There are two types of keratitis: ulcerative keratitis, also known as corneal ulcer, and non-ulcerative keratitis, or deep keratitis. It is caused by different factors such as internal and external causes. Inflammation caused by corneal trauma, bacterial and viral invasion of the cornea. The affected eye has a foreign body sensation, stinging pain or even burning sensation. Mixed congestion on the surface of the bulbar conjunctiva with photophobia, lacrimation, visual impairment and increased secretion. The corneal surface is infiltrated with ulcer formation. Ulcerative keratitis, also known as corneal ulcer, is overwhelmingly caused by exogenous factors, i.e. inflammation that occurs when infectious agents invade the corneal epithelial cell layer from outside.
Etiology
I. Exogenous factors
Most corneal infections due to exogenous factors require two conditions.
a. Damage to corneal epithelial cells, shedding.
b. Co-infection at the same time. Only when these two conditions are present, infectious corneal ulcers are likely to occur.
Second, the endogenous cause
This refers to endogenous disorders from the whole body. The cornea has no blood vessels, so acute infectious diseases do not easily invade the cornea. However, corneal tissue is involved in the immune response of the whole body, although the degree of immune response is lower than that of other tissues, but because it is not vascular, metabolism is more sluggish, so that this immune response changes for a long time, the cornea is in a sensitive state for a long time, so it is easy to occur metabolic disorders, such as vesicular keratitis.
Third, the spread of neighboring tissues
Because of the embryological homologation and anatomical continuity, most of the disorders that spread to the corneal epithelium come from the conjunctiva, such as severe conjunctivitis combined with superficial keratitis.
Course of disease
I. Initial inflammation
When the inflammation first starts, there is more or less irritant and mobile cell formation infiltration in the corneal tissue, while the corneal tissue is filled with fluid, thus the affected area is swollen and cloudy, and sometimes even higher than the surface, which is called the corneal infiltration stage.
Second, corneal infiltration
Corneal infiltration: its main symptom is grayish-yellow cloudy, cloudy, lusterless, and higher than the surface of the cornea.
Third, progressive corneal ulcer
Progressive corneal ulcer:The progressive end of corneal infiltrate has two.
a. The infiltrate is absorbed. When the corneal infiltration has not yet reached its peak, the inflammatory phenomenon is subsided, the corneal luster is restored, completely transparent (this end is not common in the clinic).
b. Infiltrate suppuration. In general, the corneal tissue is lysed immediately after infection, and the epithelium and even the superficial parenchyma are shed due to necrosis, resulting in the formation of an ulcer. The edges of the ulcer are initially cloudy, followed by further deterioration in and around the middle of the ulcer. The ulcer has a gray base, is not flat, and has indistinct margins, which is known as an unclean or progressive ulcer. When progressive, the ulcer may extend to one side or the periphery; it may also progress to the deeper layers, or to the periphery or deeper layers simultaneously. This is the case with gonorrheal corneal ulcers, for example, which progress not only to the periphery of the cornea, but also to the deeper layers, penetrating the cornea and even destroying the cornea in its entirety.
Fourth, degenerative corneal ulcers
Degenerative corneal ulcers: The most common corneal ulcer is a partially necrotic, partially detached corneal ulcer, with the undetached portion connected only to the center of the base. This condition indicates that toxins are concentrated in the middle of the ulcer, which has been surrounded by multinucleated leukocytes at the periphery. These leukocytes phagocytose the bacteria and lyse the necrotic tissue. At this point, the epithelial cells surrounding the ulcer progress rapidly toward the center of the ulcer, and the epithelial cells proliferate and extend very rapidly (usually fully recovered within 24 hours of scraping the corneal epithelium), while the necrotic portion of the ulcer continues to shed until the cloudiness of the ulcer gradually decreases and disappears. The base of the ulcer and its margins tend to smooth out, clear, and enter the clean phase. This is the degenerative stage.
V. Corneal scar
Corneal scar: When the corneal ulcer reaches the clean stage, the connective tissue in the cornea proliferates and repairs the defect, the ulcer heals and a scar is formed. In cases where the ulcer is small and shallow involving only the epithelial cell layer, the cornea can be completely clear again. If the anterior elastic membrane and superficial layers of the corneal parenchyma are involved, a dense, cloudy scar remains. The clouding is initially dark and then increases in intensity, but never crosses the ulcerated edge. The disappearance of corneal scarring is limited to mammary children, which is not possible at older ages and inevitably leaves a permanent scar that causes visual impairment. After the scar has begun to form and the destroyed portion has not fully recovered its original curvature, but the fluorescein is no longer staining, a small depression forms in the cornea called the microsurface. Eventually the small surface disappears and the cornea regains its normal curvature. In some cases, however, the corneal microsurface remains permanently intact. The size and thickness of the corneal scar varies according to the severity of the ulcer. The thin ones are cloudy and shallow, called corneal clouding, the slightly thick ones are called corneal opacities, and the thickest and densest ones are called corneal white spots.
