Cornea is located at the forefront of the eyeball, which not only protects the contents, but also is an important part of eye refraction, just like the lens of a camera. Therefore, corneal diseases will directly affect vision. The so-called "black eyes" are displayed through the transparent cornea, iris and pupil; Therefore, the transparency of cornea is very important in the beauty of facial appearance. There are many factors affecting corneal transparency, among which keratitis ranks first.

Section 1 Overview of Keratitis

Because the anatomical position of cornea is in direct contact with the outside world, it is easily affected by various external factors, especially the producers directly engaged in industry and agriculture. The cornea itself has no blood vessels, and its nutrient source is not only aqueous humor supply, but also the peripheral cornea mainly depends on the limbal vascular network.

First, the causes and complexity of corneal inflammation, except for the unknown reasons, mainly include the following aspects.

(1) Trauma and infection are the most common causes of keratitis. When corneal epithelium is damaged by mechanical, physical and chemical factors, bacteria, viruses and fungi take the opportunity to enter and be infected. Invasive pathogenic microorganisms can not only come from trauma, but also from various pathogenic bacteria hidden in eyelids or conjunctival sac, especially chronic dacryocystitis, which is a risk factor for corneal infection.

(2) Systemic diseases are internal factors. Such as allergic keratitis caused by tuberculosis, rheumatism and syphilis. General malnutrition, especially keratomalacia caused by vitamin A deficiency in infants and neuropathic keratitis caused by trigeminal paralysis. In addition, there are autoimmune diseases such as silkworm erosion corneal ulcer with unknown causes.

(3) The influence of diseases near the cornea, such as acute conjunctivitis, can cause superficial punctate keratitis, scleritis can cause sclerosing keratitis, and uveitis can also cause keratitis. Exposed keratitis can occur when eyelid defect is combined with incomplete closure of eyelid fissure.

Second, the course of disease and pathological changes

After keratitis occurs, its course of disease and pathological changes can generally be divided into three stages: inflammatory infiltration stage, progressive stage and recovery stage. On the one hand, the outcome of inflammatory diseases depends on the strength of pathogenic factors and the body's resistance; On the other hand, it also depends on whether medical measures are timely and appropriate. The list is summarized as follows.

(1) In the infiltration stage, when pathogenic factors invade the cornea, the first thing is corneal limbal vasodilation and congestion (ciliary congestion, if accompanied by conjunctival vascular congestion, it is called mixed congestion). Due to the role of inflammatory factors, the permeability of vascular wall increases, and plasma and leukocytes, especially neutrophils, move into the lesion site, forming a gray-white turbid lesion with unclear boundaries in the corneal injury area. Peripheral corneal edema is called corneal infiltration. The infiltrated cornea loses its luster due to edema. The size, depth and shape of corneal infiltration vary with the severity of the disease. After treatment, the infiltration can be absorbed by itself or by itself, and the corneal transparency is restored and cured. If the condition is serious or the treatment is not timely, the inflammation will continue to develop.

(2) In the late stage, if the inflammation in the infiltration stage is not controlled, the infiltration will spread and expand, and then new blood vessels will extend into the infiltration area, especially the surrounding area. Neutrophils dissolve in the infiltration area, releasing lysosomal particles containing hydrolase. Hydrolase reacts with corneal protein, resulting in corneal epithelial layer, anterior elastic layer and matrix layer necrosis and shedding in the infiltration area, corneal tissue defect, and corneal ulcer, also known as ulcerative keratitis, with gray or grayish yellow edge. If the ulcer develops deep, it will form a deep ulcer with uneven bottom. Due to the stimulation of toxins, iridocyclitis can be complicated; In severe cases, a large amount of fibrin exudate accumulates in the lower part of the anterior chamber, forming hyphema. When the corneal stroma is completely destroyed and the ulcer spreads to the posterior elastic layer, due to the decrease of local resistance, intraocular pressure can make the posterior elastic layer and endodermis bulge forward, which is called posterior elastic layer prolapse. During clinical examination, the "black" transparent vesicle-like process can be seen at the bottom of the ulcer. This is a sign that the cornea is about to perforate. At this time, if the eyeball is oppressed, such as rubbing eyes, colliding, sneezing, coughing hard, constipation, etc. , can cause sudden perforation of the cornea. At the moment of perforation, the patient can feel sudden and severe pain in the eyes and tears (that is, aqueous humor) flow out. Perforation can cause a series of complications and sequelae.

Infiltration in corneal stroma may not cause ulcer, which is called ulcerative keratitis, and lymphocyte infiltration is the main factor. This type of keratitis is mostly related to the allergic reaction of the body, such as corneal stroma.

