Clinical manifestations
(a) Symptoms, the disease is insidious and is often detected when the other eye is covered. Patients often complain of
Patients often complain of blurred vision, central dark spot, and distortion of vision. Visual acuity is usually 0.02~0.5, with an average of 0.1.
(B) Fundus manifestation and clinical stage, according to the fundus manifestation in different stages of idiopathic macular fissure formation process.
Gass divided it into four stages
Stage I: At the beginning of the disease, the vitreous cortex in front of the central macular sulcus contracts spontaneously, causing traction in the tangential direction of the retinal surface, resulting in the detachment of the central sulcus, the disappearance of the reflection of the central sulcus in the fundus, and the appearance of yellow dots (100~200mm) on the surface of the retinal pigment epithelium (RPE) in the central sulcus, which is stage Ia; the vitreous cortex in front of the central sulcus contracts further, the central macular sulcus detaches, and a Both stage Ia and stage 1b are not accompanied by the separation of vitreous and macular central concavity, and there is no “true” full-layer macular hole, which is clinically called aura macular hole, and the visual acuity is mildly reduced to 0.3~0.8, and fluorescein fundus angiography can show slight hyperfluorescence of macular central concavity. Fluorescein fundus angiography may show slight hyperfluorescence of the central macula.
Stage II: A few days~months after the onset of the disease, the tangential direction of the vitreous is further stretched and a macular hole is formed at the edge of the central notch, which gradually enlarges and develops from crescent-shaped to horseshoe-shaped, and finally forms a round hole, 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 an uncovered hole. In recent studies, it has been found that there is no loss of central retinal sulcus tissue during the formation of idiopathic macular fissure, and the so-called “pre-fissure lid” is the concentrated posterior vitreous cortex. The subretinal fluid rim is visible around the macular fissure, and there are yellow vitreous wart-like deposits at the fissure, and the visual acuity is reduced to 0.1~0.6. Fluorescein fundus angiography may show moderate hyperfluorescence.
Stage II: After 2~6 months of the above lesions, due to the contraction of retinal tissue, the macular fissure enlarges to 400~500μm, with or without capping, at this time, it is stage III macular hole. Yellow vitreous wart-like deposits with subretinal fluid rim can be seen, cyst-like changes around the central small concavity, and the visual acuity decreases to 0,02~0,5.
Stage IV: Early manifestation is the anterior displacement of macular hole cover film, late manifestation is the complete separation of vitreous and macula and optic nerve papilla, at this time is stage 4 macular hole.
(C) Natural course of disease
Stage I macular hole (aura hole): about 50% of the cases develop into full macular hole, 50% of the cases spontaneously resolve after the separation of vitreous and macular central hollow.
Stage II macular hole: most cases develop to stage 3 hole after 2~6 months. The size of macular hole develops to more than 400mm in most cases.
Stage III macular hole: Less than 40% of cases progress to stage VI macular hole. 80% of cases have relatively stable visual acuity. The RPE depigmentation of the retinal detachment area usually occurs after 1 year, and the pigment demarcation line can appear after 6 months. In many cases, the retinal adventitia is present. Occasionally, spontaneous retinal repositioning occurs, and retinal detachment may also occur.
(iv) Contralateral eye
(1) Separation of the vitreous from the central macular sulcus: no risk of macular hole formation.
(2) No separation of vitreous humor and central macular sulcus: the possibility of macular hole formation is <15%.
(3) Macular anterior membrane covering the central concave area, often accompanied by yellow dots: the possibility of macular hole formation <1%.
(4) Star-shaped clouding in front of the central macular sulcus with radial folds of the retina: no risk of macular hole formation.
(5) If yellow dots or rings appear in the macular area, and combined with other manifestations of the aura macular hole, it indicates a high risk of macular hole formation.
(5) Diagnostic points
Since the introduction of fundus coherence optical tomography (OCT), the diagnosis of macular hole is no longer difficult. The diagnosis can be confirmed by OCT scan when the suspicious macular hole is detected by fundoscopy.
(VI) Differential diagnosis
1.Differentiation of etiology: It is necessary to exclude the causes other than idiopathic macular hole, such as trauma, inflammation, high myopia, cystoid macular edema, fundus vascular disease, degenerative diseases, secondary macular edema caused by eclipse retinopathy, etc.
2. Morphological differentiation: It should be differentiated from 2 other kinds of vitreous traction macular lesions.
(1) Idiopathic macular anterior membrane: sometimes combined with macular fissure, fundus and OCT examination can be clearly diagnosed.
(2) Vitreous macular traction syndrome: It often leads to macular traction deformation and macular edema, sometimes coexisting with macular fissure, and OCT examination can confirm the diagnosis.
(3) Laminar macular fissure: OCT examination can clarify whether the macular fissure is total or laminar.
(4) Macular fissure retinal detachment: It often occurs in high myopia. Idiopathic macular fissure often appears as a shallow detachment halo with hole source warped around the macular fissure, but rarely occurs as a true retinal detachment.
Treatment principles and progress
1.Surgical treatment of macular hole
Previously, it was 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 hole, it is recognized that the formation of macular hole is closely related to the traction of vitreous body on the tangential direction of macular central recess. Therefore, removal of the vitreous cortex in front of the central sulcus by vitrectomy has been widely carried out to treat macular holes.
The aim of the surgery is to relieve the vitreous macular traction. In stage I patients, removal of the vitreous body, especially the posterior vitreous cortex in front of the macular area, can reset the detached central macular notch. For patients with full macular hole formation, the surgical objectives are multifaceted, including relief of vitreous macular traction, detachment of the anterior macular membrane or inner retinal boundary membrane associated with macular hole development, and intraocular gas filling to allow macular hole closure. For refractory macular hole (e.g., large or recurrent hole), the use of autologous serum, β2 transforming growth factor (TGF-β2) or autologous concentrated platelets applied to the macular hole may increase chorioretinal adhesions in the hole area and induce the hole to close and heal.