Classification
Keratitis is the growth of a “white star” on the black eye, the patient feels pain, fear of light and tears, vision loss. There are many types of keratitis, and their naming and classification are complex. There are classifications based on the anatomical location of the inflammation, the shape of the inflammation, and the presence or absence of ulcers and internal and external causes, but none of them can include all clinical types.
The following methods of classification by etiology are described.
(1) viral keratitis: the most common is herpes simplex keratitis, caused by herpes simplex virus; followed by herpes zoster keratitis, cowpox vaccine keratitis and punctate keratitis caused by adenovirus; and trachoma virus-induced keratitis.
(2) bacterial keratitis: the common bacteria that cause this disease are S. pneumoniae, Staphylococcus, Streptococcus, etc. Due to the strong virulence of bacteria, rapid progress, often causing acute purulent corneal ulcers, clinically known as “creeping corneal ulcers”; followed by corneal ulcers caused by Pseudomonas aeruginosa.
(3) fungal keratitis: the common causative fungus is Aspergillus, followed by Fusarium. Because of the early symptoms of this disease is light, slow development, often misdiagnosed, the formation of corneal ulcers, the ulcer surface is toothpaste-like or tongue-like appearance for its characteristics.
(4) Allergic keratitis: caused by congenital and allergic factors, including fascicular keratitis, deep keratitis, sclerosing keratitis, and parenchymal keratitis.
(5) Traumatic and trophic keratitis: including corneal epithelial detachment, corneal chondromalacia, neuropathy keratitis and exposure keratitis.
(6) Keratitis of unknown etiology: including erosive corneal ulcer, coiled filiform keratitis and punctate corneal epithelial exfoliation.
Symptoms
With the exception of paralytic keratitis, most patients with keratitis have intensely inflammatory symptoms such as pain, shyness, lacrimation and blepharospasm. This is due to inflammatory stimulation of the trigeminal nerve endings in the cornea, which causes reflex contraction of the orbicularis oculi and excessive tear production. The cornea is a non-vascular tissue, but the adjacent areas are rich in blood vessels (corneal limbus and iris-ciliary body vessels), and when inflammation involves the adjacent tissues, there is congestion and inflammatory exudation. Thus, patients with keratitis have not only ciliary congestion, but also iris congestion. The latter manifests as iris discoloration and pupil narrowing.
The exudate comes from the same source. In severe patients, the bulbar conjunctiva and even the eyelids become edematous. Corneal infiltration occurs due to the movement of leukocytes toward the corneal lesion as a result of congestion at the corneoscleral rim. When corneal inflammation reaches the regressive stage, the clinical irritation is greatly reduced.
Corneal inflammation inevitably affects vision to a greater or lesser extent, especially if the inflammation invades the pupil area. The corneal scar formed after the ulcer heals not only prevents light from entering the eye, but also changes the curvature and refractive power of the corneal surface, so that objects cannot be focused on the retina to form a clear image, thus reducing visual acuity. The extent of visual acuity depends on the location of the scar, which may be small but may have a significant impact on vision if it is located in the middle of the cornea.
Complications
I. Anterior chamber pus accumulation
Severe cases are often combined with iridocyclitis. This is called anterior chamber pus due to the clouding of the anterior chamber water by leukocytes exuding from the iris ciliary body and depositing in the lower part of the anterior chamber angle. It is horizontal because it is liquid. When the head is tilted, the fluid gradually changes direction to the lower part. The amount of pus in the anterior chamber is highly variable, with only a yellow crescent-shaped line in the lower corner of the anterior chamber in mild cases, or filling the anterior chamber in severe cases. The pus in the anterior chamber may be completely absorbed (the thinner it is, the more easily it is absorbed). The fibrous exudate may form connective tissue, producing anterior or posterior adhesions around the iris and even atresia of the pupil. The posterior corneal wall has deposits in those with ciliary involvement.
