(A) Disease Introduction
Retinal detachment is a pathological state in which the retinal neuroepithelium and pigment epithelium are separated from each other. In embryogenesis and histology, there is a potential gap between the retinal neuroepithelium and the pigment epithelium. Under normal conditions, through a series of physiological and biochemical mechanisms, the retinal neuroepithelium and the pigment epithelium adhere to each other to ensure the normal physiological function of the retina. After retinal detachment occurs, due to the damage of photoreceptor cell nutrition, if it is not reset in time, the retina will be atrophied and degenerated, and the visual function will be seriously damaged.
(B) Disease classification
According to the different pathogenesis of retinal detachment, it is divided into two categories: pore-derived and non-pore-derived retinal detachment, and the latter is further divided into retinal detachment by retraction and retinal detachment by exudation. The most common one is foraminogenic retinal detachment.
1.Pore-derived retinal detachment
Pore-derived retinal detachment is the most common type of retinal detachment. Due to the presence of retinal fissure (atrophic hole or retraction tear hole), when there is also vitreous pulling factor on the retina, the liquefied vitreous enters the subretina, resulting in the separation of retinal nerve retinal layer and pigment epithelium layer.
2.Exudative retinal detachment
Exudative retinal detachment or serous retinal detachment occurs in the course of certain diseases, but does not combine with fissures. It is common in cases of retinal vascular or retinal pigment epithelial damage. Exudative or serous retinal detachment can occur secondary to inflammatory disease, retinal vascular disease, tumors of the retina and choroid, and hemorrhage.
Subretinal fluid movement is characteristic of exudative retinal detachment, where the flow of subretinal fluid is in the same direction as gravity. For example, in the sitting position, the lower retina detaches; in the supine position, the subretinal fluid flows toward the back of the eye. The smooth surface of the detached retina is another characteristic of exudative retinal detachment. Retinal surface wrinkles and fixed folds also rarely occur with long duration of disease.
Treatment includes etiological treatment, condensation, laser photocoagulation, radiotherapy and surgery. Surgical treatments include scleral buckling or subretinal fluid drainage.
3. Retinal detachment by traction
Retinal neuroepithelium is pulled apart from pigment epithelium by intravitreal proliferative membrane due to proliferative retinopathy or penetrating eye trauma. Retinal detachment is slow in progression and may be asymptomatic in the early stages of the disease. When the retinal detachment has reached a certain level or extent, the patient may experience severe vision loss or visual field loss. The retina may be flattened and elevated at the site of retinal detachment, with twisted and distorted vessels, poor retinal mobility, mostly smooth surface, but also with retinal folds, usually without retinal fissures, subretinal hyperplasia and subretinal deposits or a small amount of vitreous blood. In some cases of retinal detachment due to severe vitreous opacification, the fundus cannot be seen preoperatively and ultrasonography should be performed. In some cases, retinal fissures are caused by retraction, in which case the fundus manifestations include both foraminogenic and retinal detachment of retinal origin, called retinal detachment of retraction-porous origin. Treatment includes scleral buckling surgery, vitrectomy or combined intraocular filling.
(iii) Causes and pathogenesis
The three elements of foraminogenic retinal detachment are: (1) retinal fissure; (2) vitreous traction on the retina; and (3) continuous fluid flow through the retinal hole into the subretina. Although retinal lacunae are an important factor in the development of foraminogenic retinal detachment, only about 1 or 4% of patients with retinal lacunae develop retinal detachment. The reason for this is that under normal conditions, there are mutual apposition forces between the retinal neuroepithelium and pigment epithelium, including the osmotic pressure between the choroid and vitreous, the pump mechanism of the retinal pigment epithelium, the presence of acidic mucopolysaccharide (which acts as a glue) between the outer segment of the retinal photoreceptors and the retinal pigment epithelium, and the mutual misalignment between the retinal pigment epithelium and the photoreceptors. Therefore, in order for retinal detachment to occur, the above mutual apposition between retinal neuroepithelium and pigment epithelium must be overcome. When there is a pull around the retinal fissure, if the liquefied vitreous comes into contact with the retinal fissure, the combined effect of these two factors will lead to the occurrence of hole-derived retinal detachment.
1. Vitreous degeneration and detachment
Retinal traction during posterior vitreous detachment is one of the common causes of retinal fissure formation, while posterior vitreous detachment is mostly the result of vitreous liquefaction or degeneration. Initially, vitreous liquefaction occurs centrally and superiorly, gradually forming a liquefied cavity that extends from the optic nerve papilla to the base, and eventually, posterior vitreous detachment occurs. A posterior vitreous cortical fissure usually occurs in the macula, and the liquefied vitreous passes through the posterior cortical fissure between the posterior vitreous cortex and the retina, resulting in a large posterior vitreous detachment. Complete posterior vitreous detachment is age-related, occurring in 27% of people aged 60-69 years and in 69% of those aged 70 years and older.
