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12 Subretinal Fluid andRetinal Detachment
foveal choroidal thickness is a good prognostic
indicator for response to treatment with antiVEGF agents in eyes with retinal vein occlusion
(RVO) that shows SRF [91]. Increased vascular
permeability due to high vitreous levels of VEGF,
soluble intercellular adhesion molecules
(sICAM), and downregulation of pigment
epithelial- derived growth factor (PEDF) may
result in the formation of SRF in eyes with RVO
[92, 93]. The visual acuity is mainly affected by
macular oedema (ME) in RVO than by the presence of SRF, which often accompanies the ME
[94]. Both IVT Eylea and IVT DEX implants
lead to the resolution of the SRF in CRVO, but
the visual results are superior with Eylea [95].
Eylea is also more effective in BRVO with SRF
than Lucentis [96]. Triamcinolone acetonide
(TA) is also effective in resolving SRF in eyes
with RVO [97]. While TA led to a better morphological outcome in BRVO eyes with ME and
SRF, the visual outcome was good irrespective of
the presence of SRF [98].
12.4.5 Subretinal Fluid inMalignant
Hypertension
Recognizing exudative retinal detachment as a
manifestation of malignant hypertension (MH) is
vital. An undiagnosed patient may rst present
with sudden onset of bilateral loss of vision due
to exudative retinal detachment. For more than
125 years since Liebreich’s rst description of
‘albuminuric retinitis’ in MH, retinal arteriolar
changes in hypertension had remained the focus
of physicians’ attention until Hayreh rst
described choroidopathy as a manifestation of
accelerated hypertension in a monkey model of
renal hypertension [99]. Exudative retinal detachment and RPE infarction were the most characteristic feature of hypertensive choroidopathy.
The changes were rst detected after a median
interval of 36days after clamping the renal artery
when the systolic blood pressure (BP) reached a
median of 180–190 mmHg. There was widespread occlusion of the choroidal arteries, infarction of the choriocapillaris and RPE, and
exudative retinal detachment. On FFA, there was
delayed lling of the choroid, mainly in the postpole. Multifocal, small, round pale or white RPE
changes were seen in the macula or temporal to
the macula, which leaked uorescein in the late
phase and showed dye pooling in the subretinal
space. The choroidal vasculature is under autonomic control. The renin-angiotensin- aldosterone
system is the primary regulator of blood pressure
control. Hayreh, in his experiments, produced
acute ischaemic injury of the kidney by clamping
one or both renal arteries, which led to the release
of renin. This proteolytic enzyme cleaves angiotensin I from angiotensinogen, further converted
by the angiotensin-converting enzyme to angiotensin II.Angiotensin II has widespread activity
in the sympathetic system and promotes the
release and potentiation of norepinephrine- induced
vasoconstrictor activity. It ultimately leads to the
occlusion of arterioles.
Papilloedema and exudative retinal detachment besides the cotton wool spots and the retinal
haemorrhages characterize the fundus changes in
malignant hypertension (see Chap. 8, Fig. 8.7a–
d). If the fundus examination is unavailable, high
blood pressure (usually systolic BP>200mmHg
and diastolic BP >120mmHg) with at least three
end-organ damage, including kidneys, heart, and
brain and thrombotic microangiopathy. Despite
the availability of potent antihypertensive therapy
for more than four decades, the incidence of MH
has not decreased, especially in underserved
regions and communities. Three-fourths of the
MH is caused by essential hypertension. The less
common causes include oestrogen contraception,
renal artery stenosis, primary hyperaldosteronism, IgA nephropathy, and pheochromocytoma
[100]. The end-organ damage due to MH in the
eyes, kidneys, and brain shows a high degree of
concurrency. It is believed to be due to
hyperperfusion- induced capillary leakage, which
causes posterior reversible encephalopathy syndrome, proteinuria, and exudative retinal detachment. These changes are reversible with the
control of BP (see Chap. 8, Fig. 8.7e–h). The
reversible damage is due to an elevated BP
beyond the autoregulatory control of the arterioles leading to capillary hyperperfusion. The
choroid already has the highest blood ow tissue
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in the eye. A laser speckle owgraphy has shown
increased choroidal blood ow when the
untreated blood pressure is very high [101, 102].
