Laser-induced macular holes have beenwell reported in literature.(94–104) Neodymium doped Yttrium Aluminium Garnet(Nd:YAG) lasers (including Titanium-Sapphire lasers) and handheld lasers arethe major culprits. Macular lesions occur mostly accidently during laser calibration,adjustment and alignment in occupational settings. A few cases are alsoreported after ND: YAG capsulotomy and tattoo removal in dermatology clinics. Liet al reported macular hole formation in around 2% of patients undergoing Nd:YAG capsulotomy.(104)Alaser injury may cause a full-thickness macular hole immediately after injuryor after several days, depending upon the laser injury mechanism. Nd: YAG laserinduced macular holes occur due to their photo disruptive effect on the retinaltissues.
(94) Nd: YAG lasers of very short laserpulses duration (1 microsecond or shorter) cause plasma formation and expansivemicro explosions. Q-switch mode (few nanoseconds to a few microseconds) runlasers deliver huge amount of energy in a shorter duration and are moredangerous.(103) Macular hole in such cases developinstantaneously with tissue disruption. Handheld lasers can be either low-poweror high-power pointer lasers. Low power lasers are often used in toys andduring conferences while high power lasers are used in occupational setting. High-powerhandheld laser (up to1200 mW) causes photocoagulation at the site of lesion.
The lesions expand during the initial few days and later atrophic hole maydevelop.Theseverity of retinal injury and resulting visual impairment is determined mainlyby the duration and amount of energy delivered and the location of the lesion(distance from centre of fovea). (105) The minimum cumulative laser energy required to cause a macular hole is around 1–3 mJ.(106)The characteristic clinical features of these holes include a photocoagulationlike scar in crater like MH with surrounding pigmentation. The OCT features inmost eyes include cystic margins, disrupted outer retinal layers, and RPEdisruption in the crater of MH. Intense laser injury can breach the Bruch’s membrane-choriocapillariscomplex and lead to CNV formation later in course.(107) Thenatural history of laser induced MH is very variable. Spontaneous closure canoccur due to induced ILM contraction, fibroglial proliferation and retinalpigment epithelial hyperplasia.
(103,108) This mostly occurs in smaller holes(<180 ?m), but often this is delayed for 8-12 weeks and associated withsevere permanent loss of visual acuity.(97,102,109) Most studies report enlargement of laserinduced MH and worsening of visual acuity without surgery.(96,101)The standard treatment for idiopathicMH i.e.
vitrectomy with ILM peeling and gas tamponade works best for these MHas well. Anatomical closure rates of upto 78.6% to 100% have been reported inlarge case series on surgical management on laser induced MH with singlesurgery.(100,101) Visual acuity improves invariablyafter successful MH repair, but is not always similar. Laser injury is often associatedwith a thermolitic distruction of retina and RPE, which limits the visualrecovery.(102).
Better post-operative BCVA bears nocorrelation with the pre-operative size of MH.(100) However, it depends proportionallyto the residual foveal thickness and thinness of subfoveal defect. Finallylaser energy and distance of lesion/ MH from the fovea are important prognosticfactors of visual recovery.