Laser-induced low-power or high-power pointer lasers. Low power lasers

Laser-induced macular holes have been
well reported in literature.(94–104) Neodymium doped Yttrium Aluminium Garnet
(Nd:YAG) lasers (including Titanium-Sapphire lasers) and handheld lasers are
the major culprits. Macular lesions occur mostly accidently during laser calibration,
adjustment and alignment in occupational settings. A few cases are also
reported after ND: YAG capsulotomy and tattoo removal in dermatology clinics. Li
et al reported macular hole formation in around 2% of patients undergoing Nd:
YAG capsulotomy.(104)

A
laser injury may cause a full-thickness macular hole immediately after injury
or after several days, depending upon the laser injury mechanism. Nd: YAG laser
induced macular holes occur due to their photo disruptive effect on the retinal
tissues.(94) Nd: YAG lasers of very short laser
pulses duration (1 microsecond or shorter) cause plasma formation and expansive
micro explosions. Q-switch mode (few nanoseconds to a few microseconds) run
lasers deliver huge amount of energy in a shorter duration and are more
dangerous.(103) Macular hole in such cases develop
instantaneously with tissue disruption. Handheld lasers can be either low-power
or high-power pointer lasers. Low power lasers are often used in toys and
during conferences while high power lasers are used in occupational setting. High-power
handheld laser (up to1200 mW) causes photocoagulation at the site of lesion.
The lesions expand during the initial few days and later atrophic hole may
develop.

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The
severity of retinal injury and resulting visual impairment is determined mainly
by 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 photocoagulation
like scar in crater like MH with surrounding pigmentation. The OCT features in
most eyes include cystic margins, disrupted outer retinal layers, and RPE
disruption in the crater of MH. Intense laser injury can breach the Bruch’s membrane-choriocapillaris
complex and lead to CNV formation later in course.(107)

The
natural history of laser induced MH is very variable. Spontaneous closure can
occur due to induced ILM contraction, fibroglial proliferation and retinal
pigment epithelial hyperplasia.(103,108) This mostly occurs in smaller holes
(<180 ?m), but often this is delayed for 8-12 weeks and associated with severe permanent loss of visual acuity.(97,102,109) Most studies report enlargement of laser induced MH and worsening of visual acuity without surgery.(96,101) The standard treatment for idiopathic MH i.e. vitrectomy with ILM peeling and gas tamponade works best for these MH as well. Anatomical closure rates of upto 78.6% to 100% have been reported in large case series on surgical management on laser induced MH with single surgery.(100,101) Visual acuity improves invariably after successful MH repair, but is not always similar. Laser injury is often associated with a thermolitic distruction of retina and RPE, which limits the visual recovery.(102). Better post-operative BCVA bears no correlation with the pre-operative size of MH.(100) However, it depends proportionally to the residual foveal thickness and thinness of subfoveal defect. Finally laser energy and distance of lesion/ MH from the fovea are important prognostic factors of visual recovery.