Lattice degeneration

Introduction

Introduction Plaid-like degeneration: lattice-like degeneration is most closely related to retinal detachment. The resulting retinal tears account for 40% of the pore-derived eyes, and about 7% of the normal eyes have lattice-like degeneration. It is more common in the temporal or temporal quadrant between the equatorial part and the serrated edge. It has a fusiform or strip shape. The long axis is parallel to the serrated edge. The retina in the lesion is thin and has many white lines, which are staggered into a grid. These lines are actually peripheral blood vessels that have been occluded or have a white sheath. Pigment clusters are sometimes seen in the lesion and are derived from the retinal pigment epithelium.

Cause

Cause

(1) Causes of the disease

It is related to the condition of the retina itself, the vitreous condition, the eyeball itself and even genetic factors.

(two) pathogenesis

1. Retinal degeneration and tear formation

Due to the complex structure of the retina, the blood supply is unique and it is easy to cause degeneration due to various reasons. The peripheral part and the macula are well-denatured parts. Retinal degeneration is the basis of retinal tear formation. The following changes are common before the hole occurs.

(1) Lattice-like degeneration: lattice-like degeneration is most closely related to retinal detachment. The resulting hole is 40% of the hole. Also visible in normal eyeballs, about 7%. There is no racial and gender difference in the incidence of lattice-like degeneration, which invades both eyes, and its formation and location are often symmetrical. It is more common in the temporal and temporal quadrants between the equator and the serrated margin. It has a fusiform and strip-like, edge-clear island-like lesion. The long axis is parallel to the serrated margin. The lesion area varies greatly. The long right is from 1DD to 1/ Above 2 circumferences, the width varies from 0.5DD to 2DD. The lesion retina is thin. There are many white lines that are staggered into a grid facade. This line is connected to the retinal blood vessels outside the lesion and is actually a peripheral blood vessel that is occluded or has a tubular white sheath. The distribution of white pigment clusters, sometimes called pigmentary lattice-like degeneration, is sometimes found in the lesions, and the pigment is derived from the retinal pigment epithelial layer.

(2) cystic degeneration: occurs in the vicinity of the macula and the inferior margin of the incision, the edge is clear, round or round, dark red. Small cavities can be fused into a large cystic cavity, so the size varies greatly. The reticular sac-like degeneration that occurs in the peripheral part of the fundus becomes a small red dot that is clustered and slightly raised, and the vitreous or granular opacity is nearby. The cystic degeneration of the macula is a small honeycomb cavity at the beginning, which is especially obvious when there is no red light examination. The small cystic cavities of the peripheral or macular portion gradually merge into each other to form a large cystic cavity. The anterior wall is often broken by the vitreous traction, but only when the front and rear walls are broken, it becomes a true hole and causes retinal detachment.

Cystic degeneration affects the metabolic metabolism of the retina by various causes (such as senile changes, inflammation, trauma, high myopia, etc.), causing the breakdown of its neural components, thereby forming a cavity in its inner plexiform layer or inner and outer nuclear layers. A change in the gap. The cavity is filled with a liquid containing a mucopolysaccharide component.

(3) Frosty degeneration: mostly occurs near the equator and the serrated edge, and some areas covered by fine white or slightly yellow shiny particles are visible on the surface of the retina. The thickness is uneven, as if the retina is covered with a frost. This degeneration can occur alone. It can also exist simultaneously with lattice-like degeneration and cystic degeneration. Frost-like degeneration is close to the equator and merges into a band, also known as snail trace degeneration.

(4) paving stone degeneration: generally seen in myopia patients over 40 years old. More common in both eyes. Occurs in the lower part of the fundus, showing a pale yellow round or rounded, clear-cut multiple lesions with pigmented edges. Large and small lesions are grouped together. Paved stone. The choroidal capillary network in the central part of the lesion is atrophied, exposing the choroidal large blood vessels or even the pale white sclera. The degeneration area is caused by the vitreous traction, which leads to the formation of retinal tears.

