bubble_chart Overview

In daily industrial and agricultural production as well as everyday life, it is not uncommon for chemical substances to accidentally come into direct contact with the eyes, causing eye injuries. According to some statistics, chemical ophthalmic injuries (chemical injuries of the eye) rank third among industrial eye injuries. Chemical eye injuries account for about 10% of all eye injuries. Chemical substances often cause severe damage to eye tissues. If not treated properly in time, the prognosis is poor, and in severe cases, it may even lead to blindness or loss of the eyeball. Among chemical-induced eye injuries, 17% are caused by solid chemicals, 31% by liquid chemicals, and 52% by chemical fumes. These injuries can result from direct contact of chemicals with the eyes or through systemic absorption via the skin, respiratory tract, or digestive tract, affecting the eyes, visual pathways, or visual centers and causing injury.

bubble_chart Etiology

There are numerous types of chemical eye irritants, and only the common ones are classified as follows:

1. Corrosive Irritants

1.1 Acidic Irritants

(1) Inorganic salts and their compounds: sulfuric acid, phosphoric acid, chromic acid, hydrogen sulfide, fluorides, etc.

(2) Organic acids: carbolic acid, acetic acid, phosphoric acid, chromic acid, hydrogen sulfide, fluorides, etc.

(3) Others: acetic anhydride, phenol, zinc chloride, sodium dichromate, acetone, ammonium sulfate, etc.

1.2 Alkaline Irritants

(1) Alkali metals and their compounds: sodium, potassium, potassium hydroxide, etc.

(2) Alkaline earth metals and their compounds: calcium, strontium, calcium chloride, etc.

(3) Others: ammonia, lysol, brine, etc.

1.3 Non-metallic Corrosives: arsenic, selenium, phosphorus, nitrogen, sulfur, silicon compounds, calcium oxide, etc.

2. Cytotoxic Substances

Hydrocarbons, alcohols, aldehydes, ketones, esters, ethers, and organic oxidizers.

bubble_chart Pathogenesis

The Mechanism of Chemical Burns

1. The penetration of chemicals into the eye is closely related to the physiological characteristics of the eye's surface tissues. The corneal epithelium and endothelium are lipophilic, while the corneal stroma and sclera are hydrophilic, similar to the conjunctiva and corneal epithelium. Liposoluble substances easily penetrate the corneal epithelium and accumulate in the corneal stroma, whereas water-soluble substances struggle to pass through the corneal epithelium but can easily traverse the stroma. Therefore, unless the epithelial tissue is damaged, water-soluble substances find it difficult to enter the cornea.

The water balance and metabolism of the corneal stroma primarily depend on the functions of the corneal epithelium and endothelium, with the endothelium playing a more critical role. Electrolytes do not easily permeate the epithelial and endothelial tissues. When the integrity of the epithelium or endothelium is compromised, the cornea can develop edema and opacity.

The cornea's nutrition mainly comes from the uvea, diffusing into the cornea through the aqueous humor via the corneal endothelium. The surrounding vascular network plays only a supplementary role. A healthy cornea does not rely on it; it becomes significant only under pathological conditions. For instance, when the corneal stroma becomes opaque, the opacity gradually clears and becomes transparent only when new blood vessels grow into the cornea from the surrounding vascular network.

2. The injurious effects of chemicals: The solubility of chemicals is crucial for assessing the extent of damage they can cause to eye tissues. Acids are water-soluble. Alkalis, sulfur dioxide, ammonium hydroxide, and mustard gas possess both water-soluble and liposoluble properties, giving them exceptional penetration and destructive capabilities. Many organic solvents, such as formaldehyde, chloroform, alcohol, acetone, and ether, are highly liposoluble and can cause temporary damage to the corneal epithelium. The dehydrating (water-absorbing) effect of acidic and alkaline chemicals is less significant than their necrotic impact on tissues.

