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11.4 Causes ofMacular Oedema
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multifactorial interventions over 4–6 weeks
before subjecting them to focal/grid laser photocoagulation. Of those who achieved complete
control of the target values, 29% of the eyes had
improvement in VA by three lines or more versus
21% of those with incomplete control [96].
Elevated HbA1C is known to increase the risk
of DME.Often the focal DME is accompanied
by massive hard exudates (HEX). There is a risk
of subfoveal migration of hard exudates following laser therapy. The HEX under the fovea can
damage photoreceptors and promote subfoveal
brosis. The use of statins before focal laser photocoagulation is known to reduce the severity of
HEX even before the laser and prevent subfoveal
migration [97]. Statins reduce the risk of progression of diabetic retinopathy and DME.They also
reduce the need for laser photocoagulation, any
treatment for diabetic retinopathy, and vitreous
surgery in these patients [98, 99]. Diabetes is a
systemic disease, and its comorbid systemic
associations profoundly affect the progression of
diabetic retinopathy. It needs a multidisciplinary
team approach for preventing, progressing, and
controlling diabetic retinopathy. Control of blood
sugar levels and hypertension signicantly
impacts the course of diabetic retinopathy and the
need for therapeutic interventions [100].
11.4.2 Macular Oedema inRetinal
Vein Occlusions
Retinal vein occlusions, the branch as well as the
central retinal vein, and the hemispheric retinal
vein occlusion are the second most common
cause of macular oedema. Macular oedema is the
commonest cause of visual disturbance in these
patients (Fig. 11.8). By 3 months of the onset,
most of the retinal haemorrhages get absorbed by
the usual phagocytic mechanisms and depending
upon the net balance of uid leakage from the
broken/decompensated endothelial cell barrier
and the capacity of the collateral vessels that
form in deep capillary plexus to drain it; macular
oedema may resolve or continue to persist. There
are no collateral channels identied on OCTA in
the supercial venous plexus. The uid moves in
the interstitial tissue from the SCP to the
DCP.The uid rst collects in the INL and then
moves to the OPL.A pioneering study showed
that compared to 0.3mg, the effect of IVT injection of 0.5 mg Lucentis in reducing ME was
quicker and lasted longer. Moreover, there is a
direct correlation between the severity of ME and
the baseline aqueous humour VEGF levels, suggesting that VEGF was a major driver of ME and
laid grounds for establishing the role of antiVEGF therapy for the resolution of macular
oedema, albeit for a short duration (~1month) in
both the BRVO and the CRVOs [101].
11.4.2.1 Macular Oedema inBranch
Retinal Vein Occlusions
The visual acuity improves spontaneously in
many BRVO eyes without intervention. Still,
improvement beyond 20/40 visual acuity is
uncommon [102].
In the natural course, the median time to
resolve macular oedema was 18months in the
macular vein occlusion and 21 months for the
major BRVO [103]. Major BRVO eyes show a
abc
Fig. 11.8 A 54-year-old man presented 4 months after a
left eye upper temporal branch vein occlusion. He showed
residual linear haemorrhages and an incomplete ring of
hard exudates around an area of macular oedema (a). FFA
showed telangiectatic vessels and multiple microaneu-
rysms (b) and diffuse staining of the macula in the affected
quadrant in the late frames of FFA (c). Such macular
oedema in branch retinal vein occlusion will only rarely if
at all show a spontaneous resolution
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11 Macular Oedema
higher aqueous VEGF and inammatory cytokine level than the macular BRVO. The major
BRVO eyes also show a higher chance of DRIL,
EZ disruption, and SRF and require several antiVEGF injections [104]. In terms of visual
improvement, in the branch vein occlusion study,
a multicentric controlled trial, there was spontaneous improvement ≥20/40 in 34% of the
untreated eyes versus 60% who had undergone a
grid laser photocoagulation in the area of macular oedema [105]. The persisting macular oedema
does not follow a zonal distribution and collects
in the centre of the macula. Spontaneous resolution in up to 40% of the affected eyes may restore
near-normal visual acuity [103]. However, with
the anti-VEGF treatment, ME may resolve completely, persist, or recur after initial resolution.
