| disease | Primary Retinal Detachment |
| alias | Retinal Detachment |
Primary retinal detachment is a common clinical condition, with a higher incidence in males than females at a ratio of approximately 3:2. Most patients are adults over 30 years old, and it is rare in children under 10 years old. There is no significant difference between the left and right eyes, with bilateral incidence accounting for about 15% of the total cases. It frequently occurs in myopic eyes, especially high myopia.
bubble_chart Etiology
Primary detachment is the result of the combined action of two factors: retinal degeneration and vitreous degeneration. In other words, primary detachment must have these two prerequisites, and neither can be omitted.
1. Retinal Degeneration and Hole Formation Due to the complex structure and unique blood supply of the retina, it is prone to degeneration due to various reasons. The peripheral and macular regions are common sites for degeneration. Retinal degeneration is the basis for the formation of retinal holes. Before the occurrence of holes, the following changes are often observed:
⑴ Lattice Degeneration: Lattice degeneration is most closely related to retinal detachment. It accounts for 40% of rhegmatogenous detachment cases. It can also be seen in normal eyes, with an incidence of about 7%. Lattice degeneration shows no racial or gender differences, affects both eyes, and often exhibits symmetry in formation and location. It is commonly found in the temporal or superotemporal quadrant between the equator and the ora serrata, appearing as spindle-shaped or strip-like, well-defined island-like lesions. The long axis is parallel to the ora serrata, and the lesion size varies greatly, ranging from 1DD to more than half the circumference in length and from 0.5DD to 2DD in width. The retinal tissue in the lesion becomes thin, with numerous white lines arranged in a grid-like pattern. These lines are connected to retinal vessels outside the lesion and are actually occluded or sheathed peripheral vessels. Sometimes, white pigment clumps are seen within the lesion, referred to as pigmented lattice degeneration, with the pigment originating from the retinal pigment epithelium.
⑵ Cystoid Degeneration: This commonly occurs near the macula and the inferotemporal ora serrata, presenting as well-defined, round or oval, dark-red lesions. Small cavities may merge into larger cysts, resulting in significant size variation. Reticular cystoid degeneration in the peripheral fundus appears as clustered, slightly elevated small red dots, with nearby vitreous showing fibrous or granular opacities. Early macular cystoid degeneration manifests as honeycomb-like small cavities, particularly evident under red-free light examination. Small cavities in the periphery or macula gradually merge into larger cysts. The anterior wall may rupture due to vitreous traction, but only when both anterior and posterior walls rupture does it become a true hole leading to retinal detachment.Cystoid degeneration is caused by various factors (e.g., aging, inflammation, trauma, high myopia) affecting retinal metabolism, leading to the breakdown of neural components and the formation of cavities in the inner plexiform layer or inner/outer nuclear layers. These cavities are filled with fluid containing mucopolysaccharides.
⑶ Frost-like Degeneration: This mostly occurs near the equator and ora serrata, where the retinal surface shows areas covered with fine white or slightly yellow shiny granules. The thickness varies, resembling frost on the retina. This degeneration can occur alone or coexist with lattice or cystoid degeneration. When frost-like degeneration near the equator merges into a band-like pattern, it is also called snail-track degeneration.
⑷ Paving Stone Degeneration: This is typically seen in myopic patients over 40 years old, often bilaterally. It predominantly occurs in the inferior peripheral fundus, presenting as multiple, well-defined, round or oval, pale-yellow atrophic lesions with pigmented borders. The lesions vary in size and appear like paving stones. The central part of the lesion shows atrophy of the choriocapillaris, exposing larger choroidal vessels or even pale sclera. If the degenerated area is subjected to vitreous traction, it may lead to retinal hole formation.
(6) Dry retinal membrane longitudinal folds: The folds extend from the interdental spaces of the serrated margin toward the equator. They are folds of overgrown retinal membrane tissue. Generally, no treatment is required, but there is a possibility that a hole may develop at the posterior end of the fold due to vitreous traction.