On the other hand, many believe that lesions of
hypertensive choroidopathy are due to ischaemic
insult [103, 104]. Multimodal imaging shows
SRF and the presence of hyperreective deposits
on Bruch’s membrane, which persist after the
resolution of the SRF. The OCT angiography
also shows the hyperreective deposits in the
choriocapillaris layer. These are seen as autouorescent spots on FAF and are likely due to brin
deposits [105, 106]. The electron microscopy in
the monkey model of hypertensive choroidopathy also showed brin deposits [107]. On OCT
angiography, the retinal circulation showed
extensive ow voids in the choriocapillaris of a
patient with MH who showed massive
SRF. Concurrent with the normalization of BP,
the perfusion in the choriocapillaris improved,
SRF resolved, and the visual acuity improved but
ow decit persisted in the retina [108].
Reperfusion of choriocapillaris was also seen in a
patient with pregnancy-induced hypertension
[109]. Hypertensive choroidopathy frequently
complicates pregnancy-induced hypertension
(preeclampsia). These patients develop choroidopathy at a BP lower than in age-matched
non-pregnant hypertensive patients who present
more often with hypertensive retinopathy. On
OCT angiography, these patients may not have
complete reperfusion of choriocapillaris. Both
ischaemic and hyperperfusion mechanisms may
likely be responsible for hypertensive choroidopathy [110]. Patients with end-stage renal disease
who are on dialysis have a higher risk of developing serous retinal detachment, perhaps because of
hyperperfusion in the choroid [111].
12.4.6 Subretinal Fluid inUveitis
The most common cause of SRF/exudative retinal detachment (ERD) is VKH disease which
accounts for nearly 40% of the cases of ERD in
uveitis. The other less common causes are panuveitis (15%), posterior scleritis (4%), necrotizing
scleritis (2%), retinochoroiditis (2%), and sympathetic ophthalmia (1%) [112].
The SRF develops in around 40–65% of eyes
with uveitis CME [113]. Unlike other causes of
ME (RVO; Irvine-Gass syndrome) that show the
presence of hyperreective deposits in the SRF,
only a minority of uveitis ME (UME) does so
[114]. In patients with uveitis who develop cystoid macular oedema (CME), SRF appears rst
before they develop CME [115]. It is an early
sign of UME and generally carries a favourable
prognosis. Patients with worse vision and thicker
retinas on presentation respond well to treatment
with improved visual acuity [113]. They respond
well to periocular or IVT corticosteroids. Macular
oedema affects vision more than SRF.The SRF
does not appear to have a direct effect on visual
acuity. However, eyes with ME with SRF respond
better to treatment than eyes with intraretinal
thickening without SRF [116]. However, increasing central subeld thickness (CST) had a greater
chance of disruptions of EZ and the interdigitating zone (IZ), leading to irreversible visual loss
[117].
The OCT has shown that more than 80% of
the eyes with juvenile idiopathic arthritisassociated chronic uveitis (JIA uveitis) may be
associated with macular oedema and show SRF
in 18% [118]. SRF may be the only manifestation, or it may be associated with perifoveolar
macular thickening or CME. Patients respond
well to increased immunomodulatory therapy
[119].
Even Bartonella henselae neuroretinitis rarely
may present as a monofocal choroiditis lesion
with overlying serous detachment in the macula
appearing as a helioid lesion (SUN-like) [120,
121].
The patients with VKH disease show thickening of the choroid due to inltration by granulomatous inammatory cells (Fig.12.6). FFA and
the ICG angiography show initial delayed lling
of the choroid and pinpoint leakage from the RPE
in mid-phase with pooling of the dye in multifocal SRF pockets.