Second, posterior elastic membrane bulge
Because corneal ulcers can progress to a deeper level, when the cornea is about to perforate, a thin layer of clear tissue may appear at the base of the ulcer, shaped like a “black” vesicle protruding forward, surrounded by a gray ulcer. This bulge is formed by the posterior elastic membrane, hence the name posterior elastic membrane bulge. This is because the posterior elastic membrane is tough and elastic, which not only resists damage from inflammation, but also resists intraocular pressure. Because the posterior elastic membrane is thicker in older people than in younger people, posterior elastic membrane bulges can persist for several weeks in some older patients. This is rarely seen in young and young children, as it is often punctured by transient increases in intraocular pressure such as coughing, sneezing, or eyelid spasm. It is also common for the eyelid to be punctured by forceful separation during examination.
Corneal perforation
When the cornea is perforated, the patient feels severe pain and hot tears (atrial fluid), but the original painful symptoms disappear; after the perforation, the atrial fluid overflows, first the anterior chamber becomes shallow or even disappears, then the iris and lens are displaced forward and come into contact with the posterior wall of the cornea, and the eye becomes soft. The pupil narrows at this point, although it has been dilated with atropine in the past. After corneal perforation, the outcome varies according to the size and location of the perforation.
IV. Anterior pole cataract
If the perforation is small and located in the central part of the cornea, the iris may begin to heal without detachment. When the atrial water flows out and the perforation is not yet blocked by thick enough fibrous exudate, the lens is in continuous 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 anterior capsule surface and subcapsular tissues in the central part of the lens have become permanently clouded, forming an acquired anterior pole cataract.
V. Iris detachment
If the perforation occurs far from the central cornea, the iris is bound to block the ruptured hole. In larger perforations, the iris is pushed forward by the fluid from the posterior chamber, etc., into the rupture hole and prolapses. Initially, the prolapsed portion is often brownish-black, and soon a fibrous exudate forms on its surface, resembling a small grayish-yellow cap, covering the prolapsed portion and forming a partial iris prolapse. At this point the exudate fuses with the edge of the ulcer and fixes it, isolating the anterior chamber from the outside world. At this point the anterior chamber rapidly recovers and scarring begins to form. The iris prolapse gradually heals and tapers off. The iris is permanently fixed within the perforation. Although the clinical picture is of a corneal scar, part of the iris actually becomes scarred as well. Sometimes the embedding is so minimal that it cannot be seen with the naked eye (if a brownish-yellow pigmented spot is found on the corneal white spot, this indicates that the iris is embedded within the scar). In some cases, the scar is thick and self-limiting, and this is called a corneal adhesion leukoplakia.
In severely enlarged corneal ulcers, when the iris is prolapsed, the entire iris, along with the pupil, is pushed forward, occupying almost all of the corneal surface, which is called total iris prolapse. Despite this name, this is not actually the case, as the limbus is never destroyed and the pupil is closed by fibrous exudate at the same time. When the cornea is perforated, there is a sudden drop in intraocular pressure, which ruptures the anterior segment vessels of the eye and hemorrhage occurs. In a small number of patients, the lens or vitreous comes out when the iris is completely detached. In severe cases, even expulsive hemorrhage may occur.
Generally speaking, perforation is beneficial for corneal ulcers. Not only does the ulcer stop progressing immediately after perforation, but it begins to heal. Except for very virulent infections, sepsis rarely extends to the interior and rarely causes endophthalmitis or total ocular septicemia.
The iris-corneal adhesions are not limited to the area of iris adhesions; as the iris is pulled forward, peripheral anterior adhesions with the anterior chamber angle tissue also occur. This adhesion area may be so wide that it affects atrial aqueous drainage, resulting in secondary glaucoma.
Sixth, corneal chylomicron
After corneal ulcer perforation and iris detachment, normal intraocular pressure is sufficient to cause the detached iris to protrude from the corneal surface. During the healing period, the scar can be fixed in place, so that there is a half spherical or conical bulge on the normal corneal surface, which is gray in color, called partial corneal staphyloma. This lesion mostly occurs near the edge of the cornea, while the pupil is normal or only partially involved, with reduced visual acuity and no high intraocular pressure.
If the detached iris is completely scarred and bulges into a hemisphere or cone, it is called a complete corneal staphyloma. The color varies according to the thickness of the scar, and can be grayish white, porcelain white, or blackish blue. In older cases, rough blood vessels are often seen on the surface of the staphyloma. In addition, the scar may turn yellow due to glassy degeneration. Sometimes the staphyloma is highly protruding from the lid fissure, the surface resembles skin tissue, is red and dark, and there is exposed corneal dryness, and vision is only light perception or even blackness. If the pressure in the eye decreases, the staphyloma shrinks and becomes completely small and flat, known as a flat cornea. At this point, the eye shrinks and forms a consumption of the eye.