2. Vitreous Degeneration: Another Key Factor Leading to Retinal Detachment Under normal circumstances, the vitreous is a transparent gel-like structure that fills 4/5 of the posterior cavity of the eyeball, providing support for the adhesion of the retinal neuroepithelial layer to the pigment epithelial layer. Except for adhesions at the pars plana of the ciliary body to the ora serrata, around the optic disc, and the retina, other areas are only tightly attached to the inner limiting membrane of the retina without adhesion.
Before retinal detachment occurs, common vitreous degenerative changes include interrelated vitreous detachment, liquefaction, opacities, membrane formation, and condensation.
(1) Vitreous Detachment (detachment of vitreous body): Vitreous detachment refers to the appearance of gaps between the vitreous interface and the tissues it closely contacts. It is more common in highly myopic eyes and elderly patients. Detachment can occur at any external interface of the vitreous, with posterior and superior vitreous detachment being the most common and closely related to retinal detachment.
The primary cause of vitreous detachment is the depolymerization and dehydration of hyaluronic acid in the vitreous, forming one or more small liquefied cavities that merge into larger spaces. If the fluid in these spaces breaks through the external vitreous interface and enters the front of the retina, separation occurs between the vitreous and the inner limiting membrane of the retina. If pathological adhesions exist at the detachment site, retinal tears may occur due to traction.
(2) Vitreous Liquefaction (fluidity of vitreous body): Vitreous liquefaction is the transformation of the vitreous from a gel state to a dissolved state, caused by the disruption of colloidal balance due to metabolic dysfunction. It is also common in highly myopic and elderly patients. Liquefaction typically begins at the center of the vitreous, forming an optical space that gradually enlarges, or multiple small liquefied cavities may merge into a larger one. Semi-transparent gray-white filamentous or flocculent materials float within the liquefied cavities.
(3) Vitreous Opacities and Concentration (vitreous opacities and concentration): Vitreous opacities have many causes, but those related to primary retinal detachment result from the destruction of the vitreous scaffold structure, often coexisting with vitreous detachment and liquefaction. The opacified fibrous strands may lead to retinal tears.
The so-called vitreous concentration is also a form of vitreous opacity, occurring when the scaffold structure dehydrates and degenerates during advanced liquefaction, forming an opaque body, hence termed atrophic concentration. Compared to the membrane-like opacities at the external interface during vitreous detachment or the filamentous/flocculent opacities in liquefied cavities, there is no significant qualitative difference, only a more severe degree, increasing the risk of retinal detachment.
(4) Vitreous Membrane Formation: Also known as massive periretinal proliferative membrane, its formation mechanism is highly complex and not yet fully understood. It may involve glial cells, free pigment epithelial cells, transformed macrophages, fibroblasts, and others. The proliferative membrane grows along the anterior or posterior retinal interface or the external vitreous interface. Upon contraction, it can pull the retina, causing folds, forming fixed adhesive folds or star-shaped folds, or even shrinking the entire posterior retina into a closed funnel shape.
This proliferative membrane is observed in patients before retinal detachment, during detachment, or in cases of long-standing detachment. When occurring before detachment, it is also a significant cause of retinal detachment.
Membrane formation is classified into three grades based on severity, as detailed later.
In summary, the so-called primary detachment is merely a conventional term, as it is actually secondary to degeneration of the retina and vitreous. Retinal holes, along with vitreous liquefaction, detachment, and pathological adhesions to the retina, are two indispensable conditions for causing primary retinal detachment—neither can be omitted. For instance, clinically, some cases exhibit clear retinal holes, yet as long as the vitreous remains healthy, retinal detachment does not occur. Similarly, when only vitreous degenerative changes are present without retinal holes, retinal detachment also does not occur. For example, observations show that 65% of individuals aged 45–60 have posterior vitreous detachment, yet only a minority develop retinal detachment. This further illustrates that retinal detachment results from the mutual influence and combined effects of retinal degeneration and vitreous degeneration. Retinal holes often form due to various manifestations of degenerative changes in the upper layers, exacerbated by pathological vitreous adhesions and traction. Vitreous liquefaction and detachment, on one hand, weaken the supportive force that adheres the retinal neuroepithelial layer to the pigment epithelial layer, while on the other hand, liquefied vitreous may infiltrate beneath the neuroepithelial layer through the holes.
