I. Disease Introduction Macular lysis is a tissue defect that occurs from the inner border membrane of the retina to the photoreceptor cell layer in the macula, which severely impairs the patient’s central vision.Knapp and Noyes first reported traumatic macular lysis in 1869 and 1871, respectively, and Kuhnt reported non-traumatic macular lysis for the first time in 1900, since then, macular lysis of various causes has been recognized successively. The prevalence of the disease is low, about 3.3 per 100,000 of the population, with unexplained idiopathic macular lentigines being the most common (about 83%), often occurring in healthy women over 50 years of age (average age 65 years, F:M = 2:1), and in 6% to 28% of those with bilateral disease. It also occurs in younger patients. Classification of diseases: 1. According to the etiology: (1) idiopathic macular cleft; (2) traumatic macular cleft; (3) highly myopic macular cleft; (4) other secondary macular cleft. 2, according to the morphology of macular lentigines: (1) whole macular lentigines; (2) laminar macular lentigines. Third, the cause of morbidity In addition to idiopathic macular cleft, the etiology of other causes are clearer, such as trauma, high myopia, cystoid macular edema, inflammation, retinal degeneration-like diseases, macular anterior membranes, and eclipsing retinopathy. The understanding of idiopathic macular schisis, on the other hand, went through a long period of more than a century until 1988, when Gass proposed that the tangential direction of retinal surface pulling in the macular region was the main cause of idiopathic macular schisis formation, providing a theoretical basis for the treatment of macular schisis using vitreous surgery. The proposed theory is based on the anatomical relationship of the vitreoretinal interface of the ratio derived from the fact that in the aging process of the human body, due to vitreous liquefaction and the occurrence of postvitreous detachment. So that the retinal surface often residual part of the vitreous cortex, due to these residual vitreous cells in the posterior cortex of the value-added, in the macular center concave area of the retinal surface parallel to the retinal surface of the formation of the retinal surface of the tension, initially occurring in the center of the macula small concave detachment, then the center of the concave detachment, and ultimately the formation of the whole macular lentigo. Pathogenesis The pathogenesis of macular schisis is not completely clear. Early reports in the literature suggested that trauma was the main cause of macular lentigines, however, with the increase in case reports, it was found that only about 5% to 15% of macular lentigines were caused by trauma. At the beginning of this century, some authors suggested that cystoid macular degeneration was the main cause of macular lentigines, and some suggested that age-related vascular changes led to macular atrophy and eventual formation of macular lentigines, but none of these ideas could explain the pathogenesis of idiopathic macular lentigines.In 1924, Lister suggested for the first time that vitreous pulling was closely related to macular lentigines, and since then, the role of vitreous in the pathogenesis of macular lentigines had been noticed. In 1988, Gass revolutionized the pathogenesis of idiopathic macular lentigines by suggesting that vitreous tangential pulling in front of the central macular pucker was the main cause of idiopathic macular lentigines, which provided a theoretical basis for the use of vitreous surgery in the treatment of macular lentigines (Figs. 31-32), and a theoretical basis for the use of vitreous surgery in the treatment of macular lentigines (Figs. 31-33). theoretical basis for the use of vitrectomy in the treatment of macular lentigines (Fig. 31-3). Since then, there have been increasing reports on the use of vitrectomy in the treatment of macular lentigines. Vitrectomy, especially the removal of the posterior vitreous cortex and the anterior retina to loosen the vitreomacular pull, resulted in the closure of the lacunae in the majority of cases, with significant improvement in visual acuity in some cases, and in 1995, through clinicopathologic studies and on the basis of the fact that visual acuity could be improved after vitreous surgery, Gass further pointed out that idiopathic macular lentigines were formed without loss of the neural tissue of the central pits, thus explaining why the surgery was performed without loss of neural tissue of the central pits. This explains why vision can be restored after surgery. Pathophysiology The clinicopathology of macular schisis can be manifested as follows: 1) macular hole size of 400-500 μm; 2) “detachment” around the macular schisis in the range of 300-500 μm; 3) photoreceptor cell atrophy; 4) macular cystic changes; 5) yellow dot-like deposits similar to vitreous warts attached to the RPE surface; 6) the presence of retinal neural tissue loss; 7) the appearance of retinal neural tissue loss; 8) the appearance of retinal neural tissue loss. 6. Pre-retinal astrocyte membranes appear. Clinical manifestations The disease is insidious and is often detected only when the other eye is covered. Patients often complain of blurred vision, dark spots in the center, and distorted vision. Visual acuity is generally 