Spotted dark gray opacities on the cornea

Introduction Due to corneal opacity, there is a point-like dark gray turbidity on the cornea. The cornea is a transparent tissue with avascular structure. Transparency is the greatest feature of corneal tissue and is an essential element of its physiological function. Once it is affected by trauma or harmful factors, its transparency is lost and turbidity can cause visual impairment. The transparency of the cornea is primarily dependent on the optical consistency of its tissue structure. Therefore, the integrity of the epithelium and endothelium, the alignment of the corneal stroma plate, the proper water content of the corneal tissue, and the avascular tissue of the cornea can maintain its transparency. Therefore, if some factors undermine the above basic conditions, corneal opacity can be caused. For example, inflammation leads to cell infiltration or opaque substance deposition, excessive moisture infiltrates into the corneal parenchyma through the damaged corneal endothelium, and corneal neovascularization or scar tissue caused by certain lesions destroys the regularity of the corneal plate and epithelial arrangement.

Cause

1. Congenital.

2. Infectivity. Including keratitis caused by bacteria, fungi, viruses, corneal ulcers.

3. Traumatic. Corneal perforation, contusion, blast injury, chemical burn, hot burn, etc.

4. Allergic reactivity. Such as vesicular keratitis.

5. Denaturation or malnutrition. Such as corneal old ring. Corneal band degeneration, lattice dystrophy, corneal softening, etc.

6. Scarring. Corneal cloud, leukoplakia, adhesion blood spots, corneal staphyloma and so on.

7. Corneal tumors. The originator is rare, and most of it originates from the conjunctiva or limbus.

8. Others. Corneal opacity is one of the signs of other eye diseases. Such as corneal edema, corneal depression, corneal neovascularization. Corneal blood staining, Keyier (Kayser-Fleischer referred to as KF ring) pigment ring, pterygium and so on.

an examination

Related inspection

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Corneal opacity is generally seen by visual inspection. Lighter like a veil, the screen is slightly foggy, and the heavy one is magnetic white. However, very slight turbidity needs to be checked by special inspection. Corneal opacity can be all or limited. As long as turbidity is found, its properties should be further understood.

First, medical history

To understand the eye, time of onset, and detailed symptoms. Such as corneal opacity with redness, shame, tearing, pain, vision loss is the characteristics of corneal inflammation. If there is a history of trauma, you should ask about the specific circumstances of the injury, such as crop wounds, it may be a fungal infection. With a history of corneal foreign body removal, corneal ulcers progress rapidly, pay attention to Pseudomonas aeruginosa infection. If the cornea is mostly opaque, has no irritation and has a family history, there is a possibility of corneal degeneration. Has a history of trauma or keratitis, no irritating symptoms, only visual impairment, it may be a corneal scar.

Second, physical examination

Some corneal lesions are caused by other diseases of the body. Such as a cold can cause rash keratitis, herpes zoster can spread to the cornea, malnutrition in infants and young children due to vitamin A deficiency can cause corneal softening. Therefore, we should pay attention to the whole physical examination, which is conducive to diagnosis.

Eye examination: Corneal lesions can be examined with a 10x magnifying glass with a flashlight. Detailed lesions still need to be observed by slit lamp microscope combined with fluorescein staining. For example, keratitis opacity is mainly cell infiltration and edema, so the boundary of the turbid area is unclear, and the surface is tarnished with ciliary congestion. If it is a corneal scar, there is no ciliary congestion, the corneal turbidity is clear, and the surface is shiny. The fluorescent staining of the inflammatory person was stained, and the scar was not stained due to the integrity of the epithelium. Calcium deposition, etc. on the basis of the original white class, is corneal degeneration or malnutrition.

Third, laboratory inspection

1. Scrape and culture: corneal ulcer scraper quickly understand the pathogenic bacteria, conjunctival sac secretions for bacterial or fungal culture.

2. Cytological examination: Cytological examination of ulcer scraping, the virus is a three-dimensional oval. The cytoplasm and nucleus infected under the fluorescence microscope showed yellow-green fluorescence.

3. Serological examination: meaningful for the diagnosis of herpes simplex keratitis.

Fourth, equipment inspection

Slit lamp microscopy combined with fluorescein staining is helpful for diagnosis.

