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
320
https://t.me/medicina_free
12 Subretinal Fluid andRetinal Detachment
variations. The formation rate of aqueous humour
varies from 3μL/min in the morning to 1.5μL/
min at night [3]. The non-pigmented ciliary epithelium forms most of the aqueous humour by
secretion, which is actively transported by the
aquaporin water channels. The aqueous humour
is responsible for maintaining homeostasis in the
anterior segment. The bulk of the aqueous
humour follows a pressure gradient. It ows
through the anterior route via the trabecular
meshwork at the anterior chamber’s angle
and ~40% through the uveoscleral outow
through an osmotic gradient through the anterior
face of the ciliary muscles into the suprachoroidal space [4]. Contrary to popular belief held till
recently that there is no posterior aqueous ow,
current evidence suggests that almost the same
amount of aqueous ows out (2.5 μL/min)
through the vitreous cavity as the anterior route.
The posteriorly directed uid moves through the
neurosensory retina (NSR), is pumped out by the
RPE, and nally exits the eye through vortex
veins [5].
12.3 Factors That Keep theRetina
Attached toRPE
andtheAccumulation
ofSubretinal Fluid (SRF)
The photoreceptors contact the microvilli of the
RPE through interdigitation. On the OCT, it is
seen as the zone of interdigitation. An interphotoreceptor protein matrix consisting of glycoproteins and proteoglycans with high
concentrations of glycosaminoglycans acts as a
glue between the photoreceptor outer segments
and the RPE microvilli [6, 7]. The NSR and the
RPE remain adherent throughout life despite the
absence of anatomic adhesions. However,
within no time of the eye removal or death, the
NSR can be easily peeled off from the RPE at
37°C.Metabolic activity and oxygen are crucial
in maintaining the adhesion of the NSR and the
RPE [8]. Lowering the temperature to 4 °C
makes it difcult to peel off the NSR, possibly
because of the shutting down of the Na+pump,
which causes cellular swelling and thus tightens
the grip of microvilli on the outer segments of
the photoreceptors [9]. Several factors play a
role in keeping the subretinal space dry. The
most important is an active pump located at the
apical aspect of the RPE cells capable of pumping balanced salt solution uid from the subretinal space at a rate of 0.12μL/mm2/h. The RPE
pump removes 70% of the SRF.The rest of the
uid moves into the choroid because of the high
oncotic pressure in the choroid [10]. A posteriorly directed pressure gradient is created by
maintaining a posteriorly directed uid ow. In
addition to these factors, the retina offers resistance to uid ow, and the intraocular pressure
pushes the retina posteriorly against the eye
wall [7].
The fact that the retina offers resistance to the
uid ow across the retina has become a matter
of debate. The outow rate from the RPE is
almost the same as the anterior route outow. In
patients with retinal detachment subjected to pars
plana vitreous surgery, the vitreous cavity is often
lled with silicone oil as a vitreous substitute.
Many of these eyes show a rise in IOP.The IOP
rises because the normal posterior outow channel through the retina is no longer available.
Apart from the anterior outow, the ow of aqueous humour through the retina also plays a crucial role in maintaining IOP. The pressure
gradient across the NSR and RPE cannot be easily measured [5]; thus, there is no way of knowing whether uid is transported across the
NSR.Some uid, albeit small in quantity, generated in the NSR from the very high cellular metabolic activity is undoubtedly transported across
NSR through the retinal Muller glial cell processes. The Muller cell processes link with the
photoreceptors to form the outer retina’s external
limiting membrane (ELM).
It has been estimated that in non-drainage retinal detachment surgery, 261μL/mm2/day can be
transported by the RPE and absorbed by the choroid, which is half the volume of the vitreous cavity suggesting a very active RPE pump for
removal of SRF [11].
