Keratitis: There are two kinds: ulcerative keratitis, also known as corneal ulcer, and non-ulcerative keratitis, namely deep keratitis.
Ulcerative keratitis
Etiology:
1. External causes: Most corneal infections caused by external causes must meet two conditions:
A. damage and shedding of corneal epithelial cells,
B. concurrent infection. Only when these two conditions are met can infectious corneal ulcer easily occur.
2. Internal cause: refers to internal diseases from the whole body.
There are no blood vessels in the cornea, so acute infectious diseases are not easy to invade the cornea. However, corneal tissue is involved in systemic immune response. Although the degree of immune response is lower than other tissues, it is precisely because it has no blood vessels and its metabolism is relatively slow, so this kind of immune response changes for a long time. Cornea is in a sensitive state for a long time, which is prone to allergic diseases, such as bullous keratitis.
3. Because of the homologous relationship in embryology and anatomical continuity, the adjacent tissues spread, and the diseases that spread to the corneal epithelium mostly come from conjunctiva, such as severe conjunctivitis and superficial keratitis.
Ulcerative keratitis, also known as corneal ulcer, is mostly caused by external factors, that is, inflammation caused by infectious pathogenic factors invading corneal epithelial cells from the outside.
Course of disease: At the beginning of inflammation, there are more or less irritants and swimming cells in the corneal tissue, and the corneal tissue is full of liquid, so the affected area is swollen and turbid, sometimes even higher than the surface, which is called corneal infiltration period.
Corneal infiltration: Its main symptoms are grayish yellow, cloudy and dull, which is higher than the corneal surface.
Progressive corneal ulcer: the progress of corneal infiltration has two results:
A. the infiltration was absorbed. When the corneal infiltration has not reached the peak, the inflammation disappears, the corneal luster recovers and it is completely transparent (this outcome is rare in clinic).
B. Infiltration and suppuration. Generally speaking, corneal tissue dissolves immediately after infection, and epithelial cells and even superficial parenchyma fall off due to necrosis, thus forming ulcers. The edge of the ulcer is cloudy at first, and then it becomes more serious in the middle and around. The ulcer base is gray, uneven and unclear, which is called unclean stage or progressive ulcer. When it progresses, the ulcer can spread to one side or around; You can also progress to the depths, or to the surroundings or depths at the same time. For example, gonorrhea and corneal ulcer are like this. It will not only bypass the cornea, but also go deep, pierce the cornea and even destroy the whole cornea.
Degenerative corneal ulcer: the most common corneal ulcer is local necrosis and partial shedding, and the undiluted part is only connected with the center of the basement. This situation shows that the toxin is concentrated in the middle of the ulcer, and its periphery has been surrounded by polynuclear white blood cells. These white blood cells devour bacteria and dissolve necrotic tissue. At this time, the epithelial cells around the ulcer quickly progress to the center of the ulcer, and the epithelial cells proliferate and spread very quickly (usually corneal epithelial cells can be completely recovered within 24 hours after scraping), and the necrotic part of the ulcer continues to fall off until the ulcer turbidity gradually decreases and disappears. The base of ulcer and its edge tend to be smooth and transparent, and enter the cleaning period. This is the stage of degeneration.
Corneal scar: when corneal ulcer reaches the cleaning period, connective tissue in cornea proliferates, repairs the defect, and the ulcer heals to form scar. If the ulcer is small and shallow and only involves the epithelial layer, the cornea can be completely transparent. If the anterior elastic membrane and the superficial layer of corneal parenchyma are involved, dense and turbid scars will be left. At first, the turbidity is dim, then the concentration increases, but it will never cross the edge of the ulcer. The disappearance of corneal scar is limited to infants, and it is impossible when they are old, which will inevitably leave permanent scars, thus causing visual impairment. At the initial stage of scar formation, the damaged part has not completely recovered its original curvature, but fluorescein is no longer stained, forming a small depression on the cornea, which is called corneal facet. Finally, the facet disappeared and the cornea returned to normal curvature. However, in some cases, the corneal surface is permanent.
The size and thickness of corneal scar vary according to the severity of ulcer. Thin is cloud-like, slightly thicker is called corneal cloud, and the thickest is called corneal leukoplakia.