Persistent or recurrent ME is associated with collateral formation in the intermediate capillary
plexus and the DCP, where these capillary networks show increased density and thickening of
the retinal layer [106, 107]. Moreover, the BRVO
eyes that show recurrence of ME also show a
greater loss of the perifoveal capillary network,
especially in the DCP [108]. Eyes that show more
gap vessels (capillaries present in the SCP but
corresponding capillaries absent in the DCP) also
tend to show a persistent ME [109, 110].
Clinical diagnosis of macular vein occlusion,
especially if the patient presents late, may pose a
challenge to differentiate it from diabetic retinopathy. Notably, the retinal veins follow a strict
quadrantic pattern. The haemorrhages and the
microaneurysms, unlike macular oedema, are
strictly limited to the affected quadrant above or
below the horizontal raphe, as the case may be. In
diabetic retinopathy, the microaneurysms and
haemorrhages do not follow this rule and are seen
across the horizontal raphe. One notable exception is the formation of hard exudates in the
BRVO.If oedema persists, hard exudates may be
seen deposited in a circinate pattern around the
site of persisting retinal oedema from the decompensated capillary bed and/or microaneurysms
and cross the horizontal raphe. The formation of
microaneurysms is a risk factor for the development of refractory macula oedema [111]. In the
BRVO eyes with macular oedema and increased
subfoveal choroidal thickness, elevated levels of
VEGF and IL-8 were seen as predictors of good
outcomes following anti-VEGF therapy [112].
The BRVO eyes that show non-perfusion
areas on ultra-wide FFA show a good correlation
with the CNP in the SCP and the DCP. Thus,
OCTA alone can provide a fair idea of the ischaemic status of the eye in patients with BRVO
[113].
Optical coherence tomography (OCT) is often
used to diagnose and monitor the presence of
macular oedema (central subeld thickness,
CST). Notably, the smoothness of the interface
between INL and OPL on SD-OCT may indicate
fewer chances of ME or its recurrence [114].
Additionally, the OCT may show some structural
alterations, including disorganization of the internal retinal layers (DRIL) and disruptive changes
in the photoreceptors and the external limiting
membrane that may limit visual improvement,
including contrast sensitivity following therapeutic interventions [115, 116].
There is level 1 evidence for using pharmacotherapy to treat ME in BRVO [117]. In the last
15 years, intravitreal injections of anti-VEGF
agents have supplanted gird laser photocoagulation for treating macular oedema due to
BRVO. Many such agents have been tested in
several controlled trials. They have found almost
equivalent results using ranibizumab, bevacizumab, or aibercept that need to be given initially every month for three injections and
followed by a PRN (pro re nata) basis protocol.
Visual improvement and reduction in CST, the
usual parameters to monitor the response, have
shown more signicant results with the use of
pharmacotherapy compared to laser gird therapy
[118, 119].
A more recent Cochrane review of randomized controlled trials has endorsed the recommendations of the earlier studies that, compared
to no treatment or treatment with grid laser photocoagulation, treatment with any of the antiVEGF agents or depot corticosteroids was more
effective in improving visual acuity, the CST, and
quality of life up to 12months. Because of the
spontaneous improvement of ME in many eyes,
investigators in the past usually waited for
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3–4months before starting anti-VEGF therapy. It
has been seen that an early start of intervention
gives a superior visual outcome with a lesser
number of injections than delaying the treatment
[120]. Compared to corticosteroids, anti-VEGF
agents are more effective. Moreover, there is evidence that steroids lead to high intraocular
pressure and cataract formation [121]. Although
highly effective, these injections have increased
the burden on patients and care providers.
Additional macular laser photocoagulation can
reduce the number of intravitreal injections [122]
(Fig.11.9a, b).
11.4.2.2 Macular Oedema inCentral
Retinal Vein Occlusion
Raised intravascular pressure in the CRVO leads
to a breakdown of the blood-retinal barrier and
increased uid leakage into the retina’s interstitial tissues. Eyes with CRVO, which maintain a
foveal depression on structural OCT, have a better outcome as these require fewer injections of
IVT anti-VEGF than those without preserved
foveal depression. In CRVO, extensive RNFL
haemorrhages compared to deep retinal haemorrhages provide an easy clinical clue to the eventual worse visual outcome, severe ME, and
ischaemic complications [123].