(3) The recovery period is the stage of inflammation. After treatment, the ulcer can gradually turn clean, and healthy corneal epithelial cells around it grow rapidly, completely covering the ulcer surface. Under the cover of corneal epithelial cells, fibroblasts of corneal stroma proliferated and synthesized new collagen, which repaired the defect of stroma and cured corneal ulcer. The healing mode of central corneal ulcer is mostly non-neovascular healing; Peripheral ulcers are mostly vascular healing. The newly formed corneal stroma collagen fibers are arranged in disorder, forming opaque scar tissue. Dense scars in the central area can cause severe loss of vision in the affected eyes. Superficial ulcer, only corneal epithelial layer covers the wound surface without connective tissue hyperplasia, then a transparent concave surface is formed at the injury site, and fluorescein is not stained, which is called corneal facet. (Figure 6- 1, 6-2)

Third, clinical manifestations

(1) Conscious symptoms Because the sensory fibers of trigeminal nerve are stimulated by inflammation, patients mainly complain of fear of light, tears and pain, and in severe cases, they have irritating symptoms such as blepharospasm. When corneal epithelium falls off, it will cause serious eye pain. According to the degree and location of corneal lesions, there may be different degrees of visual impairment. Except for purulent corneal infection, there is little or no secretion in general.

1, epithelial shedding 2. Ulcer and hyphema 3. Posterior elastic layer bulging

Fig. 6- 1 corneal ulcer

Figure 6-2 Progressive Evolution of Corneal Ulcer

(2) signs

1. Keratitis with severe bulbar conjunctival edema can cause bulbar conjunctival edema in different degrees.

2. Ciliary congestion

When the cornea is inflamed, the ciliary anterior vascular network around the corneal limbus expands and becomes congested, which is called ciliary congestion. When conjunctival congestion and ciliary congestion occur at the same time, it is called mixed congestion. (See color picture 20)

3. Corneal opacity

Caused by corneal infiltration, edema or ulcer. It must be differentiated from corneal scar formed after inflammation.

Table 6- 1 Difference between corneal infiltration and scar opacity

Osmotic turbidity

Scar opacity

Stimulating symptom

Ciliary or mixed congestion

Glossy surface

Turbid boundary

Fluorescein staining

+

+

Dark, rough and dull.

vague

Corneal epithelial injury, shedding or ulcer can be colored. However, deep corneal infiltration epithelium is not stained when it is intact.

-

-

Smooth and bright

clear

ecru

4. Corneal neovascularization

In the process of corneal inflammation or ulcer, when the capillary network around the congested corneal limbus extends out of the neovascularization branch and invades the cornea, it is called corneal neovascularization Subepidermal neovascularization, derived from superficial vascular network, is dendritic and bright red, and is connected with conjunctival blood vessels. Pre-stromal neovascularization originated from deep vascular network; Posterior stromal neovascularization comes from the great ring of iris artery and the branches of radial iris blood vessels extending to the limbus of cornea. Deep neovascularization is brush-like and deep red in color. The appearance of new blood vessels on the cornea is the performance of the body's repair function.

During the inflammatory period, corneal neovascularization is easy to see. After the inflammation subsides, the new blood vessels remaining on the relatively transparent cornea are just no blood in the lumen, which is called ghost blood vessels, which is difficult to find. Corneal neovascularization, on the one hand, can make the cornea lose its transparency, on the other hand, it will make the corneal tissue undergo biochemical changes, and it will never participate in the immune response of the whole tissue, which may lead to rejection during corneal transplantation.

Fourth, corneal inflammation and sequelae.

(a) iridocyclitis and superficial corneal scar, deep corneal ulcer or corneal stromitis. In the inflammatory stage, iriditis or iridocyclitis may be complicated. If hyphema is formed at this time, it is aseptic hyphema. When corneal ulcer or stromal inflammation is healed and repaired, the opaque part formed on the cornea is called corneal scar. Its influence on vision varies with the thickness, size and location of scars.

1. corneal nerve-like corneal scar. It can be found by oblique illumination or slit lamp inspection.

2. Corneal macula is thick, gray and turbid, translucent and visible to the naked eye.

3. corneal leukoplakia

) is the thickest corneal scar, which is milky white or porcelain white and opaque.

(2) Complications and sequelae caused by corneal ulcer perforation.