Because of the strong attachment between the basal vitreous and retina, when posterior vitreous detachment occurs, a traction tear hole (retinal tears) can be produced at the base of the vitreous, which can be covered (horseshoe-shaped fissure) and adhered to the posterior vitreous surface or separated from the retina and free and adhered to the posterior vitreous surface.
2. Abnormal adhesion between vitreoretinal tears
Developmental mutations or degeneration can lead to enhanced adhesion of the vitreoretinal membrane, which is the reason why a large number of retinal fissures occur in posterior vitreous detachment. Developmental vitreoretinal variants associated with retinal fissures include closed mouth-like depressions, serrated-edge meridian retinal folds, meridian-oriented complexes, retinal capsular plexuses, and small banded tractional plexuses. Closed mouth-like depressions can be misunderstood as retinal lacunae and are associated with retinal tear holes. Meridional retinal folds do not increase the risk of retinal detachment, but retinal tear holes in retinal detachment can be located at the posterior border of the meridional retinal fold. The retinal cystoid plexus is an extra-basal damage that occurs in 5% of the population and is associated with approximately 10% of retinal detachments of foramen ovale. Retinal atrophy holes adjacent to the retinal cystoid plexus rarely result in foraminal retinal detachment. In 0,11% of cadaveric eyes there are small banded traction plexuses that rarely trigger foraminogenic retinal detachment.
Paravascular retinal vessels and the posterior edge of the vitreous base are often the site of stronger vitreoretinal adhesions, and approximately 13% of retinal tear holes are associated with paravascular vitreoretinal adhesions, which occur in posterior vitreous detachments and are often combined with vitreous hemorrhage due to retinal vessel tearing.
The most important abnormality seen that predicts the occurrence of retinal tears and retinal detachment in the fundus is retinal lattice-like degeneration, and the risk of retinal detachment in the presence of retinal lattice-like degeneration is 0,3-0,5%. Both retinal atrophy and tear holes can occur in the retinal lattice degeneration area, with atrophy holes occurring in 20% of cases. Except in young myopic patients, retinal detachment due to atrophic holes within the lattice-like degeneration zone is relatively rare, with a risk of development of only 0,247%. 2% of eyes with lattice-like degeneration develop retinal tear holes at the degeneration edge, but these tear holes are important for the development of foraminogenic retinal detachment because of the pulling factor. For symptomatic retinal tear holes, 28% to 35% of cases progress to foraminogenic retinal detachment. It is generally accepted that 30% to 40% of foraminogenic retinal detachments occur in retinal tear holes associated with lattice-like degeneration.
Other degenerations associated with foraminal retinal detachment include retinal splits and vitreoretinal abnormalities in patients with myopia. Retinal clefts can occur in the outer retinal lacunae, leading to foraminogenic retinal detachment. There are two types of foraminogenic retinal detachment associated with retinal cleavage: a limited, non-progressive detachment and a symptomatic, rapidly progressive retinal detachment. Retinal detachment in highly myopic patients occurs mostly due to vitreous liquefaction, posterior vitreous detachment, retinal lattice-like degeneration, and anterior retinal thinning. The prevalence of foraminogenic retinal detachment in patients with high myopia is 0.7%-6%.
(iv) Pathophysiology
After the occurrence of pore-derived retinal detachment, a traumatic repair response to the retinal fissure will occur, which is manifested by the occurrence of fibrous proliferative membrane in the vitreous cavity, retinal surface and subretina, and the contraction of the proliferative membrane leads to the pulling of the retina, i.e. proliferative vitreoretinopathy (PVR), which is a common complication of pore-derived retinal detachment and one of the most important reasons for the failure of retinal detachment repositioning surgery. It is also one of the most important causes of failure of retinal detachment resurfacing surgery, and in severe cases, patients may eventually lose their vision. Since the mechanism of PVR is not fully understood, it is difficult to effectively prevent and treat it.
(V) Clinical manifestations
1.Symptoms
(1) Flash sensation: It is the earliest symptom of retinal detachment, and its essence is the retinal irritation symptom produced by posterior vitreous detachment.
The essence is the retinal irritation symptom produced by the posterior vitreous detachment, which appears in 1-2 quadrants around the retina with arc light-like symptoms, and the patient can often point out the clear direction of the flash.