VII. Corneal fistula
Sometimes corneal fistulas are formed after incomplete healing of a corneal perforation. In the center of the white spot at the rupture, a small, dark black bulge appears, while the anterior chamber disappears and the eye becomes soft. The eye immediately compensates by increasing atrial aqueous production in order to maintain the normal hardness of the eye. If this bulge is closed by the new membrane, the increased atrial aqueous production will gradually increase the intraocular pressure and cause secondary glaucoma. If the pressure continues to rise, the symptoms of an acute glaucoma attack can be caused, and the membrane breaks through, the symptoms disappear, and the eye becomes soft again. However, soon after the fistula is closed again by the new membrane, and the IOP increases again. Eventually, endophthalmitis, full-blown septicemia, or intraocular hemorrhage occurs due to fierce bacterial infection, and the eye eventually atrophies. It also ends with long-term softening of the eye, flattening of the cornea, clouding of the lens, and even retinal detachment.
A corneal fistula is not a fistula, but rather a loose tissue embedded in the corneal rupture, from which the atrial fluid exudes. Corneal fistulas are most likely to occur in patients whose pupillary rim is embedded within the area of the corneal perforation. The atrial fluid often exudes along the pupil margin, and the epithelium is not easily repaired. The main signs of a corneal fistula are a dark black bulge on the corneal surface, loss of the anterior chamber, and a softening of the eye. In addition, fluorescent staining can be used to demonstrate.
Eight, the 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. Initially, the vessels advance radially toward the ulcer and then widen as the ulcer begins to heal. This is extremely important for the healing of the ulcer. However, sometimes ulcers heal without vascularization. The vessels gradually disappear after the ulcer heals, but they may never disappear, especially in the presence of preiris adhesions.
Sometimes the vessels are accompanied by inflammation, resembling exudate, into the cornea, as seen in parenchymal keratitis and corneal vascular opacification. Determining the location of the vessels is important in identifying keratoconus, and can often be used to diagnose the type of keratitis.
The former are superficial vessels that are directly connected to the conjunctival vessels, usually in the form of curved rivulets, while the latter are deep vessels that are brush or broom-shaped, not connected to the conjunctival vessels, and terminate at the corneal limbus.
Treatment
I. Methods
The basic principle of treating keratoconjunctival ulcers is to take all effective measures to control the infection rapidly, to strive for early cure, and to minimize the sequelae of keratitis. Since most ulcerative keratitis is due to external causes, it is extremely important to remove the causative external causes and eliminate the causative microorganisms. To help diagnose the cause, a smear should be taken from the proceeding edge of the corneal ulcer for bacterial culture and drug sensitivity testing (and mycobacterial culture if necessary). However, do not delay treatment by waiting for the test results, but take the necessary measures immediately. The treatment process, precautions and application methods are described as follows.
1.Heat compress
Make the eye blood vessels dilate, release congestion, while promoting blood flow, enhance resistance and nutrition, so that the ulcer can be rapidly recovered.
2.Rinsing
If there are more secretions, saline or 3% boric acid solution can be used to flush the conjunctival sac 3 or more times a day in order to flush out secretions, necrotic tissues, bacteria and toxins produced by bacteria. This will not only reduce the factors of infection expansion, but also ensure that the concentration of the topical medication is not diminished.
3. Pupil dilatation
a. Atropine is the main and commonly used drug, with a concentration of 0.25-2% solution or ointment, applied 1 to 2 times a day (pay attention to pressing the tear sac after the drops to avoid excessive absorption of the solution by the mucous membrane, causing poisoning).
b. It can be used for simple corneal ulcers or those with insignificant irritation symptoms, but must be used for ulcers with significant irritation symptoms and potential perforation. This drug has a dual role in the treatment of corneal ulcers; on the one hand, it rests the pupillary sphincter and ciliary muscles, and on the other hand, it prevents and treats iridocyclitis and its consequences. Furthermore, as the intraocular muscle spasm is released, it also has a relieving and pain-relieving effect.