Clinical manifestations: Except paralytic keratitis, most patients with keratitis have strong inflammatory symptoms, such as pain, shame, tears and eyelid spasm. This is because the trigeminal nerve endings in the cornea are stimulated by inflammation, which causes reflex orbicularis oculi muscle contraction and excessive tear secretion. Cornea is avascular tissue, but there are abundant blood vessels in the adjacent area (corneal limbus, iris and ciliary body). When inflammation involves adjacent tissues, congestion and inflammatory exudation will occur. Therefore, patients with keratitis have not only ciliary congestion, but also iris congestion. The latter is characterized by iris discoloration and pupil contraction.
The exudate comes from the same source. In severe cases, bulbar conjunctiva and even eyelid edema may occur. Corneal infiltration occurs when white blood cells move to corneal lesions due to hyperemia of corneoscleral margin. When corneal inflammation reaches the stage of regression, the clinical irritation symptoms are greatly alleviated.
Corneal inflammation will inevitably affect vision more or less, especially when inflammation invades the pupil area. Corneal scar formed after ulcer healing not only prevents light from entering the eyes, but also changes the curvature and refractive power of the corneal surface, making objects unable to focus on the retina to form a clear image, thus reducing vision. The degree of visual impairment depends entirely on the location of the scar. If it is located in the middle of the cornea, even if the scar is small, it will greatly affect vision.
Complications:
1. Severe hyphema cases are often complicated with iridocyclitis. Due to the white blood cells oozing from iris and ciliary body, the aqueous humor in anterior chamber is turbid and deposited in the lower part of anterior chamber angle, which is called hyphema. It is horizontal because it is liquid. When the head is tilted, the liquid gradually changes direction to a lower position. The amount of hyphema is extremely inconsistent, from the pale yellow crescent line in the lower corner of the anterior chamber to the severe crescent line filling the anterior chamber. The hyphema may be completely absorbed (the thinner it is, the easier it will be absorbed). Fibrous exudate can form connective tissue, produce anterior or posterior adhesion around iris, and even cause pupillary atresia. There are deposits on the posterior wall of cornea in patients with ciliary body involvement.
2. Posterior elastic membrane bulging Because corneal ulcer can progress to the deep layer, when the cornea is about to be perforated, a thin layer of transparent tissue can appear at the base of the ulcer, which looks like a "black" vesicle protruding forward and is surrounded by gray ulcer. This bulge is formed by the back elastic membrane, hence the name "back elastic membrane bulge". This is because the posterior elastic membrane is tough and elastic, which can not only resist the destruction of inflammation, but also resist intraocular pressure. Because the posterior elastic membrane of the elderly is thicker than that of the young, the posterior elastic membrane of some elderly patients can last for several weeks. This situation is rare in young people and children, because it is often worn out by sudden increase of intraocular pressure such as cough, sneezing and eyelid spasm. If you don't check carefully, your eyelids will be separated strongly, and you will often wear them.
3. Corneal perforation When the cornea is perforated, the patient feels severe pain and tears (aqueous humor) flow out, but the original pain symptoms disappear; After perforation, aqueous humor overflows, first the anterior chamber becomes shallow or even disappears, then the iris and lens move forward to contact with the posterior wall of cornea, and the eyeball becomes soft. Although atropine was used to mydriasis in the past, it will become narrower at this time. After corneal perforation, the outcome is different according to the size and location of perforation.
4. If the perforation of anterior polar cataract is small and located in the central part of cornea, iris can begin to heal without prolapse. When the perforation is not blocked by enough fibrous exudate after aqueous humor flows out, the lens keeps in contact with the posterior corneal wall. When the anterior chamber is formed and the anterior capsule of the lens is out of contact with the posterior corneal wall, the surface of the anterior capsule and the subcapsular tissue in the central part of the lens have been permanently turbid, forming acquired epipolar cataract.
5. Iris prolapse If the perforation occurs far from the center of the cornea, the iris will inevitably block the hole. In larger perforations, the iris is pushed forward by the liquid in the posterior chamber, and so on. , into the hole. The detached part is usually brown-black at first, and soon fibrous exudate appears on its surface, similar to a gray-yellow hat covering the detached part, forming a part of iris detachment. At this time, the exudate is fused and fixed with the edge of the ulcer, so that the anterior chamber is isolated from the outside world. At this time, the anterior chamber quickly recovered and scars began to form. Iris prolapse gradually healed and gradually calmed down. The iris is always fixed at the perforation. Although it is clinically found to be corneal scar, in fact, part of the iris has also become scar. Sometimes the embedding is so small that it is almost invisible to the naked eye (if there are brown spots on the corneal leukoplakia, it means that the iris is embedded in the scar). Some scars are thick and self-contained, called corneal adhesion leukoplakia.
