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6.2 Pathophysiology ofDiabetic Retinopathy
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Fig. 6.1 Fundus uorescein angiography showing areas of capillary non-perfusion (CNP) (blue arrows) in the mid
periphery of the retina in the right (a) and the left (b) eyes of a patient with diabetic retinopathy
105
a
c
b
d
Fig. 6.2 Fundus photographs showing moderate non-proliferative diabetic retinopathy (a, b). Fluorescein angiography
shows areas of capillary non-perfusion (CNP) in the nasal retina in the right and left eyes of the patient (c, d)
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6 New Vessels ontheOptic Disc andElsewhere intheRetina
of multiple biochemical pathways, including the
NF-kB activation by the reactive oxygen species,
protein kinase C activation, and dephosphorylation of the platelet-derived growth factor
receptor-β (PDGFR-β)ultimately lead to the
apoptosis of the pericytes [21].
In the endothelial cells, a number of biochemical mechanisms get activated in the hyperglycemic state, including the activation of polyol and
hexosamine pathways. Accumulation of AGE
products and activation of the PKC lead to the
induction of the enzyme, the inducible nitric
oxide synthase (iNOS). Overproduction of the
highly cytotoxic nitric oxide (NO) and release of
the reactive oxygen species ultimately lead to the
loss of endothelial cells [21]. Additionally, the
capillary endothelial cells express adhesion molecules in response to the inammatory cytokines
released by the activation of microglia, which
cause leukostasis and occlusion of the capillaries.
Furthermore, there are signicant rheological
changes in the blood ow in patients with diabetes. The release of oxygen from the RBC is
decient, especially if the HbA1C is high, as
oxygen binds more strongly with the glycated
Hb. The RBCs are swollen, lose their biconcave
shape, and hence lose their deformability and
ability to negotiate through the normal capillaries
efciently. All these factors also contribute to
retinal capillaries’ occlusion [22]. Another major
challenge in diabetes is the inability of the circulating endothelial progenitor cells to repair the
dysfunctional endothelial cells. Progressive capillary non-perfusion leads to the release of VEGF
from the neurovascular unit, the most potent
growth factor for angiogenesis and the development of abnormal new vessels in the retina and
the optic disc [11]. A signicant increase in the
aqueous humour levels of inammatory cytokines, including IL1β, IL-6, IL-8, IL-10, TNF-α,
MCP-1, and the VEGF, have been noted to correlate with the severity of peripheral retinal capillary non- perfusions areas in patients with
PDR.These proinammatory cytokines may be
responsible for the progression of diabetic retinopathy changes [23].
6.2.6 Retinal Capillary NonPerfusion andSeverity
ofDiabetic Retinopathy
In the last 50years, the areas of acellular retinal
capillaries, as discussed above, have been demonstrated in diabetic retinopathy using fundus
uorescein angiography (FFA). These capillary/
retinal non-perfusion/non-perfused regions or
areas (CNP/RNP/NPR/NPA) are not uniformly
distributed in the retina. Generally, the retinal
area within a circle of radius 10 mm from the
foveal centre is considered central, between
10–15mm as midperipheral and beyond 15mm
as the peripheral retina [24]. In the early stages of
diabetic retinopathy, CNP areas are most commonly distributed in the midperipheral retina and
are often accompanied by retinal haemorrhages,
cotton wool spots, and dilated retinal vessels
(Figs.6.1 and 6.2). The CNP areas may be less
often seen in the central retina, especially nasal to
the optic disc, and least common in the peripheral
retina. When located in the extreme periphery,
several microaneurysms may be seen around
these CNP areas without cotton wool spots or
blot haemorrhages [25]. Optical coherence
tomography angiography (OCTA) studies have
shown that smaller areas of CNP are seen next to
the retinal arterioles. However, larger areas are
near the retinal veins [26]. Eyes with nonproliferative diabetic retinopathy with a threshold of a 107-disc area of CNP, especially in the
midperiphery, are at a high risk of developing
retinal new vessels (NVE). The greater the area
of CNP in the retinal midperiphery and the central retina, the higher the chance of developing
new vessels on the optic disc (Fig.6.3) [27].
