit, after topical anesthesia, thoroughly irrigate the conjunctival sac with saline (isotonic solution preferred) and recheck pH 20 minutes after irrigation.
| Severity | Treatment strategy |
|---|---|
| Grade 1–2 | Antibiotic eye drops + steroid eye drops/ointment. Most heal with topical treatment alone. |
| Grade 3a | In addition to the above, systemic steroids (intensive for about 1 week then taper), mydriatics. |
| Grade 3b to 4 | Systemic steroids + intraocular pressure management + acute surgical treatment (amniotic membrane transplantation, Tenon’s capsule plasty) |
| Cicatricial phase | Ocular surface reconstruction (limbal transplantation, corneal transplantation, amniotic membrane transplantation) |
For mild to moderate injuries (Kinoshita classification Grade 1–2), antibiotic and steroid eye drops and ointments are prescribed to control infection and inflammation. For more severe injuries, systemic steroids are administered intensively for about one week and then tapered.
For Grade 3b or higher or with severe limbal ischemia, acute surgical treatment is added.
Tenon’s capsule plasty is a procedure that advances the Tenon’s capsule to the limbus to restore blood supply in cases of limbal and scleral ischemia, and is useful as an eye-preserving surgery in severe chemical trauma2).
In the cicatricial phase, ocular surface reconstruction is performed using a combination of limbal stem cell transplantation (autologous or allogeneic), amniotic membrane transplantation, and full-thickness corneal transplantation. In severe bilateral cases, femtosecond laser-assisted large-diameter lamellar corneal limbal transplantation is applied, and good visual improvement has been reported3).
Acidic substances denature and coagulate tissue proteins (coagulation necrosis), forming insoluble proteins. This coagulated protein acts as a barrier (self-defense membrane) that limits further penetration of the acid. Therefore, damage is often more superficial compared to alkali injuries.
However, changes in ocular surface pH and residual acid in the tissue cannot be ignored. Hydrofluoric acid has particularly high penetrance and causes extensive destruction of the cornea, sclera, and anterior segment. Strong acids (e.g., high-concentration sulfuric acid) can cause deep damage and may penetrate into the anterior chamber.
Alkali saponifies lipids in cell membranes via hydroxyl ions, causing liquefactive necrosis. Being lipophilic, it easily passes through the epithelial layer and penetrates deep into the stroma within a short time. Alkali that penetrates into the anterior chamber causes iritis, cataract, and glaucoma.
In contrast, acid-induced coagulation necrosis relatively preserves tissue structure, and hyperemia tends to be maintained in the acute phase. However, if the limbal corneal epithelial stem cells are damaged, epithelial regeneration becomes impossible, and conjunctival epithelium invades the cornea (conjunctivalization). Limbal ischemia increases the risk of limbal stem cell deficiency (LSCD), leading to corneal scarring and permanent visual impairment 2).
The course after chemical injury is classified into acute phase, early reparative phase, and late reparative phase. In the acute phase, damage to the corneal and conjunctival epithelium and inflammation occur. In the early reparative phase, epithelial regeneration and inflammatory reactions proceed in parallel. In the late reparative phase, scar formation, symblepharon, and conjunctival sac shortening occur, worsening the ocular surface environment.
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. AS-OCTA results correlate well with final visual outcomes, and integration into existing classification systems is expected 2).
Femtosecond laser-assisted large-diameter lamellar keratolimbal transplantation can simultaneously transplant corneal stroma and limbal stem cells as a one-stage surgery for severe bilateral chemical trauma. Compared with conventional manual dissection, it enables uniform lamellar incision, and good visual improvement has been reported 3).
The application of femtosecond laser is limited in the number of cases, and further research is needed to establish long-term efficacy 3). Standardization of AS-OCTA and its incorporation into classification systems remain future challenges 2).