4.Bacterial agents
a. Sulfonamide chemical agents such as 10-30% sodium sulfacetamide and 4% sulfisoxazole eye drops.
b. For gram-positive coccus infection, topical drops of 0.1% rifampicin ophthalmic solution or 0.5% erythromycin or 0.5% bacitracin ophthalmic solution 4 to 6 times daily are sufficient to control. Some broad-spectrum antimicrobials such as 0.5% chlortetracycline, 0.25% chloramphenicol and 0.5% tetracycline (0.5%) are more effective.
c. For Gram-negative bacillus infection, 1-5% streptomycin, 0.3-0.5% gentamicin, polymyxin B (20,000 units/ml), 0.25-0.5% neomycin, 0.5% kanamycin, etc. can be used.
d. For ulcers in which the results of bacterial culture and drug sensitivity tests are not yet known and the disease is more serious, a variety of broad-spectrum antimicrobials can be tried simultaneously at the beginning, alternating with one drop every few minutes or one quarter hour, and then decreasing as appropriate. In addition, subconjunctival injection can also be used as a route of administration, once a day, and for several days until the ulcer symptoms subside. Conjunctival necrosis sometimes occurs after subconjunctival injection of some drugs, which should be noted.
e. Anti-viral drugs such as 0.1% herpes net. The anti-mycotic agents are mycobacterium (25,000 units/ml), 0.1% dicloxacillin B, 0.5% trichostatin and 0.5% pimaricin, etc.
5.Wrapping and dressing
a. In order to stop the rotation of the eye and promote the early healing of the ulcer, wrapping must be carried out. This treatment is especially suitable for winter. Because it not only makes the eye not to be cold, but also happens to be hot and protective role.
b. If there is a discharge from the conjunctival sac, it should not be wrapped, but can be replaced by Buller’s (Buller’s) eye patch or dark glasses. Furthermore, if the ulcer is about to penetrate, or is about to bulge during the scarring period, a compression bandage should be applied daily, or if daytime is not possible, it should be used at night during sleep to save the adverse consequences.
6.Etiological treatment
a. While treating corneal ulcers, the cause of the ulcer must be noted and treated.
b. The most important thing to pay attention to is conjunctival disease and malnutrition. For example, trachoma vascular opacity ulcer, if not treated at the same time trachoma, ulcer is difficult to heal. Another example is corneal softening. If we don’t pay attention to the whole body nutrition and replenish vitamin A, not only the corneal softening will not be healed, but also will be worsened.
7.Stimulation therapy
When the ulcer has completely healed and scarring has begun, efforts should be made to make the scar form as thin as possible. For small, dense and centrally located corneal leukoplakia, augmentation iridectomy can be performed to improve vision. For larger white spots, corneal transplantation can be performed. Sometimes the corneal white spot is an eyesore, soot and Chinese ink can be used for corneal ink needle surgery.
Second, the corneal ulcer co-morbidity therapy
a. Emergency measures should be taken for corneal ulcers that are about to be perforated. Make the patient bedridden, give light laxatives and acetazolamide and other drugs that lower intraocular pressure, and instruct the patient to avoid sneezing or coughing and other actions that suddenly increase intra-abdominal pressure.
b. If a corneal ulcer is perforated, not only does the ulcer tend to heal, but also increases corneal nutrition. For this purpose, artificial anterior chamber perforation can also be performed. This not only allows for a slow outflow of atrial fluid, but also avoids the undesirable consequences of the ulcer piercing itself, such as iris prolapse or lens prolapse. Furthermore, anterior chamber puncture has the effect of stopping severe pain in the eye. If an anterior chamber puncture is performed at the base of the ulcer, it can be covered by a conjunctival flap. Iridotomy can be performed in cases of iris prolapse.
c. For patients with corneal fistula, cautery should be performed, along with antiglaucoma surgery and conjunctival flap masking of the corneal fistula.
d. Beta radiation can inhibit the growth of corneal blood vessels. In addition, allogeneic protein therapy and herbal treatment can enhance systemic resistance and promote healing of keratitis.
It is difficult to use a strict clinical classification of corneal ulcers to accommodate their varied clinical course. Today only according to the pathogenic point of view combined with the clinical manifestations of the classification, and an overview of its symptoms and treatment, in order to enable the reader to get a clear concept.
Viral keratitis is a disease caused by a virus.
The most common forms of keratitis are herpes simplex virus keratitis and herpes zoster virus keratitis, which seriously endanger visual function. Herpes zoster is characterized by the appearance of beads on the skin along the area of distribution of the trigeminal nerve terminals, mostly limited to the area of distribution of the first branch of the trigeminal nerve, with skin lesions not exceeding the midline of the body. This disease is mostly caused by low cellular immune function, cold and fatigue as its triggers, so it is necessary to strengthen exercise and enhance physical fitness. This disease is equivalent to the category of “poly-synovitis” in Chinese medicine. The disease is mostly caused by external wind-heat, wind-heat upward offense; or wind-cold offense to the eyes; or liver fire; or phlegm, water, dampness and heat contain steam and Yin deficiency evil stay.