Eyes that show dye leakage with a nonperfused retina (NPR) in the central retina are associated with diabetic macular oedema (DME)
(Fig.6.4). The NPR in the peripheral areas is usually not associated with dye leakage and correlates negatively with the occurrence of the DME
[28]. Recent years have seen increasing use of
wide-eld- swept-source optical coherence
tomography angiography (SS-OCTA) to quantify
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a
d
Fig. 6.3 A 60-year-old man with type 2 diabetes mellitus
presented with clinically apparent non-proliferative diabetic retinopathy in the posterior pole (a). Most microaneurysms were seen away from the fovea on Fundus
uorescein angiography of the posterior pole. A doubtful
new vessel was on the optic disc (b, blue arrow). However,
b
e
c
there was extensive capillary non-perfusion in the nasal
retina (red arrows) with new vessels (blue arrow) (c). Five
months later, despite laser pan-retinal photocoagulation,
he developed vitreous and subhyaloid haemorrhage (d,
blue arrows) A supplemental laser photocoagulation led to
resolution (e)
Fig. 6.4 Fundus uorescein angiography showing areas
of the non-perfused retina (blue arrows) in the central
retina (a) with retinal neovascularization (red arrow). Late
and analyse the retinal microvascular parameters
using semi-automated software algorithms.
Unlike the ultrawide-angle FFA that can simultaneously visualize almost 200 degrees of the ret-
phase (b) shows diffuse dye leakage with diabetic macular
edema (DME)
ina, SS-OCTA is limited by the maximum scan
area of 12×12mm2 at a time. The SS-OCTA,
however, is a non-invasive technique without
using any dye. The DCP cannot be separately
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6 New Vessels ontheOptic Disc andElsewhere intheRetina
Fig. 6.5 Left eye retina of a patient with PDR (a). Note
the extensive network of abnormal vessels (thin red
arrows) that have started bleeding (thin orange arrows).
He was the Author’s (AG) rst patient to receive an intravitreal injection of 2.5mg of Avastin in early 2006. The
same eye, as shown in (a), after 48h of Avastin injection
into the vitreous cavity, shows a dramatic disappearance
of most abnormal retinal vessels(thick red arrows) (b).
The abnormal retinal vessels need a continuous supply of
appreciated with the dye-based FFA, and dye
leakage from the permeable retinal capillaries
VEGF to sustain them. Anti-VEGF antibodies like
Avastin, Lucentis, or Eylea block the free VEGF leading
to the disappearance of the vessels. However, the effect of
one injection lasts for only 4weeks or so. (Reproduced
from Gupta, A. (2022). Bench-to-Bedside Research in
Ophthalmology. In: Sobti, R., Ganju, A.K. (eds)
Biomedical Translational Research. Springer, Singapore.
https://doi.org/10.1007/978- 981- 16- 8845- 4_5. With per-
mission of the publishers)
was observed either on the UWF-FA or on the
WF SS-OCTA [30, 31].
obscures the CNP areas. These areas cannot be
accurately quantitated.
Using wide-eld SS-OCTA, increasing RNP
areas in the peripheral retina was associated with
6.2.7 Development ofRetinal New
Vessels
increasing the severity of diabetic retinopathy.
Therefore, effective is the SS-OCTA technique
that in the future, the severity of retinopathy
grading is likely to be done by using an objective
assessment of the RNP areas [29]. Intravitreal
injections of anti-VEGF agents, such as Lucentis,
Eylea, or bevacizumab, have become the standard of care for eyes with diabetic macular
oedema, PDR, or even the NPDR (Fig. 6.5).
While using these agents slows down the progression of the CNP areas, these agents fail to
revascularize the ischaemic areas. The apparent
revascularization of the CNP noted in some
instances after using anti-VEGF agents may be
due to the unplugging of the retinal capillaries
blocked by the leukostasis. However, the capillaries that have lost their endothelial cells to
apoptosis cannot be vascularized [24]. Even after
3 months of the pan-retinal photocoagulation
(PRP) for the PDR, no change in the RNP areas
In response to chronic hypoxia in diabetic retinopathy and retinal vein occlusions, several
growth factors are produced by the neural and
glial elements of the hypoxic retina, the most
abundant of which is the vascular endothelial
growth factor (VEGF). Michaelson, in 1948, had
rst hypothesized the presence of such a diffusible factor in the eyes that developed pathological
new vessels either in the retina or in the anterior
segment of the eye. He called it ‘factor X’ [32].