A similar phenomenon is seen in the tubercular (TB) choroidal granulomas, which are
hypoxic and highly vascularized. TB granulomas
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Fig. 12.6 Multifocal pockets of subretinal uid (blue arrows) are seen in both eyes in acute VKH disease on fundus
photography (a, b) and OCT (c, d)
12 Subretinal Fluid andRetinal Detachment
are often associated with the accumulation of
SRF, leading to a variable extent of exudative
retinal detachment (see Chap. 10, Figs. 10.1b and
10.2b) [122–124]. In experimental models of TB
granulomas, the VEGF was overexpressed by the
overlying RPE of TB granulomatous choroidal
inammation [125]. On FFA, these granulomas
show initial hypouorescence followed by
intense hyperuorescence and pooling of dye in
the subretinal space. On the IC angiography,
these granulomas remain hypouorescent
throughout the study.
metastasize to the choroid because of its rich
blood supply. Nearly 28–73% present with SRF
[127]. The unrestricted proliferation of the cancer cells increases the metabolic requirements,
expresses VEGF, and forms new vessels. The
RPE barrier breaks, and the patient presents
with vision loss due to exudative retinal detachment [128]. The FFA shows early hypouorescence, multifocal pinpointing points in the
mid-phase, and hyperuorescence in the late
phase (Fig. 12.7). On ICG angiography, the
metastatic lesions remain hypouorescent
throughout the study [127]. On OCT angiography, the choroidal metastasis lesions show no
12.4.7 Subretinal Fluid inMetastatic
Cancer
ow in the mass lesion, which may be due to the
masking effect of the RPE.However, on colour
ow mapping, 100% of the metastatic lesions in
Choroid is a common and preferred site for
breast and lung cancer metastasis. Renal cell
carcinoma may metastasize to choroid years
before the rst presentation or several years
after the patient’s nephrectomy for cancer.
These metastases have a characteristic orangered colour [126]. Nearly 8–10% of all cancers
the choroid show high vascularity [129]. Several
successful cases of choroidal metastasis treat-
ment have been reported when anti-VEGF ther-
apy was combined with systemic chemotherapy
[127]. Subretinal uid may be the presenting
sign of lung cancer and renal cell carcinoma
metastasis to the choroid (Fig.12.7b, c).
ab
cd
A
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e f
Fig. 12.7 (A) A 52-year-old female, who completed che-
motherapy for breast carcinoma, presented with bilateral
exudative retinal detachment (a, b), suggestive of metastatic
cancer. FFA showed multifocal pinpoint leaking points
(blue arrows) and hyperuorescence in the late phase (c, d).
OCT showed subretinal uid (red arrows) (e, f). (B) A
48-year-old man presented three months following a total
nephrectomy for renal clear cell carcinoma. In the past, he
had received laser photocoagulation in the right eye for a
diagnosis of central serous choroidopathy (a, arrow). His
visual acuity was 6/18 and 6/9in the right and left eyes,
respectively. On uorescein angiography, there was punctate hyperuorescence between the optic disc and the fovea
with leakage of dye above the optic disc (b). The OCT scan
shows minimum subretinal uid and increased choroidal
thickness (c). The left eye showed similar changes (d–f).
There is increased choroidal thickness and intra- and subretinal uid (g). (C) A 60-year-old non-smoker presented
with 15days of diminution of vision in his left eye. Fundus
examination of the left eye showed a at subretinal lesion
(arrow), approximately one-disc diameter in size, located
upper and temporal to the optic disc (a, black arrow). The
FFA showed initial punctate hyperuorescence and faint
staining in late frames (b, arrow). Optical coherence tomog-
raphy (OCT) showed subretinal uid involving the fovea
(c). CT scan of the thorax showed a spiculated mass in the
right lower lobe extending up to the visceral pleura (d).
