Chemical eye injury

Introduction to chemical eye injury In the daily industrial and agricultural production process and daily life, it is not uncommon for the chemical substances to act directly on the eyes, causing eye damage. According to some statistics, chemical injuries of the eye accounted for the third place in industrial eye trauma, and chemical eye damage accounted for about 10% of eye injuries. Chemical substances often cause serious damage to the eye tissue. If not properly treated in time, the prognosis is poor, and even severe cases are blind or lose their eyeballs. 17% of eye injuries caused by chemical substances are caused by solid chemicals, 31% are caused by liquid chemicals, and 52% are caused by chemical smoke. In the eye injuries caused by these chemicals, chemicals can be directly contacted with eyes. It can also cause damage to the eye, the visual path, or the visual center through the systemic absorption of the skin, respiratory tract, and digestive tract. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population Mode of infection: non-infectious Complications: ball adhesion scar varus

Cause of chemical eye injury

There are many kinds of chemical scars in the eye, and only the common chemical injuries are classified as follows:

First, corrosive injuries

1. Acidic injury

(1) inorganic salts and their compounds: sulfuric acid, phosphoric acid, chromic acid, hydrogen sulfide and fluoride;

(2) organic acids: phenolic acid, acetic acid, phosphoric acid, chromic acid, hydrogen sulfide and fluoride;

(3) Others: acetic anhydride, phenol, zinc chloride, sodium heavy soy, acetone and ammonium sulfate.

2, alkaline injury

(1) alkali metals and their compounds: sodium, potassium and potassium hydroxide;

(2) Alkaline earth metals and their compounds: calcium, barium and calcium chloride;

(3) Others: ammonia, come to the brine and brine.

3. Non-metallic etchant

Arsenic, selenium, phosphorus, nitrogen, sulfur and silicon compounds, calcium oxide, etc.

Second, cytomycin

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

Mechanism of chemical burns

1. The effect of chemicals penetrating the eyeball is closely related to the physiological characteristics of the surface layer of the eyeball. The corneal epithelium and endothelium are lipophilic, the corneal stroma and sclera are water-soluble, and the conjunctiva and corneal epithelium are similar. All fat-soluble substances are easy to wear. It penetrates the corneal epithelium and remains in the corneal stroma; water-soluble substances are difficult to pass through the corneal epithelium, but easily pass through the matrix, so unless the epithelial tissue is damaged, the water-soluble substance is difficult to enter the cornea.

The water balance and metabolism of the corneal stroma mainly depend on the function of the corneal epithelium and endothelium. The role of the endothelium is more important. The electrolyte is not easy to penetrate the epithelium and endothelium. When the integrity of the epithelium or endothelium is destroyed, the cornea can edema and turbid.

Corneal nutrition mainly comes from the uveal membrane. Through the aqueous humor, the nutrients are diffused into the cornea through the corneal endothelium. The vascular network around the cornea is only an auxiliary function. The normal cornea does not need it. It only works under pathological conditions, such as when the corneal stroma is turbid. Only when the new blood vessels protrude from the surrounding vascular network into the cornea, the turbidity gradually absorbs and becomes transparent.

2, the chemical damage effect: the solubility of chemicals is of great value to estimate the degree of damage to the eye tissue, acid is water-soluble, alkali, sulfur dioxide, ammonium hydroxide and mustard oxygen are water-soluble and fat-soluble Sexuality, so it has special penetrating and damaging effects. Many organic solvents such as formaldehyde, chloroform, alcohol, acetone and ether have high fat solubility, which can cause temporary damage to the corneal epithelium and dehumidification of acid and alkali chemicals. ) does not moderate the necrosis of tissue.

Another type of heavy metal salt mainly acts as a precipitation, so-called astringent reaction. At low concentration, the surface tissue hardens the binding between the cell surface and the capillary cells due to precipitation, and the tissue becomes white and the inflammatory exudation is reduced. When the concentration is increased, it is corrosive, and the cell protein is coagulated and necrotic.

The damage of various chemical substances to the ocular tissues is vascular congestion at the beginning, and the permeability is increased. Following the tissue edema, the protein of the tissue cells is denatured and solidified and died.

