Acquired retinoschisis

Introduction to acquired retinal cleft palate Acquired retinal cleft palate (acquiredretinoschisis) The most common type of retinoschisis, also known as senileretinoschisis, but also occurs in young people after the age of 20, often due to flashing hallucinations or floaters Symptoms and visits were discovered. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population Mode of infection: non-infectious Complications: retinal detachment

Acquired retinoschisis

(1) Causes of the disease

Because the disease is occurring in the area of extensive cystic changes, most authors believe that this disease is the result of the development of small cyst fusion in the peripheral part of the retina. People of any age may have cystic degeneration in the periphery of the fundus, usually in The temporal side is most prominent. The cystic degeneration increases with age. In the same age, women are heavier than men. The most severe cystic changes can be seen by the destruction of adjacent cystic walls, but some Müller cells or glial cells are preserved. Support, such as enlargement of the cyst, more separation between the layers of the retina, this support is torn off, it develops into a cyst, more common in young people, mostly occurs in the long-term detachment of the retina, below the equator, it develops into retinal cleft palate .

(two) pathogenesis

The pathogenesis of this disease is mainly caused by retinal capillary blood supply disorder in the lesion area, leading to retinal cell death, and also providing tissue repair of glial cells and insufficient blood supply. Therefore, retinal cystic degeneration occurs, and the covered vitreous cortex shrinks. The inner layer of the cystic degeneration can be pulled into a retinal cleft palate, and the liquid generated in the cleft palate can expand the range of the cleft palate. When the cleft palate is thinned, a circular hole can be formed. It is often impossible to see the flap or the torn flap. The appearance of the inner pore has no effect on the shape of the splitting cavity.

Acquired retinal cleft palate prevention 1. Maintain an optimistic and happy mood. Long-term mental stress, anxiety, irritability, pessimism and other emotions will make the balance of the cerebral cortex excitatory and inhibition process imbalance, so you need to maintain a happy mood. 2, life restraint pay attention to rest, work and rest, life orderly, maintain an optimistic, positive, upward attitude towards life has a great help to prevent disease. Do the regularity of tea and rice, live daily, not overworked, open-minded, and develop good habits.

Acquired retinal palpebral complications Complications

The probability of retinal detachment is 77% to 96%.

Acquired retinoschisis symptoms common symptoms visual impairment visual field defect hemorrhage edema

The early lesions of the disease, often located in the periorbital part of the fundus, have no obvious relationship with the refractive status. Usually there are no obvious symptoms before the onset, most of them are found when examining the fundus. The earliest retinal cleft palate, almost always In the vicinity of the serrated margin of the temporal side, it does not affect the visual function. The indirect ophthalmoscope and scleral indenter can be used to detect early manifestations. The leading edge of the retinal cleft palate often has a narrow cystic degeneration zone connected to it. The cleft palate is separated from the serrated edge. In this period, the retinal cleft palate can develop in two directions, that is, the annular extension and the posterior extension. When the ring is advanced, a narrow and low flat cleft is extended to the nasal side and finally surrounds the fundus. Department, backward development, the most prominent quadrant of the lower quadrant, can form a spherical bulge, which is a part of the retinal palpebral fissure that is easily found, usually limited to about 1 quadrant, remains stationary or slow development, most often involving the underarm quadrant Secondly, the upper quadrant, according to statistics, about 7% of patients with retinal cleft palate over 40 years of age are progressive, more women than men.

During the stage of retinal palpebral fissure, the convex surface of the spherical bulge, that is, the inner layer of the cleft palate, is visible in the vitreous, which is a transparent and fixed bulge with a clear boundary. The position and shape do not rotate with the patient's head or eyeball. Displacement, the inner layer of the retinal cleft palate is transparent like a gauze, and its luster is like a soaked silk. This luster disappears immediately after the boundary, and the retinal blood vessels are often located on the inner layer of the cleft palate, and often have white sheaths, showing obstruction. The appearance, venules and small arteries are involved, and occasionally there are 1 or 2 retinal vessels on the outer layer of the cleft palate. If the cleft palate progresses, it will be pulled from the inside to the outside, which can rupture the hemorrhage and accumulate in the cleft palate. Blood can form a well-defined intraretinal hemorrhage plane.