1. After corneal fistula's small cornea is perforated, if corneal epithelial cells grow into the wound along the edge of the wound and hinder the healing of the perforation, corneal fistula will be formed, which will connect the inside and outside of the eyeball and easily cause intraocular infection. During the examination, a small black spot can be seen in the center of corneal opacity. The anterior chamber becomes shallow and the intraocular pressure decreases. When fluorescein drops on the cornea, aqueous humor flowing from the fistula will dilute fluorescein and form a light green trickle. If the fistula is temporarily closed by epithelial cells, a small bubble can be seen there, which will rupture when the intraocular pressure is restored or increased. So repeated, threatening the eyeball.

2. Prepolar cataract, after corneal perforation, the anterior chamber suddenly disappears, and the corneal hole directly contacts the lens. Stimulated by toxins, it can cause local metabolic disorder of the lens and local turbidity of the anterior pole of the lens.

3. When the corneal ulcer is perforated due to iris prolapse, the iris can be separated from the perforation due to the outflow of aqueous humor, and the pupil loses its roundness and is melon-seed-shaped, with its tip facing the iris prolapse (Figure 6-3). At this time, the intraocular pressure drops and the eyeball becomes soft. During the healing process, the following conditions will occur.

Fig. 6-3 schematic front view and side view of local iris prolapse.

(1) adhesive corneal leukoplakia

) After the iris prolapse, fibrin oozes from the iris surface quickly and condenses on the perforated and detached iris, fixing the edge of the ulcer and the detached iris part, so that the anterior chamber is not connected with the outside world and gradually recovers. After the ulcer healed, corneal scar tissue mixed with prolapsed iris tissue. This kind of corneal scar is called adhesive corneal leukoplakia. (Figure 6-4)

Figure 6-4 Adhesive corneal leukoplakia

(2) Corneal staphyloma If the range of corneal perforation is large, the embedded iris adheres to the cornea, forming a loose scar to close the perforation, and the pre-adhered iris hinders the drainage of aqueous humor, leading to an increase in intraocular pressure. If the scar tissue can't resist the intraocular pressure, it gradually swells out of the normal corneal surface. This swollen corneal scar is called corneal staphyloma. Among them, when the swelling is limited to a part of the cornea, it is called partial corneal staphyloma, and when all corneas swell forward, it is called total corneal staphyloma. (Figure 6-5, 6-6)

Figure 6-5 Partial corneal staphyloma

Figure 6-6 Whole corneal staphyloma

(3) Secondary glaucoma (secondary glaucoma) Because of the extensive anterior synechia of iris, the anterior chamber angle is narrowed or blocked, and the drainage of aqueous humor is blocked, which leads to the increase of intraocular pressure and the formation of secondary glaucoma.

4. suppurative endophthalmitis (suppurative cndophthalmitis) and panophthalmia (panophthalmia)

After corneal ulcer perforation, purulent bacteria can enter the ball. If the treatment is improper, or the bacterial toxicity is strong, it can cause suppurative endophthalmitis or panophthalmitis. Eventually, it will lead to eyeball atrophy or tuberculosis and blindness.

Verb (abbreviation of verb) diagnosis

(1) Clinical examination

1. Medical record

Whether there are symptoms of corneal irritation and history of trauma, whether corticosteroids have been used locally and systematically; Whether there are chronic dacryocystitis, entropion and other eye diseases and related systemic diseases.

2. Eye examination

People with severe irritation symptoms, especially children, can be examined after dripping local anesthetic. For those who are at risk of perforation, do not press the eyeball during the examination. Fluorescein staining is easy to find superficial corneal lesions, and magnifying glass or slit lamp is easier to find the position and shape of corneal lesions. Corneal perception examination and tear secretion function examination were performed when necessary.

(2) Laboratory inspection

In order to choose the most effective treatment, it is very important to determine the pathogenic factors. For bacterial or fungal corneal ulcers, curettage can often give clues. Microbial culture and drug sensitivity test are more helpful for diagnosis and treatment. It must be pointed out that before the experimental results are obtained, the necessary treatment should be given according to the clinical diagnosis, and the treatment opportunity should not be delayed.

Sixth, treatment.

The treatment of corneal inflammation should focus on removing pathogenic factors and promoting the body's repair ability.

(A) Common treatment methods

1. Eliminate the inducement, such as timely treatment and treatment of entropion, trichiasis, chronic dacryocystitis, conjunctivitis, etc.

Control infection

According to pathogenic microorganisms, appropriate antibiotics are selected and prepared into eye drops or eye ointment with different concentrations. For cases of severe infection, broad-spectrum antibiotics, such as 0.4% gentamicin, 0.5% kanamycin, 0.25% chloramphenicol and other eye drops, can be selected first. If necessary, it can be used for subconjunctival injection and systemic medication. Can be used alone or in combination.