0.02~0.5, with an average of 0.1. Fundus performance and clinical staging According to the fundus performance at different stages of idiopathic macular schisisis, Gass divided it into four phases (Fig. 31-4): Phase I: at the initial stage of the disease, spontaneous contraction of the vitreous cortex in the front of the macular central concavity causes tangential pulling of the retinal surface, which leads to the detachment of the central concavity, disappearance of the central concavity reflections at the fundus, and disappearance of retinal pigmentation on the central concavity area. In the early stage of the disease, spontaneous contraction of the vitreous cortex in front of the central concavity caused tangential traction on the retinal surface, resulting in detachment of the central minor concavity, disappearance of the central concavity reflection, and the appearance of yellow dots on the surface of the retinal pigment epithelium (RPE) of the central concavity area (100-200 mm), which was the Ia stage; further contraction of the vitreous cortex in front of the central concavity, detachment of the central concavity, and the appearance of a yellow ring on the surface of the RPE (200-350 mm), which was the 1b stage; the Ia and 1b stages did not accompany the detachment of vitreous from the central concavity of the macula and no Stages Ia and 1b are not associated with separation of the vitreous from the central macula, and there is no “true” full-layer macular hole, which is clinically known as impending macular hole, and the visual acuity decreases slightly to 0.3~0.8, and the fluorescein fundus angiography can show slight hyperfluorescence of the central macular plexus. Stage II: Days~months after the onset of the disease, the vitreous body is further pulled in the tangential direction, and a macular hole is formed at the edge of the central notch, which gradually enlarges and develops from a crescent to a horseshoe shape, and finally forms a rounded hole, which is often accompanied by a capping membrane. In a few cases, the macular hole starts to form in the center of the central sulcus and gradually enlarges to become uncovered. Recently, it has been found that there is no loss of retinal central recess tissue during the formation of an idiopathic macular hole, and that the so-called “pre-capitulum” of the hole is the condensed posterior vitreous cortex. A subretinal fluid rim is seen around the macular tear, with yellow vitreous warty deposits at the tear, and visual acuity is reduced to 0.1-0.6. Fluorescein fundus angiography shows moderate hyperfluorescence. Stage III: After 2~6 months of the above lesions, due to retinal tissue contraction, the macular fissure enlarges to 400~500 μm, with or without a capping membrane, which is then a stage III macular hole. Yellow vitreous membrane warty deposits with subretinal fluid rim were visible, cystic changes around the small central concavity, and the visual acuity decreased to 0.02~0.5. Stage IV: Early manifestation was anterior displacement of the cover membrane of the macular hole, and the late manifestation was the complete separation of vitreous from the macula and the optic nerve papilla, which was then a stage 4 macular hole. Stage I macular hole (precursor hole): about 50% of the cases develop into a full-layer macular hole, and 50% of the cases resolve spontaneously after the vitreous body separates from the macular center. Stage II macular hole: Most cases develop a stage 3 hole after 2-6 months. In most cases, the size of the macular hole develops to more than 400mm. Stage III macular hole: less than 40% of cases progress to stage VI macular hole. 80% of cases have relatively stable vision. Usually, the RPE depigmentation of the retinal detachment area occurs after 1 year, and the pigment demarcation line can be seen after 6 months. In many cases, anterior retinal membranes are present. Occasionally, retinal detachment can occur with spontaneous retinal resetting: 1, separation of vitreous and macular central concavity: no risk of macular hole formation; 2, vitreous and macular central concavity are not separated: the possibility of macular hole formation is <15%; 3, macular anterior membrane covering the central concavity area, often accompanied by yellow dots: the possibility of macular hole formation is <1%; 4, macular central concavity anterior stellate clouding accompanied by retinal radial folds: no risk of macular hole formation; 5, anterior membrane covering central concavity area: no risk of macular hole formation. If yellow dots or rings appear in the macular area and are combined with other manifestations of the precursor macular hole, this indicates a high risk of macular hole formation. VII. Diagnostic points Since the introduction of fundus coherence tomography (OCT), macular hole diagnosis has not been difficult. When funduscopic examination found that the macular area suspected of broken hole OCT scan can determine the diagnosis. Eight, differential diagnosis 1, etiological differentiation: need to except idiopathic macular hole outside the causative cause, such as trauma, inflammation, high myopia, cystoid macular edema, fundus vascular disease, degenerative diseases, eclipsing retinopathy and other causes of secondary macular edema; 2, morphology differentiation: should be differentiated from the other 2 kinds