Fine-needle biopsy of the lung mass revealed a loosely
cohesive cluster of tumour cells with moderate-to-abundant
vacuolated cytoplasm (arrow) (May Grünwald-Giemsa
stain; 40×). Inset shows a papillary cluster of tumour cells
with coarse chromatin and conspicuous nucleoli (haema-
toxylin and eosin stain; 40×) consistent with adenocarci-
noma (e). Complete lesion regression was observed on
repeat fundus examination after four cycles of chemother-
apy (f). (Reproduced with permission of the publishers from
Singh N, Kulkarni P, Aggarwal AN, Mittal BR, Gupta N,
Behera D, Gupta A.Choroidal metastasis as a presenting
manifestation of lung cancer: a report of 3 cases and system-
atic review of the literature. Medicine (Baltimore).
2012;91(4):179–194. https://doi.org/10.1097/
MD.0b013e3182574a0b. PMID: 22732948)
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ab c
de
abc
12 Subretinal Fluid andRetinal Detachment
f
g
d
Fig. 12.7 (continued)
12.5 Consequence ofSubretinal
In rhegmatogenous retinal detachment, within
24 h of separating the photoreceptor from the
RPE, the photoreceptors’ outer nuclear layer is
lost due to apoptosis [130]. In acute cases of central serous chorioretinopathy (CSC), if the outer
border of the photoreceptor layer is smooth, with
minimum thinning of the foveal ONL compared
to the normal contralateral eye, they usually have
good vision. On the other hand, patients with
thickening of the outer border or granular appearance (shaggy border) have thinning of the foveal
Fluid
e f
ONL and have loss of vision. The worst outcome
is seen in those who show granular deposits on
the ELM and have a maximum thinning of the
foveal ONL [131].
12.5.1 Tractional Retinal Detachment
The simultaneous upregulation of the broblastic
growth factor and the vascular endothelial growth
factor (VEGF) in response to the ischaemic retina
leads to the development of new retinal vessels
accompanied by brous proliferation. The most
common causes of retinal neovascularization
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335
Fig. 12.8 Tractional retinal detachment (TRD) in the
right eye of a patient with proliferative diabetic retinopathy along the major vascular arcades (a). The macula is
include proliferative diabetic retinopathy (PDR),
branch retinal vein occlusion, retinopathy of prematurity (ROP), familial exudative vitreoretinopathy (FEVR), sickle cell anaemia, and ischaemic
retinal periphlebitis. Effective treatment strategies to regress the new vessels include ablation of
the ischaemic retina with laser photocoagulation
or intravitreal injections of anti-VEGF agents.
However, the accompanying brous tissue does
not regress. TRD develops along the major vascular arcades in PDR and lifts the macula into a
table-top TRD (Fig.12.8a). Fibrous proliferation
on the posterior hyaloid surface of the vitreous
leads to the formation of a taut posterior hyaloid
membrane which causes macular oedema with a
shallow macular detachment. Post-treatment
with either PRP or anti-VEGF therapy, there is
often a visible regression of the new vessels. Still,
the brous membranes lying at on the posterior
pole are only sometimes evident on clinical
examination. In such cases, the OCT can show
the presence of brous membranes, their adherence to the underlying retina, and the extent of
the retina elevation.
There is as yet no medical treatment available
not only to prevent the formation but also the
contraction of these brous membranes. The
brous membranes are rmly anchored to the
new vessels’ growth sites and grow along the
posterior hyaloid surface, which provides a scaffold for these proliferating brocytes. The
growth of the new vessels along the posterior
lifted (black arrow) into a table-top TRD.Following pars
plana vitrectomy, the retina was attached with laser scars
in periphery (b)
hyaloid face leads to partial vitreous detachment
and contraction of the posterior hyaloid face.
The contracting brous membranes exert anteroposteriorly or tangentially oriented forces that
overcome the adhesion forces between the NSR
and the RPE and form tractional retinal detachment (TRD). Clinically, the TRD appear taut and
concave anteriorly due to the forward pulling
traction of the brosis and the posterior pulling
forces of the RPE pump. At times, the contraction of these membranes may be so severe to create a break (hole) in the retina and develop a
combined rhegmatogenous and tractional retinal
detachment.