(2) Flying mosquitoes: It is also one of the symptoms of posterior vitreous detachment, and can also be caused by blood cells entering the vitreous after the rupture of retinal vessels.
It can also be caused by blood cells entering the vitreous after the rupture of retinal vessels. The occurrence of flash sensation and flying mosquitoes does not necessarily have retinal detachment, but because it is often a precursor symptom of retinal detachment, so it must be taken seriously, detailed fundus examination, if necessary, triple-lens examination, so as not to miss the possible occurrence of retinal fissure or detachment.
(3) Visual field defect and central vision loss: When retinal detachment occurs, the retinal field defect occurs in the area of the first detachment.
When retinal detachment occurs, the visual field defect occurs in the direction corresponding to the first detached area, and increases with the extent of retinal detachment. The retinal site where the first visual field defect occurs is often the site of the retinal fissure, which is important when taking a medical history. When the retinal detachment involves the macula, there is a severe loss of central vision. Occasionally, due to the slow development of retinal detachment, patients do not come to the clinic until after the central vision is involved, and by then it is already an old retinal detachment.
2.Fundus manifestation
(1) Vitreous: It is manifested as vitreous liquefaction and clouding, and posterior vitreous detachment is manifested as a denser ring-shaped clouding in front of the optic papilla.
The posterior vitreous detachment shows a dense annular clouding in front of the optic papilla (Weiss ring). Vitreous hemorrhage can be seen when the retinal vessels are ruptured. In old retinal detachments, coarse pigment particles in the vitreous cavity can be seen under slit lamp. In advanced retinal detachment, proliferative membranes can be seen in the vitreous due to the development of proliferative vitreoretinopathy (PVR).
(2) Retina: Retinal detachment varies in form, the mildest being subclinical detachment next to the retinal fissure.
The mildest is a subclinical detachment next to the retinal fissure, which appears as a pale gray bulge around the fissure. As the extent of detachment increases, the retina becomes a greenish-gray elevation with an undulating retinal surface and tortuous blood vessels. In fresh retinal detachments, the characteristic wave motion may be seen if the detachment is extensive, but in limited superficial detachments, the motion is less extensive. Small foci of hemorrhage are sometimes seen in fresh retinal detachments near the retinal fissure, which may be due to retinal vascular traction during posterior vitreous detachment. Proliferative membranes, including subretinal proliferation, retinal surface or full-length fold formation, are seen in old detached retinas, in which case retinal mobility is diminished during eye movement.
Finding retinal fissures is critical to the success or failure of surgery for foraminogenic retinal detachment. In the vast majority of cases of foraminifacial detachment, retinal fissures can be found. In a few cases, they can be found under indirect inspection in combination with scleral compression. Retinal lacunae are described in several different ways:
I Depending on the morphology of the fissure, it can be described as a tear (tear), an atrophy (hole), or a serrated edge detachment.
II According to the location of the fissure: ① According to the latitude of the fissure, it is described as distal peripheral part, peripheral part, or posterior pole (mostly seen in macular fissure). ② According to the meridian or quadrant where the fissure is located, describe as superior temporal, inferior temporal, superior nasal, and inferior nasal quadrant fissures.
III According to the size of the fissure, describe as small fissure, large fissure (greater than 3 PD), or giant fissure (greater than or equal to 90°).
IV Depending on the number of fissures, they are described as single fissures or multiple fissures.
There is a pattern to finding the lacunae: ① Based on the history, the retinal area where the visual field defect first appears is usually where the lacunae are located, but due to gravity and fluid flow, the retinal detachment that occurs below can also be caused by the retinal lacunae above, when the retinal detachment above is not obvious. Patients complaining of rapid progression of visual field defects that quickly lead to loss of central vision are most likely due to superior lacunae. (2) The prevalent sites of the fissure are superior temporal, inferior temporal, superior nasal, and inferior nasal quadrants in order of preference, mostly in the peripheral part of the retina. The location of the fissure is inferred from the age of the patient. The serrated edge detachment occurs most often in young people and is mostly located in the infratemporal or inferior part of the retina. According to the refractive status of the patient, the superior temporal quadrant is most frequently involved in patients with high myopia, and it is important to pay attention to both horseshoe fissures in the peripheral retina and the presence of atrophic fissures in the degenerative zone. If the retinal detachment is asymmetrical on both sides, the retinal detachment is located on the side with high upper boundary; if the retinal detachment is located on the vertical midline, the retinal detachment is flattened. The retinal detachment is symmetrical on both sides. In the case of posterior pole retinal detachment, it is mostly caused by macular fissure. (6) In cases of retinal detachment after vitrectomy, attention should be paid to the presence of a fissure near the scleral puncture opening during vitreous surgery, which is usually caused by repeatedly entering and exiting the instrument and pulling the vitreous during surgery. (7) In patients with recurrent foraminogenic retinal detachment, we should carefully check whether the original fissure is closed, whether there are missed fissures or whether new fissures are created, and especially pay attention to the lattice-like degeneration area. (8) In patients with retinal detachment who have undergone laser photocoagulation, attention should be paid to the possibility of retinal fissures caused by excessive laser energy, which are difficult to detect and require careful examination of each photocoagulated spot. In rare patients, the fissure cannot be found after repeated examinations. If necessary, the fissure may be detected when the retina is flattened by wrapping both eyes in bed for one to two days; it can also be examined quadrant by quadrant during surgery through indirect ophthalmoscopy combined with scleral compression. (⑩ More than half of the patients with retinal detachment have multiple fissures, so it is important not to miss them during the examination, so that the way to seal them can be designed before and during the operation.