of vitreous traction macular lesions. (1) idiopathic macular anterior membrane: sometimes combined with macular lentigo, fundus and OCT examination can clarify the diagnosis; (2) vitreomacular macular traction syndrome: often lead to macular traction deformation, macular edema, sometimes coexisting with macular lentigo. oCT examination can confirm the diagnosis; (3) laminar macular lentigo: OCT examination can clarify whether the macular lentigo is full or laminar; (4) macular lentigo retinal detachment: Often occurs in high myopia, idiopathic macular lacunae often appear around the macular lacunae with a shallow detachment halo of aperture origin warping, but rarely occurs in the real sense of retinal detachment. IX. Treatment principles and progress 1. Surgical treatment of macular holes used to be a forbidden area, and was only considered when there was a large range of peripheral retinal detachment. In recent years, due to the research on the pathogenesis of macular holes, it is recognized that the formation of macular holes is closely related to the traction of vitreous body on the tangential direction of macular central concavity. Therefore, removal of the vitreous cortex in front of the center concavity by vitrectomy has been widely performed to treat macular holes. The aim of the procedure is to relieve vitreomacular traction, and in stage I patients, removal of the vitreous, especially removal of the postvitreous cortex in front of the macular area, can reset the detached macular central pucker. In patients who have developed a full-layer macular hole, the surgical aims are multifaceted, including relief of vitreomacular macular pull, stripping of the pre-macular or intraretinal border membrane associated with the development of the macular hole, and intraocular gas tamponade to allow closure of the macular hole. For refractory macular holes (e.g., large or recurrent holes), the use of autologous serum, β2 transforming growth factor (TGF-β2), or autologous platelet concentrates applied to the macular holes may increase the choroidal retinal adhesions in the area of the holes, prompting the holes to close and heal. 2.Indications (1) Therapeutic vitrectomy: The aim is to induce closure of the macular hole and reset of the shallow retinal detachment around the hole. A. Those who are clearly diagnosed as stage II~IV idiopathic macular lacunae, with significant loss of visual acuity (0.05~0.4) and obvious visual distortion. B. Those who have macular lentigines formed within one year and are willing to undergo surgery. (2) In Gass's staging of macular schisis, stage I macular schisis did not form a full-layer macular hole, and about 1/2 of the patients with stage I macular schisis can be spontaneously relieved, so most do not advocate surgery for stage I macular schisis, and surgery can be carefully selected for patients with high risk of developing a full-layer macular hole. Whether vitrectomy can prevent the formation of a full-length macular hole is inconclusive. In a multicenter, randomized, controlled clinical study in the United States, for patients with stage I macular lentigines, the incidence of total macular lentigines in the vitrectomy group compared with the non-operated observation group was 37% and 40%, respectively (P=0.81), and the efficacy of prophylactic surgery cannot be confirmed at this time because the number of cases observed is still small. Therefore, the pros and cons of prophylactic vitrectomy for the treatment of stage I macular tears need to be weighed against the "pros" of the procedure, which are the relief of the mechanical pull of the vitreous body on the macula, and the "cons" of the possible risks of the procedure, which include the possibility of a total macular tear, a peripheral retinopathy, a peripheral retina, and the possibility of a peripheral retina. The "disadvantages" are the risks associated with the surgery, including: surgical operation may cause total macular tear, peripheral retinal medical source of tear, retinal detachment, infection, lens clouding and so on. 3, Surgical methods and progress Traditional surgical techniques are standard three-incision transciliary flat vitrectomy, artificial vitreous post-detachment, sub-total removal of the vitreous body, stripping of the macular anterior membrane or inner retinal border membrane in the macular area, or supplemented with biological agents to close the macular hole. Expanded gas/air exchange was performed with 20% to 25% SF6 gas. After the operation, the patient was placed in prone position for about 14 days, the gas in the vitreous cavity was absorbed and normal position was restored. (1) Mini-incision vitreous surgery In 2002, the 25G transconjunctival sutureless vitrectomy system was introduced, and in 2003, the 23G sutureless vitrectomy system was used for vitreous surgery. Currently, these two vitrectomy devices have been used in idiopathic macular hole surgery. In China, Zhao Mingwei et al. proposed the 20G maneuver for small incision vitreous surgery, which also achieved good results and reduced the cost of surgery. (2) Internal Border Membrane Staining Technique The internal border membrane is mostly removed using the internal border membrane staining technique, and the staining agents include trypan blue, brilliant blue G, bromphenol blue, BPB, Chicago