3. mydriasis

All symptoms of scleral stimulation, such as pupil shrinkage, slow response to light, complicated with iridocyclitis, etc., should be dilated. Commonly used mydriatic drugs are 0.5 ~ 3% atropine and eye ointment; If necessary, midazolam can be injected under the conjunctiva.

4. Wet and hot compress can dilate ocular blood vessels, promote and improve local blood circulation, relieve irritation symptoms, promote inflammation absorption and enhance tissue repair ability. Hot compress can be applied 2 ~ 3 times a day, each time 15 ~ 20 minutes.

5. The application of corticosteroids is limited to allergic keratitis or corneal ulcer healing, and corneal stroma still has infiltration and edema. For corneal epithelial injury or corneal ulcer caused by various reasons, corticosteroids are prohibited in principle, so as not to aggravate the ulcer or delay the healing of epithelial injury.

6. Covering the affected eyes with sterile gauze can avoid light stimulation, reduce the friction between eyelid and corneal surface, protect ulcer wound, relieve pain, promote ulcer healing and prevent secondary infection. You can also wear therapeutic soft contact lenses, but those with conjunctivitis and purulent secretions are prohibited. Wear colored glasses if necessary.

7. Multivitamins, such as vitamins C, E and AD, can be used to support therapy.

(2) treatment of refractory corneal ulcer

1. Corneal cautery Under topical anesthesia with 0.5% caine, the area of ulcer (that is, the area to be cauterized) was determined by 1% fluorescein staining. You can choose 10 ~ 30% trichloroacetic acid, 5 ~ 7% tincture of iodine, 20% zinc sulfate or pure carbolic acid to cauterize the ulcer surface, so that pathogenic microorganisms and necrotic tissues on the ulcer surface will coagulate and fall off. Pay attention to protect the healthy cornea when cauterizing. It can be cauterized once every 2 ~ 3 days, and 4 ~ 5 times is 1 course of treatment.

2. After surface anesthesia by freezing method, the freezing range was determined by fluorescent staining. Freezing with a freezing head at -60 ~-80℃. The freezing time is generally 5 ~ 10 second; The freezing point depends on the size of the ulcer, and generally does not exceed 10 freezing point at a time.

3. The application of collagenase inhibitors

Recent studies have proved that the level of collagenase in alkali burned rabbit cornea and herpes simplex keratitis increases. Collagenase can destroy collagen fibers and affect ulcer healing. Therefore, for corneal ulcers that cannot be cured for a long time, you can try to drop collagen inhibitors. Such as 2 ~ 3% cysteine, 0.5 ~ 2.5% EDTA-Na (Ca), 0.5% zinc sulfate, etc. You can also use your own blood, penicillamine, glutathione and other eye drops.

4. Operation (1) small conjunctival flap covering. When corneal ulcer is in danger of perforation, the affected eye should be lightly bandaged or wear contact lenses; Oral antihypertensive drugs can reduce intraocular pressure, prevent perforation, and cover it with conjunctival flap if necessary. If there is perforation and iris prolapse, iridectomy and conjunctival flap covering can be performed. Covering surgery depends on the location and area of membranous ulcer. (Figure 6-7)

Figure 6-7 Different conjunctival flaps are used to cover corneal ulcers in three different parts.

1. bag shape; 2. The petal shape of the bridge; 3. Wallet-shaped

(2) Therapeutic corneal transplantation

For intractable corneal ulcer, the visual acuity is below 0. 1 and the corneal posterior layer is normal, so it is feasible to carry out therapeutic lamellar keratoplasty. For patients who are at risk of perforation or have been perforated, penetrating keratoplasty is feasible when fresh corneal materials are available.

(3) Application of medical adhesive For perforation cases within 2 mm, adhesive can be tried to promote healing.

(III) Treatment of corneal scar

1. At present, there is no ideal medicine to promote scar absorption. Generally, 1 ~ 5% dionin solution can be used for eye drops (starting from a low concentration and then gradually increasing the concentration) three times a day. Traditional Chinese medicine has been recorded for a long time and is still under study. The Chinese medicine "Huayunning" eye drops made by our scientific research have achieved initial effect in clinical application.

2. According to the location, range and thickness of corneal scar and the degree of influence on vision, laser iridectomy, optical iridectomy or corneal transplantation can be performed. For secondary glaucoma caused by adhesive corneal leukoplakia, anti-glaucoma surgery can be performed.