MH with vitrectomy and suggested that MH

MH is occasionally associated with
retinal vascular conditions, such as macular telangiectasia, coats disease,
retinal artery macro aneurysm, diabetic retinopathy, hypertensive retinopathy,
and congenital arterio-venous communications.

Macular Telangiectasia

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Macular, juxtafoveal, or perifoveal telangiectasia
also known as mac tel type 2 is a bilateral, acquired form of perifoveal
telangiectasia of unknown etiology with characteristic changes in the macular
area (loss of retinal transparency, right-angled venules, superficial retinal
crystalline deposits, and pigment clumping) and neurosensory retinal
degeneration.(41) Probable patho mechanisms include
chronic low grade leakage from abnormal perifoveal capillaries, neuro-glial
tissue degeneration, and vascular insufficiency.(41–44)

OCT shows outer retinal disruption
with intraretinal cystic spaces and a bridging thin paper like inner retinal
tissue often called as ILM drape.(42) Olson et al were the first to report
MH formation in such eyes following degeneration of cystoid spaces.(44) Koizumi et al proposed Muller cell
loss to be the reason as Muller cell cone provides structural support to the
macula.(45) Also the inner layer (presumed ILM)
may get torn by vitreous traction leading to MH formation.(42,43) Although Charbel et al proposed VMT
as an additional factor, vitrectomy did not show any anatomical or functional
improvement.(42) However Shukla et al reported
improvement with vitrectomy and suggested that MH with edematous edges and VMT
may behave similar to idiopathic holes and are better candidates for surgery as
compared to atrophic holes.(43) Most cases reported were in their
sixth- seventh decade.

Given that subtle macular changes in
Mac Tel may be easily missed on biomicroscopic examination, Mac Tel as the
cause for MH may be underestimated. Fluorescein angiography, blue reflectance
imaging and OCT angiography may help in identification of characteristic Mac
Tel changes in eyes where etiology of MH cannot be ascertained.(46,47) Screening of fellow eye for Mac Tel
changes cannot be stressed more in this regard.

Retinal artery

retinal macroaneurysms are fusiform dilations of the retinal arterioles that
occur in the posterior pole, affecting patients in their sixth-seventh decade
often in the presence of systemic conditions like hypertension, diabetes and
hypercholesterolemia.(48) Rupture of macroaneurysms can result
in hemorrhage into the subretinal space, into the retina, beneath the internal
limiting membrane, or into the vitreous cavity. Subretinal hemorrhage and
exudation from the lesion can lead to outer retinal layer degeneration. Macular
hole formation following rupture is not uncommon.(48–52) In majority of the cases, MH are not
detected early due to overlying sub ILM or vitreous hemorrhage, and are noted
intra-operatively during vitrectomy performed for removal of premacular bleed. Tashimo
et al. studied 75 eyes with RAM and found MH in four (5.9%) out of 68 eyes which
developed rupture.(48) They suggested two types of hole
based on the onset: early onset type occurs immediately after rupture due to
sudden elevation of pressure in subretinal space with hemorrhage and dehiscence
of the fovea; late onset type occurs due to ongoing structural retinal damage
from subretinal bleed which weakens the fovea. Colucciello et al. and Mitamura
et al. suggested another mechanism for late MH formation, wherein the vitreous
hemorrhage causes PHM contraction and the resulting traction on fovea (both
tangential and antero posterior) in turn contributes to MH formation.(50,52)

Hole closure frequently occurs with
vitrectomy alone in these eyes.(48,49,51) Sato et al. reported macular hole
closure and significant visual recovery in 2 out of 3 eyes with ruptured RAM
with MH.(49) Tashimo et al noted anatomical
closure in 3 out of four eyes with vitrectomy alone.(48) Surgical modification in these cases
included gentle passive suction of premacular bleed with soft-tipped canula
avoiding inadvertent touch of the macular tissue. However the visual prognosis
was guarded with final BCVA less than 20/100. Nevertheless, as vitrectomy is
the standard approach for removal of premacular hemorrhage in these eyes, MH
should be carefully looked for.

Diabetic retinopathy

retinopathy, especially maculopathy is a rare but important cause of secondary
MH.(53–57) Amemiya et al. first reported it in
3 eyes with DR and proposed that fibrous proliferation exerts traction on
edematous macula, thereby leading to MH formation.(54) Brazitikos et al. studied 8 such
eyes and highlighted causes other than macular edema like intraretinal
exudation, and vitreous traction during vitrectomy for PDR.(55) Kurihara et al. found persistent
edema in all 3 of their cases at the edge of hole and disapproved of vitreous
traction as the cause.(56) In the largest case series of 23
eyes by Ye PT et al., thick fibro vascular proliferation was noted to exert
traction at the edges of MH and removal of this traction with vitrectomy led to
hole closure in 19 eyes (82.6%).(57) Final BCVA was governed by baseline
visual acuity and degree of macular elevation in their study. ILM peeling did not significantly affect
MH closure in their study. Presence of hard exudates at fovea has been
found to be a risk factor for non closure of MH.(53)

Retinal venous occlusion

contraction leading to MH formation has been reported by Cohen et al in a 22
year old male with chronic renal failure with vitreous hemorrhage secondary to
hypertensive retinopathy.(58) Khakima et al. reported an unusual
case of foveal horse shoe tear due to vitreous traction in a 53 year adult with
recurrent vitreous hemorrhage secondary to macular branch venous occlusion.(59) Surgical removal of traction led to
anatomical closure but visual improvement was limited. Associated macular edema
and ischaemia may have compromised the foveal structural integrity in both
these cases.

Other extremely rare vascular causes
for MH include peripheral retinal telangiectasia, coats disease, congenital
retinal arterio-venous communication, and central retinal artery occlusion.(60–63) Peripheral retinal telangiectasia
with chronic exudation, whether idiopathic or secondary to chronic RD/
retinoschisis may cause PVD induction and resulting vitreomacular traction may
lead to MH formation.(61)