![]() It helps to prognosticate pre-operatively and follow up postoperatively. It gives the three-dimensional cross-sectional picture of the hole and associated abnormality i.e., epiretinal membrane (ERM) or VMT mainly. OCT is the gold standard in the diagnosis, management, and follow-up in MH. But as it is a disease of old age, associated cataract or other media opacities make it harder for the surgeon sometimes. Associated features are also evident usually in the clinical examination. PVD, if present, carries a lower risk of development of macular hole, if not present already.Ĭlinical examination is the mainstay of diagnosis of macular hole (MH). The fellow eye must be examined for the presence of similar changes. Depending on the stage of development, a yellowish cuff of fluid may be visible with yellowish dots in the center. Īssociated features may be evident in the form of epiretinal membrane i.e., perilesional puckering, involutional thinning, cystoid changes, complete posterior vitreous detachment (PVD), retinal pigment epithelium changes, pseudo-operculum, vitreomacular traction (VMT), and others. Varying sized laser-aiming beam (50 micrometers, 200 micrometers) if projected on the center of the macula in cases of a pseudo hole, can be seen but can not be detected by the patients with macular hole. Patients with a pseudo hole may describe as thinning of the slit in the center, or a bend at the center with no discontinuity. After focussing a thin slit-lamp beam on the fovea with a fundus viewing lens, if the patient is asked to describe the thin slit, typically the patient describes a discontinuity or break in the midline i.e., Watzke-Allen test positive suggestive of full-thickness macular hole. Two different easy and simple examinations by slit lamp and laser-aiming beam can easily distinguish between a full-thickness macular hole and pseudo hole. Usually, slit-lamp biomicroscopy with +90D/+78D fundus viewing lenses confirms the diagnosis of FTMH as a red central spot. Visual acuity reduction varies mildly in partial-thickness (PT) to markedly in a full-thickness macular hole (FTMH). Initially, during the early stage of development of macular hole, vision may be mildly affected, but as it progresses visual problem increases. The painless, gradual diminution of central vision with or without distorted vision is the main complaint. Īn idiopathic macular hole is a disease of elderly individuals, mostly in their 6th to 7th decade of life, and females are more affected. The loss of photoreceptors in the area of hole formation is another characteristic feature. This cystoid change is mainly due to the lamellar separation of retinal layers caused by vitreous traction. Cystoid changes around the macular hole at any stage are well known due to preexisting vitreofoveal traction. We often get the epiretinal membrane attached to the vitreoretinal interface. The pseudo-operculum over the macular hole consists of vitreous condensation without neurosensory retinal components. Very minimum cellular proliferation usually takes place before the onset of a macular hole with minimum hypertrophy and hyperplasia of the retinal pigment epithelium. Posterior cortical vitreoschisis occurs before macular hole formation, which leaves a hypocellular vitreous attached to the macula. ![]() This also suggests that direct foveal traction has a role in the pathogenesis of macular holes. True opercula (39%) - contains both glial tissue and neural tissue (cones) due to avulsion of neuroretinal tissue from full-thickness foveal tear. Other pathologies of macula or retina associated with macular hole formation are usually related to vitreoretinal interface abnormality. Myopia is another cause leading to abnormal vitreoretinal physics, which causes the macular holes in a setting of retinal thinning in the center. Trauma, in young patients with a gel vitreous body, causes sudden vitreomacular traction followed by forceful separation of them, leading to the formation of the macular holes. The successful anatomical closure of the macular hole after surgical removal of the vitreous indirectly proves its pathologic role. ![]() This abnormal tangential vitreous traction is the product of fluid movement in the vitreous with cellular proliferation suggested by a study conducted by W.R.Green. This tractional force may be tangential traction by pre-existing epi-retinal membrane or vertical by vitreomacular traction. Involutional foveal thinning also plays a role. Vitreo-retinal interface abnormality along with its tractional forces play a major role in the development of macular holes. But recent advances in the section of ocular diagnostics in the form of spectral-domain optical coherence tomography (SD-OCT) have made a big impact. The exact pathophysiology behind the development of idiopathic macular holes is unknown. ![]()
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