Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2589_Библиотеки_им_академика_М_И_Перельмана
.pdf
ab
cd
11.4 Causes ofMacular Oedema
https://t.me/medicina_free
279
Fig. 11.2 Fluorescein angiography showing diffuse macular oedema in both eyes (a, b). OCT shows corresponding
cystoid spaces in both eyes (c, d)
DME should be classied based on whether there
was signicant involvement of the central 1mm
(central subeld). In patients with no or minimal
diabetic retinopathy and who did not have clinically detectable DME, the mean central subeld
thickness (CST) was 270μm on SD-OCT, which
was 70μm higher than the Stratus OCT [40]. It
was proposed that any thickness above two standard deviations of the mean thickness taken as
320 μm for men and 305 μm on SD-OCT
(Spectralis, Heidelberg Engineering, Heidelberg,
Germany) be classied as centre-involving DME
(CI-DME). Values less than these are considered
non-centre-involving DME (nci-DME). Notably,
the errors in automated measurements of DME
were minor even with the Stratus OCT, compared
to the manual technique used earlier, and were
not likely to affect the results of trials. Thus, there
was no need to send the OCT images to the centralized reading centres [41].
11.4.1.7 The OCT Biomarkers inDME
Till the availability of the OCT, patients with
DME who did not respond to the then standard of
care focal/grid laser photocoagulation were
labelled as recalcitrant macular oedema. One of
the primary reasons for the recalcitrance was the
presence of a thick glistening membrane in the
macula labelled as a taut posterior hyaloid membrane (PHM), which caused signicant traction
on the macula. These taut membranes often
accompany the regressed proliferative diabetic
retinopathy. No amount of laser photocoagulation was effective in such patients. It required
pars plana vitreous surgery to release the traction
on the macula (Fig.11.3a–d). These taut hyaloid
membranes were only sometimes discernible on
clinical biomicroscopic examination. Even the
rst-generation TD-OCT could easily detect all
the vitreoretinal interface abnormalities, including thickening of the PHM, posterior vitreoschi-
280
bc
https://t.me/medicina_free
11 Macular Oedema
a
de
Fig. 11.3 A taut posterior hyaloid membrane (TPHM) is
a thick membrane (red arrows) in the macula that causes
signicant traction on the macula and is often responsible
for recalcitrant diabetic macular oedema (a). A 62-yearold woman with type 2 diabetes for 15 years had undergone pan-retinal photocoagulation in both eyes for
proliferative diabetic retinopathy. She was pseudophakic
in both eyes and had DM for 15 years. Her visual acuity in
the left eye was 6/60. She had a clinically unapparent taut
post-hyaloid membrane (b), which on OCT showed traction on the macula. Macular thickness was increased to
726 μm (c). She underwent pars plan vitreous surgery to
remove the taut posterior hyaloid membrane. At 18
months, her visual acuity had improved to 6/18, there was
no CME (d), and OCT showed a normal foveal contour,
and macular thickness had reduced to 226 μm (e). Another
patient with an apparent taut posterior hyaloid membrane
(TPHM) was already treated for proliferative diabetic retinopathy with PRP in the right eye. Visual acuity was
reduced to counting ngers at one metre. The OCT
showed tractional macular detachment with complete disturbance of the macular architecture (f, h). She underwent
pars plana vitreous surgery for removal of the tractional
elements and at 3 weeks improved to 6/24 visual acuity
with restoration of the foveal contour (g, i)
hi
11.4 Causes ofMacular Oedema
https://t.me/medicina_free
281
f
g
Fig. 11.3 (continued)
sis, and tractional detachment of the macula. It is,
thus, essential rst to rule out these tractional elements in DME because no pharmacotherapy is
effective in such cases, and they require surgery.
The SD-OCT and the SS-OCT give highly accurate and reproducible measurements of the CST,
which is a measurable critical parameter to study
the therapy outcome.
Leakage from MAs in the deep capillary
plexus (DCP) leaks into the outer plexiform layer
and in the ONL, which on OCT is seen as hyporeective comparatively large cystic cavities.
Intraretinal uid in the inner nuclear layer appears
as smaller hyporeective cystic spaces due to a
breakdown of BRB in the supercial capillary
plexus (SCP) and DCP.Later, cysts appear in the
OPL as well. Fluid may also accumulate in the
potential space between the outer nuclear layer
and the RPE layer, termed the subretinal uid
[42]. The SRF may be present in 25–30% of the
eyes with DME.The signicance of SRF is still
not clearly understood. It may result from either
a failure of the RPE pump or the breakdown of
tight junctions of the RPE. Larger intraretinal
cysts are associated with chronic DME [42].
