Macular hole

Introduction to the macular hole Macular hole refers to the tissue defect in the retinal inner membrane to the photoreceptor layer of the macula, which seriously impairs the central vision of the patient. Knapp and Noyes first reported traumatic macular retinal tears in 1869 and 1871, respectively. Kuhnt first reported non-traumatic macular holes in 1900. Since then, various causes of macular holes have been recognized. The prevalence of the disease is not high, accounting for 3.3% of the population, of which the most common idiopathic macular hole is unexplained (about 83%), often occurring in healthy women over 50 years old (average 65 years old, female) : Male = 2:1), 6% to 28% of patients with both eyes. Some also occur in younger patients. The disease is insidious and often found when the other eye is covered. Patients often complain of blurred vision, dark spots at the center, and distortion of vision. basic knowledge The proportion of sickness: 0.01%-0.05% Susceptible people: healthy women who are more than 50 years old Mode of infection: non-infectious Complications: macular hole retinal detachment extraocular myopathy and amblyopia retinal detachment optic nerve disease retinal tear

Cause of macular hole

In addition to idiopathic macular hole, the causes of other causes are clear, such as trauma, high myopia, cystoid macular edema, inflammation, retinal degeneration, macular epiretinal membrane and eclipse retinopathy.

The understanding of idiopathic macular holes has been going on for more than a century. Until 1988, Gass proposed that the tangential direction of the macular area of the retina is the main cause of idiopathic macular hole formation, in order to treat the macula by vitreous surgery. The split hole provides a theoretical basis. The theory is based on the adjacent anatomical relationship of the vitreoretinal interface, in the aging process of the human body, due to vitreous liquefaction and posterior vitreous detachment. The retinal surface often remains in the vitreous posterior cortex. Due to the increase in vitreous cells in these residual posterior cortex, a tension parallel to the surface of the retina is formed on the retinal surface of the fovea in the fovea, initially the foveal detachment of the macular center, followed by a fovea Detach, eventually forming a full-thickness macular hole.

The pathogenesis of macular holes is not fully understood. The earliest literature reported that trauma is the main cause of macular hole formation. However, with the increase in case reports, it was found that only about 5% to 15% of macular holes were caused by trauma. At the beginning of this century, some authors suggested that cystoid macular degeneration is the main cause of macular hole. Some people think that age-related vascular changes lead to macular atrophy and eventually form macular hole, but these views can not explain the pathogenesis of idiopathic macular hole. . In 1924, Lister first proposed that vitreous traction is closely related to the formation of macular hole. Since then, people have begun to notice the important role of vitreous in the pathogenesis of macular hole, and gradually believe that the longitudinal traction of the vitreous to the macular retina is a macular hole. The cause of the disease. In 1988, Gass proposed a revolutionary insight into the pathogenesis of idiopathic macular holes. It is believed that the anterior vitrectomy of the macular fovea is the main cause of idiopathic macular hole formation, providing vitreous surgery for macular hole. The theoretical basis. Since then, reports of vitrectomy have been reported to treat macular holes. Through vitrectomy, especially the posterior vitreous cortex and the anterior membrane of the retina, the vitreous macular debridement is released, and the hole is closed in most cases. In some cases, the visual acuity is obviously improved. In 1995, through clinical pathology studies and visual acuity after vitreous surgery, Gass further pointed out that idiopathic macular hole formation is not accompanied by loss of foveal retinal nerve tissue, thus explaining why visual acuity can be restored after surgery. .

The clinical pathology of macular hole can be expressed as 1 macular hole size 400~500m. 2 The disengagement around the macular hole ranges from 300 to 500 m. 3 Photoreceptor cells shrink. 4 cystic changes in the macula. 5 A yellow point deposit similar to the glass film is attached to the RPE surface. 6 The pre-retinal astrocyte membrane appears.

Macular hole prevention

For the presence of a non-essential macular hole with a clear cause, the occurrence of macular hole can be prevented by treating the primary disease and closely following the examination. There is currently no effective prevention method for idiopathic macular hole.

Macular hole complication Complications: macular hole retinal detachment extraocular myopathy and amblyopia retinal detachment optic nerve disease retinal tear

Blurred vision may cause macular hole retinal detachment, extraocular muscle disease and amblyopia, retinal detachment, optic nerve disease, retinal tears and so on.

Macular hole symptoms Common symptoms Visual acuity often foggy vision Vision vision changes visual distortion

The disease is insidious and often found when the other eye is covered. Patients often complain of blurred vision, dark spots at the center, and distortion of vision. Vision is generally 0.02~0.5, with an average of 0.1.