Chemical eye injury prevention

Eye chemical injury is the first emergency in ophthalmology. On-site first aid for eye chemical eye injury is very important. Whether the first aid is timely and completely has a great relationship with the prognosis. The main point of first aid is to count every second, to take materials locally, rinse thoroughly, and after injury. Immediately flush the eyes with plenty of clean water at the scene. The more quickly and thoroughly the rinse, the better. If there is no disinfected clean water on the spot, use tap water or any other clean water. Do not treat any chemical eye trauma. With the patient everywhere to find a doctor or remote referral, so that chemical substances stay in the eye for a long time, continue to produce chemical damage, increase the degree of eye damage.

Chemical ocular trauma complications Complications, sacral adhesion, scarring, varus

Eyeball adhesions, scars, meaty vasospasm, corneal leukoplakia and dry eyes.

Symptoms of chemical ocular trauma Common symptoms Conjunctival congestion, lens opacity, corneal ulcer, corneal opacity, dystrophic dysfunction, secondary infection, bilateral valgus, conjunctival hemorrhage, alkali burn

First, the category of chemical eye damage

1. Chemical eye immersion and staining: Due to prolonged exposure to chemicals, visible chemical substances are deposited in the eyelid skin, conjunctiva, cornea, crystal, vitreous, retina, etc., and the surface of the eye is colored, often due to long-term direct contact with chemicals. As a result, the chemical deposits in the eye are mostly chemically absorbed by the skin, the respiratory tract and the gastrointestinal tract, and then deposited in the eye. For example, silver stains are exposed to silver dust for a long time, and the cornea and conjunctiva may develop taea and silver deposit. .

2, chemical eye irritation or burns: chemicals that do not cause irritation to the skin, can also cause damage to the cornea and conjunctiva, often cause irritation, such as tobacco, alcohol, mercury, asphalt and hydrogen sulfide, can cause conjunctiva Congestion, papillary hyperplasia or conjunctivitis can also cause corneal epithelial damage.

3, chemical-induced eye allergic reactions: this kind of reaction, multi-surface is eyelid skin inflammation and conjunctival congestion and edema, each with a thorny skin foreign body sensation.

4. Ocular lesions caused by chemical poisoning: toxic chemicals are absorbed by the body and cause lesions in the eye tissue. There may be ophthalmoplegia, lens opacity and chemical deposition, uveal and retinopathy, optic neuropathy, In addition to eye symptoms, there may be symptoms of poisoning in other parts of the body.

Second, the factors that determine the degree of eye chemical damage

The severity of damage caused by chemical substances on the eye tissue is determined by factors such as the toxicity of the chemical, physical and chemical properties, contact time, contact area, amount and concentration of chemicals, and timely and reasonable first aid after injury.

1. Physical and chemical properties of the wound

The chemical damage to the tissue is mainly to destroy the physical and chemical state of the protein of the body, causing degeneration and solidification and necrosis. After the contact of the chemical with the tissue, the result is different due to the chemical reaction. In general, Gas damage to tissue is lighter than liquid, liquid is lighter than solid, because gas is easily diluted by air, and liquid is easily diluted and washed by tears. The concentration of chemical is proportional to the degree of damage to tissue, and the penetration is large and the solubility is large. Its organizational damage is also heavier.

2. Time and area of contact between the chemical and the eye tissue

When the chemical is in contact with the eye tissue for a long time, the tissue damage is heavy, and the contact area between the chemical and the eye tissue is large, and the damage is also serious.

Third, the stage and division of chemical burns

In order to observe the changes and treatment of the disease, the alkali burns were staged and indexed.

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

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

Repair period: 1 day to 2 weeks after injury.

Complication period: 2 to 3 weeks after injury.

2. Indexing: According to the national eye disease occupational eye disease group's indexing standard, combined with skin burn classification method, the eye burn is divided into 4 degrees.

Area calculation:

+: Total burn area of each organization 14

++: 1/4 injury area 12

+++: 12<burn area 34

++++: all burns

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

Fourth, the clinical manifestations of chemical burns

Because acid and alkali are widely used in industry and daily life, it is quite common for acid and alkali to cause eye burns.