The formation of a hole in the retina allows the
aqueous uid to go behind the retina, with a consequent change in the conguration of the RD.This
phenomenon is seen in diabetic retinopathy more
commonly than other causes of TRD.
Patients of DR who reach a stage of TRD generally have poor systemic health. The 5-year
mortality in these patients after surgery varies
from 25.3% [132] to 57% [133].
Patients with BRVO, sickle cell retinopathy,
and FEVR often develop peripheral TRDs. The
ischaemic peripheral vasculitis produces highly
complex peripheral TRD.In contrast to the diabetic TRDs that form in the posterior pole or the
post-equatorial retina, the post-vasculitic TRDs
are often pre-equatorial. If not treated in time,
preterm babies with ROP develop peripheral
tractional retinal detachment that involves the
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12 Subretinal Fluid andRetinal Detachment
macula. Eventually, the contracting brous tissue may detach the entire retina, causing total
retinal detachment to lie just behind the crystalline lens.
In juvenile idiopathic arthritis-associated
uveitis, brous membranes are often formed on
the peripheral retina and the ciliary body. These
form brous cyclitic membranes that cause tractional detachment of the pars plicata and peripheral tractional retinal detachment. Inferior
traction retinal detachment may develop in the
retina’s inferior periphery, complicating longstanding pars plana exudates in intermediate
uveitis.
The larva migrans of Toxocara canis often
present as a peripheral TRD or a juxtapapillary
TRD.
12.5.2 Myopic Tractional
Maculopathy
For the clear perception of objects, the parallel
rays of reected light from the objects located at
innity (the far point of the normal eye, generally
taken as 6 m) must be sharply focused on the
NSR.The light rays from objects closer than 6m
are divergent, but the accommodative power of
the crystalline lens focuses the image on the NSR
(the eye’s focal point). Many factors contribute to
the focus of the image on NSR.The axial length
of the eyeball is the most important of all. If the
eyeball’s size is longer than average, the eye’s
focal point moves anterior to the NSR, the light
rays from the far point are focused in front of the
retina, and the image is perceived as a blur. This
error of refraction is called myopia. Myopia is
corrected by placing a minus-powered (diverging) lens to move the far point to innity. The
average axial length of the emmetropic eye is
23mm (22–24mm). An increase in the eyeball’s
axial length by 0.35 mm leads to an error of
refraction −1D [134]. The newborns are born
with a short eye which continues to grow in size
till it achieves most of the emmetropic size by 3
years and, after that, slowly continues to grow till
adolescence. Myopia is fast emerging as a public
health challenge in Asian countries where
80–90% of school-leaving children have myopia,
and 10–20% have pathological myopia [135].
High myopia is dened when a≥6D minus lens
must be placed in front of the cornea to focus the
image on the NSR.In many patients, axial length
elongation leads to sight-threatening pathological changes in the retina, namely the myopic
crescent, chorioretinal atrophy, cracks in the
Bruch’s membrane (Lacquer cracks), subfoveal
choroidal neovessels, macular hole, macular
schisis or macular traction retinal detachment,
and outpouching of the posterior sclera (posterior
staphyloma). If any of these changes are present,
it is called ‘pathological myopia’ [135]. More
than the axial length, the eyeball’s abnormal
shape is responsible for pathological changes
[134].
One-third of the patients with high myopia
may show tractional maculopathy. In myopic
tractional maculopathy (MTM), the posterior
hyaloid membrane is thickened and rmly
adherent to the NSR.Due to the abnormal shape,
two opposing forces are generated in the vulnerable eyes, laterally directed tangential and
anterior- posterior traction by the post-hyaloid
face of the vitreous. The relatively rigid ILM
and anterior retina stretch across the posterior
staphyloma while the more compliant outer retina lines the staphyloma leading to tractional
detachment of the anterior retinal layers. Vertical
stretching of Henle’s bres gives the appearance
of a schisis- like appearance. The inner retina
may show cystic changes. The macular hole
may develop in some patients. The MTM was
only recognized after the availability of OCT.
