Corneal burn

Introduction Corneal burns include many types, common with corneal chemical burns, corneal thermal burns. Chemical burns are the local damage of chemicals, mainly cell dehydration and protein denaturation, and some produce heat and aggravate burns. Some chemicals can be poisoned after being absorbed. Alkaline eye chemical burns are one of the most common clinical treatments for thorny eye injuries. Aseptic corneal corneal ulceration, perforation, eyeball adhesion and secondary glaucoma after injury are common causes of eye disability. The chemical burn of the eye, the treatment of alkali burns, is a major problem in the ophthalmology field; early correct treatment is very important for restoring visual function and reducing complications as much as possible. Thermal burns are caused by high temperatures such as hot water, steam, flame, and electric current.

Cause

Corneal alkali burns are mostly caused by strong alkaline substances (PH >11.5). The damage of alkaline substances to the eyes is mainly due to the biphasic solubility of these substances, water solubility and fat solubility, so it is easy to pass the epithelial barrier. An aqueous solution of an alkaline substance, the hydrogen cation ion and the lipid saponification, bind to the tissue protein to form a basic protein, thereby destroying the structure of the cell membrane, entering the cell and rapidly destroying the intracellular structure and causing intracellular necrotic damage. .

It manifests as tissue dissolution, which produces a large amount of alkaline substances that penetrate into the tissue. Corneal acid burns mainly refer to the damage of strong acidic substances (PH<3) to the eyes. Low-concentration water-soluble acidic substances generally cannot damage the fat-soluble barrier of the corneal epithelium, and most of them do not cause serious corneal damage. The high concentration of acidic substances has strong corrosion, and once contacted with the eyeball, it can damage the corneal epithelium and invade the corneal stroma, causing the protein in the corneal tissue to coagulate and denature, forming an insoluble acidic protein compound, resulting in cornea or other Destructive damage to the wall tissue of the eye.

On the other hand, due to the denaturation and solidification of the tissue protein, a thick insoluble barrier can be formed, which in turn can hinder the acidic substance. Therefore, the damage of the acidic substance to the cornea is mostly limited and the boundary is clear, the penetration is relatively advanced, and severe necrotizing ulcers are less likely to occur. Corneal thermal burn refers to (direct) contact damage to the cornea by high temperature molten iron, boiling oil, etc. First, the corneal epithelial cell layer and the anterior elastic layer are involved, which can lead to degeneration and necrosis of the stromal fibers. When the damage affects the endothelial cell layer, the cornea becomes edematous, and finally leads to corneal ulcer and perforation. In the repair stage, scar formation is accompanied by neovascularization. .

an examination

Related inspection

Corneal examination

After the alkaline substance enters the eye, it will quickly produce a necrotic reaction. The more serious reaction can cause irreversible damage within a few minutes. The symptoms are almost the same as the acid burn. But more intense, especially pain and swelling are more obvious. Clinically, according to the degree of ocular tissue damage and the nature of the lesion, it is divided into 3 phases and 4 degrees:

1, the acute phase: within a few seconds to 3 days after the burn, the early manifestations of the formation of the knot, corneal necrosis, pain and eye irritation symptoms.

2, nutritional disorders: 3 days to 3 weeks after burns, early manifestations of corneal edema degeneration, and gradually developed into non-inflammatory necrotic ulcers. In the later stage, a large number of new blood vessels grew in, and some tissues began to repair, and gradually reduced gradually.

3, scar stage: burns for 3 weeks to manifest as corneal leukoplakia or vascular sinus cornea. Various eye complications have appeared one after another, and the ocular ball adhesion has increased intraocular pressure or the eyeball has atrophy.

Once the acidic substance enters the eye, it can immediately cause an damaging reaction to the tissue. The symptoms of the symptoms are severe pain in the eyes, stinging in the burning, obvious irritation in the front of the eyes, and a sharp drop in vision.

Eye examination: often mixed with eyelid skin and conjunctival burns. Corneal burns first show that the adhesion of the corneal epithelium to the anterior elastic membrane is weakened, resulting in large epithelial shedding, followed by corneal edema thickening, showing grayish white turbidity, and serious visual loss if the pupil area is involved. In most cases in the late stage, a large number of neovascularization of the cornea can be formed, and the cornea is white. Severe cases can be treated as extensive sputum adhesions and pseudo-sick scorpions.

According to the indexing standards adopted by the Collaborative Group on Ocular Trauma and Occupational Ophthalmology in 1982, I divided into: I degree: epithelial injury, epithelial opacity, but the front elastic layer and corneal stroma were not damaged, leaving no trace after healing. II degree: only the shallow edema of the stroma, not involving the deep layer, so the deep layer remains transparent. III degree: parenchymal superficial edema, turbidity is significant, the cornea is ground glass, and the deeper corneal parenchyma is also damaged, and the iris is faintly visible. IV degree: the whole layer of the cornea is involved, it is porcelain white turbid, and the iris is invisible.