Only after four decades, this factor was identied
as VEGF [33–35].
The VEGF is the gene involved in normal
organogenesis, embryogenesis, and development
of normal blood vessels. After the embryogenesis
is over, the role of the growth factors is limited to
menstruation and the heart and skeletal muscles
during strenuous exercise. Another growth factor
from the VEGF family was discovered in
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109
1991[36], called the placental growth factor
(PlGF), which also plays a signicant role in
pathological angiogenesis.
Soon after the discovery of VEGF, it was
detected in the eyes of a primate model of diabetic retinopathy [37] and the ocular uids of
patients with diabetic retinopathy [38]. Injecting
VEGF into non-human primate eyes led to a clinical picture mimicking diabetic retinopathy [39],
establishing VEGF as the primary growth factor
in the pathogenesis of diabetic retinopathy.
6.2.8 Intraretinal Microvascular
Abnormalities (IRMA)
VEGF released from a hypoxic retina is responsible for developing intraretinal microvascular
abnormalities (IRMA) and is an attempt to revascularize the ischaemic area. Muraoka and
Shimizu [40] followed their patients of the NPDR
and PDR eyes on FFA for up to 4years and demonstrated attempts to form zigzag or hairpin
loops in a single area of CNP and called this
intraretinal neovascularization (IRNV) (Fig.6.6).
These dilated capillary segments always arose
from the retinal veins and did not leak uorescein. On average, 2–3 such IRNV were seen per
eye, but as many as 12 lesions have been seen.
The concept of IRMA as collateral vessels was
Fig. 6.6 Intraretinal neovascularisation (IRNV) or intraretinal microvascular abnormalities (IRMAs) seen as hairpin loops (blue arrows) are formed as an attempt to
revascularize the ischaemic retina in diabetic retinopathy.
Also seen are neovascularisation of the optic disc (black
arrow) and vitreous and subhyaloid haemorrhages (green
arrows)
initially based on fundus pictures [40]. In any
case, the term IRMA continues to be the preferred term.
Increasing retinal hypoxia results in more retinal haemorrhages, venous dilatation, and the formation of IRMAs. The early treatment diabetic
retinopathy study (ETDRS) group classied the
presence of more than 20 retinal haemorrhages in
all four quadrants of the retina, the venous dilation and beading in two quadrants or the presence
of IRMA in one quadrant as severe nonproliferative diabetic retinopathy (NPDR), the
rule of 4-2-1 [41, 42]. All of these signs are strong
risk factors for the development of proliferative
diabetic retinopathy. The simultaneous presence
of two or more signs was classied as moderately
severe NPDR and portended an imminent development of proliferative diabetic retinopathy
(PDR). IRMAs are much better delineated on the
depth-resolved OCTA than on the 2-D FFA.The
IRMAs are dilated capillary segments that arise
from the retinal vein and loop back into the vein.
These are located on the border of the nonperfused area; on OCTA, most of the IRMAs are
seen to arise in the inner plexiform layer or sometime in the ganglion cell layer or the nerve bre
layer. These remain within the retina and only
breach the ILM once they develop into NVE.On
FFA, these generally do not leak except occasionally at the tips (Fig.6.7) [43].
Recently, the behaviour of the IRMAs before
and 3months after laser pan-retinal photocoagulation (PRP) prompted a further characterization
of these vessels as unchanged, tufting, reperfusion, mixed, and worsening types. Some of these
IRMAs did not change or even showed reperfusion of the NPAs. Most interesting was the tuft
type, wherein the tips of the irregularly dividing
capillary network were twice the calibre of the
capillaries, had a bulbous ending, and were seen
to elevate the ILM (outpouching of ILM).