Additionally, it has been observed that retinal breaks often occur at locations corresponding to the attachment points of the superior and inferior oblique muscles in the fundus, leading to the speculation that these breaks are related to the traction caused by the movement of these muscles. Others have noted that many patients recall a history of minor trauma to the fundus, suggesting that detachment may be associated with trauma. In reality, except for a few special cases such as severe blunt trauma to the eye, the traction of the oblique muscles and trauma can only be considered as predisposing factors for retinal detachment.
bubble_chart Clinical Manifestations
1. Symptoms and findings of visual function examination
(1) Central vision impairment: Varies depending on the location and extent of retinal detachment. When the posterior pole is detached, vision suddenly and significantly declines. In peripheral detachment, central vision is initially unaffected or minimally affected. Central vision impairment only occurs when the detachment extends to the posterior pole.
(2) Metamorphopsia: Occurs when peripheral detachment spreads to the posterior pole, causing shallow detachment. In addition to decreased central vision, symptoms such as distorted or shrunken vision may appear.
(3) Floaters: Seen in vitreous opacities caused by various factors. A sudden increase in floaters should raise suspicion of being a precursor symptom of retinal detachment.
(4) Photopsia: The most important symptom of retinal detachment, which may serve as a precursor. In cases of vitreous degeneration with pathological adhesion to the retina, traction from the vitreous during eye movement stimulates photoreceptor cells, causing flashes of light. If flashes persist and are localized to a specific area of the visual field, retinal detachment may occur soon. Photopsia can also occur in patients with existing retinal detachment, caused by liquefied vitreous entering the sub-neurosensory layer through a retinal tear and stimulating retinal cells.
(5) Visual field changes: In peripheral retinal detachment, patients may notice shadows or visual field defects in the corresponding opposite area. However, in temporal retinal detachment, the nasal visual field defect falls within the binocular visual field and may go unnoticed by the patient, only being detected during visual field testing.
Retinal detachment involves the neurosensory layer, and due to nutrient supply issues, photoreceptor cells are the first to be damaged. Photoreceptor cell impairment primarily affects blue color vision. In normal eyes, the blue visual field is larger than the red visual field. When examining the visual field with white, blue, and red targets in a detached eye, not only are there form visual field defects in the corresponding area, but also a crossover between blue and red visual fields.
2. Intraocular pressure (IOP) In early stages with limited detachment, IOP is normal or slightly low. As the detachment expands, IOP decreases further. Detachments exceeding one quadrant result in significantly reduced IOP, sometimes too low to measure with a tonometer. The drop in IOP may be related to the hydrodynamic changes in the detached eye. In the posterior segment, there is a misdirected flow of aqueous humor from the posterior chamber through the vitreous and retinal tear into the sub-neurosensory space, transported by the pigment epithelium, and eventually drained by the choroidal vascular system.
3. Findings on slit-lamp microscopy and ophthalmoscopy The anterior segment is generally normal. The anterior chamber may be slightly deeper. Prolonged detachment can cause mild uveal inflammation, with weak Tyndall phenomenon in the aqueous humor and brown punctate deposits on the corneal endothelium.