2.Indications
(1) Therapeutic vitrectomy: The purpose is to induce macular hole closure and repositioning of superficial retinal detachment around the hole.
A. Clearly diagnosed as stage II~IV idiopathic macular fissure, with obvious loss of visual acuity (0.05~0.4) and obvious visual deformation.
B. Those who have macular fissure formation time within one year and are willing to undergo surgery.
(2) Staging of macular fissure in Gass: Stage I macular fissure has not formed a full-layer macular hole, and about 1/2 patients with stage I macular fissure can spontaneously remit, so surgery for stage I macular fissure is mostly not advocated, and surgery can be carefully chosen for patients with high risk of developing a full-layer macular hole.
Whether vitrectomy can prevent the formation of total macular fissure is inconclusive. In a multicenter, randomized, controlled clinical study in the United States, for patients with stage I macular fissures, the incidence of total macular fissures was 37% and 40% in the vitrectomy group compared with the non-operated observation group (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 the proposed prophylactic vitrectomy for stage I macular fissure need to be weighed. The “pros” of the surgery are to relieve the mechanical pull of the vitreous on the macula, while the “cons” are the possible risks associated with the surgery.
These include: surgical operation may cause total macular fissure, peripheral retinal fissure of medical origin, retinal detachment, infection, lens clouding, etc.
3.Surgical methods and progress
The traditional surgical technique is standard three-incision vitrectomy through the flat part of the ciliary body, with posterior detachment of the artificial vitreous, sub-total removal of the vitreous, stripping the anterior macular membrane or the inner retinal boundary membrane of the macula, or closing the macular hole with biological agents. Expansion gas/air exchange with 20%-25% SF6 gas is performed. After the operation, the patient was placed in prone position for about 14 days, and the gas in the vitreous cavity was absorbed and normal position was restored.
(1) Microincision 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 use of 20G maneuver small incision vitreous surgery also achieved good results and reduced the cost of surgery.
(2) Internal boundary membrane staining technique
Most of the staining techniques are used to remove the inner border membrane, and the staining agents are Taipan Blue, Brilliant Blue G (BBG), Bromophenol Blue (BPB), Chicago Blue (CB), Tretinoin (TA) and Indocyanine Green (ICG). Tretinoin cannot color the inner border membrane, but it can make it easily recognizable.
4.Surgical complications
The surgical complications of treating idiopathic macular fissure are similar to those of ordinary vitrectomy surgery, including nuclear cataract, transient high intraocular pressure, medically induced retinal fissure production, macular fissure enlargement, retinal pigment epitheliopathy caused by phototoxicity, vascular obstruction, and endophthalmitis. The incidence of nuclear cataract is the highest, up to 12-90%. The literature reports that cataract extraction and IOL implantation are required in about 33% of cases 5-16 months after the first surgery, and in eyes with closed macular fissures, vision returns to previtreous surgery vision or better. Transient high intraocular pressure occurs in about 17 or 4% of operated eyes, mostly within 3 weeks after surgery, mainly due to gas filling, and is usually treated symptomatically. If a medically induced fissure occurs, laser sealing should be used instead of condensation sealing whenever possible to reduce the occurrence of postoperative complications such as macular anterior membrane.
Surgical evaluation and prognosis
The main causes of macular fissure vision loss are as follows
(1) There are no retinal photoreceptor cells at the fissure.
② Superficial retinal detachment around the fissure.
(3) Cystoid edema around the lacunae.
④ Different degrees of degeneration of the optic cells around the lacunae.
The cause of the disease can be eliminated by loosening the pull in the anterior and posterior directions of the lacunae as well as in the tangential direction through vitrectomy, and the macular lacunae can be closed by gas filling and biologic factors to promote the repositioning of the retinal neuroepithelium, thus improving the visual acuity and visual distortion and other symptoms.
The following factors affect the prognosis of surgery.
①Whether the fissure is closed or not. Poorly closed lacunae do not restore visual acuity satisfactorily. Whether the fissure is completely closed after surgery may depend on whether the anterior macular vitreous cortex is cleared during surgery, whether the membrane around the fissure is removed, whether there is still tension around the fissure, and whether the patient’s head position is maintained after surgery.
(2) Postoperative complications may also have an impact on the recovery of vision, such as cataract formation and the appearance of preretinal hyperplasia after scleral freezing in the case of medical source hole.
(3) Intraoperative operations in the macular hole area should be performed with care to avoid instrumentation damage to the retinal tissue in the macula.
With the progress of OCT technology, the prognosis of idiopathic macular hole has been better understood. Inoue et al. examined 53 patients with postoperative macular hole closure using frequency-domain OCT and found that the connection between the inner and outer segments of the photoreceptors may play an important role in the recovery of visual acuity after macular hole surgery. The more severe the postoperative defect of the inner and outer intersegmental connections, the worse the visual prognosis. As time progresses, the inner and outer intersegmental connections can be partially restored in some patients, while in others they persist.
Disease prevention
For non-idiopathic macular fissures with a clear etiology, prevention of macular fissures can be achieved through treatment of the primary cause and close follow-up examinations. There is no effective prevention method for idiopathic macular fissures.
Disease care
Macular fissure surgery requires prone position due to intraocular gas filling, the duration of prone position depends on the type of gas filling in the eye. The duration of prone position depends on the type of intraocular gas filling, usually 1-2 w. At this time, the care is carried out according to the routine of intraocular filling care after vitreous surgery.