In patients with long-standing DME, there are
often disruptions of the inner retinal layers
(DRIL), a signicant biomarker for predicting
the visual outcome following any therapeutic
intervention. It is proposed that DRIL develop
when the thickening of the retina stretches the
bipolar cells beyond their limit of elasticity.
DRIL of ≥50% of the central 1-mm area (CSF)
carries an inferior visual outcome. DRIL is present if the boundaries between the various retinal
layer interfaces in the inner retina cannot be identied, for example, between ganglion cell layer
(GCL), IPL, and INL or INL and OPL or OPL
and ONL.These are present irrespective of the
cystic cavities in the retina [43]. Any improve-
282
https://t.me/medicina_free
11 Macular Oedema
ment or worsening in the DRIL >300μm in the
CFS was associated with long-term improvement
or worsening, respectively. DRIL may represent
the retinal cells’ disorganization that hinders the
photoreceptors’ signal transmission to the ganglion cells [43]. After the resolution of DME in
patients with DRIL, increased FAZ in both supercial and deep capillaries is seen, suggesting that
DRIL is possibly caused by ischaemia [44]. The
other OCT parameters associated with DRIL are
disruption of the ELM and EZ.
Small, round, or oval hyperreective foci
(HRF) in the retinal layers and choroid also predict visual outcomes in DME.These are believed
to be activated microglia and are also present in
inammatory diseases and age-related macular
degeneration. These could also represent migrating RPE cells, lipid-laden macrophages, extracellular proteinaceous, or lipid material. However,
HRFs are usually less than 30μm in size without
any shadowing and are more likely to be of
inammatory origin [45]. These HRFs are not
visible on biomicroscopy or the fundus photographs till they become conuent. They are seen
on the outer border of the ONL and OPL and
detected within the walls of the retinal MAs and
may thus be the microglia lled with lipids [46].
The higher number of HRF in the outer retinal
layers is also a predictor of poor visual outcomes
[45]. These must be differentiated from the hard
exudates, which are larger and generally show a
shadow. Baseline higher numbers of HRF in the
choroid and a low choroidal vascularity index,
both indicating inammatory activity, predict a
good response to the treatment of DME with
uocinolone acetonide (FA) inserts [47]. If associated with DME, the hard exudates respond
better to intravitreal (IVT) injection of corticosteroids than the anti-VEGF agents [48].
11.4.1.8 OCT Angiography inDiabetic
Macular Oedema
OCT angiography (OCTA) is a non-invasive
technique of visualizing the depth-resolved ow
of RBCs in the regular or abnormal retinal/choroidal vessels without injecting any dye. The
OCTA seeks to replace the FFA in day-to-day
clinical practice. It has several advantages over
the conventional FFA as the segmented en face
view can show layer by layer the retinal capillaries and larger vessels that were not seen in FFA
because of the obscuration of the deeper vessels
by the dye. It has been shown that MAs in the
deep capillary plexus are majorly responsible for
DME.Wide-angle OCTA can quantify the extent
of ischaemia in DR (Fig.11.4). It can show the
extent of the ischaemic macula at the SCP and
DCP layers, which carries signicant prognostic
implications for the visual outcome.
Several OCTA parameters are larger in DME,
such as FAZ area and irregularity of its contour,
average vessel calibre, higher vessel tortuosity,
and a low vessel density (VD) in the SCP.Higher
VD in SCP carries a better visual outcome following anti-VEGF therapy [49]. Large cystic
spaces in DME introduce artefacts and pose a
signicant challenge in interpreting the OCTA
images in ~25% of the DME eyes [50]. The VD
in DCP may artifactually show a higher VD in
eyes with DME [51]. Patients with DME, nonresponders to anti-VEGF treatment, have capillary non-perfusion in the DCP layer and more
MAs in this layer [52]. The OCTA does not show
any signicant reperfusion of the ischaemic areas
of the retina following the use of the anti-VEGF
agents for DME [53]. On the other hand, it has
been claimed that IVT corticosteroids (Iluvien)
may reopen capillaries blocked by leukostasis
and improve perfusion in DME [54]. Although
anti-VEGF therapy has become the gold standard
treatment for DR, there is some evidence that
using anti-VEGF agents may affect retinal perfusion in the DCP [55].