3. Other ocular manifestations
(1) Low intraocular pressure: Patients with retinal detachment usually have lower intraocular pressure, probably due to intraocular fluid crossing the retinal fissure.
This may be caused by the posterior drainage of intraocular fluid through the retinal fissure across the retinal pigment epithelium, or it may be related to the reduced secretion of atrial fluid.
(2) In the late stage of retinal detachment, chronic uveitis, post-iris adhesions, pupil atresia and cataract formation may occur.
Cataract formation and eventual atrophy of the eye.
(6) Diagnostic points
The key is to find the retinal fissure, which is both the basis for the diagnosis of pore-derived retinal detachment and a necessary condition for successful surgery. Occasionally, patients who cannot find the fissure even after careful examination can still be diagnosed as retinal detachment of pore origin by combining the medical history and retinal detachment morphology, and it is necessary to continue the search under parietal pressure intraoperatively.
(VII) Differential diagnosis
(a) Exudative retinal detachment: see previous section in this section.
(ii) Retinal detachment by retraction: see earlier in this section.
(iii) Retinal splitting (retinoschisis): retinal splitting is an interlaminar splitting of the retinal neuroepithelium itself. Retinal detachment, on the other hand, is a separation between the neuroretina and the pigment epithelium. Acquired retinal clefts develop in the outer plexiform layer adjacent to the inner nuclear layer, often on top of cystic degeneration of the peripheral retina in older individuals, and are therefore also known as senile retinal clefts or degenerative retinal clefts. In congenital retinal clefting, the lesion is located in the retinal nerve fiber layer. Retinal splits may be accompanied by retinal detachment. Early lesions of acquired retinal cleft, often located in the temporal periphery of the fundus, often appear asymptomatic until the progressive phase. During the progressive phase of the cleft, a spherical bulge is seen in the vitreous, the inner layer of the cleft, which presents as a delimited, more transparent and fixed bulge that does not shift in location or shape depending on the patient’s head position or eye rotation. The inner layer of the retinal cleft is transparent, and the retinal vessels are often located on it, with snowflake-like white spots. The outer layer of the retinal cleft is difficult to identify when it is not separated from the retinal pigment epithelium. On closer inspection, foveal or sieve-like garden or oval shaped holes of varying size and shape are visible in the pinkish weakness. In approximately 25% of cases, the pores appear in both the inner and outer layers of the cleft. The inner pores are often located at the most elevated part of the cleft, while the outer pores are often present singly and are larger than the inner pores, and may have a rolled edge, resembling a retinal tear. If there is only an outer layer without an inner layer, only a limited retinal detachment is likely to occur. In about 40% of the eyes with this disease, both the inner and outer layers of the cleft have holes, which can easily develop into retinal detachment.
(d) Choroidal detachment: According to the causes, there are primary and secondary choroidal detachment. Primary choroidal detachment is caused by unexplained spontaneous leakage of the choroid, while secondary choroidal detachment is mostly caused by surgery, trauma, intraocular inflammation, uveal tumor, retinal detachment, etc. The fundus manifestation of choroidal detachment is different from that of retinal detachment, which is mostly brown or gray spherical elevation, with smooth and wrinkle-free surface, retinal vascular crawling, clear edges and darker color, mostly in front of the equator. The choroidal detachment is divided into several spherical bulges due to the restriction of the vortex vein. Pore-derived retinal detachment can be combined with choroidal detachment, which is called choroidal detachment retinal detachment, and the prognosis is bad because of low intraocular pressure and heavy uveal reaction.