IFN-γ is a signicant regulator on the posterolateral aspect of the RPE cells that keeps the subretinal space dry. IFN-γ is activated by nitric
12.4 Causes ofSubretinal Fluid
https://t.me/medicina_free
oxide, continuously produced in the retina and
the choriocapillaris [12].
Acetazolamide, when systemically administered, also enhances the apical to basal uid ow
in the RPE by blocking the cell membrane carbonic anhydrase and lowering the pH in the subretinal space [13, 14]. However, it is more
effective in drying SRF due to RPE dysfunction
than the macular detachment due to retinal vessel
leakage.
12.4 Causes ofSubretinal Fluid
The major causes of the accumulation of uid in
the subretinal space (SRF) are (A) exudative, (B)
tractional, and (C) rhegmatogenous retinal
detachment. Besides, several systemic diseases
present with subretinal uid accumulation. See
Box 12.1.
A. Exudative (serous) retinal detachment
1. Central serous chorioretinopathy; pachychoroid spectrum disorder in young
2. Neovascular age-related macular degeneration in old
3. Retinal disorders—diabetic macular
oedema; retinal venous occlusions; retinal angiomas; Coats’ disease; and retinal
inammations
4. Malignant hypertension and pregnancyinduced hypertension
5. Uveal inammations (anterior uveitis;
choroiditis; choroidal granulomas;
inammatory choroidal neovascular
membrane)
6. Choroidal metastatic lesions; choroidal
tumours
B. Tractional causes of retinal detachment
1. Proliferative diabetic retinopathy
2. Branch retinal vein occlusion
3. Retinopathy of prematurity; familial exudative vitreoretinopathy (FEVR)
4. Retinal vasculitis; sickle cell retinopathy
5. Myopic tractional detachment
C. Rhegmatogenous retinal detachment
321
Box 12.1 Systemic Disorders Associated with
Serous Macular Detachment
1 Malignant hypertension
2 Diabetes mellitus
3 Pregnancy-induced hypertension
4 Systemic lupus erythematosus
5 Chronic renal disease/end-stage renal
6 Drug-induced: phosphodiesterase type 5
7 Hypercortisolism: endogenous or
8 Disseminated intravascular coagulopathy
9 Thrombocytopenic purpura
10 Systemic vasculitis
11 Paraproteinemias/hyperviscosity
12 Glomerulonephritis; IgA nephropathy
13 Metastatic disease; leukaemias
a
Wolfensberger and Tufail [170]
b
Roos etal. [171]
c
Jabs etal. [172]
d
Chang etal. [111]
e
da Cruz etal. [173]
f
Fortes etal. [174]
d
disease
inhibitors; anticancer drugs
exogenous (corticosteroids)
syndromes
a
a
a
b
c
e,f
a
a
a
a
a
a
12.4.1 Central Serous
Chorioretinopathy
Central serous chorioretinopathy is a common
idiopathic condition seen at least six times more
common in men <50years of age who present
with acute onset of metamorphopsia and blurring
of vision. In a nationwide study of the Japanese
population over 8 years, 76% were men, and 24%
were women. The incidence rate of CSC was
54.2 and 15.7 per 100,000 population in men and
women, respectively. The mean age at onset was
higher in women at 54.7 ± 13.5 vs
50.5 ± 12.5 years in men, the peak incidence
being in 40–44years in men and 50–54in women
[15]. Forty percent of patients with CSC have
bilateral disease [16]. A 3D single-layer RPE
scan on SD-OCT has shown RPE bumps in 94%
of the asymptomatic eyes [17].
Fundus examination reveals a serous detach-
ment of the macula from the subretinal uid
322
A
https://t.me/medicina_free
12 Subretinal Fluid andRetinal Detachment
(SRF) collection (Fig.12.1). Most patients show
spontaneous resolution within 6 months without
a
any intervention. On fundus uorescein angiography, following an initial delay in the choroidal
lling, there is either a single or multiple points of
uorescein leakage, which increases in size as an
ink blot or has a classical smoke stack appearance
as the dye is seen rising as a plume of smoke
under the retina and lls a sharply dened PED
and late pooling of the dye in the subretinal space.