Following the laser PRP, the tufts seemed to
regress, and IRMAs appeared like pruned
branches of a tree. The tuft-like IRMA appears to
be the precursor of the NVE [44]. Prospectively
followed on the OCTA, IRMA has been shown to
develop into NVE [30, 31]. Interestingly, post
hoc analysis of the CLARITY trial (comparing
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6 New Vessels ontheOptic Disc andElsewhere intheRetina
Fig. 6.7 Venous dilatation, retinal haemorrhages, hard
exudates, and cotton wool spots seen in non-proliferative
diabetic retinopathy (a). Fundus uorescein angiography
PRP vs Intravitreal aibercept in severe NPDR)
found that while intravitreal aibercept injections
led to improvement in the severity score of the
diabetic retinopathy in 75% of the eyes, including the deep retinal haemorrhages and the IRMA,
there was no change in the venous beading [45].
It is likely that while anti-VEGF agents lead to a
cosmetic improvement in the appearance of diabetic retinopathy, there is no reversal of hypoxia
or decrease in the area of RNA.
(b) showing IRMAs (blue arrows) at the border of the
non-perfused retina and no dye leakage
that venous dilatation in the peripheral retina
(outer zone), although not related to the retinal
non-perfusion area, is perhaps more sensitive in
predicting the progression of diabetic retinopathy. Moreover, the narrowing of the retinal arterioles in the outer zone, but not in the inner zone,
was related to the retinal non-perfusion area and
the progression of the retinopathy [47]. The retinal venous dilatation/ beading reects the degree
of retinal hypoxia in the retinal periphery and is a
strong predictor of the development of PDR
(Figs.6.3 and 6.8). Almost 50% of the eyes with
6.2.9 Retinal Veins Dilatation,
Beading, andRisk
ofProgression
PDR show venous beading, while less than 10%
with NPDR show such abnormality (Fig. 6.8).
These are seen more often in the temporal half of
the retina and the secondary branches rather than
In the early treatment diabetic retinopathy study
(ETDRS) report #12, the group identied the
severity of haemorrhages/microaneurysms,
IRMA, and venous beading as the most signicant risk factors for the progression of retinopathy [41, 42]. In prospective studies, a 10 μm
increase in the central retinal vein equivalent over
4years predicted the progression of diabetic retinopathy development of PDR and DME.However,
such an association was not seen with a change in
the calibre of the central retinal arterioles [46].
More recently, using UWF-FFA, while con-
rming the above observations, it was suggested
in the primary, tertiary, or smaller branches [48].
There may be ethnic differences as in a Chinese
population, venous beading in >2 quadrants was
seen in only 6% and 2% of eyes with moderately
severe and severe NPDR, respectively, and none
in the NPDR eyes. The authors felt that >2 quad-
rants of venous beading is too strict a criteria to
diagnose severe NPDR [49]. While the retinal
loops may be seen in 25% of the eyes with PDR,
duplication of the veins is uncommon. If a venous
loop is seen clinically, it is almost always sugges-
tive of PDR, and a thorough search is done to
locate new vessels using FFA (Fig.6.9) [48]. The
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111
c
Fig. 6.8 (a, b) Venous fullness and beading in the retinal
veins with retinal haemorrhages and a few cotton wool
spots (a) in a patient with moderate NPDR.Funds uorescein angiography (b) shows extensive capillary nonperfusion and venous beading (blue arrows). (c, d)
d
Peripheral retina as seen on fundus photography (c) and
uorescein angiography (d). Note the IRMAs (green
arrows), neovascularization of the retina elsewhere (NVE,
red arrows), and vast areas of capillary non-perfusion
(blue arrows)
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Fig. 6.9 The presence of a venous loop (blue arrows) seen clinically (a) is almost always suggestive of proliferative
diabetic retinopathy, as conrmed by uorescein angiography (b)
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6 New Vessels ontheOptic Disc andElsewhere intheRetina
venous loops and duplication are proposed to
result from a non-thrombotic occlusion of the
large retinal vein and the opening of the collateral
channels [50]. The availability of wide-eld fundus imaging may show nearly 40% more lesions
that are not captured on the standard 7-eld fundus photographs [51]. Eyes with diabetic retinopathy that predominantly show peripheral lesions
have an increased risk of retinopathy progression, and the progression of these peripheral
lesions enhances the risk of the development of
PDR [52].