Another category includes heavy metal salts, which primarily act through precipitation, known as the astringent reaction. At low concentrations, surface tissues undergo precipitation, hardening the intercellular substance between cell surfaces and capillary cells, causing the tissue to turn pale and reducing inflammatory exudation. At higher concentrations, these salts exhibit corrosive effects, leading to the coagulation and necrosis of cellular proteins.

bubble_chart Pathological Changes

In the initial stage of chemical injury to eye tissues, the first stage involves vascular congestion and increased permeability, followed by tissue edema, protein denaturation, coagulation, and ultimately cell death.

bubble_chart Clinical Manifestations

1. Types of Chemical Eye Injuries

1. Chemical deposition and staining in the eye; Due to prolonged exposure to chemicals, visible chemical deposits may occur on the eyelid skin, conjunctiva, cornea, lens, vitreous body, retina, etc. Staining of the eye surface tissues is often caused by long-term direct contact with chemicals. Deposition of chemicals in intraocular tissues is mostly due to absorption through the skin, respiratory tract, or gastrointestinal tract, followed by deposition in the eye. For example, long-term exposure of silver workers to silver dust can lead to gray-brown silver deposition in the cornea and conjunctiva.

2. Chemical eye irritation or burns: Chemicals that do not cause irritation symptoms on the skin can still injure the cornea and conjunctiva. These often cause irritation symptoms, such as tobacco, alcohol, mercury, asphalt, and hydrogen sulfide, which can lead to conjunctival congestion, papillary hyperplasia, or conjunctivitis, as well as corneal epithelial injury.

3. Allergic reactions in the eye caused by chemicals: These reactions often manifest as eyelid skin inflammation and conjunctival congestion with edema, accompanied by a prickly sensation of foreign bodies on the skin.

4. Eye lesions caused by chemical poisoning: Toxic chemicals absorbed by the body can cause lesions in eye tissues. These may include eye muscle paralysis, lens opacity and chemical deposition, uveal and retinal lesions, and optic nerve lesions. In addition to eye symptoms, systemic poisoning symptoms may also occur in other parts of the body.

2. Factors Determining the Severity of Chemical Eye Injuries

The severity of injury caused by chemicals acting on eye tissues depends primarily on the toxicity of the chemical, its physicochemical properties, duration of exposure, area of contact, quantity and concentration of the chemical, and whether prompt and appropriate first aid was administered after the injury.

1. Physicochemical properties of the injurious substance

Chemical injury to tissues mainly disrupts the physical and chemical state of the body's proteins, causing denaturation, coagulation, and necrosis. The outcome varies depending on the chemical reaction triggered when the injurious chemical comes into contact with tissues. Generally, gaseous chemicals cause less injury to tissues than liquids, and liquids cause less injury than solids. This is because gases are easily diluted by air, while liquids are diluted and washed away by tears. The degree of tissue injury is directly proportional to the concentration of the chemical. Chemicals with high permeability and solubility cause more severe tissue damage.

2. Duration and area of contact between the injurious chemical and eye tissues

Prolonged contact between the chemical and eye tissues results in more severe injury. A larger contact area between the chemical and eye tissues also leads to more severe injury.

3. Staging and Grading of Chemical Burns

To facilitate observation of disease progression and treatment, alkali burns are staged and graded.

1. Staging: According to the Hughes method, it is divided into three stages:

Acute phase: From a few minutes to 24 hours after injury.

Repair phase: From 1 day to about 2 weeks after injury.

Complication phase: From 2 to 3 weeks after injury.

2. Grading: Based on the grading standards of the National Occupational Eye Disease Group for Eye Trauma and combined with the classification method for skin burns, eye burns are divided into 4 degrees.

Area calculation:

+: Total burn area of all tissues ≤ ¼

++: 1/4 ≥ burn area ≤ ½

+++: ½ < burn area ≤ ¾

++++: Total burn

Note: The conjunctival area is calculated mainly based on the bulbar conjunctiva.

4. Clinical Manifestations of Chemical Burns

Due to the widespread use of acids and alkalis in industry and daily life, chemical burns to the eyes caused by acids and alkalis are quite common.

1. Acid burns: Injury to the eye caused by acidic substances is called acid burns (acid burns). Acidic substances are divided into two major categories: organic acids and inorganic acids, which are soluble in water but insoluble in fat. Acidic substances are easily blocked by the corneal epithelium because the corneal and conjunctival epithelium are lipophilic tissues. However, when high-concentration acids come into contact with tissues, they cause tissue protein coagulation and necrosis, forming a scab membrane that prevents the remaining acid from penetrating deeper. Inorganic acid molecules are small, structurally simple, highly active, and easily penetrate tissues. Therefore, tissue injury caused by inorganic acids is more severe than that caused by organic acids.