11.4.1.9 Role ofVascular Endothelial
Growth Factor inDME
The discovery of VEGF in 1989 [56] and its
humanized antibody in 1997 [57] brought about a
paradigm shift in managing several eye disorders,
including ARMD, DME, retinal vascular occlusion, and proliferative diabetic retinopathy. The
VEGF mRNA levels were nearly 3.2 times higher
in the retina of a diabetic rat model, and the retinal vascular permeability was 1.8 times higher in
the diabetic rats versus the control animals.
Highly specic antibodies against the VEGF
ab
cd
11.4 Causes ofMacular Oedema
https://t.me/medicina_free
283
Fig. 11.4 Fundus photographs of right (a) and left (b)
eyes of a patient with proliferative diabetic retinopathy.
Montage of OCT angiography, a dyeless angiography,
blocked the increased permeability. The authors
concluded that anti-VEGF antibodies could
become a potent tool for treating patients with a
blood-retinal barrier breakdown [58]. Earlier, it
had been shown that intravitreal injection of
VEGF led to overexpression of intercellular
adhesion molecules (ICAM) on the retinal vascular endothelium promoting leukostasis in retinal
capillaries [59]. Moreover, vitreous levels of
VEGF, ICAM-1, IL-6, and monocyte chemotactic protein-1(MCP-1) were signicantly higher in
patients with DME than in non-diabetic controls.
quantifying the extent of ischaemia (blue arrows), and
retinal neovascularization (red arrows) in both eyes (c, d)
Of these, the VEGF and the ICAM-1 level were
also signicantly associated with the severity of
DME [60, 61].
11.4.1.10 Anti-VEGF Therapy
inDiabetic Macular
Oedema
Many patients who have CI-DME still maintain a
visual acuity of 20/20. Such patients should be
followed every 2–3months, and treatment should
be instituted if the VA drops to 20/30 or worse
[62]. In a prospective, controlled trial, patients
284
https://t.me/medicina_free
11 Macular Oedema
with CI-DME but visual acuity ≥20/25 randomized to receive either aibercept every 4 weeks or
laser photocoagulation or observation had visual
acuity of 20/20in 77%, 71%, and 66%, respectively, at the end of 2 years. By this time, the
probability of receiving aibercept as a rescue
treatment in the laser and observation group was
26% and 36%, respectively [63]. Interestingly,
nearly two-third of the patients in the observation
group maintained their visual acuity and giving
them injections would have been unnecessary.
Thus, patients with CI-DME and good visual
acuity should be observed [64]. Besides the cost
factor, IVT interventions carry a denitive, minimal risk of endophthalmitis. Thus, these patients
must be counselled to maintain control of their
HbA1c and other comorbid conditions to delay
injections and maintain good vision as long as
possible [65].
A sham-controlled, masked, double-blind
controlled trial in DME (VA 20/32–20/160)
showed that IVT injection of 0.5 mg ranibizumab administered every month led to ≥15
ETDRS letter improvement in 22.6% of the eyes
and 53% achieved ≥20/40 at the end of 1 year
compared to 8.2% and 23.6% eyes, respectively,
by the laser photocoagulation alone. There was
no advantage to combining laser therapy with
ranibizumab [66]. Two parallel multicentric
phase 3 RISE (NCT00473330) and RIDE
(NCT00473382) pivotal trials established the
role of IVT injections of ranibizumab 0.3 or
0.5mg every month for treating DME.Seventy
percent of the patients who were followed up to
4 years showed a sustained effect of 0.5 mg
ranibizumab given on a PRN basis after the initial 1-monthly dosage schedule [67]. The US
FDA approved IVT Lucentis 0.3 mg (ranibizumab) prelled syringe to treat DME in August
2012.
A novel anti-VEGF molecule was created by
fusing VEGFR1 and VEGFR2 receptors to the Fc
region of the human IgG.In addition to binding
all isoforms of VEGF, it also bound the placentaderived growth factor and was called VEGFTrap. Not only it prevented the activity of VEGF
on its receptors in the endothelial cells, but it also
reversed the leukostasis [68]. This novel antiVEGF agent, named aibercept (Eylea), was US
FDA approved in 2019 for the treatment of DME
following two phase 3 parallel randomized controlled trials, VIVID and VISTA, in which more
than 40% of patients showed ≥15 letters of
improvement in visual acuity score compared to
the laser photocoagulation. Intravitreal injections
of Eylea 2.0mg/0.05mL given every 8/16weeks
for moderately severe or severe DR without DME
have also resulted in consistent improvement in
DR severity scores (DRSS) and prevented the
development of DME (Fig.11.5). Eighty percent
of the eyes which received IVT Eylea injection
every 8 weeks and 65% of eyes every 16weeks
had improvement in DRSS by ≥2 steps.
