[Non-surgical treatment of vitreomacular traction and macular hole].

Macular hole (MA) is a significant cause of visual acuity (VA) loss in patients over 50 years in our environment. The traction by the vitreous, particularly the posterior hyaloids, on the retina surface plays a leading role in the etiopathogeny of MA. The collagen fibers that comprise the posterior vitreous are firmly joined to the macula and connecting to the internal limiting membrane by means of a sort of biological adhesive made up by proteoglycans, laminin and fibronectin.1 With aging, the vitreous gel becomes progressively liquid and vitreoretinal adherence weakens to the point that the vitreous detaches from the retina, known as posterior vitreous detachment (PVD). However, PVD may not be complete: a portion of the vitreous may remain adhered to the macular surface, which is known as vitreomacular adhesion (Fig. 1). When the traction increases due to anteroposterior or tangential stress, vitreomacular traction (VMT) takes place. VMT can be asymptomatic in the form of metamorphopsia and loss of central VA (Fig. 2). In addition, VMT can produce cystic spaces in the retina and involve the formation of MA.2 Typically, MA is classified in 4 stages depending on partial thickness without involving the external layers (i), full thickness with VMT (ii), full thickness without VMT and without PVD (iii) and full thickness without VMT and with PVD (iv) (Fig. 3).3 In the treatment of MA, observation is recommended with frequent supervision for stage i, while surgery is recommended for the remaining stages. At present, recommended