The increased pressure interferes with the perfusion in the retinal tissues, especially in the
DCP. It leads to hypoxia and the release of
hypoxia-inducible factor 1-alpha, causing overexpression of the vascular endothelial growth
factor (VEGF). Discovered in 1989, the VEGF is
expressed in response to hypoxia and is a potent
endothelial cell-specic stimulant that causes
increased vascular permeability, endothelial cell
proliferation, formation of new vessels, and
recruitment of leukocytes [124].
Vascular endothelial growth factor (VEGF)
was found elevated in the ocular uids in the
patients with proliferative diabetic retinopathy
and CRVO [125, 126] and related with the severity of the retinal vein occlusion [127]. Although
initial reports had found elevated VEGF levels in
the RVOs, it was unknown how much of the uid
in the interstitial uid is contributed by the
increased hydrostatic pressure or the cytokines in
the retina. The discovery of VEGF led to the
development of an antigen-binding protein
against VEGF (bevacizumab) and later a special
antigen-binding fragment (ranibizumab), especially for intraocular use [57, 128]. Initial small,
controlled trials with 3-monthly IVT injections
of ranibizumab, an anti-VEGF agent, led to
remarkable improvement in the vision and the
reduction in central retinal thickness irrespective
of the duration of the RVO.
One of the earliest studies found vitreous levels of IL-6 and VEGF elevated in eyes with
CRVO [129]. Subsequently, aqueous humour levels of sVEGFR-1 and sVEGFR-2, placental
growth factor (PlGF), and platelet-derived growth
factor (PDGF) and inammatory cytokines were
also found elevated in the CRVO eyes and related
to ME [130]. The inammatory cytokines keep
increasing in the CRVO and account for persistent and refractory ME.Moreover, the blood ow
velocity of leukocytes slows, converting many
non-ischaemic CRVO into the ischaemic variety
[131]. There is level 1 evidence that early treatment with anti-VEGF agents is a safe and effective therapy in CRVO. It needs to be initiated
early rather than late. It has also been shown that
anti-VEGF therapy leads to decreased retinal
venous pressure in eyes with CRVO [132].
Several controlled clinical trials have been
done both with anti-VEGF agents that last about
1 month and intravitreal injections of depot steroids (triamcinolone acetonide, 1mg Kenalog) or
sustained-release dexamethasone implants
(Ozurdex) to overcome the increased burden of
the monthly injections [133].
There is a signicant risk of cataract formation
and raised intraocular pressure with intravitreal
depot steroids. The anti-VEGF agents to date
remain the rst line of therapy for persistent macular oedema in RVOs, depot steroids being reserved
only for patients who are resistant to the antiVEGF agents [134]. A post hoc analysis comparing the efcacy of Avastin, Eylea, and Lucentis in
CRVO ME showed that ~61% of eyes still showed
recurrent ME, 28% were completely dry, and 11%
had persistent ME at the end of 2years. Of the
three agents, persistent ME was seen in ~18% of
eyes treated with Avastin, compared to 8% with
Lucentis and 5% with Eylea [135]. There is strong
evidence for a treat and extend strategy as only ~8
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11 Macular Oedema
injections were required in the rst year and 13 by
the end of second year of therapy [136].
However, most patients continue to receive
injections even after 5 years [137] and still
require at least four injections per year at the
end of 8years [138]. The search for innovative
drug delivery systems continues in an attempt
to reduce the treatment burden (Fig.11.9a, b).