In a severely enlarged corneal ulcer, when the iris is prolapsed, all the iris and pupils move forward, occupying almost all of the corneal surface, which is called total iris prolapse. Although it is named like this, it is actually not the case, because the limbal part of the cornea will never be destroyed, and the pupil will be closed by fibrous exudate at the same time. When the cornea is perforated, the intraocular pressure suddenly drops, leading to the rupture and bleeding of the anterior segment. In a few patients, when the iris is completely detached, the lens or vitreous body is also detached. In severe cases, there may even be drainage bleeding.
Generally speaking, perforation is beneficial to corneal ulcer. After perforation, the ulcer not only stopped progressing immediately, but also began to improve. Except for highly toxic infection, suppuration rarely spreads to the inside, and rarely causes endophthalmitis or panophthalmitis.
The adhesion between iris and cornea is not limited to the iris adhesion area, because the iris is pulled forward, and its peripheral part and anterior chamber angle tissue also have peripheral anterior adhesion. This adhesion area may be very wide, affecting aqueous humor excretion and leading to secondary glaucoma.
6. Corneal staphyloma after corneal ulcer perforation and iris prolapse, normal intraocular pressure can make the detached iris protrude from the corneal surface. In the healing period, the scar that can be formed is fixed in place, which makes the normal corneal surface appear hemispherical or conical protrusions with gray color, which is called partial corneal staphyloma. This kind of lesion mostly occurs near the corneal edge, but the pupil is normal or only partially involved, and the vision is reduced and the intraocular pressure is not high.
If the detached iris is completely scarred and bulges into a hemispherical or conical shape, it is called complete corneal staphyloma. Its color varies according to the thickness of the scar, including grayish white, porcelain white or black and blue. When you are ill for a long time, you often see blood vessels with rough surface of grape swelling. In addition, the scar turned yellow because of hyalinization. Sometimes the staphyloma is highly prominent in the palpebral fissure, the surface looks like skin tissue, the color is red and dark, and the exposed cornea is dry, and the vision is only light or even dark. If the intraocular pressure decreases, the staphyloma shrinks and becomes completely smaller and flatter, which is called flat cornea. At this time, the eyeball shrinks and forms eyeball tuberculosis.
7. corneal fistula sometimes forms corneal fistula due to incomplete healing after corneal perforation. A small dark bulge appeared in the center of the white spot, while the anterior chamber disappeared and the eyeball became soft. At this point, the eyeball immediately compensates and increases the output of aqueous humor to maintain the normal hardness of the eyeball. If this swelling is sealed by a new membrane, the increase of aqueous humor will inevitably increase intraocular pressure and cause secondary glaucoma. If the intraocular pressure continues to rise, it can cause the symptoms of acute glaucoma, and when this membrane breaks through, the symptoms disappear immediately and the eyeball becomes soft again. But soon after, the fistula was closed by a new membrane and the intraocular pressure increased again. Repeatedly, severe bacterial infection will eventually lead to endophthalmitis, panophthalmitis or intraocular bleeding, and finally eyeball atrophy. It also ended because of long-term softening of eyeball, flattening of cornea, opacity of lens and even retinal detachment.
Corneal fistula is not a fistula, but loose tissue embedded in corneal perforation, and aqueous humor seeps from the fissure. Corneal fistula is most likely to occur in patients whose pupil edge is embedded in corneal perforation area. Aqueous humor often extravasates along the pupil edge, and epithelial cells are not easy to repair. Therefore, the main symptoms of corneal fistula's disease are dark protrusion on the corneal surface, disappearance of anterior chamber and softening of eyeball. In addition, it can also be proved by fluorescence staining.