The inner layer of the retinal palpebral fissure often has tiny white spots like snow flakes, which may appear early in the course of the disease, but are more pronounced when the spherical cleft palate bulges into the vitreous cavity. The snowy white spots are located behind the retinal blood vessels, indirectly. Under the ophthalmoscope, through the scleral indentation method, sometimes there are white fiber strips between the inner and outer layers of the retinal cleft palate, suspended in the cleft palate cavity, and the outer layer of the retinal cleft palate is difficult to identify when it is not separated from the retinal pigment epithelium. Sometimes it can be seen that there is a slight gray halo in this area, which is the only feature that distinguishes the disease. The lesions are carefully identified. In the pink weakness, honeycombs or mesh-like circles or ovals with different sizes and shapes can be seen. Holes, which are gray and thick in appearance, are often the nerve connective tissue pillars that connect the inner and outer layers. When the spherical part of the retinal cleft palate reaches the equator, the development is relatively fast. Once it reaches the posterior pole, the development speed slows down. When it is near the fovea, it can remain stable for several years.

The outer layer of the retinal cleft palate can be seen as a red spot, such as the appearance of a cluster of fish eggs. The posterior edge of the cleft palate sometimes shows the pigmentation boundary. The macula often has cystic degeneration and pigmentation, and can appear in front of the fly, and the sense of flash and Vision loss, but retinal palpebral invasion of the macula is rare, the retinal palpebral fissure around the fovea often combined with peripheral retinal palpebral fissure, the patient's central vision is reduced, and there is a paracentral dark spot, the slit lamp front mirror can be found The foveal fovea of the macula are flat and edema, but the paracentral fossa is bulged like a ring-shaped cake. It is speculated that the retina at the fovea is still intact, and the cleft palate is in the periphery of the fovea.

Retinal tears can occur in the inner and outer layers of the cleft palate. The inner pores are almost always located at the most bulge of the cleft palate. They are usually multiple small holes. They are located at the highest point of the bulge, which is small and can be multiple. Due to acquired retinal cleft palate Located in the deep layer of the retina, the outer pupil is common and large, located at the posterior edge of the cleft palate, multiple or single, round or oval, and the outer outer perforation is curled in the edge, which is larger than the inner hole. The hole is caused by the elastic contraction of the outer layer. The outer hole often appears along the trailing edge of the cleft. The leading edge is rare. Because the outer layer of the cleft is in contact with the pigment epithelium, the hole is difficult to identify. Sometimes it is used. Indirect ophthalmoscope plus scleral depression is also difficult to ascertain. If there is only an outer hole without an inner hole, localized retinal detachment may occur, but about 40% of the disease is in the cleft palate, on the outer layer. There are holes in the hole, which can easily lead to extensive retinal detachment.

Retinal palpebral fissure usually has many years of quiescent period, spontaneous collapse can occur, but rarely occurs. In some cases, retinoschisis is spread in three directions: toward the back hole, along the retina serrated edge and toward The vitreous cavity increases the height of the bulge. In the initial stage, the retinal cleft palate forms a large fixed spherical bulge in the inner layer, which is almost transparent. The inner surface is smooth and has no undulations. The outer retina often has a cluster of fish or scorpion-like a large number of red dots, the inner retina is usually characterized by pits in the back, and the inner rupture alone does not cause retinal detachment. The outer layer or double layer rupture can cause retinal detachment. When the retinal cleft palate extends The pole, which usually causes visual field defects, usually occurs in the nasal upper quadrant. In contrast, retinoschisis is located in the inferior quadrant, and the lesion originating from retinal detachment has a slope boundary unless the detachment is long.

The disease is usually accompanied by vitreous degenerative diseases, such as liquefaction, post-detachment, slit lamp biomicroscopy, often found in the retinal palpebral eye caused by degeneration of vitreous liquefaction, 60% have vitreous detachment, in addition, in the cleft palate There are also various changes in the vitreous body. The vitreous body adjacent to the cleft palate area seems to be concentrated, and a distinct fibrous-like structure is visible. The vitreous cortex, which is located on the cleft palate area, is pulled, like a brush-like short-wool fiber, and some are not attached to The inner layer is now curled, and the splitting of the inner layer of the fissure can be accompanied by detachment of the vitreous. The inner and outer layers have cracks. The posterior layer of the inner layer often has vitreous detachment. The vitreoretinal traction may be the main reason for the gradual progression of the cleft palate. After the posterior vitreous body is separated from the cleaved inner layer, the cleft palate can be changed from progressive to static.