Fundus manifestation and clinical staging

According to the fundus performance at different stages of idiopathic macular hole formation, Gass divides it into four phases:

Stage I: In the early stage of the onset, the vitreous cortex in the fovea of the macula spontaneously contractes, causing the reticular line of the retina to be pulled, resulting in the detachment of the central fovea, the foveal reflex of the fundus disappears, and the yellow spot on the surface of the retinal pigment epithelium (RPE) in the fovea ( 100~200m), at this time, it is stage Ia; the vitreous cortex in the fovea is further contracted, the fovea is detached, and a yellow ring (200~350m) appears on the surface of RPE, which is 1b. Ia and 1b were not associated with the separation of vitreous and macular fovea, nor did there appear "true" full-thickness macular hole, clinically known as impaired macular hole, with a slight decrease in visual acuity to 0.3-0.8. Fluorescein fundus angiography can show a slight high fluorescence of the fovea.

Stage II: After several days to several months of onset, the tangential direction of the vitreous is further pulled, forming a macular hole at the edge of the central fovea, gradually expanding, from crescent to horseshoe, and finally forming a circular hole, often accompanied by a cover film . In a few cases, the macular hole begins to form in the center of the fovea and gradually expands to become a capless hole. Recent studies have found that there is no loss of foveal tissue during the formation of idiopathic macular holes. The so-called "frontal lamella" is a concentrated posterior vitreous. The edge of the subretinal fluid is visible around the macular hole, and there is a yellow glassy membrane-like deposit at the hole, and the visual acuity drops to 0.1-0.6. Fluorescein fundus angiography can be moderately high fluorescence.

Stage III: After 2 to 6 months of the above lesions, due to contraction of the retinal tissue, the macular hole expanded to 400-500 m, with or without a cover membrane, and this is a stage III macular hole. It can be seen that the yellow glass membrane is like a sediment and the edge of the subretinal fluid. The cystic around the central fovea changes, and the visual acuity drops to 0.02~0.5.

Stage IV: It is characterized by the separation of vitreous and macula. The early manifestation is the anterior displacement of the macular hole, and the late stage is the complete separation of the vitreous and macular, optic nerve head. At this time, it is a stage 4 macular hole.

Natural course

Stage I macular hole (prodigal hole): About 50% develop into full-thickness macular hole, and 50% of cases spontaneously relieve after separation of vitreous and macular fovea.

Stage II macular hole: Most cases develop to stage 3 hole after 2 to 6 months. In most cases, the macular hole size has developed to more than 400 m.

Stage III macular hole: less than 40% of cases develop to the stage VI macular hole. 80% of cases have relatively stable visual acuity. Usually, after 1 year, the RPE depigmentation in the retinal detachment area can occur after half a year. The retinal anterior membrane appears in many cases. Retinal detachment can also occur by accidental spontaneous retinal reattachment.

Contralateral eye symptoms

(1) Separation of vitreous and macular fovea: no risk of macular hole formation.

(2) The vitreous and the macula are not separated: the possibility of macular hole formation is <15%.

(3) The macular anterior membrane covers the fovea, often accompanied by yellow spots: the possibility of macular hole formation is <1%.

(4) Star opacity in the central fovea of the macula with radial retinal folds: no risk of macular hole formation.

(5) If a yellow spot or ring appears in the macula, and other manifestations of the macular hole are combined, it indicates a high risk of forming a macular hole.

Macular hole examination

Ophthalmic examination: fundus examination, fundus fluorescein angiography, ophthalmologic examination, direct ophthalmoscopy.

Diagnosis and differentiation of macular hole

Diagnostic points

Since the advent of fundus coherence tomography (OCT), there has been no difficulty in the diagnosis of macular hole. The OCT scan can be used to determine the diagnosis when ophthalmoscopy reveals a suspicious hole in the macular area.

Differential diagnosis

1. Etiology identification: need to exclude idiopathic macular hole other than the cause of the disease, such as trauma, inflammation, high myopia, cystoid macular edema, fundus vascular disease, degenerative diseases, eclipse retinopathy, etc. Macular edema.

2. Morphological identification: should be differentiated from the other two vitreous traction macular lesions.

(1) idiopathic macular epiretinal membrane: sometimes combined with macular hole, fundus and OCT examination can be clearly diagnosed.

(2) vitreous macular traction syndrome: often lead to macular traction deformation, macular edema, and sometimes with the macular hole. OCT examination can confirm the diagnosis.

(3) lamellar macular hole: OCT examination can determine whether the macular hole is full or lamellar.

(4) macular hole retinal detachment: often occurs in high myopia, idiopathic macular hole often appears in the macular hole around the hole source lifted shallow detachment halo, but rarely occurs true retinal detachment.

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