(5) Retinal pressure whitish and non-pressurized whitish: After the sclera is depressed, the bulge of the fundus becomes opaque grayish white, which is called pressurized whitening. When the lesion is further aggravated, it is grayish white even if it is not pressurized, and it is called non-pressurized whitish, and a trailing edge sometimes forms a clear sputum. More common in the peripheral part of the upper fundus, is considered an indication of vitreous traction. If the vitreous body is detached, the trailing edge can be torn to form a slit.

(6) Dry retinal longitudinal folds: wrinkles extend from the edges of the serrated edges toward the equatorial direction. It is a fold of overgrown retinal tissue. Generally, there is no need for treatment, but there is also the possibility that the vitreous body is pulled at the back end of the crease and the hole is broken.

2. Vitreous degeneration

Another key factor for causing retinal detachment. Under normal circumstances, the vitreous is a transparent gel-like structure, which is filled in the cavity of the posterior 4/5 of the eyeball, and has a supporting effect on the retinal neuroepithelial layer attached to the pigment epithelial layer. Except for the flat part of the ciliary body to the serrated edge and the adhesion around the optic disc and the retina, the other parts are only closely attached to the inner limiting membrane of the retina, but there is no adhesion. Before the occurrence of retinal detachment, common changes in vitreous degeneration include: interrelated vitreous detachment, liquefaction, turbidity, membrane formation, concentration, and the like.

(1) detachment of vitreous body: vitreous detachment refers to the occurrence of a gap between the critical surface of the vitreous and the tissue in close contact with it. More common in high myopia and elderly patients, the external interface of the vitreous body can be detached, the posterior vitreous detachment, upper detachment is common, and the relationship with retinal detachment is also relatively close.

The reason for the vitreous detachment is mainly the depolymerization and dehydration of hyaluronic acid in the vitreous, forming one or more small liquefied cavities in the vitreous body, and merging with each other to form a large cavity. If the liquid in the cavity breaks through the external interface of the glass and enters the retina, the separation between the vitreous and the inner limiting membrane of the retina occurs. If the detachment has some pathological adhesion to the retina, retinal tears may occur due to traction.

(2) Fluidity of vitreous body: The vitreous liquid is a colloidal equilibrium damage caused by a new metabolic disorder of the vitreous. It is also common in high myopia and elderly patients. Liquefaction generally begins at the center of the vitreous, an optical space appears, gradually expanding, or a plurality of smaller liquefied cavities can be fused into a larger liquefaction chamber. The liquefied cavity has a translucent grayish white tow or a floc floating.

(3) Vitreous opacities and concentration: There are many reasons for vitreous opacity, but those associated with primary retinal detachment are caused by the destruction of the vitreous scaffold structure, so they often detach from the vitreous and liquefy. The turbid fiber strands have the potential to cause retinal tears.

The so-called vitreous concentrating is also a vitreous turbidity. It is an opaque body formed by dehydration and denaturation of the scaffold structure when the vitreous is highly liquid, so it can be called atrophic concentration. Compared with the membrane turbidity of the outer interface, the tow-like or the flocculation turbidity in the vitreous liquefaction chamber, there is no significant difference in the nature of the detachment of the anterior vitreous body, only the degree of severity is more serious, and the risk of retinal detachment is caused. It is also more intense.

(4) Vitreous membrane formation: The mechanism of co-formation of the massive perietinal proliferative membrane is also very complicated and is not fully understood. There may be glial cells, free pigment epithelial cells and their transformed macrophages, fibroblasts and the like. The proliferative membrane grows along the anterior and posterior interface of the retina or the external interface of the glass. After contraction, the retina can be stretched to form some fixed adhesion folds or star-shaped folds. Even the entire posterior retina is collapsed together to form a closed funnel.

Such proliferative membranes are seen in patients with detachment of the retina, detachment, and old detachment. Occurred in the former, is also an important cause of retinal detachment.

In summary, the so-called primary detachment is only a idiom, in fact, it is secondary to the degeneration of the retina and vitreous. Retinal tears and vitreous liquefaction, detachment and pathological adhesion to the retina are two essential conditions for primary retinal detachment, which are indispensable. For example, some cases have been found to have clear retinal tears in the clinic. As long as the vitreous is healthy, retinal detachment will not occur. Similarly, retinal detachment does not occur when the vitreous degeneration is changed and the retina has no reaming. For example, it is observed that 65% of people aged 45 to 60 have posterior vitreous detachment, and only a few of them have retinal detachment. This also shows that retinal detachment is the result of a mutual interaction between retinal degeneration and vitreous degeneration. Retinal tears are often formed by the pathological adhesion of the vitreous on the basis of a variety of manifestations of degeneration. The liquefaction and detachment of the vitreous body on the one hand weakens the supporting force for attaching the retinal neuroepithelial layer to the pigment epithelial layer, and on the other hand, the liquefied vitreous is perfused into the neuroepithelial layer from the ruptured pore.