Vitreous opacities and liquefaction are inevitable in primary detachment. These changes are more clearly visible under slit-lamp microscopy. Liquefied cavities appear as structureless optical spaces. Between these cavities, dehydrated and atrophied vitreous scaffold tissue forms silk-like opacities. Sometimes, brown or gray-white opacities are present within the liquefied cavities or silk-like opacities. As liquefied cavities expand and merge, liquefied vitreous passes through the outer boundary into the space between the retina and the vitreous surface, leading to vitreous detachment. Depending on location, vitreous detachment can be anterior, superior, lateral, or posterior, with superior and posterior detachments being most closely related to retinal detachment. Vitreous detachment often involves varying degrees of pathological adhesion to the retina, termed incomplete detachment. Traction at adhesion sites can lead to retinal tears. Under slit-lamp examination, the detached vitreous interface appears as an uneven, veil-like opacity. In posterior detachment, a gray-white annular vitreous posterior interface tear may be seen. This annular opacity results from the detachment of the vitreous from the optic disc margin. Over time, it may become crescent-shaped, irregular, or condense into an opaque mass.
The various lesions of the vitreous body mentioned above can also be observed under a direct ophthalmoscope. However, they are not as clear, well-layered, or three-dimensional as when examined with a slit-lamp microscope.
Under direct ophthalmoscopy, the detached retina appears undulating and elevated, moving in a wave-like manner with eye movement. In fresh detachments, the neuroepithelial layer and the subretinal fluid are transparent, allowing visualization of the yellowish-red or pale-red choroidal hue beneath the retinal pigment epithelium, though the choroidal texture remains indistinct. Retinal vessels crawling over the detached surface act as light-blocking structures, appearing as dark-red lines, making it difficult to distinguish arteries from veins. Occasionally, vessel shadows corresponding to the retinal vessels may also be observed. In longer-standing detachments, the neuroepithelial layer becomes semi-transparent, resembling paraffin paper. The detached arteries and veins become distinguishable. In chronic detachments, the subretinal fluid, due to choroidal exudative reactions and increased fibrin, turns light brown and viscous, with yellowish-white punctate deposits on the posterior surface of the neuroepithelial layer.
Retinal breaks are often found in areas of detachment, numbering from 1 to several. The superotemporal quadrant is a common site for breaks, but due to gravity, the subretinal fluid settles, leaving the break area either minimally detached or undetached.
With a direct ophthalmoscope, up to 70º of the fundus can be examined after full pupil dilation and eye rotation. Breaks beyond this 70º periphery are harder to detect and require binocular indirect ophthalmoscopy, sometimes supplemented with scleral depression. Alternatively, a slit-lamp microscope with a three-mirror lens and scleral depression can be used to examine breaks near the ora serrata, the pars plana, or degenerative changes at the vitreous base.
4. Retinal Breaks Theoretically, primary detachments should reveal breaks in 100% of cases. However, due to various clinical factors, even with advanced diagnostic methods, the detection rate remains around 90%.
Breaks within the central 70º of the fundus are easier to detect than those in the far periphery. Larger breaks are also more readily identified than smaller ones. Small breaks, often near retinal vessels, can be mistaken for hemorrhages and require repeated, careful observation for differentiation.
Round breaks are more common. Those located at the macula are termed macular holes, as previously described. They may also appear in the peripheral fundus, either as single or clustered lesions, or scattered. The edges are sharp. Breaks caused by cystoid degeneration lack a membrane-like operculum corresponding in size. Those caused by vitreous traction may show an operculum (torn neuroepithelial layer).
Horseshoe-shaped or similar breaks (e.g., crescent-shaped, tongue-shaped, or gaping breaks) are the most prevalent, accounting for 25–68% of rhegmatogenous retinal detachments, with single breaks being particularly common. These breaks also result from vitreous traction on the retina, with broader adhesion areas compared to round breaks. The size of the break correlates with the extent of adhesion and traction force. Since one end of the traction adheres to the retina and the other to the vitreous, the base of a horseshoe-shaped break always faces the periphery, with the apex pointing toward the posterior pole. Larger horseshoe breaks often have a rolled posterior edge and a lifted flap, making the actual break area larger than what is seen under ophthalmoscopy.