The treatment of MTM involves 3-port PPV
with posterior hyaloid removal. It has excellent
outcomes following pars plana vitreous surgery
to relieve macular traction with complete
resolution of the MTM and improve visual acuity
[136, 137]. The ILM is not peeled over the foveal
centre for fear of creating an iatrogenic macular
hole. Fovea-sparing ILM peeling leads to signicant visual improvement compared to when the
ILM over the fovea is also peeled [138, 139].
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12.5.3 Treatment ofTractional
Retinal Detachment
Treating TRD, epiretinal brous membranes, or
the taut hyaloid membranes requires surgical
intervention. The complexity of the surgery varies from case to case, and the surgical plan is
individualized. The basic steps of surgery involve
a three-port pars plana vitreous (PPV) surgery to
remove the entire vitreous gel, release all the
brous tractional membranes and bands, remove
the posterior hyaloid face, obtain haemostasis,
and close all the preexisting or iatrogenic retinal
holes with the application of laser photocoagulation. If there are no retinal breaks, often releasing
the tractional forces will lead to reattachment of
the NSR to the RPE (Fig. 12.8b). However, it
may take several months to completely absorb
the SRF [140].
Surgery of TRD is highly variable in complexity; iatrogenic breaks are not uncommon and may
be seen in nearly 25% of the eyes. The surgery
requires careful removal of the posterior hyaloid
face and the scar tissue. To ensure complete reattachment of the retina on the table, some surgeons prefer to create retinal breaks to drain all
the SRF during the uid gas exchange and replace
the vitreous cavity with a long-acting gas or silicone oil. Some surgeons may place a 360° scleral
buckle to counteract unseen residual traction.
Any residual traction on the retina will not allow
the entire retina to reattach. If the residual TRD is
in the periphery or in the nasal retina, many surgeons prefer to leave it as such if it is not compromising the vision.
The single surgery success rate in diabetic
TRD has improved over the years and is ~85%
[141, 142]. The PPV with suture less 25G+ technique also was effective and safe in reaching success in 91% [143] to 99% [144].
Despite excellent surgical outcomes, visual
acuity better than 20/50 was achievable only in
23% [142]. Postoperative vitreous haemorrhage
is a signicant complication of PPV in diabetic
TRD.To reduce the risk of postoperative haemorrhage, many surgeons favour preoperative or
intraoperative use of intravitreal injection antiVEGF agents [145]. The current surgical tech-
niques show a signicant decrease in
postoperative haemorrhage at 13%. However,
visual acuity better than 20/50 was achieved in
only 19.5% of eyes, although it stabilized in 96%.
Only 1.2% lost light perception [146]. Instead of
leaving the eye lled with a balanced salt solution
at the end of the surgery, replacing it with 20–30%
SF6 gas reduced the postoperative haemorrhage
from 33% to 11% [147].
In a series of 74 eyes with post-retinal vasculitis RD, one-third were combined tractional and
rhegmatogenous RD.Although 90% of the eyes
achieved anatomical success following pars plana
vitreous surgery, signicant visual acuity
improvement was seen only in 70% of the eyes
[148].
Conuent laser photocoagulation of the ischaemic retina with or without concurrent use of
intravitreal anti-VEGF therapy is highly effective
in preventing the progression of ROP to stage 4,
i.e. peripheral TRD without (4A) or with macular
involvement (4B). Bilateral sequential lens sparing 25/27G PPV in the same surgical session is a
highly effective strategy in stage 4 ROP.In one
such series, the macula was still attached in 90%
of eyes, and complete resolution of TRD was
achieved in 63% of eyes at the end of 45weeks of
surgery [149]. A Turkish group obtained similar
results and achieved anatomical success in 96%
of 4A and 85% in 4B ROP [150]. This strategy
was found highly effective in the paediatric age
group PPV to achieve anatomical success in 90%
of cases [151].