ab
cd
ef
Fig. 11.9 A 65-year-old man presented with left eye nonischaemic central retinal vein occlusion with CME and
visual acuity of 6/24 (a, b). He received intravitreal inj bevacizumab and showed incomplete resolution of haemorrhages
and a normal foveal contour on OCT at 4 weeks (c, d). Six
weeks later, the CME returned, and he received another IVT
bevacizumab (e, f). He received seven injections in the rst
year of CRVO on a pro re nata basis. Course during the second year shown (g–j) and the third year (k–m). In 34months
of follow-up, he required bevacizumab injections in decreasing frequency, totalling ten injections. He maintained a visual
acuity of 6/6 and a dry macula
11.4 Causes ofMacular Oedema
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ij
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Fig. 11.9 (continued)
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k
m
l
Fig. 11.9 (continued)
11.5 Macular Oedema inUveitis
Macular oedema in uveitis is a leading cause of
blindness in the industrialized world and may
account for 10–15% of blindness [139, 140]. One
of the most frequent causes of impaired vision in
uveitis is the development of cystoid macular
oedema (CME), which may occur in >40% of the
eyes [140, 141]. The CME is often seen in older
patients with long-duration chronic uveitis,
uncommon in acute cases (Figs. 11.10 and
11.11). Smoking is a signicant risk factor for the
development of uveitis CME [142]. The most frequent anatomical location of uveitis complicated
by the development of CME is intermediate uveitis, posterior and pan uveitis, the least common
being anterior uveitis. The estimates of the prevalence of CME for each anatomical location have
varied widely. The prevalence of CME in uveitis
has varied from 9% to 28% in the anterior, 25%
to 70% in intermediate uveitis, 19% to 34% in the
posterior, and 18% to 66% in the posterior [140,
143–145]. There are many reasons for these vari-
ations. Unlike macular oedema with a clear
media in DM, vascular occlusions, or cataract
surgery, uveitis CME (UME) is difcult to diagnose clinically as the media is often hazy due to
vitritis, posterior synechiae, complicated cataract, hypotony, or band-shaped keratopathy. The
latter is a frequent complication of juvenile idiopathic arthritis-associated uveitis in young
children.
ab c
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d
ef
g
Fig. 11.10 A 56-year-old woman presented with a diminution of visual acuity in BE for 6 days. She had been
treated for uveitis 18years ago with oral steroids. Visual
acuity was 6/18, and vitreous cells and CME in the right
eye (a). FFA showed a petaloid pattern of dye collection
and perivascular leak from retinal vessels (b). The OCT
showed CME (c). Her tuberculin skin test was positive at
+20×23mm. Since she showed no response to oral corticosteroids and anti-TB therapy, she was given an Ozurdex
implant. CME resolved at 1 week (d) and remained CMEfree till 12weeks (e, f) with Ozurdex, but CME recurrence
started at 16weeks (g)
11.5.1 Diagnosis ofMacular Oedema
inUveitis
Apart from the biomicroscopic examination, the
FFA and OCT are employed frequently to diagnose UME.However, in uveitis, the dye leakage
from retinal vessels on FFA does not always
increase macular thickness on the OCT, especially
if the macula is already atrophic or if the leakage is
only mild. Concordance between the FFA and
OCT may be seen only in half of the patients. In
birdshot chorioretinopathy, an autoimmune panuveitis, FFA shows mild leakage from the retinal
vessels, but the OCT may not show increased cen-
tral subeld thickness (CST). On the other hand, in
intermediate uveitis, the OCT shows the presence
of CME, but the FFA may not show any leakage
[146]. If the media is clear, over 80% of uveitis
eyes may show concordance between FFA and
OCT observations [147] (Figs.11.10 and 11.11).
Generally, uveitis eyes with diffuse macular
oedema have a poorer outcome than those with
CME.Since ~10% of eyes may also show SRF, it
creates a challenge in estimating the exact CST
[147]. Of the three modalities, helpful information
for CME diagnosis was obtained in 90% with
Stratus-3 OCT, 77% with FFA, and 76% with the
biomicroscopic examination. Nearly one-third of
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c
Fig. 11.11 Fundus photograph of a 46-year-old woman
with decreased vision of 6/24in right eye showing media
haze due to vitritis and a dull foveal reex (black arrows)
the patients with uorescein leak did not show
macular thickness on OCT, and one-third of those
with macular thickness did not show uorescein
leakage. Therapeutic decisions should ideally be
made after obtaining information from FFA and
OCT [148].
(a). Diagnosis of cystoid macular oedema was conrmed
by uorescein angiography (red arrows) that also showed
leakage from retinal vessels (b), and OCT (c)
UME.It led to a reduction of ≥20% in UME or
resolution (≤320μm without cysts) in 69% and
43%, respectively, by 3 months. The rise of IOP
in 11% of the eyes above 24mm Hg was a signicant concern, and these eyes need to be
watched [150].
Resolution of UME is a reasonable goal of
treatment efcacy in non-infectious uveitis.