Irregular breaks in the peripheral retina are rare, appearing as linear or irregular shapes. If the lines are very fine and the surrounding retina is not detached, they may be mistaken for peripheral vessels.
Dialysis of the ora serrata occurs at or near the ora serrata (vitreous base) and represents the largest type of retinal break, often located in the inferotemporal quadrant. The dialysis line runs parallel to the limbus, spanning a quadrant, half the circumference, or even the entire circumference. The term "dialysis" is used because these large breaks lack an anterior edge, with the posterior edge of the retina retracting and curling into a grayish-white arc, contrasting sharply with the dark-red area devoid of retina. Ora serrata dialysis is more common in young individuals, often with a history of blunt ocular trauma, and may also occur secondary to retinoschisis.
5. Vitreous membrane formation and its grading The formation of a vitreous membrane actually includes membrane-like proliferation on the inner and outer surfaces of the retinal neuroepithelial layer. Its formation mechanism has been mentioned earlier. The severity of vitreous membrane formation is of great significance in terms of retinal detachment formation, surgical approach selection, and prognosis. The commonly used grading systems in China are the grading method proposed by Zhao Dongsheng and the grading method proposed by the International Retinal Association.
Zhao Dongsheng Classification:
Grade 0: Vitreous liquefaction and posterior detachment are present, but no proliferative changes.
Grade I: The wall of the vitreous liquefaction cavity thickens, and posterior holes form. The vitreous base shifts posteriorly. Membrane proliferation occurs near the ora serrata and the edges of lattice degeneration. Horseshoe tears have opercula and membrane-like traction bands on the posterior lip, while round tears have opercula anteriorly. Membranes form in the vitreous and can float significantly.
Grade II: In addition to Grade I changes, fixed retinal folds or annular folds appear. The folds are located at or anterior to the equator. Annular folds may represent further progression of the posterior shift of the vitreous base.
Grade III A: Fixed folds are located posterior to the equator, approximately near the superior and inferior vascular arcades of the retina. The vitreous shows condensation changes. Annular folds reach the equator.
Grade III B-1: Fixed folds and annular folds extend near the optic disc, forming a shallow funnel shape. The vitreous is condensed.
Grade III B-2: The same folds form a deep funnel shape. Proliferative membranes cross the funnel, and the vitreous is condensed. There is extensive adhesion between the retina and vitreous.
Grade III B-3: The same folds form a funnel, the funnel closes, the optic disc becomes invisible, and the vitreous is condensed.
International Retinal Society Classification:
Grade A: Vitreous condensation and pigment clumps are present in the vitreous.
Grade B: The inner retinal surface shows folds and/or rolled edges of retinal breaks, with marked vascular distortion at the folds.
Grade C: Full-thickness fixed retinal folds are present, subdivided into three levels: C 1 , fixed folds occupy one quadrant; C 2 : fixed folds involve two quadrants; C 3 , fixed folds extend to three quadrants.
Grade D: Fixed folds involve all four quadrants, manifesting as radial folding centered on the optic disc or massive star-shaped folds covering the entire retina. Further divided into three levels: D 1 is a wide funnel shape; D 2 is a narrow funnel shape (under indirect ophthalmoscopy, the anterior opening of the funnel is within a 45º range of a +20D lens); D 3 the funnel is very narrow or closed, and the optic disc is not visible.
Several Special Types of Retinal Detachment:
1. Congenital Choroidal Coloboma with Retinal Detachment Congenital choroidal coloboma results from incomplete closure of the fetal fissure during embryonic development. The neurosensory retina in the coloboma area is prone to detachment. Beneath the transparent retina in the coloboma lies the white sclera, and retinal breaks are often undetectable in most patients. If hemorrhage is present in the choroidal coloboma, breaks are usually nearby. During surgery, attention should be paid to sealing the posterior edge of the choroidal coloboma, but due to the large extent of the defect, outcomes are poor.