12.5.4 Rhegmatogenous Retinal
Detachment
Rhegmatogenous retinal detachment (RRD) is a
collection of uid between the neurosensory retina and the RPE caused by a retinal tear or a hole
(Fig.12.9). RRD is a common cause of sudden
loss of vision in older people. The main symptom
of acute RD is a dark curtain rising in front of the
eye.
The mere presence of a retinal hole is not
enough to create an RRD, as the hole remains
plugged by a healthy vitreous. Typically, the corti-
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Fig. 12.9 Subretinal uid in an eye with rhegmatogenous
retinal detachment, caused by a retinal tear or a hole
(black arrows)
cal vitreous is rmly adherent at the optic disc
margins and the vitreous base where it straddles
the ora serrata (transition from the NSR to the nonpigmented ciliary epithelium). The vitreous is also
lightly attached to the retinal surface over the macula and the retinal vessels. The cortical vitreous
adheres rmly to areas of retinal degeneration,
especially at the borders of the lattice degeneration. It is also adherent at sites of chorioretinal
scars. Nearly one-third of the patients with myopia
of ≥6D–8D and 6–10% of the normal population
have circumferentially or occasionally radially
oriented patches of lattice degeneration. These
areas of retinal atrophy, crisscross white lines, and
variable pigmentation may have atrophic holes.
Nearly 54% have lesions in both eyes, equally distributed among men and women [152].
The vitreous gel undergoes syneresis (liquefaction) with old age. In eyes with high myopia,
vitreous liquefaction occurs at a much younger
age. There is also a thinning out of the posterior
cortical vitreous in front of the macula where an
opening may form, allowing the misdirected
aqueous to move behind the posterior hyaloid
membrane, peeling it off from the ILM.The agerelated liquefaction of the anterior vitreous may
weaken Wiegert’s ligament attachment on the
posterior surface of the crystalline lens. The misdirected aqueous then gets access to ow through
the Cloquet’s canal to the Martegiani space in
front of the optic disc to communicate with the
pocket of liqueed vitreous in front of the macula
12 Subretinal Fluid andRetinal Detachment
[153]. Movement of the partially detached PHM
due to saccadic eye movements of the eye exerts
a constant force on its posterior attachment to the
optic disc margin. Separation of the vitreous
attachment to the optic disc margin is an acute
event termed posterior vitreous detachment
(PVD) and is a common phenomenon between
the ages of 45 and 65.
The PVD happens earlier in myopic eyes and
post-trauma [154]. Following uneventful cataract
surgery, nearly 75% of eyes without preexisting
PVD developed PVD within 5 years and, more
often, if they had preexisting asymptomatic lattice degeneration [155].
The patients often become aware of the PVD
by the sudden appearance of a oating partial or
complete ring shadow (Weiss ring) and dark
spots (oaters) in their eld of vision. A sudden
movement of the head may bring on a lightning
streak. The lightning streak appears due to the
pull on the retinal elements by the still adherent
vitreous strands. The light ashes in themselves
are not signicant except when oaters accompany these. Opacities cause oaters in the vitreous due to leakage of blood from the rupture of
retinal capillaries, especially in areas where the
vitreous is rmly attached to the retina. The
leaked blood is seen as a thin horizontal layer
inferiorly on the retina’s surface. The PVD needs
urgent consultation with a retina specialist for
binocular indirect ophthalmoscopy with scleral
depression to rule out the presence of a retinal
tear, especially if there are pigmented cells or
blood in the vitreous cavity or retina. These
symptomatic tears lead to retinal detachment in
the next few days. However, if it is detected and
sealed with laser photocoagulation, the development of RRD can be prevented.