11.5.2 OCT Biomarkers inUveitis
Macular Oedema
Patients who participated in the multicentric
uveitis steroids treatment trial (MUST)
received either an intravitreal Retisert implant
In non-infectious uveitis, the most critical OCT
biomarkers to predict VA improvement are the
intact ellipsoid zone and cystic spaces in the macula’s central subeld (CSF) and the subretinal uid
(SRF). OCT biomarkers, including disruption of
the retinal inner layers in both horizontal and vertical extent, CST, presence of intraretinal cysts, disruptions of the ellipsoid zone and ELM, and
presence of hyperreective foci, are signicant surrogate markers for VA improvement in UME [149].
(Fluocinolone acetonide 0.59mg) or oral corti-
costeroids (Fig.11.12). The cumulative UME
resolution rate was seen in 94% of the eyes
with initial UME (dened on TD-OCT as
≥240μm), followed by annual OCT measure-
ments up to 7 years. However, >40% of eyes
had recurrences. The VA improved if the CST
improved, but not otherwise. An epiretinal
membrane had a lower likelihood of improving
the CST [151].
Steroid-sparing antimetabolite treatment
improved macular thickness at 6 and 12months
11.5.3 Treatment ofUveitis Macular
Oedema
of initiation, but 50% of the eyes still had persis-
tent UME [152].
Triamcinolone acetonide suspension (TA)
Topical treatment with diuprednate 0.05% is a
reasonably good rst line of therapy for treating
delivered as a periocular or intravitreal injection has been used for a long time in treating
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abc
Fig. 11.12 A case of uveitic cystoid macular oedema (a). Following an injection of intravitreal dexamethasone implant
(b), and the macular oedema remains resolved at 3months (c)
UME. Development of ptosis in the former
and a rise in intraocular pressure in both techniques have been significant challenges. By
24months with one or more IVT-TA, the incidence of raised IOP >21mmHg had increased
to ~45% [153]. Fifty-three percent of the eyes
had resolution of UME following a single
injection of 1 mL of periocular TA (40 mg/
mL) at 1 month. More than 40% required
repeat injections. Of those which had shown a
good initial response, more than 50% of eyes
had a recurrence of UME in a median time of
20weeks. Nearly 16% of eyes developed ptosis, and 59% had IOP rise beyond 22mm of
Hg, half above 30mm of Hg [154]. While the
IVT-TA (4mg/0.1mL) was a reasonably safe
option to treat UME, half the eyes had persistent UME at the mean follow-up of 18months.
Nearly 20% of eyes had shown cataract progression [155].
In the POINT trial, the head-to-head efcacy
of three common strategies to treat UME,
namely the posterior subtenon TA, IVT-TA, or
IVT Dexa implant, was tested. All eyes showed
a reduction in CST.At 8 weeks, the CST reduced
from the baseline by 23%, 39%, and 46%,
respectively. PST treatment strategy was inferior to both IVT treatment strategies but showed
a lower rise in intraocular pressure compared to
the IVT groups [156].
11.5.4 Sustained-Release
Corticosteroid Implants
Presently, three sustained-release corticosteroid
implants are available.
11.5.4.1 Biodegradable
Dexamethasone Implant
These include a slow-release biodegradable dexamethasone implant (DEX implant, Ozurdex,
Allergan, Inc., Irvine, California) injected into the
vitreous cavity through a preloaded 22-gauge
syringe. In patients with non-infectious uveitis, it led
to a signicant reduction in the vitreous haze score.
There was a mean reduction of the CST by >90μm
at 8 weeks, but by the end of the study at 26weeks,
the mean reduction was only 50μm. This study had
no signicant incidence of cataract formation or rise
in IOP [157]. US FDA approved Ozurdex in
September 2010 for the treatment of non-infectious
uveitis. The Ozurdex was designed to release dexamethasone over 6 months. Still, in practice, the effect
did not last that long and required repeated IVT
implantation at 3–4months for sustained effect on
control of inammation. It reportedly controlled
inammation in 72% of the eyes and was considered
a valuable adjunct to systemic therapy [158]. 85% of
the eyes sustained improvement in VA and decreased
CST over the 5-year follow-up. However, 30% of
eyes had raised IOP [159].
In refractory UME in both adults and children,
the IVT Ozurdex was a safe and effective adjunctive therapy [160].