Moreover, only 16% of patients developed DME
at the end of 1year versus 50% in the untreated
control group [69].
a
c
Fig. 11.5 OCT showing bilateral diabetic macular oedema (DME) at presentation (a, b) and resolution of DME 2 years
following anti-VEGF therapy with aibercept (c, d)
b
d
11.4 Causes ofMacular Oedema
https://t.me/medicina_free
285
Bevacizumab (Avastin) is the rst anti-VEGF
agent developed for oncology use. It is available
as 40mg/mL vial. Fractionated from this vial, a
1.25mg/0.1mL dose has improved or stabilized
the visual acuity of patients with DME [70]. It
has to be sourced from compounding pharmacies. Although not approved by the FDA for IVT
injections, being the most cost-effective antiVEGF, it remains the most commonly used IVT
anti-VEGF agent worldwide. A head-to-head
comparison of bevacizumab (Avastin), ranibizumab (Lucentis), and aibercept (Eylea) in a
randomized control trial (DRCR-protocol T) did
not show any difference in the visual outcome or
safety in patients with DME at the end of 2years
if the initial VA was 20/40 or better. However, in
patients with 20/50 or worse, Eylea was superior
to Avastin. However, 64%, 52%, and 41% of eyes
required focal laser photocoagulation for persistent DME beyond 6 months in the eyes that
received Avastin, Lucentis, and Eylea, respectively [71].
Moreover, a post hoc analysis of this study
revealed that the CST contributed only a small
part to the improvement in visual acuity and cannot be a surrogate marker for evaluating the
visual acuity change following IVT anti-VEGF
therapy in DME [72]. Nearly two-third of the
patients in protocol T were followed up for 2
years and received treatment at the investigator’s
discretion for the next 3 years. While the reduced
macular thickness obtained at 2 years was maintained at 5 years, there was a mean loss of 4.6
letters of visual acuity between the 2 and 5years.
The results emphasized the need for better strategies for the long-term management of DME [73].
The DRCR Retina network protocol W looked
at whether aibercept could prevent the development of PDR and CI-DME in patients who had
only NPDR and NCI-DME.At the end of 2 years,
there was a three-fold decrease in the risk of
developing CI-DME or PDR compared to the
sham group, which received aibercept only as
rescue therapy. However, after 4 years, although
a signicant risk reduction in sight-threatening
DR was evident, there was no meaningful visual
gain from using aibercept as a preventive strategy [74].
11.4.1.11 Newer Therapeutic
Paradigms
fortheTreatment ofDME
The major challenge of using anti-VEGF agents
in treating DME is the treatment burden for the
patients and the healthcare systems as the disease
they treat is chronic, and the effect of the antiVEGF agents is short-lived and does not last
beyond 4 weeks. Thus, there has been a continuous search for new treatment paradigms and
drugs. In recent years, the angiopoietin-Tie signalling pathway has emerged as an effective
mechanism for controlling endothelial barrier
function [75]. Angiopoietin-Tie (tunica interna
endothelial kinase) signalling pathway controls
vascular endothelial permeability and stability.
Ang-1 is a natural ligand for Tie-2 (a transmembrane receptor on vascular endothelial cells). By
binding Tie-2, it activates it by phosphorylation
and promotes the endothelial cells’ viability,
junctions, and barrier functions. Vascular endothelium protein tyrosine phosphatase (VE-PTP)
and Ang-2 are upregulated in hypoxia and
inammation.