Acid burns result in relatively shallow wounds with clear boundaries, and necrotic tissue tends to slough off and heal more easily. Concentrated sulfuric acid has strong dehydrating properties, turning organic matter into black charcoal. Nitric acid initially causes yellow wounds that later turn yellowish-brown. Hydrochloric acid is less corrosive and also produces yellowish-brown wounds. Among organic acids, trichloroacetic acid is the most corrosive, causing tissue to turn white and necrotic.

2. Alkali Burns: In ocular chemical injuries, alkali burns (alkaline burns) progress rapidly, have a prolonged course, involve multiple complications, and carry a poor prognosis.

Common alkalis include potassium hydroxide, sodium hydroxide, calcium hydroxide, ammonium hydroxide (ammonia water), and sodium silicate (water glass).

(1) Mechanism of Alkali Injury to Ocular Tissue: Alkalis react with lipids in cell membranes through saponification and simultaneously form water-soluble alkaline proteins with tissue proteins. The resulting compounds exhibit biphasic solubility—both water- and lipid-soluble—thus disrupting the corneal epithelial barrier and rapidly penetrating all layers of the eyeball. Once inside cells, the pH rises sharply, making compounds formed between alkaline substances and cellular components more soluble. Additionally, the alkaline environment promotes the emulsification of cell membrane lipids, leading to membrane destruction.

Alkaline cellular proteins are highly destructive, damaging enzymatic and structural proteins. Mild alkali burns affect enzyme proteins, inhibiting cellular life processes, while severe burns directly destroy cell membrane proteins, rapidly causing widespread tissue coagulation necrosis. Alkaline compounds often induce thrombosis and necrosis in the corneal limbal vascular network, severely impairing corneal nutrition and reducing resistance, making secondary infections, ulcers, or perforations more likely.

(2) Changes in Generation and Transformation of Alkali Burns: Normal corneal epithelium lacks collagenase, but alkali-burned corneal epithelium and ulcerated tissue from other causes contain large amounts of collagenase, which digests and breaks down collagen. The peak period for collagenase release is between the 2nd week and 2nd month post-burn, increasing the risk of ulcer perforation. Corticosteroids can enhance collagenase activity, so topical use of such medications should be avoided during this period.

After alkali burns, prostaglandin levels in the aqueous humor significantly increase, causing local vasodilation, capillary congestion, increased blood flow, and elevated intraocular pressure. Symptoms resemble acute angle-closure glaucoma.

Alkali burns reduce levels of ascorbic acid, riboflavin, and glucose in ocular tissues, impairing normal metabolic processes.

(3) Clinical and Pathological Course: Alkali burns often involve a complex and prolonged pathological process. Based on Hughes' staging and domestic research, it can be divided into three phases.

I. Acute Phase: From seconds to 24 hours post-burn. Alkalis typically penetrate the cornea into the anterior chamber within minutes. Manifestations include corneal and conjunctival epithelial necrosis, sloughing, conjunctival edema, ischemia, corneal stromal edema and opacification, extensive thrombosis and hemorrhage in the limbal and adjacent vessels. Severe cases may present with acute iridocyclitis, leading to heavy fibrinous exudate in the anterior chamber. In grade III alkali burns, the cornea appears porcelain-white, obscuring intraocular structures. Due to ischemia and necrosis of the iris and ciliary body, aqueous production decreases, causing markedly reduced intraocular pressure.

II. Repair Phase: Around 5–7 days to 2 weeks post-injury, corneal epithelial regeneration begins, with neovascularization gradually invading the cornea, and iridocyclitis subsiding.

III. Complication Phase: Beginning 2–3 weeks post-burn, this phase often involves recurrent, persistent sterile corneal ulcers, frequently leading to perforation. Necrotic tissue in the palpebral and bulbar conjunctiva sloughs off, resulting in scar formation, shrinkage, shortened or obliterated fornices, symblepharon, corneal leukoma, vascularized nebula, or even ankyloblepharon. This may progress to xerophthalmia, uveitis, leukocoria, glaucoma, or phthisis bulbi.

(4) Prognosis: The prognosis of ocular alkali burns depends on the severity of the burn and whether the treatment is timely and appropriate. Roper-Hall classified alkali burns into 4 grades based on the extent of corneal limbus and conjunctival injury; grades 1 and 2 are mild with a better prognosis, while grades 3 and 4 are more severe with a poorer prognosis. For clinical convenience, it is simplified into mild, moderate, and grade III.