8. Formation of corneal blood vessels Corneal inflammation is often accompanied by vascular proliferation, mostly reticular, which occurs at the corneal margin near the ulcer. These are superficial blood vessels, but deep ulcers also have deep blood vessels. At first, the blood vessels radiate to the ulcer,
When the ulcer begins to heal, it will widen. This is extremely important for the healing of ulcers. But sometimes ulcers heal without vascular proliferation. Blood vessels gradually disappear after ulcer healing, but some will never disappear, especially when there is anterior synechia of iris.
Sometimes blood vessels are accompanied by inflammation, similar to exudate, which enters the cornea and is seen in corneal parenchymal inflammation and pannus. Determining the location of blood vessels is very important for differentiating keratitis and can often be used to diagnose the types of keratitis.
The new blood vessels can come from the vascular network at the corneal limbus or the blood vessels deeper at the corneal limbus. The former is a shallow blood vessel directly connected with conjunctival blood vessels, which is generally curved like a river, while the latter is a brush-like or broom-like deep blood vessel, which is not connected with conjunctival blood vessels and ends at corneal limbus.
Treatment: The basic principle of treating corneal ulcer is to take all effective measures to quickly control infection, strive for early cure and reduce the sequelae of keratitis to a minimum. Because most of ulcerative keratitis is caused by external factors, it is extremely important to remove external factors and eliminate pathogenic microorganisms. In order to help the etiological diagnosis, smear, bacterial culture and drug sensitivity test (mold culture if necessary) should be taken from the progressive edge of corneal ulcer. But don't delay treatment by waiting for the test results, and take necessary measures immediately. The treatment process, precautions and usage are as follows:
1. Hot compress: dilate eye blood vessels, relieve stagnation, promote blood flow, enhance resistance and nutrition, and make ulcers recover quickly.
2. Flushing If there are many secretions, the conjunctival sac can be flushed with normal saline or 3% boric acid solution three times or more a day to flush out secretions, necrotic tissues, bacteria and toxins produced by bacteria. This not only reduces the factors of infection expansion, but also ensures that the local drug concentration will not decrease.
3. mydriasis:
Methatropine is the main commonly used drug, and its concentration is 0.25 ~ 2% solution or ointment, and it is dripped 1 ~ 2 times a day (after dripping, pay attention to pressing the lacrimal sac to avoid poisoning caused by excessive absorption of the solution by mucosa).
B can be used for simple corneal ulcer or those whose irritation symptoms are not obvious, but it must be used for ulcers with obvious irritation symptoms and potential perforation. This medicine has a dual effect on the treatment of corneal ulcer: on the one hand, it can rest the pupil sphincter and ciliary muscle, on the other hand, it can prevent and treat iridocyclitis and its consequences. Furthermore, because the muscle spasm in the eye is relieved, it also has the effect of relieving and relieving pain.
4. Microbial preparations:
10 ~ 30% sulfonamides such as sodium sulfacetamide and 4% sulfaisoxazole eye drops.
B. For the infection of Gram-positive cocci, 0. 1% rifampicin eye drops, 0.5% erythromycin or 0.5% bacitracin eye drops can be controlled four to six times a day. Some broad-spectrum antibiotics, such as 0.5% chlortetracycline, 0.25% chloramphenicol and 0.5% tetracycline (0.5%), are more effective.
C 1 ~ 5% streptomycin, 0.3 ~ 0.5% gentamicin, polymyxin b(20000 units /ml), 0.25 ~ 0.5% neomycin and 0.5% kanamycin can be selected for the infection of gram-negative bacilli.
D. For the ulcer with serious illness whose bacterial culture and drug sensitivity test results are unknown, a variety of broad-spectrum antibiotics can be tried at the beginning, and 1 drop is alternately dropped every few minutes or 1 minute, and then reduced as appropriate. In addition, subconjunctival injection, 1 time, daily 1 time, can also be used for several days until the ulcer symptoms subside. Conjunctival necrosis sometimes occurs after subconjunctival injection of some drugs, which should be paid attention to.
E antiviral drugs are 0. 1% herpes simplex, etc. The antifungal agents are nystatin (25,000 units/ml), 0. 1% amphotericin b, 0.5% trichostatin and 0.5% pitamycin.
5. Bandages and dressings:
A. In order to prevent eyeball rotation and promote early healing of ulcer, it must be wrapped. . This therapy is especially suitable for winter. Because it can not only prevent the eyeball from catching cold, but also has the function of hot compress and protection.