The ICG shows increased hyperpermeability of
the choroidal vessels. In most acute cases of CSC,
there is an associated single or multiple leaks in
pigment epithelial detachments (PEDs) overlying
b
the area of choroidal hyperpermeability [18, 19].
The yellow dot-like precipitates seen in the SRF
of CSC correspond to hyperautouorescent dots
seen in CSC and represent the outer segments of
photoreceptors [20]. On resolution, the NSR
quickly establishes contact with the microvilli of
the RPE.The hyperautouorescent shed photoreceptor outer segments in the SRF may remain visible for a long time under the NSR.Exposure to
corticosteroids leads to massive exudation in CSC
[21]. Subretinal brinous exudation with or without corticosteroid exposure, especially in the
young, is often associated with RPE rips, which
may be giant at times [22–26].
12.4.1.1 Risk Factors forCSC
The risk factors for CSC include male gender,
hyperopia, short axial length [27], thick sclera,
type A personality [28], corticosteroid use and
pregnancy [29], and stress [30] (Fig.12.1b, c).
Frequent and vigorous physical activity increases
the risk of CSC. Increased blood pressure and
sympathetic activity due to vigorous exercise
might contribute to decompensating the choroidal vessels [31]. Exercise is known to activate the
renin-angiotensin-aldosterone pathway and
induce hypertension. The choroid may be the target organ for frequent attacks of exercise-induced
hypertension variability. The sclera is signicantly thinner in the steroid-associated CSC than
in the non-steroid-associated CSC, suggesting
that steroid-associated CSC is unrelated to
Fig. 12.1 (A) Serous retinal detachment in the macula
(black arrows) in a 32-year-old man suggestive of acute
central serous chorioretinopathy (CSC) in the left eye (a).
OCT shows subretinal uid (blue arrows) (b). (B) A
44-year-old man presented with a diminution of vision in
the right eye and had received corticosteroids elsewhere
with a mistaken diagnosis of choroiditis. The right eye at
presentations showed subretinal uid with massive
yellow- coloured subretinal brin (a). FFA shows an area
of hyperuorescence (red arrow) and outlining of the pigment epithelial detachments (PEDS), white arrows in (b).
Late frames of FFA show lling of the PEDs and a reverse
smokestack hyperuorescence from the site of leakage
shown in ‘b’ with a red arrow (c). He was asked to stop
oral corticosteroids which led to spontaneous resolution
of the SRF and left behind only a streak of brin (blue
arrow) (d). (C) A 42-year-old woman had a diminution of
vision in both eyes for 3 months. She had been diagnosed
with bilateral choroiditis elsewhere and treated with oral
corticosteroids, leading to further vision deterioration in
both eyes. The right eye posterior pole shows subretinal
uid, folds of the internal limiting membrane and subretinal brin. Note clear dot-like spaces in the brin (a, red
arrows). Similar subretinal brin and exudative detachment are seen in the left eye (b). On FFA, the right eye
shows expanding dots of uid leakage (c, d). Note that the
red arrows in ‘c’ correspond to the clear dots in the brin
seen in ‘a’. FFA in the left eye also shows similar expanding dots and pooling uorescein dye under the retina
(e–h). (i, j) The patient was advised to stop oral corticosteroids which led to resolution of the subretinal uid in
both eyes. The right eye shows a subretinal residual contracted brinous membrane (red arrows)
ab
cd
B
C
12.4 Causes ofSubretinal Fluid
https://t.me/medicina_free
323
a
b
c
d
Fig. 12.1 (continued)
324
https://t.me/medicina_free
12 Subretinal Fluid andRetinal Detachment
e
g
f
h
ij
Fig. 12.1 (continued)
increased scleral thickness [32]. Proportionately,
more women than men are affected in steroidassociated CSC. The precise mechanisms that
cause CSC with steroid use are not known. It may
be due to sympathetic overactivity. Stress and
type A persons are long-recognized risk factors
for CSC. The choroidal blood supply is autonomic and responds to parasympathetic and sympathetic control. Applying topical 2%
homatropine increased subfoveal thickness
within 30–60 min [33]. In anecdotal reports,
recurrent PED has followed the application of
topical phenylephrine 2.5% [34, 35].