Grade I: Corneal epithelial injury, erosion, Grade I corneal opacity, but the iris texture is clearly visible, and the corneal limbus shows no ischemia or ischemia less than 1/3. If it progresses further, corneal epithelial detachment and Grade I stromal edema may be observed. With appropriate treatment at this stage, corneal ulceration can be avoided. Complete repair can be achieved within 1–2 months, with the opacity absorbed, and corneal thickness and transparency returning to normal or leaving only slight nebula and minimal neovascularization. Visual function is largely or fully restored.

Grade II: Most or all of the corneal epithelium is detached, with significant corneal edema and opacity. The iris and pupil are faintly visible, while the conjunctiva and corneal limbus show partial ischemic necrosis, ranging from 1/3 to ½. This type involves severe corneal limbus injury, with extensive and deep corneal lesions, leading to a slow repair process. Improper management may result in corneal ulceration, anterior chamber exudation, recurrent ulcers causing corneal thinning or even perforation. After healing, corneal opacity and vascular nebula may persist, and symblepharon may form, significantly impairing visual function. Clinical recovery typically takes 4–6 months.

Grade III: The cornea is completely opaque, appearing milky white or porcelain white, obscuring intraocular structures. The corneal limbus and conjunctiva exhibit extensive ischemic necrosis, leading to nutritional impairment of all corneal layers. Combined with collagenase activity, this results in persistent sterile corneal ulcers. Complications such as corneal perforation, leukoma, glaucoma, or eyeball atrophy often occur. Complete repair of corneal ulcers may take over half a year. Ultimately, the cornea is covered by a thick fibrovascular membrane, with vision reduced to only hand motion or light perception.

bubble_chart Treatment Measures

The treatment of chemical burns to the eye can be divided into two stages: early and advanced stage. The early stage primarily involves emergency treatment and preventing further progression of necrotic lesions, restoring nutritional supply to the injured tissue, preventing infection, and reducing complications and sequelae. The advanced stage focuses on treating sequelae such as symblepharon, scarring, vascular nebula, corneal leukoma, and xerophthalmia.

1. Emergency and early treatment for chemical burns to the eye: Immediately remove toxic substances to reduce tissue reaction.

(1) Irrigation: Act without delay to remove chemical substances and minimize their contact with ocular tissues, thereby reducing the severity of the burn. All chemical burns should be irrigated on-site with clean water or by immersing the face in a basin of water, opening both eyes, and continuously moving the head to ensure thorough irrigation. After emergency treatment, the patient should be sent to the hospital.

Medical facilities should always have 25mg of potassium permanganate powder on hand. In emergencies, dissolve it in 500ml of sterile saline to prepare a 1:20,000 concentration solution for immediate irrigation lasting 10–15 minutes. Potassium permanganate solution releases active oxygen, stimulates intracellular respiration, and has detoxifying and antiseptic effects. This irrigation must be completed within minutes of the injury to be effective. Necrotic tissue on the cornea and conjunctiva should also be irrigated with the 1:20,000 potassium permanganate solution, and this should be repeated during daily dressing changes until all necrotic tissue is removed. For lime burns, a 1%–2.5% disodium edetate (EDTA-2Na) solution can be added to wash out calcium deposits in the cornea. Frequent instillation of collagenase inhibitors such as 2.5%–5% cysteine can effectively treat corneal ulcers caused by alkali burns.

(2) Subconjunctival injection of autologous whole blood or serum: This dilutes toxins, separates tissues, prevents the burn from penetrating deeper, improves corneal nutrition, promotes tissue regeneration, and helps prevent symblepharon. Berman et al. noted that α₂macroglobulin in human serum can inhibit corneal collagenase.

(3) Anterior chamber paracentesis: Generally, this should be performed within 1–2 hours after the injury. Grant found that the aqueous humor pH rises to 10 but returns to normal within 15–45 minutes, so performing the procedure too late has limited clinical value. Anterior chamber paracentesis not only removes toxic substances but also allows newly produced aqueous humor, which has anti-inflammatory and nutritional effects, to aid in tissue repair.

(4) Conjunctival incision: Radial incisions in the conjunctiva, followed by slight separation and irrigation, help drain alkaline fluid from the subconjunctival space, remove toxins, reduce tension, and improve corneal blood supply.