Differential diagnosis

Acidic burns and alkaline burns differ in their examination and clinical performance and need to be identified. In general, in acid burns, the burn boundary of the cornea and conjunctiva is clear, the coagulation membrane on the surface of the tissue, the conjunctival blood vessels are dark, and there may be subconjunctival hemorrhage, and the severe blood vessels may be completely occluded. In the case of alkali burns, the conjunctiva is congested and the corneal epithelium is shed. In slightly heavier, the conjunctival ischemic, the blood vessels become darker or occluded, and the cornea is turbid. In severe cases, the conjunctival blood vessels disappear and the cornea is completely turbid. The eyeball is porcelain white with no symptoms. And irritating symptoms.

Corneal burns and scratches: Sunlight or some external objects, especially those with rough surface, can cause different degrees of abrasion of the cornea, such as corneal epithelial defects or exfoliation.

Corneal ulcer: an eye disease caused by infections such as bacteria, viruses, and fungi. When the pathogenic factors invade the cornea, the limbal vascular network first expands and is congested, called ciliary congestion. Inflammation oozes, white blood cells invade the lesion, causing edema and edema of the epithelium and stroma, called corneal infiltration. If the condition cannot be controlled, the infiltration will continue to worsen, and degeneration, necrosis, and tissue shedding will occur, and corneal ulcers will form. The infiltrated base is grayish white and the edges are unclear. If the treatment is appropriate, the inflammation is controlled, the base and edges of the ulcer are gradually cleaned, the boundary is clear, the surrounding epithelium is regenerated, and the connective tissue proliferates to form different scars.

Corneal erosion is a symptom of superficial punctate keratopathy. Superficial punctate keratopathy is a general term for three types of lesions of the corneal epithelium: punctate epithelial keratitis, punctate epithelial erosions, and punctate subcutaneous infiltration (punctate). Subepithalial infiltrates), they often exist at the same time, but the weight and extent of the lesion are biased and different.

Corneal opacity: The cornea is a transparent tissue with no vascular structure. Transparency is the greatest feature of corneal tissue and is an essential element of its physiological function. Once it is affected by trauma or harmful factors, its transparency is lost and turbidity can cause visual impairment. After the alkaline substance enters the eye, it will quickly produce a necrotic reaction. The more serious reaction can cause irreversible damage within a few minutes. The symptoms are almost the same as the acid burn. But more intense, especially pain and swelling are more obvious. Clinically, according to the degree of ocular tissue damage and the nature of the lesion, it is divided into 3 phases and 4 degrees:

1, the acute phase: within a few seconds to 3 days after the burn, the early manifestations of the formation of the knot, corneal necrosis, pain and eye irritation symptoms.

2, nutritional disorders: 3 days to 3 weeks after burns, early manifestations of corneal edema degeneration, and gradually developed into non-inflammatory necrotic ulcers. In the later stage, a large number of new blood vessels grew in, and some tissues began to repair, and gradually reduced gradually.

3, scar stage: burns for 3 weeks to manifest as corneal leukoplakia or vascular sinus cornea. Various eye complications have appeared one after another, and the ocular ball adhesion has increased intraocular pressure or the eyeball has atrophy. Once the acidic substance enters the eye, it can immediately cause an damaging reaction to the tissue. The symptoms of the symptoms are severe pain in the eyes, stinging in the burning, obvious irritation in the front of the eyes, and a sharp drop in vision. Eye examination: often mixed with eyelid skin and conjunctival burns. Corneal burns first show that the adhesion of the corneal epithelium to the anterior elastic membrane is weakened, resulting in large epithelial shedding, followed by corneal edema thickening, showing grayish white turbidity, and serious visual loss if the pupil area is involved. In most cases in the late stage, a large number of neovascularization of the cornea can be formed, and the cornea is white. Severe cases can be treated as extensive sputum adhesions and pseudo-sick scorpions.

According to the indexing standards adopted by the Collaborative Group on Ocular Trauma and Occupational Ophthalmology in 1982, I divided into: I degree: epithelial injury, epithelial opacity, but the front elastic layer and corneal stroma were not damaged, leaving no trace after healing. II degree: only the shallow edema of the stroma, not involving the deep layer, so the deep layer remains transparent. III degree: parenchymal superficial edema, turbidity is significant, the cornea is ground glass, and the deeper corneal parenchyma is also damaged, and the iris is faintly visible. IV degree: the whole layer of the cornea is involved, it is porcelain white turbid, and the iris is invisible.

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