Differential diagnosis

First, keratitis

(a) superficial keratitis

1 The primary lesion can be caused by a virus. Epidemic keratoconjunctivitis caused by adenovirus type VII, epidemic hemorrhagic conjunctivitis caused by enterovirus. It can cause inflammatory infiltration under the corneal epithelium and epithelium. Fluorescein staining is punctately colored with varying thicknesses. In the case of herpes simplex epithelial infection, it is punctate, star-shaped or linear, and gradually develops into dendritic or map-like opacity.

2 secondary to the inflammation of adjacent tissues, such as heavier acute conjunctivitis, invading the peripheral part of the cornea, superficial corneal infiltration, edema, epithelial exfoliation, and more point-like opacity. Fluorescein staining was positive. If the lower third of the cornea has dense punctate dermatitis and erosion, often associated with staphylococcal eyelid inflammation.

(B) corneal stroma

Most of them are immune reactions, and can also be caused by direct invasion of pathogenic microorganisms. Congenital syphilis is the most common cause, tuberculosis, herpes simplex, banded sores, etc. can also cause the disease. A deep keratitis, the lesion is located in the deep layer of the corneal stroma, infiltrating turbidity and edema. The lesions are thickened with a posterior elastic layer wrinkle and have a frosted glass appearance. Vision loss, ciliary congestion, may be associated with iridocyclitis. In the late stage, the neovascularization is surrounded by the corneal stroma, which is brush-like and rarely branched. The cornea can still return to transparency after the inflammation of the light is subsided. If the substrate layer is necrotic, deep scars of varying thickness will be left behind.

(three) corneal ulcer

The cornea has a gray-white infiltration, the boundary is not clear, the surface is tarnished, followed by tissue defects forming ulcers, and fluorescein staining is positive. The severe irritant symptoms are obvious, the ciliary congestion is significant, the ulcer is large and deep, with anterior chamber empyema, and can be perforated.

1. Claudication corneal ulcer: an acute suppurative corneal ulcer. More common in the elderly or have chronic dacryocystitis. Acute onset, often 1-2 days after corneal trauma, eye pain, photophobia, tearing, decreased vision. Ciliary congestion or mixed hyperemia. The cornea has a gray-yellow dense infiltrating foci with blurred boundaries and a rapid formation of ulcers. The base of the ulcer is filthy, covered with necrotic tissue, and the edge of the ulcer is sneak-extended to the surrounding and deep. Fluorescein staining was positive. Often accompanied by iridocyclitis, a large amount of cellulose-like exudate and empyema in the anterior chamber. The pupil is small and sticks behind. The severe cornea is easy to perforate, or even develop into endophthalmitis. Pathogens can be found by scraping or culturing. Such as pneumococcus, hemolytic streptococcus, Staphylococcus aureus and so on.

2. Pseudomonas aeruginosa corneal ulcer: a severe suppurative keratitis caused by Pseudomonas aeruginosa infection. Often caused by trauma, corneal foreign body removal, or using equipment contaminated with Pseudomonas aeruginosa, syrup (such as fluorescein), contact lens. Rapid onset, more than a few hours or 1-2d, severe pain, decreased vision, swelling of the eyelids, conjunctival congestion and edema, yellowish white necrosis on the cornea, slightly bulging on the surface, rapidly expanding, surrounded by a dense annular infiltration. The anterior chamber has a large amount Corneal necrotic tissue shedding forms a large area of ulcers and produces a large amount of yellow-green viscous secretions. If not controlled quickly, all perforations are dissolved within 1-2d. A bacteriological examination of the scraper can be found in Gram-negative bacilli. The culture of Pseudomonas aeruginosa can be clearly diagnosed.

3. Fungal corneal ulcer: There are often agricultural corneal trauma, and the incidence of high-temperature season is high. It is characterized by slow onset, long course of disease, and irritating symptoms are heavier than the former two. The color of the ulcer is white, the surface is dry and rough, and it is like "tongue" or "toothpaste". It seems to have a dry and hard feeling and is easy to scrape. "Pseudo-foot" or "satellite stove" is sometimes seen around the central lesion. There is a flaky gel-like deposit on the posterior wall of the cornea. The anterior chamber has thick empyema. The scraper can find the hyphae and the diagnosis can be established. Culture of visible pathogenic fungi. Such as Fusarium, Aspergillus, Penicillium, Candida albicans, yeast and so on.

Second, corneal trauma and foreign body retention

Mechanical or chemical damage, may have epithelial edema, exfoliation. Corneal opacity in the area of injury. Severe cases have major tissue damage, even corneal perforation, with adjacent tissue damage. Corneal foreign body survivors. In addition to the turbidity of the foreign body tissue, there is turbidity or pigmentation around the foreign body. Metal foreign matter can be seen in metal rust. It can be identified by a magnifying glass or a slit lamp microscope.