B. If there is secretion in the conjunctival sac, it should not be bandaged. Buller eye patch or black glasses can be used instead. Furthermore, if the ulcer is likely to break through or bulge during the scarring period, it should be bandaged with a pressure bandage every day. If it is impossible during the day, it should be used at night to save the bad consequences.
6. Etiology treatment:
A. While treating corneal ulcer, we must pay attention to the causes of ulcer and treat it.
B. The most important thing to pay attention to is conjunctival diseases and malnutrition. For example, trachoma pannus ulcer is rarely cured if trachoma is not treated at the same time. Another example is keratomalacia. If you don't pay attention to the whole body nutrition and supplement vitamin A, it will not be cured, but will be aggravated.
7. Stimulation therapy: When the ulcer has completely healed and started to scar, try to make the scar as thin as possible.
For small, dense and central corneal leukoplakia, iridectomy can be performed to improve vision. For larger leukoplakia, corneal transplantation can be performed. Sometimes corneal leukoplakia is unsightly, soot and China ink stick can be used as corneal ink needle surgery.
8. Treatment of corneal ulcer complicated with diseases:
A. Emergency measures should be taken for corneal ulcer about to be perforated. Put the patient in bed, give laxatives and acetazolamide to reduce intraocular pressure, and guide the patient to avoid sneezing or coughing and other sudden increases in intra-abdominal pressure.
B. If corneal ulcer is perforated, it will not only tend to heal, but also increase corneal nutrition. In order to achieve this goal, artificial anterior chamber puncture can also be used. This can not only make aqueous humor flow out slowly, but also avoid the adverse consequences of ulcer itself, such as iris prolapse or lens prolapse. In addition, anterior chamber puncture can also stop the severe pain of the eyeball. If puncture is performed at the bottom of the ulcer, it can be covered with conjunctival flap. Iris prolapse can be treated by iridectomy.
C for patients with corneal fistula, cautery should be performed, and at the same time, anti-glaucoma surgery and conjunctival flap covering corneal fistula method should be performed.
D.β rays can inhibit the growth of corneal blood vessels. In addition, exogenous protein therapy and traditional Chinese medicine therapy can enhance systemic resistance and promote the healing of keratitis.
Corneal ulcer has strict classification in clinic, and it is difficult to adapt to its different clinical processes. This article only classifies them according to their etiology and clinical manifestations, and summarizes their symptoms and treatments in order to give readers a clear concept.
Non-ulcerative keratitis
Corneal parenchymal inflammation refers to diffuse inflammation in corneal parenchyma. Most of them are manifestations of antigen-antibody reaction, such as congenital syphilitic keratitis. But it can also be seen in tuberculosis, viruses and some mold infections. The following is only about congenital syphilitic keratitis.
The cause is generally considered to be allergic reaction, that is, antigen-antibody reaction caused by Treponema pallidum in cornea. Most of them are 5-25 years old, with more women than men. At the same time, other symptoms of congenital syphilis can be seen, such as forehead protrusion, saddle nose, broad face, deafness, Hutchinson's teeth, cleft palate, cervical lymph node enlargement, tibial periostitis and so on. In addition, according to the history of acquired syphilis and parents' abortion, as well as syphilis seropositivity, it is also helpful for diagnosis. This disease is usually a binocular disease, sometimes at the same time, but it is often one after another, sometimes several years apart, and it is easy to recur.
Subjective symptoms of clinical manifestations include pain, shame, tears, blurred vision, and even light perception in severe cases. The disease is mostly chronic, and corneal endothelial edema and a small amount of fine deposits can be seen under slit lamp at the earliest stage. There is slight cell infiltration in parenchyma. With the appearance of symptoms, patients may have blepharospasm and ciliary congestion.
Corneal lesions can start from the peripheral or central part of the cornea. But the former is more common.