In addition, it has been observed that retinal tears occur in the corresponding points of the oblique and oblique points of the fundus, so it is speculated that the holes are related to the traction of these muscles. It has also been found that most patients recall a history of minor trauma at the bottom of the eye and believe that detachment is associated with trauma. In fact, except for a few special cases such as severe eyeball blunt trauma, oblique muscle traction and trauma can only be considered as the cause of retinal detachment.

3. Risk factors

(1) Relationship with myopia: Retinal detachment occurs mostly in patients with myopia. In the case of larger samples of rhegmatogenous retinal detachment, there were many patients with myopic diopter above -6.00D. The age of onset of rhegmatogenous retinal detachment in myopia is lighter than that of emmetropia. The lesions of myopia are mainly in the posterior segment of the eyeball. Starting from the equator, the posterior segment of the eyeball gradually expands. The capillary layer of the choroid shrinks and even disappears. The retina also undergoes degeneration and atrophy, and the vitreous also appears liquefied. Retinal detachment is prone to occur with these pathogenic factors.

(2) The effect of extraocular muscle movement: the end of the four rectus muscles is located in front of the serrated edge, and its movement has little effect on the retina. The oblique muscle stops at the back of the eyeball, and the superior oblique muscle pulls the eyeball down, and then the gravity of the vitreous body may be related to the easy formation of a hole in the supracondylar quadrant. The macula is prone to cystic degeneration and can be secondary to a hiatus. Some people think that it is also related to the traction of the inferior oblique muscle. The distribution of the holes in 286 cases of retinal detachment was observed. It was found that 68.4% of the holes were in the temporal side of the retina, and 47.49% of them corresponded to the position of the upper and lower oblique muscle ends, that is, the hole was in the upper quadrant and the right eye was more. Focus on 10 to 11 o'clock, 1 to 2 o'clock in the left eye, 13 to 15 mm behind the limbus. In addition, often at 11 to 1 o'clock, large horseshoe-shaped holes appear 16 to 22 mm behind the limbus. The pupils of the inferior quadrant are concentrated in the right eye at 8 to 9 o'clock and the left eye at 3 to 4 o'clock, and after the limbus at 16.46 to 26 mm.

(3) Relationship with ocular trauma: After the eyeball is blunt, the sawtooth edge breaks off and can develop into retinal detachment. The prevalence of ocular trauma in adolescents is higher in retinal detachment, accounting for 18.71% to 20%. Animal experiments have confirmed that at the moment of eyeball contusion, eyeball deformation can cause tearing in the distal part of the retina. In addition, severe trauma can produce retinal tears directly in the equator. Trauma of the posterior capillaries caused by trauma, retinal oscillations and vitreous traction can occur in macular holes or from macular degeneration and then into pores. In addition to these retinal detachment, which has a clear relationship with trauma, most of the other cases, the retina and vitreous have been degenerated or adhered, and have the intrinsic factors of retinal detachment. Trauma only induces retinal detachment as a cause.

(4) Relationship with heredity: Some cases of retinal detachment occur in the same family, indicating that the disease may have hereditary factors, and there may be recessive or irregular dominant inheritance. Most pathological myopia has a more positive hereditary nature, and more retinal detachment occurs. In addition, in patients with bilateral retinal detachment, the lesions on both sides of the fundus are mostly symmetrical, which indicates that some retinal detachment may be closely related to congenital growth and development factors.

Examine

an examination

Related inspection

Ophthalmoscopy and CT examination of the eye

1. Microscopic examination: Under the condition of full dilation, the indirect ophthalmoscope combined with scleral depression or slit lamp and contact lens can be used to check the appearance of the surrounding membrane.