2. Retinal Detachment in Aphakic Eyes Detachment occurs 1 to several years after cataract surgery. Due to the anterior shift of the iris-lens barrier, especially in cases with intraoperative vitreous loss, posterior vitreous detachment often develops postoperatively. Retinal breaks are round, ranging from 1 to several, and may be scattered across quadrants, mostly in the peripheral fundus. Sometimes, vitreous adhesions may be observed.
Based on the above clinical findings, the diagnosis is not particularly difficult, but small peripheral shallow detachments are often easily misdiagnosed as fistula disease, especially detachments in the extreme periphery, which cannot be detected by direct ophthalmoscopy. They must be confirmed through repeated and careful examination using binocular indirect ophthalmoscopy or a three-mirror lens combined with scleral depression.
Identifying retinal breaks is not only the basis for diagnosing primary detachment but also the key to surgical success. Therefore, it is crucial to accurately and thoroughly detect all breaks. Approximately 80% of breaks occur in the peripheral retina, with the superotemporal quadrant being the most common, followed by the inferotemporal, superonasal, and finally the inferonasal quadrant. When the detachment is highly elevated, these peripheral breaks are often obscured and must be meticulously searched for from various angles. If necessary, bilateral eye patching and several days of bed rest may be required to allow slight flattening of the retina before re-examination. Larger and more elevated retinal detachments often have multiple breaks. In addition to examining the detached area, attention should also be paid to non-detached or minimally detached regions, especially superior breaks, as the subretinal fluid may settle, making the detachment less apparent at the break site. The location and shape of the retinal detachment can also aid in locating breaks. For superior detachments, breaks are usually within the superior detached area; for inferior detachments, if the detachment is dome-shaped, the break may be directly above it. In cases of extensive detachment, the break may be at the higher edge of the superior margin of the detached area. If both sides are similar, the break is often located in the inferior periphery.
Patient complaints can sometimes provide clues for locating breaks. The initial position of scotomas and photopsia in the visual field often corresponds to the location of the break.
Small breaks in the detached area should be carefully distinguished from hemorrhages on the retinal surface. Within the range detectable by slit-lamp examination, the two can be easily differentiated. However, differentiation becomes more challenging, even extremely difficult, in the periphery and may require repeated observations over time to confirm.
bubble_chart Treatment Measures
To this day, primary retinal detachment is still primarily treated surgically. The surgical principle involves applying diathermy, cryotherapy, or external or internal photocoagulation to the scleral surface corresponding to the retinal break, inducing localized choroidal reactive inflammation to create adhesions between the choroid and the neurosensory layer of the retina, thereby sealing the break. To achieve this goal, it is also necessary to alleviate or eliminate vitreous traction on the retina, drain subretinal fluid, apply external scleral buckling, perform scleral shortening or encircling procedures to reduce the intraocular volume, or inject certain gases or liquids into the vitreous cavity to enhance contact between the neurosensory layer and the retinal pigment epithelium. In cases of severe vitreous traction, vitrectomy may be required. The choice of surgical approach depends on the extent of retinal detachment and the presence of vitreous membranes. Selecting the appropriate surgical method and accurately locating the retinal break are crucial.
It must be emphasized, as previously mentioned, that so-called primary retinal detachment is actually secondary, resulting from the interaction between retinal degeneration and vitreous degeneration. Therefore, strictly speaking, surgical treatment is not a cure for the underlying cause but rather a symptomatic treatment. Even after successful surgery, it remains necessary to prevent further progression of retinal and vitreous degeneration. The use of Chinese or Western medications to counteract tissue degeneration and improve choroidal and retinal microcirculation is still essential.
Generally speaking, the smaller the detachment range, the fewer the number of breaks, the smaller the area of the breaks, and the milder the vitreous membrane formation, the higher the success rate of surgery, and vice versa. For patients whose breaks cannot be found before surgery, those with extensive adhesions between the vitreous and retina that cannot be resolved, and elderly patients, the success rate is low. For highly myopic eyes, aphakic eyes, and those with congenital choroidal membrane defects, the chances of success are even lower.