1. Acid burn: acid damage to the eye is called acid burns. Acidic substances are divided into organic acids and inorganic acids. They are soluble in water and insoluble in fat. Acidic substances are easily blocked by corneal epithelium. The corneal conjunctival epithelium is a fatty tissue. However, when the high concentration of acid contacts the tissue, the tissue protein is coagulated and necrotic, forming a aponeurium membrane, which prevents the remaining acid from continuing to penetrate into the deep layer. The inorganic acid molecule is small, the structure is simple, and the activity is strong. It easily penetrates into tissues, so tissue damage caused by inorganic acids is heavier than organic acids.

The wounds of acid burns are shallow, the boundary is clear, the necrotic tissue is easy to fall off and repair, the concentrated sulfuric acid has strong water absorption, the organic matter can be turned into charcoal black, the nitric acid wound surface is yellow at first, and then turned into yellow brown; hydrochloric acid is poorly corrosive. It is also yellowish brown. The organic acid has the strongest corrosiveness of trichloroacetic acid, which can make the tissue appear white necrosis.

2, alkali burns: in the chemical burns of the eye, alkali burns (alkaline burns) develop fast, long course of disease, more complications, poor prognosis.

Common alkaline substances are potassium hydroxide, sodium hydroxide, calcium hydroxide, ammonium hydroxide (ammonia) and sodium silicate (sodium silicate).

(1) Mechanism of alkali damage to ocular tissues: Alkali can react with lipids in cell tuberculosis, and form a water-soluble basic protein with tissue proteins. The formed compounds have biphasic solubility; they are soluble in water. It is also fat-soluble, which destroys the corneal epithelial barrier and quickly penetrates the layers of the eyeball. After the alkali enters the cell, the pH rises rapidly, making the compound formed by the alkaline substance and the cellular component more soluble, and In an alkaline environment, it is advantageous for the emulsification of cell membrane lipids, which in turn leads to destruction of cell membranes.

Alkaline cell proteins have a strong role in destroying the enzymes and structural proteins of cells. Light alkali burns affect enzyme proteins and inhibit the life process of cells. Heavy alkali burns can directly destroy cell tuberculosis proteins and rapidly lead to extensive tissue. Coagulation necrosis, alkaline compounds often occur in the thrombus formation and necrosis of the limbal vascular network, which seriously affects the corneal nutrition to reduce the resistance of the cornea, and easily secondary infection, causing ulceration or perforation.

(2) Biochemical changes of alkali burns: normal human corneal epithelium has no collagenase, but alkali burned corneal epithelium and other causes of corneal ulcer tissue contain a large amount of collagenase, which can digest and decompose collagen, the second week after alkali burn February is the peak period of corneal collagenase release, easy to form ulcer perforation, corticosteroids can enhance the dissolution of collagenase, so this drug should be banned.

The prostaglandin content in the aqueous humor after alkali burns is significantly increased, causing local vasodilation, capillary network congestion, increased blood flow, and elevated intraocular pressure. The symptoms are similar to acute angle-closure glaucoma.

After alkali burn, the content of ascorbic acid, riboflavin and glucose in the eye tissue can be reduced, which affects the normal metabolism of the tissue.

(3) Clinical and pathological processes: Alkali burns are often a complex and lengthy pathological process. The Hughes staging method and domestic related materials are divided into three phases.

I acute phase: a few seconds to 24 hours after burns, generally within a few minutes after the injury, alkaline substances can penetrate the cornea into the anterior chamber, manifested as cornea, conjunctival epithelial necrosis, shedding and conjunctival edema ischemia, corneal stromal edema Turbidity, extensive thrombosis of the limbus and nearby blood vessels, hemorrhage, and even acute iritis, and even a large amount of flocculation exudation in the anterior chamber. The cornea of the severe alkali burn is porcelain white, and it is impossible to see the intraocular tissue, due to the iris and The ciliary body ischemic necrosis, the secretion of aqueous humor is reduced, and the intraocular pressure is significantly reduced.

II repair period: Generally, the corneal epithelium begins to regenerate from 5 to 7 days to 2 weeks after injury, and new blood vessels gradually invade the cornea, and iritis tends to be static.

III complication period: 2 to 3 weeks after burns enter the complication period, often with repeated and persistent aseptic corneal ulcer, each causing corneal perforation, the necrotic tissue of the deciduous conjunctiva is detached and scar healing occurs, resulting in shrinkage, Shortening or disappearing, sputum adhesion or formation of corneal leukoplakia, meaty vasospasm, and even eyelid atresia, develop into dry eye, uveitis, cataract, glaucoma or eyeball atrophy.