In the past, there have been contradictory
reports on the blood ow in patients with diabetic
retinopathy. An increase in the ow due in the
early stages of diabetic retinopathy may be due to
autoregulatory control, the failure of which in the
late stages of retinopathy may account for
reduced ow in the retina. Previously, blood ow
measurements could not be done in smaller vessels. Using more current techniques like multiplane Doppler spectral domain OCT, the blood
ow in the early stages of diabetic retinopathy
was comparable to the normal population but was
reduced in patients with PDR [53, 54]. Using
adaptive optics scanning laser ophthalmoscopy
and OCT angiography, retinal blood ow can
now be measured in SCP, DCP, and across major
retinal vessels. This technique showed that in a
normal population, there is an increase in the
blood ow and velocity with the increasing size
of the blood vessels. There is an increase in the
blood ow in vessels up to 60μm size in patients
with diabetes with no retinopathy and a decreased
ow in those with retinopathy. It was hypothesized that increased blood ow and velocity in
retinal vessels coupled with increased shear rate
before the onset of diabetic retinopathy led to
capillary endothelial damage resulting in capillary closure and hence the decreased ow and
velocity once the retinopathy had set in [55]. At
3months following laser photocoagulation, there
was a signicant increase in the oxygen saturation of both the retinal arterioles and retinal veins.
There was a reduction in the calibre and the blood
ow in the retinal arterioles and the veins.
However, this reduction in calibre was more signicant in the retinal veins. Reduced ow in the
post-PRP eyes does not appear from the restoration of the normal autoregulatory mechanisms
but is likely due to the elimination of hypoxic
areas [56]. Using adaptive optics technology, it is
now possible to measure the thickness of the wall
of retinal arterioles and the diameter of their
lumen. Following pan-retinal photocoagulation,
while the external diameter of the retinal arterioles remained the same, a signicant increase in
the wall-to-lumen ratio (WLR) in eyes with PDR
compared to that in the normal, no diabetic retinopathy or NPDR may be responsible for the
decreased ow rate in these eyes. The increased
WLR was also associated with hypertension [57].
6.2.10 New Vessels ontheRetina
Elsewhere (NVE) andtheOptic
Disc (NVD)
New vessels on the retina or/and optic disc mark
the proliferative stage of diabetic retinopathy.
The NVE is seen more frequently than the NVD,
although the NVD signies a more severe PDR
(Fig.6.10). The NVE accompanies NVD in the
majority of eyes. The ETDRS report #10 dened
the clinical signs of diabetic retinopathy, including the NVE and NVD.On stereoscopic fundus
photograph examination, the NVE (irregularly
arborizing vessels) should lie on the retina’s surface or into the posterior vitreous.
In contrast, those on the optic disc surface or
growing into the vitreous or within one disc
diameter of the optic disc margin were dened as
NVD.If vessels grow on the retina elsewhere and
reach within 1/2 to 1 DD of the optic disc margin
and no new vessels grow on the optic disc, these
would be labelled as NVE.The severity of the
NVE was further graded into ve levels based on
the absence, doubtful presence, or denitive presence and the area covered by the NVE (scale of
1/2 DA) in the retinal elds 1, 3–8, and severity
graded as per the standard fundus photograph 7A
[41, 42]. Likewise, the new vessels on the optic
disc (NVD) were evaluated in eld 1, standard
photographs 10A and C (which are centred on the
optic disc of the fundus), and ve severity grades
were dened based on the presence/absence and
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Fig. 6.10 The neovascularization of the optic disc (NVD, blue arrow) in the right (a) eye of a patient with insulin-
dependent diabetes mellitus. The NVD in the left eye (b) is obscured by the large subhyaloid haemorrhage
Fig. 6.11 Neovascularization of the retina elsewhere
(NVE, red arrows) seen nasal to the optic disc in left eyes
of two different patients (a, b), along with areas of capil-
the area of the new vessels. Grade 0 was no NVD,
grade 1 questionable NVD, and grade 2 NVD
less than that shown in standard photograph
10A.NVD in the standard photograph 10A was
one third of the disc area. Grade 3 NVD was
equal to or more than the NVD shown in standard
photograph 10A but less than the NVD shown in
standard photograph 10C, and grade 4 was equal
to or larger than the NVD shown in standard photograph 10C. New vessels within the one disc
diameter were also dened as NVD [41, 42].
