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Fig. 3.15 Colour fundus photographs of a patient with HIV, with a normal right eye (a) and a single cotton wool spot
with retinal haemorrhage (black arrow) in the left eye (b)
3 Retinal Cotton Wool Spots
Fig. 3.16 Multiple cotton wool spots and retinal haemorrhages in right (a) and left (b) eyes of a patient with HIV
3.4 Imaging oftheCWS
show a corresponding relative arcuate scotoma
on perimetry. At the same time, the site of the
On fundus uorescein angiography, the CWS
show non-lling of the retinal capillaries in the
territory of the occluded vessel. At the junction of
the capillary non-perfused areas and the normally
perfused capillaries, stumps of the normal capillaries are often mistaken for retinal microaneurysms [1]. On OCT, CWS shows hyperreectivity,
known as the ‘Hyperreectivity sign’, which persists even after CWS is resolved [27]. The persistent hyperreectivity is likely due to the
replacement of RNFs with glial scars at the site
of the CWS.It is to be noted that the axons passing through the CWS do not transmit signals and
CWS has an absolute scotoma. Some axons
passing through the CWS are likely to survive the
hypoxic insult [28].
The CWS due to HIV, when followed for several years, show highly signicant thinning of the
inner retina, which is maximum in the ganglion
cell layer, besides signicant thinning of the
RNFL, the inner plexiform layer, the inner
nuclear layer, and the outer plexiform layer [29].
Upon resolution, the CWS in hypertension leave
behind localized RNF layer defects (RNFLD).
Such RNFLDs in young people have been associated with higher glycated haemoglobin levels
ab
3.5 Paracentral Acute Middle Maculopathy (PAMM)
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(HbA1c), higher mean and daytime 24-h systolic
and diastolic blood pressures, and lower estimated glomerular ltration rates. The RNFLDs
are associated with a higher 10-year atherosclerotic heart disease at 9.7% in the middle and
25.6% in the older age group. Thus, any patient
with CWS or their remnants—the RNFLD must
be evaluated for cardiovascular disease [30].
CWS, supercial linear haemorrhages, and hard
exudates characterize hypertensive retinopathy
[30]. Uncontrolled accelerated hypertension may
also develop characteristic lesions of hypertensive choroidopathy and optic neuropathy. Even
though blood pressure in these patients can be
successfully controlled with medical treatment,
these patients show a signicant loss of the RNFL
thickness when seen later [31]. Microperimetry
studies show permanent relative scotomas, denser
in diabetes than hypertension, at the site of CW
spots even after their resolution. Interestingly, the
uninvolved surrounding retina in diabetic eyes
shows lesser sensitivity compared to hypertensive eyes [32].
3.5 Paracentral Acute Middle
Maculopathy (PAMM)
The retina’s blood supply is organized into three
layers. The outermost layer comprising the RPE
and the outer nuclear layer get the micronutrients
and oxygen from the choriocapillaris, the middle
retinal layers comprising the outer plexiform
layer, inner nuclear layer, and the inner plexiform
layer from the intermediate and DCP of the central retinal arterial (CRA) system, and the innermost retinal layers comprising the ganglion cells
and the retinal nerve bre layer get their vascular
supply from the SCP of the CRA [33]. Unlike the
CWS, which results from non-perfusion of the
SCP and the radial peripapillary capillaries that
lie in the RNF layer and the ganglion cell layer,
ischaemic insult to the intermediate and DCP that
supply the inner nuclear layer and the inner and
outer plexiform layers results in the opacication
of the middle layers of the retina, namely, the
inner nuclear layer and the inner and outer plexiform layers. It is to be noted that these plexuses
are downstream in the hierarchy of the blood supply and represent a watershed in the anteroposterior axis of the blood supply of the retina and thus
vulnerable to hypoperfusion and hypoxic insult
[34]. The availability of advanced imaging techniques in recent years, such as optical coherence
tomography (OCT) and OCT angiography, has
made it possible to observe paracentral acute
middle maculopathy (Figs. 3.17 and 3.18).