(5) Subconjunctival neutralization injection: For acid burns, inject 5% sulfadiazine sodium solution (1–12ml per dose). For alkali burns, inject 5% vitamin C (2ml), repeating the injection after most of it is absorbed, and continue 1–2 times daily for 3–4 days. Vitamin C not only neutralizes but also plays a crucial role in corneal collagen synthesis. However, experimental reports indicate that multiple subconjunctival injections of ascorbic acid can irritate the conjunctiva post-burn and worsen symblepharon. Therefore, intravenous injection can be used concurrently—40ml of 50% glucose with 1g or 2g of ascorbic acid once daily—which is beneficial for treating scorbutic conditions of the cornea and conjunctiva.

(6) Anti-inflammatory and infection prevention: After alkali burns, anti-inflammatory measures and prevention of secondary infection are essential. Topical antibiotics and atropine for mydriasis are recommended. Oral corticosteroids and non-steroidal anti-inflammatory drugs (e.g., indomethacin) for seven days can help reduce corneal edema and anterior chamber exudation. However, topical corticosteroids should be avoided as they may worsen corneal ulcers, risk perforation, and lead to secondary bacterial or fungal infections.

(7) The role of collagenase inhibitors: Currently, drugs such as disodium edetate, cysteine, penicillamine, and medroxyprogesterone can deactivate collagenase to delay or prevent the occurrence of corneal ulcers. High concentrations of collagenase inhibitors have certain toxicity to the cornea, which may cause corneal edema and opacity, and delay epithelial formation. Collagenase inhibitors should be administered starting 2 weeks after the injury.

⑻ Subconjunctival injection of heparin: Once daily, 500–625u (0.4–0.5ml) per dose can dissolve marginal corneal thrombi, with certain efficacy in restoring circulation. However, some hold differing opinions.

⑼ Conjunctival or mucosal transplantation: For large-area grade III chemical burns, excision of necrotic conjunctiva and superficial sclera followed by transplantation of conjunctiva from the other eye or autologous mucosa can prevent corneal perforation and symblepharon. Fresh tissue serves as a favorable foundation for neovascularization, and the transplanted conjunctiva or mucosa acts as a bridge, accelerating regeneration of injured tissue and blood vessels while improving nutrition. Mucosal transplantation is generally recommended within 48–72 hours post-injury. To prevent symblepharon, apply abundant antibiotic ointment in the conjunctival sac, using a glass rod to separate the upper and lower fornices.

⑽ Corneal transplantation: Therapeutic lamellar corneal transplantation may be performed for impending corneal ulcer perforation.

2. Advanced-stage treatment of ocular chemical burns: Eliminate symblepharon to create conditions for vision recovery.

⑴ Severe alkali burns extensively damage conjunctival goblet cells and lacrimal gland duct orifices, leading to reduced or absent tear production, resulting in xerophthalmia and symblepharon. Artificial tears only alleviate symptoms. Parotid duct transplantation is problematic as its secretions contain amylase, which digests corneal stromal glycosaminoglycans, potentially compromising future corneal grafts. Hydrophilic soft contact lenses, combined with artificial tears and punctal occlusion, can also mitigate xerosis.

⑵ Corneal transplantation: Post-alkali-burn corneal transplantation carries significant risks and complications, including poor wound healing, graft infection, graft autolysis due to rejection, protracted uveitis, and phthisis bulbi. However, in early-stage burns, therapeutic lamellar corneal transplantation may be urgently performed if corneal ulcer perforation is imminent. For thinned corneas with dense neovascularization or thickened corneas with extensive scar proliferation and vascularized nebula, penetrating keratoplasty is unlikely to succeed. Wait at least 1 year until inflammation subsides completely. Treat neovascularization with β-irradiation (total dose 400–420γ) or argon laser photocoagulation to induce regression. Six months post-treatment, perform lamellar keratoplasty to normalize corneal thickness. Only after another year may small-diameter penetrating keratoplasty be considered. For monocular patients, exercise extreme caution; under the above conditions, prioritize full-thickness lamellar keratoplasty. Use fresh corneal tissue with preserved epithelium, ultra-fine sutures, and postoperative corticosteroids and collagenase inhibitors for optimal outcomes.

Artificial corneal transplantation: Still in experimental stages globally. For failed or unsuitable corneal graft cases, artificial corneal transplantation may occasionally yield remarkable but often transient results, as eventual graft detachment leads to failure. This method is under ongoing refinement.