12.5.5 Pathogenesis
ofRhegmatogenous Retinal
Detachment
The formation of a round atrophic hole does not
always lead to retinal detachment. Acute ap tears
develop during acute PVD, and adherent vitreous
pulls on the degenerated/atrophic retina. The vitreous strands can be seen attached to the apex of the
12.5 Consequence ofSubretinal Fluid
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arrowhead-shaped ap, with its apex directed posteriorly. These tears tend to extend anteriorly
towards the ora serrata; hence, if detected before
they result in RRD, they should be sealed using
laser photocoagulation that must extend anteriorly
up to the ora serrata. The raised ap sets up eddy
currents during the saccades and facilitates entry
of the misdirected aqueous into the subretinal
space. In the past, only the liqueed vitreous was
believed to have entered the subretinal space.
However, it needs a more accurate explanation as
the RPE constantly absorbs the SRF, and the fresh
one moves in, a phenomenon impossible with a
limited quantity of the vitreous [153].
12.5.6 Risk Factors
forRhegmatogenous Retinal
Detachment
Myopia with lattice degeneration is the most signicant risk factor; nearly 20–30% with RRD
show this sign. Familial cases of RRD are seen in
Stickler’s syndrome, a genetic disorder with
defective collagen production, and Wagner’s syndrome, an autosomal dominant disorder. Clear
lens extraction as treatment of very high myopia
also raises the risk of RRB fourfold [156]. Nearly
1% of the patients undergoing cataract surgery,
especially those with axial myopia or intraoperative complications like capsular dehiscence or
vitreous loss, may also develop RRD [154].
Nd:Yag laser capsulotomy led to a fourfold
increase in the risk for RRD, especially in young
people [157], and led to RRD in 2% of eyes
[158]. RRD may follow trauma to the eye from
tears in the vitreous base. Lateral eyeball expansion following blunt trauma may cause disinsertion of the vitreous base and retinal dialysis or
giant retinal tears [159].
12.5.7 Clinical Diagnosis
ofRhegmatogenous Retinal
Detachment
Unlike the exudative retinal detachment with a
smooth elevation, fresh RRD appears as an
undulating semitransparent membrane with folds
of the outer retina, giving it a corrugated appearance [160, 161]. These have a highly characteristic appearance on the OCT and are likely due to
the hydration of the interphotoreceptor matrix
proteins [162]. The SRF arising from the retinal
tears above the horizontal meridian (superior retinal breaks/tears) rst appears around the retina
break, extends up to the ora serrata, and then
gravitates inferiorly to give a bullous appearance
to the RRD. These RRDs rapidly expand to
involve the macula. In contrast, those arising
from the inferior breaks are generally shallow,
expand slowly, and do not show a corrugated
appearance. These are called inferior RRDs and
may show high water marks at the upper border.
The most critical step in managing RRD is locating all the retinal breaks. The contours of the
RRD are drawn on an Amsler chart using a binocular indirect ophthalmoscope with a +20D
condensing lens [163].
The key to locating a retinal break is rst to
determine if it is a bullous RRD or a shallow RD,
i.e. whether it is arising from a superior break or
an inferior break, respectively, and draw the contours of the subretinal uid. Next is to nd out
whether the RRD is total or subtotal and, if subtotal, the number of quadrants involved, and
whether the macula is ‘On’ or ‘Off’. Most of the
retinal breaks are located in the upper temporal
quadrant. There may be more than one retinal
break, and all-out efforts are made to locate all
the breaks.
The superior RRD in the early stage may be
localized to only one quadrant. The most superior
break dictates the conguration of the RRD and
generally follows Lincoff’s rule [164]. In brief, if
the bullous RRD is located in the superior half,
determine which side has the lower SRF level. In
the superior breaks, generally, the uid will not
cross the midline, gravitate inferiorly, rise on the
opposite inferior quadrant, and then move up.
The retinal break is located on the side with a
higher uid level. However, if the retinal break is
located at the 12 O’clock meridian, the uid level
crosses the midline, and the inferior uid levels
are the same on either side. In the inferior bullous
RRD, the retinal break is located on the side,
which shows a higher uid level and shall always
be above the horizontal meridian. In shallow
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