On the contrary, a controlled study has shown
that topical tropicamide 1% and phenylephrine
2.5% decreased the subfoveal choroidal thick-
ness [36]. Epinephrine has been used to create an
animal model that mimics CSC [37]. In vitro
12.4 Causes ofSubretinal Fluid
https://t.me/medicina_free
325
experiments have shown that epinephrine causes
apoptosis of RPE cells by elevating the cyclic
adenosine monophosphate in the RPE [38].
Dexamethasone, when applied directly to the
RPE cells, did not cause apoptosis, but cortisols
work by upregulating the β-adrenergic receptors
on a variety of cells. It has long been known that
endogenous blood and urine cortisol levels are
higher in patients with CSC [39].
12.4.1.2 OCT inCSC
Nearly 50% of the CSC eyes may show a microrip in the RPE corresponding to the FFA leak.
Spontaneous closure of the micro-rip leads to
the resolution of the SRF [40]. Others have
noted a lower incidence of micro-rips and seen
them more often in chronic CSC (6%) than in
acute CSC (2%) [41, 42]. One of the earliest
studies using enhanced depth imaging on
SD-OCT revealed increased subfoveal choroidal thickness and decreased innermost choroidal layer. A double- layer sign consisting of
undulating RPE and intact Bruch’s membrane
was seen in 75% of the eyes with chronic CSC
[42], which shall now be interpreted as representing a polypoidal choroidal vasculopathy
(PCV). PCV is considered a stage in pachychoroid syndrome. PCV has been mimicking the
CSC in the past [43].
12.4.1.3 Pathogenesis ofSRF inCSC
The source of the SRF can be either the NSR or
the choroid. The increased hydrostatic pressure
under the RPE because of a choroidal pathology
may overcome the adherence forces that keep
the NSR and the RPE in contact. The serous retinal detachment develops when the RPE barrier
breaks, and the uid leaks through the RPE into
the subretinal space. It is usually seen in all those
conditions with increased hydrostatic pressure in
the choroid, such as venous outow choroidopathy, pachychoroid spectrum disorders, or choroidal inammations. A normal functioning RPE
will dry out this leakage of SRF in no time.
However, it is not the case in patients with
CSC.The persistent SRF indicates a more widespread metabolic dysfunction of the RPE that
fails to pump out the SRF.An equilibrium may
reach when the inow into the subretinal space
matches the outow. It is hypothesized that
increased choroidal pressure and choriocapillaris ischaemia, coupled with an RPE metabolic
dysfunction around the leak’s site, allow the
uid accumulation in the subretinal space. It
may accumulate far away from the site of leakage [44].
It is believed that acute CSC is the rst stage
of a pachychoroid spectrum disease. Notably, the
sclera in CSC eyes is signicantly thickened
compared to non-CSC eyes [45]. Recently, ~20%
of the eyes with CSC were shown to have ciliochoroidal effusion. Ciliochoroidal effusion and
exudative retinal detachment are features of uveal
effusion syndrome (UES) [46]. Hyperopia, short
axial length and increased scleral thickness are
risk factors for both UES and CSC. Increased
scleral thickness suggests that CSC, like UES,
may be the outcome of venous outow choroidopathy [47].