From the periphery, the corneal edge darkens first, and there is slight turbidity, which starts from the top of the cornea and gradually expands to the center. This turbidity lives in the deep layer and is grayish white. Epithelial edema may form blisters. The adjacent ciliary vessels immediately became congested and began to develop inward from the corneal edge. The corneal limbus is swollen due to edema, which looks like an officer's epaulettes called epaulettes pannus. When the edema around the cornea subsided, the ciliary vessels quickly disappeared. But the deep blood vessels at the limbus of cornea extend to the center of cornea, which seems to push the opacity forward. These blood vessels live in the deep layer of cornea, which are typical brush-like or broom-like, straight and parallel, and do not match. It can last for more than ten years and eventually harden. At the same time, similar opacity appeared in other parts of the corneal limbus and developed towards the center. This diffuse opacity develops rapidly and widely, so that the whole cornea darkens and loses its luster. If examined by slit lamp, corneal edema becomes thicker; The dark gray opacity of the cornea is snowflake-like, tiny points or lines. It reached its peak after 2 ~ 4 weeks. At this time, the corneal surface is cloud-like, very similar to ground glass. In severe cases, the cornea is extremely turbid, and even the iris is completely covered and invisible. This progress period can also be extended for several months to reach its peak.
From the center, it first invades the middle of the cornea, and gray snowflake, punctate or linear opacity appears in the deep layer of the cornea. The corneal surface is smooth and dark, with no light reflection, and the opacity gradually increases, progressing from the center to the periphery, and finally reaching the edge, making the cornea completely turbid. Even so, the central part is still denser than the peripheral part. When the opacity reaches the edge, blood vessels begin to enter the limbus from all directions. These are deep blood vessels, which are brush-like or broom-like. When the inflammation reaches its peak, the cornea is completely turbid. Because the deep layer of cornea is covered with blood vessels and covered by gray opacity of cornea, it is uniformly dirty red, such as red cloth. At this time, it is difficult to see the iris tissue, and at the same time, the vision drops to pre-exponential or manual. The peak of inflammation takes about 2 ~ 4 months to enter the regression period. The opacity first subsided from the corneal edge, the cornea gradually returned to transparency, and the blood vessels became thinner or even occluded. Only the opacity in the middle lasts the longest and finally subsides, leaving only a small amount of mild opacity and some deep blood vessels, which has little effect on vision. After many years, the patient can still be diagnosed with this disease according to the deep corneal opacity and brush blood vessels left behind. It will take half a year or even a year or more for the return period to end.
The above clinical course does not represent the course of all cases, and some cases are mild, and the turbidity is not only less, but also completely subsides after a short course; But there are also serious cases, and the turbidity does not fade; It even becomes soft, and due to eyeball pressure, the cornea expands, causing irregular astigmatism, which greatly affects vision. Sometimes, in the worst case, the cornea becomes flat, and sometimes the vision is completely lost.
Irisocyclitis is a common complication, which is characterized by iris congestion, corneal endothelial edema, posterior elastic layer deposition and wrinkles. In severe cases, posterior iris adhesion, pupillary membrane closure or plastic iridocyclitis can occur, and finally eyeball atrophy can be seen.
Intraocular pressure generally decreases, and in the late stage of the disease, intraocular pressure may increase and secondary glaucoma may occur, resulting in corneal dilatation. Sometimes suffering from peripheral choroiditis. This kind of inflammation is naturally invisible when the cornea is completely turbid. However, when the pupil is dilated at the end of the disease, most of the melanin spots can be seen in the peripheral part, and sometimes peripheral choroiditis can be seen when the other eye is not inflamed. The prognosis of this disease is good, and most patients can recover useful vision.
treat cordially
1. Treat according to the cause, such as expelling plum.
2. The application of corticosteroid local drip or subconjunctival injection can obtain obvious curative effect, which can not only improve symptoms quickly, but also inhibit the development of the disease and the invasion of blood vessels and promote the absorption of lesions. External use of 0.5% cortisone eye drops 4 ~ 6 times a day, or 0. 1% flumethasone eye drops 4 times a day. The frequency of subconjunctival injection can be determined according to the severity of the disease. If necessary, it can be injected once every other day, with 0.3 ml each time.
3. Others include local hot compress, mydriasis, systemic support therapy, oral vitamin or heterosexual protein therapy. When the intraocular pressure increases, acetanilide can be added to reduce the intraocular pressure. In order to obtain the maximum corneal transparency in the process of regression, irritating drugs such as mercuric chloride ointment and dionin solution can be used. Pericorneal threading therapy can also be used in the regression period to promote the absorption of turbidity.
4. When the turbid spots left in the central part of the cornea after surgical treatment persist after two years of treatment and have a great impact on vision, penetrating keratoplasty can be used.
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