Binocular indirect retinoscopy scleral compression The initial retinal palpebral fissure showed a flat, smooth retinal bulge, representing the bulging retina of the inner retinoschisis, usually including retinal blood vessels, some appearing white around, in the hemisphere The inner wall of the bulging bulge is thin and transparent, so the surface is water-smoothed with a smooth watered silk appearance. These spots represent the footprint of the Müller cell. The front pole of the cleft is connected to the serrated edge, and the trailing edge is clearly defined. The retinal blood vessels attached to the inner wall have a vassel shadow on the outer wall, a white line of the retinal blood vessels, and a parallel sheath, etc., and white bright snow flakes are widely visible on the inner wall. The spot is the attachment point of the broken end of the columnar cable. In addition, if the inner surface of the inner wall is carefully observed under the ophthalmoscope with a slit lamp, some fine hemispherical concave surfaces can be seen, like the beaten metal appearance. This is a trace of microcapsule-like degeneration. The photoreceptor layer remains attached to the pigment epithelial layer and becomes a cleft palate. Under the ophthalmoscope, it is difficult to see. However, with the scleral compressor, the sclera can be lightly pressed, and the outer wall of the pressed ridge can be seen as white turbidity, called white withpressure, cleft or inner wall. Circular small holes can occur. The inner wall holes are usually close to the peripheral part of the serrated edge. They are small, and the outer wall's holes are larger behind. The splitting edge is at the junction with the normal retina, and the so-called boundary line with pigment is included. Line).

Because the lesion is confined to the peripheral part, the patient often does not consciously. Only when the cleft palate extends beyond the equator, especially the photoreceptor layer is separated from the bipolar cell layer, and the neuron is detected after the neuron is cut off. Defects, as long as the lesion has not invaded the macula, can still maintain good central vision, but for this disease, if there is no retinal detachment, it is extremely rare to extend to the vicinity of the macula.

Acquired retinal cleft palate

No special laboratory tests.

Double eye ophthalmoscopes and slit lamp microscopes are used to examine the fundus in detail, which can be characterized.

Diagnosis and diagnosis of acquired retinal cleft palate

Diagnosis can be made based on clinical manifestations and characteristic changes in the fundus. Binocular indirect ophthalmoscopy and slit lamp indirect ophthalmoscopy for detailed examination of the fundus are helpful for diagnosis. Extensive retinal detachment and posterior retinal palpebral fissure can cause permanent vision. Defect, regardless of whether the patient has visual impairment.

Differential diagnosis

Such cases should be differentiated from young retinal detachment patients with signs of exudation without retinoschisis, which should be identified with the following diseases:

Congenital retinoschisis

Although the performance of the fundus is different, it is mainly the age of onset, congenital onset, found in children around the age of 10, has a family history, limited to men, due to macular cleft palate, high visual acuity, acquired in the sex Adults over the age of 20, those over 40 years old are more common, no family history, both sexes can occur, the macula is generally unaffected, and often maintains a good central vision.

2. Retinal cyst

Retinal cleft palate and retinal cysts are developed on the basis of cystic degeneration. Retinal cysts are more common in young people, mostly in the long-term detached retina, located near the equator. Isolated retinal cysts are very rare, often with retinal detachment. Occasionally, this type of cyst has a small pedicle that protrudes into the vitreous cavity and floats with the movement of the eyeball. The retinal cleft palate is one or two flat-topped ridges connected to the non-augmented zone, extending around the peripheral fundus and retinal cysts. There are no holes in the two layers of the wall, and the effusion in the cyst is watery; the inner and outer layers of the retinal palpebral can be cracked, and the liquid in the cleavage chamber is thicker.

3. Primary retinal detachment

For example, in the retinal palpebral fissure, there are holes on the outer layer, then retinal detachment can occur. At this time, the transparency of the retina is reduced and wrinkles are formed, and there is a certain degree of mobility. After the retinal detachment occurs, the visual field has a cleft palate. In addition to the corresponding absolute dark spots in the region, there are also relatively dark spots corresponding to the retinal detachment zone. If the spherical detachment merges with the horseshoe-shaped rupture, the retinal detachment is often the cause of retinal detachment. , and the identification of primary retinal detachment.

4. Malignant melanoma of the choroid The literature has reported a case of choroidal malignant melanoma and retinoschisis. There are occasional cases of misdiagnosis of the two, with indirect ophthalmoscopy combined with scleral pressure examination It is not difficult to identify, the inner wall of retinoschisis is a translucent membrane, the cavity is a liquid, sometimes the choroidal texture can be seen through the sclera, and the choroidal malignant melanoma is easily found under the indirect ophthalmoscope. Uplift, light inspection to opaque.

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