Moreover, thick sclera and increased subfoveal choroidal thickness are associated with
pockets of uid in the outer choroid, indicating
that CSC is a stage in the pachychoroid spectrum
[48, 49]. Plasma leakage into the choroidal interstitial tissue likely leads to decreased blood ow,
raising the pressure in the Haller vessels and consequent dilatation of these vessels (pachyvessels), a thick choroid and compression of the
choriocapillaris [50]. The loculation of uid in
the posterior choroid may be due to a decrease in
the trans-scleral outow of uid due to a thick
sclera.
In the choroid, the venous drainage is segmental. It drains into the vortex veins, each segment
drained by 1–2 vortex veins. The availability of
wide-angle ICG has made it possible to study the
vortex veins. An outow obstruction in the vortex
veins leads to congestion of the choroidal veins.
Intervortex veins form anastomotic channels
across the horizontal watershed to compensate
for the congested veins. These vessels are dilated
(pachyvessels) and show hyperpermeability on
ICG.Given the similarity of imaging features in
CSC and obstruction in the vortex vein blood
ow outside the eye as in carotid-cavernous stula (CCF), a view is emerging that CSC is likely
326
https://t.me/medicina_free
12 Subretinal Fluid andRetinal Detachment
an outcome of venous overload choroidopathy
[51, 52].
12.4.1.4 Formation ofChoroidal New
Vessels inCSC
One of the consequences of pachyvessels is the
compression of the choriocapillaris, causing
ischaemia [53]. It is evident on ICG angiography;
all eyes with pachyvessels show patchy delayed
lling of the choriocapillaris, and new vessels
(pachychoroid neovasculopathy) were seen in all
areas that showed delayed lling [54]. In patients
who present with a clinical picture consistent
with type I CNV without drusen, the characteristics of their CNV are more like polypoidal choroidal neovasculopathy (PCN). Patients with
chronic CSC may either present with PCN or
develop this complication after an interval varying from 7 to 365months [55].
The development of CNV is a sight- threatening
complication in the so-called benign spontaneously resolving disease. The anti-VEGF therapy
treats CNV successfully. It needs a high suspicion index, especially in older patients and those
with a chronic course of CSC.In the past, using
ICG angiography, the formation of choroidal new
vessels (CNVs) was seen in ~9% of patients.
Patients older than 50, chronic CSC patients, and
patients who showed thickened RPE, pigmentary
changes, and subretinal lipid deposits developed
CNV [56]. The diagnosis of CNV in chronic CSC
is difcult as the clinical picture of the two overlaps. On FFA, there is no specic leakage pattern
of the CNV to differentiate it from the CSC leaks.
The FFA, therefore, has poor sensitivity and only
moderate specicity to detect CNV [57]. On
OCT angiography, the incidence of CNV has varied from 21% to 23% [57, 58]. However, in CSC
lasting more than 6 months, as many as 30% of
eyes had CNV [59]. Ill-dened leakage on FFA
and irregular at PED on structural OCT and
OCTA ndings can help detect CNV in CSC
[58]. Non-homogeneous hyperreectivity either
in the choriocapillaris layer or under a shallow
irregular pigment epithelial detachment of any
length and height may be used as a marker of
CNV and treated with ant-VEGF therapy [60–
63]. While two-thirds of the chronic CSC fellow
eyes may show irregular shallow PED, internal
hyperreectivity in these lesions suggests
CNV. Nearly one-fourth of the fellow eyes of
chronic CSC may also show an asymptomatic
CNV network on the OCTA. Hence, OCTA
should always be done in both eyes, even if only
one is symptomatic. Notably, these networks are
difcult to be picked up on conventional angiography [64].
12.4.1.5 Treatment ofCSC
Most patients show spontaneous resolution and
are usually watched without intervention
(Fig. 12.2). Lifestyle changes are suggested to
reduce stress. Previously, mild focal laser photocoagulation was applied to non-resolving CSC
patients. Various cells in the retina and choroid
express mineralocorticoid (MR) and glucocorticoid receptors (GR). While aldosterone is a natural ligand for the MR, cortisol also binds the
MR.Because cortisol levels are often raised in
CSC and get aggravated by corticosteroids,
blocking the MR is a logical approach to treating
patients with CSC. However, there are no biomarkers to know either the MR pathway’s activation or their antagonists’ bioavailability in various
eye compartments [65].