blue, CB, triamcinolone, TB, TB, TB, TB, TB, and TB. Triamcinolone (TA) and indocyanine green (ICG). Triamcinolone does not color the inner border membrane, but it can make it easily recognizable. Figure 7 After surgery in the patient in Figure 1, the macular hole was closed and the macular central concavity morphology was restored 4. Surgical complications The surgical complications of treating idiopathic macular schisis are similar to those of ordinary vitrectomy, including nuclear cataracts, transient hypermetropia, medically induced retinal schisis production, enlargement of the macular schisis, phototoxicity-induced retinal pigment epitheliopathy, vascular occlusion, and endophthalmitis. The incidence of nuclear cataracts is the highest, ranging from 12% to 90%, and the literature reports that cataract extraction and IOL implantation is required in about 33% of cases 5 to 16 months after the initial surgery, and that in eyes with a closed macular fissure, visual acuity is restored to pre-vitreous surgery visual acuity or better. Transient hypertension occurs in about 17.4% of operated eyes, mostly within 3 weeks after surgery, mainly due to gas filling, and is usually treated symptomatically. During the operation, we try to avoid the occurrence of medical retinal tears. If medical retinal tears occur, laser sealing should be used instead of condensation sealing as far as possible to minimize the occurrence of postoperative complications such as macular anterior membranes. X. Surgical evaluation and prognosis The main reasons for vision loss in macular lacunae are as follows: 1. absence of retinal photoreceptor cells at the lacunae; 2. shallow detachment of the retina around the lacunae; 3. cystic edema around the lacunae; 4. different degrees of degeneration of the optic cells around the lacunae. Through vitrectomy surgery to loosen the anterior and posterior direction of the fissure as well as the tangential direction of the pull, so as to eliminate the cause of the disease; through the gas filling and biological factors to make the macular fissure closed, to promote the reset of the retinal neural epithelium, and thus can improve the visual acuity and vision distortion and other symptoms. The efficacy of different surgical methods in treating macular schisis varies from study to study. kelly (1991) et al. used vitrectomy alone (52 cases), the rate of schisisis closure was 58%, and the improvement of visual acuity by more than 2 rows was 42.3%, and the cumulative number of cases by the same author reached 170 cases 2 years later, at which time the rate of schisisis closure was 73%, and the improvement of visual acuity by more than 2 rows was 55%. In recent years, it has been found that the use of autologous platelets, autologous serum, transforming growth factor β2 (TGF-β2), and fibrinogen to fill in the macular fissure during surgery increases the healing of choroidal retinal adhesions at the fissure and effectively improves visual acuity. The literature reports that the closure rate of the macular slit using vitrectomy combined with TGF-β2 is 91% to 100%, and the visual acuity improves by more than 2 lines of 83% to 90.1%, but there are some patients who failed to repeat the same results and found that the postoperative intraocular pressure increase response is obvious. Recently, Thompson et al. reported that there was no significant difference in anatomical restoration of the macular fissure and improvement of visual acuity when using TGF-β2 versus placebo, and Gaudric (1995) et al. were the first to report on the use of autologous platelet concentrates to close the macular fissure, and the use of vitrectomy alone as a control (20 cases each), which resulted in 95% fissure closure rate in the platelet group, 85% improvement in vision over 2 rows, and 85% improvement in vision over 2 rows in the platelet group. In the platelet group, the closure rate was 95%, and the visual acuity improved by more than 2 rows was 85%, while the closure rate of the macular slit in the simple vitrectomy group was only 65%. In recent years, as surgical techniques continue to improve, there is increasing evidence that the use of vitrectomy alone in combination with endothelial membrane peeling can achieve a high surgical success rate.The results of a randomized controlled clinical trial by Christensen et al[10] showed that for stage 2 versus stage 3 idiopathic macular holes, the rate of macular hole closure after endothelial membrane peeling was significantly higher than that in the group with no endothelial membrane peeling (stage 2 macular hole For stage 2 and stage 3 idiopathic macular holes, the rate of macular hole closure was significantly higher after endostealing than in the group without endostealing (stage 2 macular holes, 100% versus 55%, stage 3 macular holes, 91% versus 36%). Disease prevention For non-idiopathic macular lentigines with a clear etiology, macular lentigines can be prevented by treating the primary disease and by close follow-up examinations. There is no effective prevention method for idiopathic macular lentigines. Twelve, disease care macular cleft surgery due to intraocular gas filling, postoperative prone position, prone duration depends on the type of intraocular gas filling. Generally 1-2 w. At this time, according to the vitreous surgery after intraocular filling nursing routine care.