Clinically, these areas may vary in size and
appear to have a very subtle colour change of
retina to apparent opacication [35]. On structural OCT, PAMM lesions are seen as a hyperreective band at the level of the inner nuclear layer
Fig. 3.17 Right eye of a patient with Purtscher’s retinopathy following trauma in a road trafc accident. Extensive
pale lesions located deep in the retina with sparing of the
retinal vessels. Some linear retinal haemorrhages are also
seen (a) and after 2 months (b). Most of these lesions
appear to be PAMM lesions. The images are from a preOCT era, which were erroneously diagnosed as cotton
wool spots in the absence of the OCT
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3 Retinal Cotton Wool Spots
c
d
Fig. 3.18 A 19-year-old male presented with non-ischemic central retinal vein occlusion (yellow arrow) in the
right eye (a). The SD-OCT showed hyperreectivity of
the inner nuclear layer, corresponding to the opacied
macula, suggestive of Paracentral Acute Middle
Maculopathy (PAMM) (b), which corresponded with a
and the inner and outer plexuses. On OCTA,
these lesions show non-perfusion of the intermediate and deep capillary plexuses. Very subtle
PAMM lesions may be picked up on fundus autouorescence imaging as hypoautouorescent.
The acute lesions of deep capillary ischaemia
that result in PAMM lesions appear as deep
opacication of the involved retina, which disap-
superior half scotoma in the macula (c). OCT angiography
with enface imaging showed disruption of the DCP (d)
contrasting from the dilated capillary bed in the SCP (e).
(Images courtesy Dr. Alok Sen, Sadguru Netra Chikitsalya,
Chitrakoot, MP, India)
more recently in SARS-CoV-2 infection [39]
(Fig.3.15).
Unfortunately, the PAMM lesions, due to
compromised circulation in the deep capillary
plexus of the middle retinal layers, are not delineated on fundus uorescein angiography. Hence,
this entity’s discovery was delayed until SD-OCT
imaging was available.
pear over the next few weeks and are hard to
detect.
In contrast to the CWS, the PAMM lesions
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layers. These contrast with CWS, which show
thinning of the RNFL with the preservation of the
middle retinal layers [37]. The PAMM lesions
have been seen in sickle cell disease, hypertensive retinopathy, compressive injury of the globe,
Purtscher’s retinopathy (Fig. 3.13), post H1N1
vaccine, migraine, occlusive retinal vasculitis,
following an upper respiratory infection [38],
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Retinal Hard Exudates
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4.1 Introduction
The presence of retinal hard exudates is most
often a sign of an underlying serious systemic
disease. The appearance of hard exudate in a
patient with diabetes who, till then, had shown
only retinal microaneurysms (MAs), the hallmark of diabetic retinopathy, indicates that the
patient has moved to the next level in the severity
of diabetic retinopathy (Fig.4.1). While evaluating fundus images in telemedicine units, it may
not be possible to see tiny red microaneurysms,
and the retinal hard exudates may be the only
visible sign of diabetic retinopathy. To maintain
transparency of the retina, the retinal blood vessels are endowed with tight endothelial junctions, which do not allow leakage of uid or
macromolecules into the extravascular space.
Retinal hard exudates are almost always accompanied by thickening of the retina. They are seen
in any disease that breaks down the tight endo-
4
Fig. 4.1 Hard exudates (black arrows), along with micro-
aneurysms and retinal haemorrhages, seen in a patient
with diabetes mellitus, indicating the presence of moderate non-proliferative diabetic retinopathy
thelial junctions allowing the extravasation of
uid and macromolecules into the extravascular
space (Fig.4.2).
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. Gupta et al., Ophthalmic Signs in Practice of Medicine,
https://doi.org/10.1007/978-981-99-7923-3_4
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4 Retinal Hard Exudates
4.3 Dierential Diagnosis
ofRetinal Hard Exudates
4.3.1 Hard Exudates Versus Soft
Exudates
Retinal hard exudates are yellow-white in colour,
have a waxy glistening appearance with sharp margins, and vary in size from a pinpoint to massive
mounds measuring several disc diameters. These
exudates consist of leaked lipids and lipoproteins
or may represent the remnants of the degenerated
neural tissue. The retinal hard exudates need to be
differentiated from the cotton wool spots, previously called the retinal soft exudates, which are
greyish-white, fudgy-bordered swellings of the
b
Fig. 4.2 Colour fundus photograph (a) showing retinal
hard exudates (black arrows) in the macula. Optical coherence tomography (OCT) scan through the macula (b)
shows thickening of the retina, with hard exudates seen as
hyperreective foci (blue arrows), subretinal uid (red
arrow), and intraretinal uid (yellow arrows) suggestive
of extravasation of uid due to the breakdown of the
blood–retina barrier
4.2 Causes ofRetinal Hard
Exudates
The common causes of retinal hard exudates
include diabetic retinopathy followed by hypertensive retinopathy, branch retinal vein occlusion, central retinal vein occlusion, retinal arterial
macroaneurysm (RAM), neuro retinitis, idiopathic retinal vasculitis, aneurysms and neuro
retinitis (IRVAN), retinal vasculitis, Coats’ disease, retinitis, retinal capillary hemangioblastoma (von Hippel-Lindau’s disease), choroidal
neovascular membranes, and choroidal hemangiomas to name a few.