Third, corneal degeneration or malnutrition

(1) Old age ring

It mainly occurs in the elderly and is a lipid infiltration in the stromal layer of the cornea. Symmetrical on both sides, there is a ring of white rings at the limbus, and the ring width is about 1mm. The naked eye was observed by the naked eye to be separated from the limbus by a transparent band, and the boundary of the inner edge was unclear. Slit lamp microscopy, the optical section can be seen turbid, the deep part comes from the rear elastic layer, and the turbidity is also downward from the front elastic layer. No inflammatory irritation, does not affect vision.

(B) banded keratopathy

It is a calcium deposit located in the pre-corneal elastic layer. The cause is still unclear, which may be related to hyperthyroidism, sarcoidosis, renal calcinosis, vitamin D poisoning, and high concentrations of calcium and phosphate in blood and interstitial fluid. Or corneal water evaporation in the palpebral zone promotes an increase in local calcium salt concentration. The volatilization of carbon dioxide increases the local pH value, which is beneficial to the precipitation of calcium and phosphate. The cornea lacks blood vessels, resulting in minimal buffering of blood to pH. The clinical manifestation is that the exposed part of the corneal cleft palate shows a banded calcareous deposit. Deposited on the epithelial basement membrane, the pre-elastic membrane and the shallow matrix. There are many holes in the elastic layer in front of the belt turbid zone. The lesion spreads from the periphery to the central part and has no neovascularization. The disease should be differentiated from corneal calcium degeneration. The latter deposition of calcium involves the deep tissue of the cornea. Often for severe eye trauma, eye praise, long-term chronic iridocyclitis and secondary glaucoma.

(three) corneal dystrophy

It is a genetically related primary progressive keratopathy. Symmetrical bilateral vision, slow progression of the disease, early cases are often found in physical examination. Most types of corneal dystrophy lesions begin with a layer of tissue or cells. After years of development, it affects or affects adjacent tissues or cells, and even affects the full-thickness cornea, causing severe visual dysfunction. According to the initial anatomy of the primary lesion, it is divided into three categories, namely, the anterior cornea, stromal and posterior corneal dystrophy.

1. Map-like-point-one fingerprint-like malnutrition: a representative of malnutrition in the front. More than 30 years old. There are many gray patches, tiny cysts or tiny lines in the central epithelium of the cornea. There may be recurrent corneal epithelial exfoliation and temporary blurred vision.

2. Granular corneal dystrophy: This is representative of corneal stroma malnutrition. It is an autosomal dominant genetic disease. There is a localized dispersion of particulate transparent material in the pre-corneal stroma. The lesions are mostly in the central part. In the advanced stage, there may be visual impairment.

3. Fucha endothelial malnutrition: is the representative of malnutrition in the posterior cornea. It is an autosomal dominant genetic disease. More women. In the central corneal endothelium degeneration and loss, the posterior elastic layer thickened with small protrusions, called corneal small spots, which were clearly visible by slit lamp microscopy. Due to decompensation of the corneal endothelium, it can cause corneal stroma and epithelial edema, which makes the cornea thick and turbid, which obviously affects vision and even macrobubble degeneration. The large bubble bursts and the upper shedding causes severe pain.

(four) corneal thick opacity

It is a scar left by corneal inflammation and traumatic healing, which makes the cornea lose transparency and turbidity. No irritation and congestion, surface gloss, negative for fluorescein staining. According to the thickness of the corneal tissue turbidity and the degree of tissue damage, the following classification can be made.

1. Corneal Yunyu: The turbidity is extremely thin and the naked eye can't see clearly. It can be seen with a good oblique light or slit lamp microscope.

2. Corneal plaque: visible to the naked eye, grayish white, thicker than the clouds, thinner than white spots.

3. Corneal leukoplakia: corneal opacity is thick, porcelain white.

4. Corneal adhesion leukoplakia: in the opacity of the whole cornea, there is anterior iris adhesion and pupil deformation. Has been caused by corneal perforation.

5. Corneal staphyloma: corneal lesions, can not support a certain pressure in the eye and perforation. At the perforation and around the cornea and the pigmented membrane tissue, they appear purple and black outward, and are shaped like grapes. The heavy one can't see the pupil.

6. Corneal vasospasm: After corneal inflammation or trauma, there are new blood vessels invading the cornea from the limbus.

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