While VE-PTP inactivates Tie-2 by dephosphorylation, Ang-2 blocks its action by binding
with it, both preventing the action of Tie-2 in
keeping the vascular endothelium stable and thus
causing its instability and loss of barrier function
[76, 77]. Newer agents that target the Ang-2/Tie
pathway have been developed to regulate and stabilize the endothelial barrier [77]. In a phase II
clinical trial, monthly IVT injections of a bispecic antibody that targets angiopoietin-2 and
VEGF-A (Faricimab, 0.6mg) were found superior to ranibizumab (0.3mg) in the treatment of
DME [78]. In a phase III trial, IVT injections of
Faricimab given every 8 weeks or at personalized
intervals up to every 16weeks were found noninferior to aibercept given every 8 weeks, thus
demonstrating the possibility of extending the
treatment interval up to 16weeks. Sixty percent
of the patients in these trials could achieve a dosing interval of 16 weeks while maintaining a
durable improvement of vision and reduction in
DME at 2 years [79].
In an invitro study, a Tie-2 agonist, a Tie2.1hexamer, was effective in normalizing and stabi-
286
https://t.me/medicina_free
11 Macular Oedema
lizing the intercellular junctions of a stressed
endothelial cells monolayer. Preclinical studies
found it effectively restored barrier function in a
mouse and a non-human primate model.
Moreover, it was found effective when anti- VEGF
agents were ineffective in restoring endothelial
barrier function. It has an extended presence in
the vitreous humour and is a new potential therapeutic agent for treating DME [80]. Several trials
evaluating newer molecules and drug delivery
systems have been recently reviewed [81].
11.4.1.12 Is There aRole forLaser
Photocoagulation forDME?
Until 2010, the standard of care for DME was
focal/grid laser photocoagulation. The ETDRS
recommended focal laser photocoagulation of
MAs in focal DME and grid laser photocoagulation in diffuse DME as it prevented moderate
visual loss by 50% at the end of the 3-year follow up. Twelve percent of the DME patients who were
treated had a signicant loss of vision (≥15 letters
on ETDRS) compared to 24% who were not
treated [39]. However, laser photocoagulation led
to only stabilization of vision, and by the end of
3 years, only 44% of eyes gained ≥10 ETDRS
letters and 16% lost vision. A modied grid with
greater spacing, less intense treatment, and direct
laser photocoagulation of MAs and not treating
anywhere closer than 500μm from the foveal centre is recommended. Although no controlled trials
have been done, laser photocoagulation is recommended for NCI-DME [62]. A recent Cochrane
analysis concluded that modied laser protocol
for focal/grid laser photocoagulation prevented
further loss of vision and led to partial or complete resolution of DME compared to no intervention at 1–3 years [82]. A mild macular grid without
directly treating the MAs is not recommended as
it is not an effective strategy [83]. Following focal
laser photocoagulation, nearly 90% of the MAs
close by 3 months (Fig.11.6). The reduction of
CST on OCT rather than the MAs leakage on FFA
at 2 weeks predicts the nal CST at 3 months
[84]. One of the signicant complications of laser
photocoagulation is an expansion of the scars, and
if treatment is done too close to the foveal centre,
it may compromise the vision. Inadvertent photocoagulation of the fovea centre is a distinct possibility, especially in an eye with severe macula
oedema where the landmarks of the fovea may not
be clearly dened.
a
Fig. 11.6 A 46-year-old man with type 2 diabetes and
dyslipidaemia presented with macular oedema with massive hard exudates in the macula (a). His visual acuity was
reduced to counting ngers close to his face. He was
treated with statins, which signicantly reduced hard exudates at 6 weeks with an improvement in visual acuity to
bc d
6/60 (b). At this stage, he was treated with focal laser photocoagulation. His visual acuity had improved to 6/36
with further reduced hard exudates (c). At 18months, his
visual acuity had improved to 6/12 with the resolution of
macular oedema and minimal hard exudates (d)
11.4 Causes ofMacular Oedema
https://t.me/medicina_free
287
11.4.1.13 Role ofCorticosteroids
inDiabetic Macular
Oedema
To reduce the frequency of IVT injections, longacting corticosteroids such as triamcinolone
acetonide (TA) or sustained-release biodegradable dexamethasone implants or non-biodegradable uocinolone acetonide (FA) inserts have
been evaluated in randomized clinical trials. In
one such trial, focal laser photocoagulation
yielded better visual outcomes at the end of
2years than the TA (IVT inj of 1mg or 4mg).
Nearly 51% of the phakic eyes receiving IVT
injections of 4 mg of TA (23% in the 1 mg
group) had to undergo cataract surgery, and 33%
and 16%, respectively, in the 4 mg vs 1 mg,
developed a 10mm of Hg rise of intraocular
pressure [85]. The outcome was not changed at
3 years of follow-up [86]. However, in a subset
of the pseudophakic eyes, TA combined with
prompt focal/grid laser yielded results similar to
IVT Lucentis [87].