(4) Prognosis: The prognosis of ocular alkali burn depends on the degree of burn and whether the treatment is timely and appropriate. Roper-Hall divides alkali burn into 4 degrees according to the degree of limbal and conjunctival injury; 1 and 2 degrees are light, and the prognosis is better. Good; 3,4 degrees is heavier, the prognosis is poor, it is convenient for clinical use, and it is simplified to light, medium and severe.

I mild: corneal epithelial damage, erosion, corneal mild turbidity, but the iris texture is clearly visible, the limbus has no ischemia or ischemia range of less than 1/3, if further development, corneal epithelial exfoliation, mild edema of the matrix, this Reasonable treatment can avoid the occurrence of corneal ulcers. It can be completely repaired within 1 to 2 months, turbid absorption, corneal thickness and transparency return to normal or only a small amount of thin sputum and a small number of new blood vessels, and the function is basically normal or complete. Back to normal.

II moderate: most or all of the corneal epithelium exfoliation, corneal opacity and edema, faintly visible iris and pupil, conjunctival and corneal marginal part of ischemic necrosis, range 1/3 ~ 12, this type of limbal injury is heavier, extensive corneal lesions Deep, the repair process is slow, such as improper treatment, often leading to corneal ulcer, anterior chamber exudate, repeated ulceration caused by thinning of the cornea or even perforation, left after the cure of corneal opacity and vasospasm, and even the formation of symblepharon adhesion, visual function is significantly affected Loss, this type generally takes 4 to 6 months to reach clinical cure.

III severity: the cornea is completely opaque white or porcelain white, the eyelid structure can not be seen, the ischemic necrosis of the limbus and conjunctiva, causing dystrophic disorders in the cornea, plus collagenase causes repeated and persistent aseptic corneal ulcer, often Complications such as corneal perforation, cataract, glaucoma or eyeball atrophy often take more than half a year from injury to complete repair of corneal ulcer. The cornea is covered by a thick fibrous vascular membrane, and the visual acuity is only manual or light.

Chemical eye injury examination

1. Inquire about the history of trauma, including the cause of injury, the type, direction, speed and distance of injury, the time of injury, and identify it as mechanical or non-mechanical trauma. If it is a mechanical injury, further distinguish eyeball contusion, eyeball Perforation or adnexal injury, presence or absence of intraocular or intraorbital, foreign bodies in the eyelids, if it is a non-mechanical injury, it should be divided into physical, chemical and so on.

2. Must pay attention to the general condition, such as shock, craniocerebral trauma, infection, etc., combined with systemic trauma, should consult the relevant department for treatment, local examination must be light, can not oppress the eye, if necessary, drip surface anesthetic, such as combined with traumatic brain injury Do not divert before the neurological examination.

3. When checking the foreign body on the surface of the eyeball, special attention should be paid to the cornea, the inferior sulcus and the sacral conjunctiva.

4. For patients with eye contusion, the eye appendage and the front and back of the eyeball should be examined in detail. For patients with penetrating eye injury, the size, location, depth of the wound, presence or absence of eyeball content, eye movement disorder or foreign body retention should be checked. The time chart indicates that the thermal and chemical burns should describe the extent and extent. When the phosphorus burns, pay attention to the presence or absence of phosphorus odor on the wound surface, and check for the presence or absence of phosphorescence in the dark.

5. Check the visual acuity and function of each eye. Except for obvious eyeball penetrating injury, the fundus should be examined as much as possible, and dilated if necessary.

6. Anyone suspected of having an eyelid fracture or a foreign body in the ball should be examined by X-ray, CT or ultrasonography. When foreign bodies are found to be present, foreign body positioning should be performed.

7. Pay attention to healthy eyesight, various conditions before and after the eyeball, and whether there is sympathetic ophthalmia.

Diagnosis and diagnosis of chemical eye injury

diagnosis:

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis:

Including the cause of injury, the type of injury, direction, speed and distance, injury time, identified as mechanical or non-mechanical trauma, such as mechanical injury, further distinguish eyeball contusion, eye penetrating injury or ancillary injury, Whether there is any eye inside or inside the eyeball, foreign matter remains in the eyelid. If it is a non-mechanical injury, it should be divided into physical and chemical.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.