(e) Choroidal melanoma: solid bulge, around which can be combined with exudative retinal detachment. It is not difficult to distinguish it from retinal detachment according to fundus performance, fundus fluorescence angiography, ultrasound, CT and other examinations.
(H) Treatment principles and progress
The basic principle is to use condensation or photocoagulation to close all the fissures, release the vitreoretinal traction, and reconstruct the physiological adhesion between the retinal neuroepithelium and pigment epithelium. The main surgical methods are scleral buckling, vitrectomy combined with vitreous cavity silicone oil or expansion gas filling; for some special cases, such as macular fissure retinal detachment, intravitreal gas injection surgery is preferred.
(1) Scleral buckling surgery: The principle of surgery is to compress the sclera by placing pressure or ring ties outside the sclera to promote the apposition of the retinal neuroepithelium to the pigment epithelium and to reduce the traction of the vitreous on the retina. Surgical approaches include extra-scleral compression and scleral ring ligation. For horseshoe fissures, external pressure in the meridian direction is generally used; for serrated margin dissection or multiple fissures, external pressure in the parallel corneal margin direction may be used. The external compressions are silicon sponge, hard silicone or dura mater. Due to the better plasticity of silicone sponge, it is more commonly used at present.
(2) Simple vitreous cavity gas injection: It is the preferred surgical method for macular fissure retinal detachment. The use of bubble uplift and surface tension top pressure on the fissure makes it adhere to the RPE, and also dissociates the subtle traction of the vitreous from the macular hole edge. If the procedure fails, a vitrectomy combined with gas or silicone oil filling is then an option. It has the characteristics of simple operation, safety, less damage to retinal tissues, and can be repeated many times. For patients with macular fissure retinal detachment with short onset time, presence of posterior vitreous detachment, no clear vitreous-macular traction, and no severe PVR, simple vitreous cavity gas injection should be preferred for the first operation. In recurrent cases, vitreous cavity gas injection can be performed again or even repeatedly. Most of the intumescent gases used for surgery include SF6, C2F6, C3F8, or air if no intumescent gas is available.
(3) Vitreous surgery: For complex retinal detachment, including refractive interstitial opacities, huge fissures with combined flap flip, severe PVR, failure to release retinal traction by cingulate surgery vitreous, failure of gas injection for macular or posterior pole fissures, etc., vitrectomy combined with intravitreal silicone oil or gas filling is used to make successful surgery possible for many cases that were previously considered incurable.
(ix) Prognosis of disease
If the retinal detachment can be operated in time, the macular detachment can be reset within 5 days, and the visual function can still be restored to the level before the onset of the disease. If the retinal detachment is prolonged, even if the surgery is successful, permanent damage to the visual function will occur. “The shorter the time of detachment, the better the visual prognosis, while the longer the time of detachment, the more complicated the condition is, and the retinal atrophy and degeneration have become irreversible, so the effect of surgery is poor. Retinal detachment for more than one year, even if the surgery is successful, the visual function is not easy to recover.
(X) Disease prevention
The effective preventive treatment for retinal detachment is to prevent the formation of retinal fissures, to prevent or counteract retinal traction, and to prevent fluid from entering the subretinal space. There is no safe and reliable method to prevent posterior vitreous detachment or to prevent the occurrence of retinal degeneration.
Indications for prophylaxis include: ① A fissure that tends to develop into a retinal detachment. ② Lattice degeneration of the equatorial part of the retina. The risk of retinal detachment is increased when the following states are combined ① acute posterior vitreous detachment; ② aphakic eye; ③ highly myopic eye; ④ previous retinal detachment in the contralateral eye.
Treatment includes photocoagulation, condensation, and scleral buckling surgery. For retinal degeneration area or fissure, photocoagulation should be preferred, and argon laser, krypton laser, diode laser or YAG frequency doubling laser can be used. Photocoagulation is appropriate for the appearance of a grade III photopic response, with fusion of the photopic spot and encircling the fissure or degenerative area. In the absence of photocoagulation equipment or when photocoagulation is not possible for distal peripheral retinal lesions, condensation can be used. Condensation is performed under direct vision with an indirect ophthalmoscope, and it is appropriate for the retina to appear as a gray condensation spot, and care should be taken to prevent excessive condensation. In cases with significant vitreoretinal traction, scleral buckling surgery should be performed to relieve the traction if necessary, along with photocoagulation or condensation to treat retinal degeneration or fissures.
(XI) Disease care
After scleral cingulate surgery, rest should be taken and strenuous exercise should be avoided.
Patients with vitreous surgery combined with intraocular filling need to adopt the appropriate position as requested by the surgeon.