Despite one macular photocoagulation treatment, patients with persistent DME were randomized to a slow-release low-dose (0.2μg/day)
or high-dose (0.5μg/day) FA insert versus a sham
IVT injection. At the end of 2 years, 26% of
patients with FA receiving either insert compared
to 13% of the sham had >15 ETDRS letters
improving visual acuity. The low-dose group had
a better risk-benet prole. Of those phakic at
baseline, cataract surgery was required in
41–51% of patients in the low and high doses,
respectively. Glaucoma incisional surgery was
required in the low and high doses in 3.7% and
8.1%, respectively [88]. By the end of 3years,
the incidence of high pressure did not change
much, but practically all phakic patients had to
undergo cataract surgery. Improvement by
ETDRS ≥15 letters in 34% of treated eyes versus
13% of sham-treated eyes [89]. In a subgroup
analysis, in patients who had chronic DME (diagnosis ≥3 years), the low-dose inserts improved
VA by ≥15 ETDRS letters in 34% vs 13% in the
sham group and 22% vs 28%, respectively, in the
non-chronic DME [90]. In September 2014, the
Iluvien implant (0.2 μg/day) was US FDAapproved for patients with DME who had not
previously shown a corticosteroid-induced rise in
intraocular pressure.
A slow-release dexamethasone implant (0.7 or
0.35 mg) was tested in two randomized shamcontrolled, parallel phase 3 clinical trials. It
showed that 22% of the study eyes vs 12% of the
sham-treated eyes showed improvement in VA by
≥15 ETDRS letters at the end of 3 years. On
average, four implants were required by the end
of 3 years. The rates of cataract development
were 68%, 64%, and 20% in the high, low, and
sham groups, respectively. A signicant rise in
intraocular pressure was seen in 0.6% and 0.3%
of the high and low doses, respectively [91]
(Fig. 11.7a, b). However, when Dexa implant
(0.7 mg) was added to the continued Lucentis
treatment in patients who showed persistent macular oedema even after three injections of
Lucentis, although macular oedema improved,
there was no change in the visual acuity [92]. In a
single-centre study of recalcitrant DME, a single
IVT of Ozurdex (0.7mg) implant led to signicant improvement in the CST over 6 months. The
VA improved from a mean of 0.82 ± 0.46 log
MAR before the implant to 0.68±0.49 log MAR
at 6 months of follow-up. Maximum improvement in VA was seen at 4 weeks, and the maximum reduction in CST was at 6 weeks [93].
Corticosteroids are no longer recommended as
primary therapy in DME but are favoured as
second- line therapy in non-responders to the conventional anti-VEGF treatment [62]. Patients
with DME who are planned for cataract surgery
may be benetted from an IVT Ozurdex implant
at the time of surgery [94].
11.4.1.14 Control ofDiabetes
andOther Comorbid
Conditions
Multifactorial interventions to control blood
sugar levels, blood pressure, lipids, and proteinuria lead to a decrease in DME.If done before
treatment with laser photocoagulation, decreased
retinal thickness facilitates the application of low
energy laser beam [95] (Fig.11.6). In a prospective study, patients with DME were encouraged
to reach the target values of HbA1c, lipids, blood
pressure, Hb, and proteinuria through extensive
288
gh
ij
https://t.me/medicina_free
abc
11 Macular Oedema
d
f
e
Fig. 11.7 (A) A 56-year-old man with type 2 DM for
20years had received focal laser thrice, and multiple antiVEGF injections and yet continued to have macular
oedema in the right eye. Visual acuity was 6/24 and the
central foveal thickness was 512μm (a, d). He received an
intravitreal implant of Ozurdex (red arrow, b). A month
later, visual acuity improved to 6/18. Note a reduction in
the hard exudates and macular thickness (b, e). At 3
months, hard exudates had resolved except at the foveal
centre (f). Visual acuity improved to 6/12. Note the residual implant inferiorly (red arrow) (b, c). Four months after
the Ozurdex implant, there were no hard exudates, and
visual acuity improved to 6/12. Macular thickness had
decreased to 218μm (g, i). However, at 6 months postOzurdex implant, the macular oedema returned, visual
acuity decreased to 6/18, and the CST measured 498μm
(h, j)
Соседние файлы в папке Библиотека им академика М.И. Перельмана