The success rate is higher if the detachment time is within 2 months. The longer the time, the lower the possibility of success.
The success of the surgery is judged by whether the retina can be reattached. However, retinal reattachment does not necessarily correspond to the recovery of visual function. For example, in so-called old detachments lasting more than 6 months, because the photoreceptor cells have suffered irreversible damage, even if the retina is reattached postoperatively, visual function cannot improve, and absolute visual field defects persist. The prognosis for central vision mainly depends on whether the macula is affected (detachment, cystoid degeneration, fixed stellate folds, etc.) and the duration of the damage.
Clinically, spontaneous retinal reattachment is occasionally observed, with yellowish-white lines appearing in the original detachment area or at its edges, located beneath the neuroepithelial layer, with retinal blood vessels crossing over them, known as linear retinal lesions (historically termed linear retinitis). These lines may result from the organization of fibrin fluid beneath the neuroepithelial layer. The spontaneously reattached area also exhibits depigmented spots and pigment spots, and the overall hue differs from the non-detached area. Since spontaneous reattachment occurs only after a prolonged period following detachment, visual field recovery is impossible; if the lines cross the macula, central vision suffers irreversible and severe damage.
The incidence of bilateral primary retinal detachment is approximately 15%. Therefore, when one eye has already experienced detachment, the other eye must undergo a thorough fundus examination with full pupil dilation. If retinal degeneration, tears, or even shallow detachment are detected, prompt surgical intervention is necessary to prevent further progression of the detachment. For cases with only tears or degeneration but no significant vitreous degeneration, no adhesive traction around the tears, and no fixed-area photopsia in the patient, prophylactic surgery is generally not required. However, patients must pay attention to maintaining health, avoid heavy lifting and strenuous exercise, and may use Chinese or Western medications that resist degeneration and improve choroidal-retinal microcirculation over an extended period. Conversely, cryotherapy or photocoagulation should be considered. For tears in the posterior fundus with minimal subretinal fluid, photocoagulation can be used; for peripheral tears, cryotherapy is preferred, which can be performed without incising the conjunctiva, making the method relatively simple. Nevertheless, extreme caution is required to properly control the area and intensity of cryotherapy. For macular holes, even if shallow detachment or radial folds are observed, photocoagulation is not advisable as long as the vitreous remains largely healthy and some vision is preserved.
Primary retinal detachment needs to be differentiated from the following diseases:
1. Retinoschisis Degenerative retinoschisis is located in the inferior peripheral fundus, presenting as a hemispherical elevation that develops from cystic degeneration. The inner wall is thin and transparent, while pigment deposition may occur near the outer wall margin. If both the inner and outer walls rupture, it becomes a true hole, leading to rhegmatogenous retinal detachment. Congenital retinoschisis is often detected in school-aged children. It has a familial history, and retinal vessels often exhibit white sheathing. The lesions are located in the inferior or inferotemporal fundus and are bilateral and symmetrical. If the inner wall ruptures, forming a large hole, it resembles ora serrata dialysis, but its anterior edge does not reach the ora serrata.
2. Central serous chorioretinopathy (referred to as "CSC") "CSC" itself involves shallow detachment of the neurosensory layer in the macula or its vicinity. It is a self-limiting condition that can resolve spontaneously, differing from primary retinal detachment. If retinal detachment invades the macula, it may cause metamorphopsia and micropsia, symptoms similar to "CSC." A dilated fundus examination of the peripheral retina should be performed.
3. Uveal effusion syndrome (choroidal effusion) Often accompanied by retinal detachment, it presents as a hemispherical elevation that tends to shift with changes in body position and lacks a retinal break.
4. Solid retinal detachment Refer to the following sections or related chapters. Cases with severe vitreous opacity are more prone to misdiagnosis. Ultrasound examination or CT scanning can aid in differentiation.