2, fundus examination: visible retinal area of the retina lost normal red reflection and gray or blue-gray, slight tremor, dark red blood vessels crawling on the surface. The uplifted retina is like a hilly undulation, and the wide range of bulges can obscure the optic disc and wrinkle. Flat detachment, often missed diagnosis if not detailed examination. When the macular area is detached, the fovea of the macula has a red dot, which is in sharp contrast with the retina that is grayish-white.

3, ophthalmoscopy: the most important. Finding all retinal tears is not only the basis for diagnosing rhegmatogenous retinal detachment, but also one of the keys to success. Therefore, how to find all the holes accurately and without fail is extremely important. About 80% of the holes occur in the peripheral part of the fundus, especially on the upper side of the sac, the lower side of the squat, the lower side of the nose, and the lower side of the nose. When the retinal detachment is high, these peripheral cracks are often obscured and must be carefully searched from various angles. In the case of binocular indirect ophthalmoscope plus scleral compression can not be found, the eyes can be pressure-wrapped, the patient can be recumbent for several days, and the retina is slightly calmed down before examination.

When the retinal detachment is large and the bulge is high, there are often several holes, which cannot be satisfied with one hole, especially one small hole. In addition to looking for holes in the detachment area, it should also be noted that there is no detachment or detachment from the inconspicuous area, especially in the upper fundus, because the liquid sinks, the retinal detachment may not be visible in the hole and its vicinity. The location and shape of retinal detachment is sometimes beneficial for finding holes. The top of the fundus is detached, the hole is always out of the zone; the lower part is detached. If the detachment is a hemispherical bulge, the hole may be directly above it; if it is a general detachment below, the hole may be above the higher side of the detachment zone. If the heights of the two sides are basically the same, the holes are often at the lower periphery. Patient complaints can sometimes provide clues to finding holes. The dark space and the position where the flashing sensation first appears in the field of view, and the corresponding location is often the location of the hole.

A hole is often found in retinal detachment. Finding a hole and surgically closing a hole is the key to treating this disease. The hole is red, the surrounding retina is grayish white, more common on the sputum, followed by the armpit, the nose is the least seen. The holes in the serrated edge are mostly under or under the arm. The holes can also occur in the macular area or the retina that has not yet detached. The size and number of the holes vary. It can be a round or horseshoe-shaped split, but also has a stripe shape, a serrated edge and an irregular shape. The detached retina sometimes has a high degree of bulging to obscure the rupture, which allows the patient to change the position of the head. You can also bandage your eyes and stay in bed for 1-2 days. Check again when the degree of bulging is reduced.

Diagnosis

Differential diagnosis

Differential diagnosis of lattice-like degeneration:

(1) Dry retinal longitudinal fold: The wrinkle extends from the tooth edge of the serrated edge to the equatorial direction, which is a fold of the overgrown retinal tissue, and the back end of the fold is easily broken by the vitreous body.

(2) cystic degeneration: occurs in the vicinity of the macula and the inferior serrated margin. The edges are clear, round or round, dark red. The peripheral lesions are reticulated, which are small red dots that are slightly elevated in clusters. The cystoid degeneration of the macula is honeycomb.

(3) Frosty degeneration: mostly occurs near the equator and the serrated edge. Some areas covered with fine white or yellow particles can be seen on the surface of the retina, and the thickness is uneven, just like covering a hoarfrost. Such degeneration can occur alone or simultaneously with lattice-like degeneration and cystic degeneration. In the equator, it is fused into a band-like snail trace.

(4) paving stone-like degeneration: good for the surrounding omentum below. It is characterized by a pigmented edge, a pale yellow circle or a round shape, and a clear multiple lesion with a clear boundary. Large and small lesions are arranged in a paving stone. The choroidal capillaries in the central part of the lesion are atrophied, exposing the choroidal large blood vessels or the white sclera.

(5) Retinal pressure whitish and non-pressurized whitish: After the sclera is depressed, the bulge of the fundus becomes opaque grayish white, called pressurized whitening. When the condition is further developed, it is grayish-white without pressure, and it is called non-pressurized whitish. The trailing edge sometimes forms a clear sputum, which is more common in the upper peripheral reticular membrane and is considered as an indication of vitreous traction.

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