The possibility for the role of MR in the pathophysiology of CSC has led to using eplerenone to
block the mineralocorticoid receptors. Eplerenone
is better tolerated than another
aldosterone- blocking drug, Spironolactone. The
other drugs used to treat CSC include ketoconazole (inhibitor of steroid synthesis) and mifepristone—a glucocorticoid receptor-blocking
drug [66]. Anti- VEGF therapy has now supplanted photodynamic therapy for the treatment
of CSC neovasculopathy. Both pulse laser and
eplerenone treatment were equally effective
short-term strategies in chronic CSC in resolving
SRF [67]. However, compared to half-dose PDT,
eplerenone therapy was not well tolerated and
resolved SRF only in 17% vs 78% in the PDT
group [68]. Previously, in a randomized placebocontrolled trial, eplerenone was no better than the
placebo in improving the best corrected visual
acuity [69]. Intact EZ and outer retina may predict a good response to eplerenone [70]. Case
ab
cd
12.4 Causes ofSubretinal Fluid
https://t.me/medicina_free
327
Fig. 12.2 Fibrinous deposits (black arrows) in the fovea
in a steroid-exposed (using steroid cream for a skin disease) patient with central serous chorioretinopathy (a).
Following cessation of steroid therapy, the brinous
deposits resolved spontaneously and completely at 3
selection is a major challenge in testing any drug
therapy in chronic CSC.Most of the studies in
the past rule out neovasculopathy OCT angiography, which is a frequent complication of chronic
CSC and is unlikely to respond to MR blocker
drugs.
months (b). OCT shows subretinal brin (blue arrows)
and subretinal uid (red arrows) at presentation (c). At
3months, there was complete resolution of brin and SRF
in the macula (d)
uid formation under the RPE, termed pigment
epithelial detachment (PED) [72]. This phenomenon is akin to atherosclerosis, where the deposits
of esteried cholesterol are several times higher
than the blood levels. A free exchange of serum
lipids from the blood to the RPE cells and the cell
membrane lipids from the digested photoreceptor
segments occurs. However, the lipid in the BM is
12.4.2 Subretinal Fluid inChoroidal
In choroidal neovascular membranes, the endothelial cells activate, migrate through Bruch’s
membrane (BM), and establish contact with the
RPE cells. Capillary endothelial cells in contact
with the RPE cells express soluble VEGF, which
compromises RPE barrier function, thus causing
SRF accumulation, reversible with anti-VEGF
agents (Fig.12.3) [71]. Thickening of the Bruch’s
membrane due to the deposition of lipids (esteried > unesteried) is an age-related phenomenon. It offers resistance to the uid passage from
the subretinal space to the choroid and leads to
Neovascular Membranes
more like LDL than the membrane lipids [73].
One of the other primary functions of the RPE is
keeping the NS and the subretinal space dry with
the help of an active pump for optimal retina
functioning. Up to 150μm of the SRF on OCT in
patients with wet age-related macular degeneration has minimal impact on vision [74]. However,
beyond 200μm, the SRF affects vision only if
there is no associated outer retinal atrophy or
subretinal hyperreective material (SHRM).
However, if there is atrophy of NSR or SHRM,
the presence of SRF has no additional detrimental effect [75]. It is crucial since giving additional
injections of anti-VEGF agents in the ARMD to
completely dry out the subretinal space only adds
328
ab
https://t.me/medicina_free
cd
12 Subretinal Fluid andRetinal Detachment
Fig. 12.3 A tiny retinal haemorrhage (black arrow)
above the fovea in an eye with choroidal neovascular
membrane (CNVM) (a). Fluorescein angiography showing leak (blue arrow) from the CNVM (b). OCT angiogra-
to the treatment burden without gaining any
vision. On the other hand, treatment- resistant
SRF is protective against macular atrophy [76].
