Acquired retinoschisis

Introduction to acquired retinal palpebral fissure This disease is called senileretinoschisis, but it also occurs in young people after the age of 20, so the name of senile is not exact. The disease is a frequently-occurring disease in people over 40 years old, but it is rarely reported in Chinese and Japanese literature. There may be differences in race. More than 80% of the eyes are affected by both eyes, and the eyes are symmetrical, and there is no difference in gender. Often seen due to symptoms such as flashing illusion or flying mosquitoes, otherwise it is accidentally found when performing fundus examination for some reason. The disease occurs in emmetropic or hyperopic eyes, rarely accompanied by myopia, vitreous often without lesions, 80% involving both eyes, and bilateral symmetry, the most common site is the inferior iliac crest, the last time, the nasal side is very rare . 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 when the visual cell layer is separated from the bipolar cell layer, and the neuron is cut off, the corresponding neurological absoluteness can be detected. Defects, as long as the lesion has not invaded the macula, can still maintain good central vision, but for this disease, if the retinal detachment occurs, it is extremely rare to extend to the vicinity of the macula. basic knowledge The proportion of illness: 0.005% Susceptible people: people who are more than 40 years old Mode of infection: non-infectious Complications: retinal detachment

Causes of acquired retinal palpebral fissure

The pathogenesis of this disease is based on peripheral micro-cystoid degeneration. There is a small vesicle called Blessing-Iwanoff cavity in the pathological specimen of the retinal plexus adjacent to the serrated edge. Gray-white opaque spots under binocular indirect ophthalmoscopes or three-sided mirrors, slowly expanding and merging with age, causing cleft palate between the outer layer and the inner core layer to form a large cystic cavity, the inner wall of the cystic cavity (inner layer) due to nerve components The degeneration disappeared and became thinner. At the end, only the inner boundary membrane and gliar remained. The outer wall (outer layer) left the visual cell layer and the pigment epithelial layer. During the course of the disease, the cystic cavity continued to expand, and between the cystic cavity and the cystic cavity. The glial tissue mainly composed of Müller cells is retained as the neural pillars that maintain the inner and outer walls. After the columnar strips are broken, the stumps are attached to the inner surface of the inner wall, and the inner and outer walls are transparent. The mucus is stored, and the mucus is mucopolysacchric acid.

Acquired retinal cleft palate prevention

The disease is almost non-progressive, even if it is very slow, so it is a self-limiting benign disease, but when the splitting of the outer wall and the outer wall are formed, it is easy to cause retinal detachment. Those with ruptures have a probability of retinal detachment of 77% to 96%, accounting for 2.1% to 3.2% of the cause of retinal detachment. From this point of view, it cannot be said that there is no danger, but according to Byer's estimation, the inner and outer walls Those with ruptures were only 1.4% of all acquired retinoschisis.

Congenital retinal palpebral complications Complications

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 when the visual cell layer is separated from the bipolar cell layer, and the neuron is cut off, the corresponding neurological absoluteness can be detected. Defects, as long as the lesion has not invaded the macula, can still maintain good central vision, but for this disease, if the retinal detachment occurs, it is extremely rare to extend to the vicinity of the macula.

Acquired retinoschisis symptoms Common symptoms Visual impairment Retinal hemorrhage Retinal edema

Under the ophthalmoscope, the cleft palate is located at the periphery of the fundus. The inner wall of the hemispherical bulge is thin and transparent, so the surface is smoothed with water-smoothed watered silk appearance. The cleft palate is connected to the serrated edge. The boundary is sharp and steep, and the retinal blood vessels attached to the inner wall are visible on the outer wall. The vassel shadow is visible on the outer wall. The retinal blood vessels are white-lined, and the parallel sheath is often seen. White bright snowflakes can be seen everywhere inside the inner wall. Snow flacks, which are attached to the broken ends of the columnar strips by the seed spots. In addition, if the inner surface of the inner wall is carefully observed with a slit lamp microscope, some fine hemispherical concave surfaces can be seen, like hammered metal sheets. Beaten metal appearance, which is the trace of microcapsule-like degeneration.

The visual cell layer still adheres to the pigment epithelial layer and becomes the cleft palate outer wall. It is difficult to see under the ophthalmoscope. However, with the scleral compressor, the sclera can be lightly pressed, and the outer wall of the pressed bulge can be seen as white turbidity, called oppression. White with pressure.

Circular cracks may occur in the inner wall or the outer wall of the split, and the inner wall crack is common in the peripheral portion near the serrated edge, and the crack in the outer wall is larger behind.

The boundary between the cleft palate and the healthy retina, accompanied by a so-called demarcation line of pigmentation.

The disease occurs in emmetropic or hyperopic eyes, rarely accompanied by myopia, vitreous often without lesions, 80% involving both eyes, and bilateral symmetry, the most common site is the inferior iliac crest, the last time, the nasal side is very rare .

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 when the visual cell layer is separated from the bipolar cell layer, and the neuron is cut off, the corresponding neurological absoluteness can be detected. Defects, as long as the lesion has not invaded the macula, can still maintain good central vision, but for this disease, if the retinal detachment occurs, it is extremely rare to extend to the vicinity of the macula.

Examination of acquired retinal palpebral fissure

Dilated eye examination, fluorescein angiography, visual field examination.

Diagnosis and diagnosis of acquired retinal cleft palate

A diagnosis can be made based on the characteristic changes of the above clinical phenomena. Double-eye indirect ophthalmoscopy and slit lamp microscope for detailed examination of the fundus, help to identify acquired retinal palpebral fissure and retinal detachment and congenital retinoschisis.

Separation of the retinal sensory layer and the pigment epithelial layer due to posterior vitreous detachment of the retina or retinal atrophy (such as lattice-like degeneration) or ocular trauma.

The diagnostic basis is:

1) A history of flashing and predator symptoms, progressive visual field defects, and decreased vision.

2) Pigment particles or vitreous hemorrhage in the vitreous.

3) The retina is blue-gray or gray-white bulge, wrinkled, and the blood vessels crawl on the retina of the bulge, which is curved, and the time is hidden and the color is dark red.

4) There are holes in the retina.

5) The subretinal fluid is clear and cannot move.

6) The detached retina often has irregular wrinkles and vitreous retinal proliferative changes, called proliferative vitreoretinopathy (PVR).

Different from the identification of congenital retinoschisis, although the fundus performance is different, it is mainly the age of onset, congenital onset, found in children around 10 years old, family history, limited to men, due to macular cleft palate The vision is highly damaged. Acquired persons are seen in adults over the age of 20, and those over the age of 40 are more common. Without family history, both sexes can occur, and the macula is generally unaffected, often maintaining good central vision.

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