In a preliminary study, the IVT Ozurdex
implant at the time of cataract surgery in uveitis
eyes was as effective as oral corticosteroids in
preventing any exacerbation of inammation following surgery [161]. In a prospective controlled
study, IVT Ozurdex showed a signicant reduction of postoperative are in uveitis cataract surgery. Nearly 37% of the eyes in the standard of
care group developed UME, vs none in the Dexa
group [162]. In a meta-analysis of cataract sur-
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gery in uveitis, intravitreal therapy (TA or
Ozurdex) controlled postoperative inammation
more effectively than systemic anti-inammatory
therapy [163].
11.5.4.2 Non-biodegradable Implants
The two US FDA-approved non-degradable
inserts are similar in construct, with the core containing uocinolone acetonide (FA) 0.18 mg
(Yutiq) and 0.19mg (Iluvien). Both are inserted
into the vitreous cavity with a 25-gauge preloaded applicator. The Yutiq implant initially
releases FA at 0.25μg/day and later at 0.2μg/day
for 3 years. The Iluvien insert releases 0.2μg/
day, and the effect also lasts for 3 years.
Randomized controlled study data is available
only for the Yutiq implant. By the end of 3 years,
mean recurrences of uveitis were 1.7 per implant
eye vs 5.3 per sham-treated eye. The time to the
rst recurrence was 657 vs 70.5 days. Nearly
65.5% of the implanted eyes had a recurrence of
uveitis versus 97.5% of the sham-treated eyes.
The implant effectively resolved UME in 75% of
the eyes with UME at the baseline vs 54% in the
sham-controlled group. Only 13% of the
implanted eyes had persistent UME at the end of
3 years versus 27.3% of the control eyes.
However, by 3 years, nearly three-fourth of
patients required cataract surgery and 26%
required IOP-lowering medications. VA had no
loss or gain [164, 165].
11.5.5 Suprachoroidal Injection
ofTriamcinolone Acetonide
Suspension
the limbus of 0.1mL of the TA suspension using
a micro-needle length varying from 0.9 to
1.1mm. Suprachoroidal injections of CLS-TA, a
suprachoroidal suspension of triamcinolone acetonide, decreased CST by 154μm compared to
18μm in the control group. The VA improved
≥15 ETDRS letters in 47% of the patients in the
treatment group vs 16% in the sham-treated control group. The treatment- related rise in intraocular pressure or cataract formation was not
signicantly different in the treatment and the
control arms [166]. CLS-TA led to improvement
in the CST preceding improvement in
VA. Interestingly, the >50μm improvement in
CST at 4 weeks could predict the outcome at
24weeks [167].
11.5.6 Alternative Strategies
toTreatUME
Repeated IVT injections of bevacizumab
(1.25 mg/0.1 mL) or TA (4mg/0.1mL) were
equally effective for persistent UME [168]. In
patients with refractory UME, anti-IL-6 receptor, tocilizumab (8 mg/kg body weight), was
given as an intravenous infusion over 1h every
4 weeks for 9 months. This therapy was effective either alone or in addition to the current
immunosuppressive therapy. This therapy led to
a reduction in CST from a mean of 415 to
259μm. Sixty percent of the eyes had remission
of CME [169]. Other therapies that have been
found helpful in refractory uveitis and UME
include IVT methotrexate (400 μg/0.1 mL)
[170].
Suprachoroidal space is a potential space
between the sclera and the choroid, a nonimmune- privileged site. In recent years, this site
has been a favourite route for drug delivery,
including gene therapies. Suprachoroidal injection of triamcinolone acetonide (TA)
4mg/0.1mL in suspension form is a novel treatment modality and is FDA approved for the
treatment of ME (Xipeer®, Clearside Biomedical,
Alpharetta, GA, USA). It involves injecting the
TA in the superotemporal quadrant 4 mm from
11.6 Post-surgical Macular
Oedema
Although rst suspected on slit-lamp biomicroscopy by Irvine [171], the advent of FFA and later
the OCT in clinical practice helped dene pathogenesis mechanisms of macular oedema following surgical procedures. Cataract surgery is the
most common cause of post-surgery ME
(Fig.11.13). Patients who undergo pars plana vit-
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