The NVE is most often seen nasal to the optic
disc or along the vascular arcades in the temporal
lary non-perfusion (blue arrows) as seen on fundus uorescein angiography
retina (Fig.6.11). NVE is not seen in the foveal
area. They are seen farther from the fovea and are
larger and more in number in type 1 DM compared to type 2 DM.NVD may be seen in up to
one third of the eyes with PDR, and the new vessels are distributed most frequently along the
upper temporal region of the neuroretinal rim of
the optic disc. New vessels over the optic disc
cup are highly unusual [58]. The NVE and the
NVD are often accompanied by supporting
brous tissue seen as strands or sheets of opaque
scar tissue on the posterior hyaloid surface
(Fig.6.12).
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Fig. 6.12 Supporting brous tissue seen as strands or
sheets of opaque scar tissue (blue arrows) on the posterior
hyaloid surface, accompanying the NVE and NVD
6 New Vessels ontheOptic Disc andElsewhere intheRetina
Fluorescein angiography provides denitive
evidence of the NVE and NVD that leak uorescein dye (Figs.6.3, 6.4, 6.8, and 6.11). However,
the dye obscures the abnormal leaking vessels
and the surrounding area, making it difcult to
assess the exact size of the area occupied by the
new vessels. The IRMA’s growing tips (tufts)
may occasionally leak uorescein, adding to the
confusion. Lee etal. [59] used OCT to differentiate NVE from IRMA.While ILM pouching and
inner retina hyperreective dots were almost
exclusively seen in IRMA, ILM breach, posterior
hyaloid breach, and vitreous hyperreective dots
were signicantly common in NVE [59].
On structural SD-OCT, the NVD appears as
hyperreective tissue on the optic disc with either
an attached or a detaching posterior hyaloid. The
posterior hyaloid surface is a scaffold on which
the new vessels grow. The NVE on SD-OCT
appears as homogenous hyperreective tissue
seen breaching the ILM, growing forward onto
the posterior hyaloid or into the vitreous cavity.
These may be seen pulling the retina anteriorly
while still attached to the retina, causing a tabletop detachment of the retina [60]. Taking B scan
OCT as the standard for diagnosis of NVD, B
Scan OCTA was more sensitive to detect NVD
than the vitreoretinal slab on en face OCTA [61].
Ophthalmologists are able to detect new vessels
in PDR with equal facility in both the FFA scans
and the OCTA, making the latter a helpful noninvasive tool to study the new vessels [62]. On
the en face OCTA, the new vessels on the optic
nerve head appear as ne arborizing vessels-the
exuberant vessel proliferation or as non- exuberant
or pruned loops of abnormal vessels (Fig.6.13).
Following PRP, the original NVD assumes the
appearance of a large-trunk and branches appear
pruned, while the growing tips of any new NVD
appear more exuberant [63]. One may have to
differentiate between optic disc collateral vessels
from the NVD.The former is seen commonly in
retinal vein occlusions and only occasionally in
diabetic retinopathy. The collateral vessels form
from the existing capillary network and may vary
in size depending on the size of the obstructed
vessel. Collaterals bypass the obstructed segment
in a vein or an artery. Blood ow in these collaterals appears to be slow. These lie in the plane of
the retina. While the NVD leaks profusely on
FFA, the collateral vessels do not leak dye [64].
On the OCTA, the collateral vessels appear as
dilated looping vessels in the radial peripapillary
segment slab (Fig.6.14).
In contrast, the NVD appears as a ne meshlike vessel in the VRI slab (Fig.6.13) [65]. It has
been suggested that the NVD shows a higher
oxygen saturation than the collateral vessels that
typically arise from the venous end of the circulation, unlike the NVD that seems to arise from the
arterial end of the blood supply [66]. Study of the
en-face vitreoretinal slab on SS-OCTA is a sensitive technique to non-invasively detect and monitor the progress of NVD and NVE [67–69] and is
as sensitive as the FFA to detect new vessels [70].
In the vitreoretinal slabs of the SS-OCTA, NVE
has predominantly two morphological patterns,
namely the round pattern and the ramied pattern. The former type is associated with more
severe retinal non-perfusion areas. On OCTA, the
area of the NVE can be measured, and the progression rates calculated. The vessel density of
the NVE decreases as the NVE increases in size
[71].
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