The SRF carries a better visual outcome than
intraretinal uid (IRF) which impacts the vision
unfavourably [77]. The IRF results from damage
to the retinal Muller glial cells affecting the photoreceptor functioning and neural transmission
[78]. A breach in the external limiting membrane
(ELM) contributes to the IRF.At the same time,
an SRF indicates an intact ELM, integrity of the
ellipsoid zone, and better visual outcome [79].
phy shows the neovascular complex (red arrow) (c). OCT
shows subretinal uid (yellow arrows) along with cystic
spaces in the macula (d)
a matter of debate. The disruptions in the ellipsoid zone (EZ), ELM, the number of hyperreective foci (HRF), and increased subfoveal
choroidal thickness are signicantly associated
with the presence of SRF in DME.The increased
fovea avascular zone, either in the SCP or DCP,
has no inuence. However, whenever there was
SRF, disruptions of the retinal inner layers were
less commonly seen [80]. Signicantly patients
of DME with SRF show high vitreous levels of
IL-6, suggesting an inammatory origin of this
uid [81]. High systolic and diastolic blood pressure may be an independent and signicant risk
factor for developing SRF in DME [82].
12.4.3 Subretinal Fluid inDiabetic
Macular Oedema
The FFA in patients of DME with SRF shows
diffuse leakage from retinal vessels compared to
an ischaemic pattern in DR eyes which do not
One-third to two-thirds of patients with diabetic
macular oedema (DME) may be accompanied by
serous retinal detachment (SRD) (Fig.12.4). The
source of the SRF in these patients has remained
show SRF.When treated with intravitreal (IVT)
Lucentis, the visual gains in DME+SRF eyes are
poorer than the DME−no SRF [83]. DME eyes
that are resistant to Lucentis show resolution of
ab
12.4 Causes ofSubretinal Fluid
https://t.me/medicina_free
c d
329
Fig. 12.4 Bilateral moderate non-proliferative diabetic
retinopathy with diabetic macular oedema (a, b). OCT
shows a cone-shaped pocket of subretinal uid (red arrow)
SRF with IVT DEX implant [84]. The SRF and
the hyperreective foci (HRF) are markers of
beneath the fovea, along with intraretinal cystoid spaces
and hard exudates (c, d)
a
inammation. In eyes treated with anti-VEGF
injections, those with SRF and HRF at the baseline have signicantly more recurrences [85].
However, in treating naïve DME with inammatory markers (SRF and HRF), anatomical results
are better with IVT DEX implant, although the
visual improvement is more signicant with
Eylea injections [86]. The DME eyes with SRF,
intact EZ, and no HRF respond much better to the
IVT DEX implant compared to those who do not
have these features [87].
b
12.4.4 Subretinal Fluid inRetinal
Vein Occlusions
Macular oedema often complicates eyes with
retinal vein occlusions (RVO). In the past, exudative retinal detachments were only occasionally
reported in eyes with central retinal vein occlusion (CRVO) [88]. The availability of OCT
revealed that many more patients with branch
retinal vein occlusion (BRVO) or central retinal
vein occlusion (CRVO) develop SRF [89]. Most
RVO eyes develop SRF under the fovea as a
Fig. 12.5 Retinal haemorrhages due to macular BRVO
(a), with cystoid macular oedema (blue arrows) and a
cone-shaped pocket of subretinal uid (red arrow) on
OCT (b)
cone-shaped detachment that later becomes
dome-shaped (Fig.12.5). It is hypothesized that
this SRF may result from uid leakage through
the retinal Muller glial cells [90]. A thicker sub-
Соседние файлы в папке Библиотека им академика М.И. Перельмана