retinal nerve bre layer (axons of the retinal ganglion cells) resulting from an ischemic insult to the
retinal nerve bres which results in the blockade of
the axoplasmic ow (Fig. 4.3). The cotton wool
spots and the hard exudates are seen in the posterior
pole of the retina or the peripapillary region. Both
may co-exist in diabetic retinopathy and hypertensive retinopathy, although the hard exudates predominate in diabetics and the cotton wool spots
dominate in the hypertensives. While the cotton
wool spots are in the supercial layers of the inner
layers of the neurosensory retina, the retinal hard
exudates are present deeper in the retina. Unlike the
cotton wool spots with a short life span of
4–6weeks, the retinal hard exudates often last for
months or even years if the pathology that caused
these continues to persist. The presence of hard
exudates indicates a rather chronic process, while
the presence of the cotton wool spots indicates an
acute event that calls for urgent attention from the
physicians for appropriate intervention.
4.3.2 Hard Exudates Versus Drusen
Apart from the cotton wool spots, hard exudates
must be differentiated from drusen bodies,
mostly seen in the elderly as a manifestation of
age- related macular degeneration. The drusen
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4.3 Dierential Diagnosis ofRetinal Hard Exudates
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Fig. 4.3 Colour fundus photograph of a patient with nonproliferative diabetic retinopathy (a) and another patient
with hypertensive retinopathy (b) showing co-existing
hard exudates (black arrows) and soft exudates (red
arrows) in the posterior pole. Hard exudates are seen as
yellow-white deposits with a glistening appearance and
sharp margins, while soft exudates are seen as greyishwhite lesions with fudgy borders
abe
cdf
Fig. 4.4 Retinal hard exudates (blue arrows) in a patient
with moderate non-proliferative diabetic retinopathy (a and
b), seen as yellow-white deposits, having a waxy glistening
appearance and sharp margins. In contrast, the retinal hard
drusen (black arrows) in a patient with dry age-related macular degeneration (c and d) are seen as yellowish nodular
lesions, deeper and more discrete than hard exudates.
Optical coherence tomography (e and f) in the patient with
dry age-related macular degeneration reveals the location
of hard drusen seen as excrescences (yellow arrows) deep
to the basal cell membrane of the retinal pigment epithelium (RPE) cells in Bruch’s membrane
are seen in clusters deeper into the neurosensory
retina and typically arise as excrescences located
deep to the basal cell membrane of the retinal
pigment epithelial cells in Bruch’s membrane.
Drusen may be hard or soft. The hard drusen are
yellowish nodular lesions less than 63 μm in
size. These are discrete, variable in number, and
have sharp borders (Fig.4.4). On the other hand,
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4 Retinal Hard Exudates
Fig. 4.5 Soft drusen (black arrows) in a patient with right
eye neovascular (a) and left eye intermediate (b) agerelated macular degeneration, seen as pale-yellow deposits, larger in size and more conuent than hard drusen,
with ill-dened borders. Optical coherence tomography (c
and d) shows them as large excrescences (yellow arrows)
under the RPE cells
the soft drusen are larger pale-yellow deposits
under the RPE and have an ill-dened border
(Fig. 4.5). These may be discrete and tend to
become conuent over time. These may be associated with both hypo and hyperpigmentary
changes. The hard and the soft drusen increase
over time [1].
hard exudates; Grade 1=questionable hard exudates; Grade 2=denitive hard exudates but less
than those shown in standard fundus photograph
#3; Grade 3=hard exudates equal to or greater
than shown in standard photograph # 3 but less
than that shown in photograph # 5; Grade 4=hard
exudates equal or more than shown in photograph
# 5 but less than shown in photograph # 4; Grade
5 is hard exudates greater or equal to those shown
4.4 Classication ofRetinal Hard
in photograph 4; and Grade 8=cannot grade.
Exudates [2]
Retinal hard exudates are classied according to
the modied Airlie House classication based on
standard stereoscopic fundus photographs. The
area occupied by hard exudates in the standard
fundus photographs 3, 4, and 5 are used for evaluating the severity of hard exudates. Grade 0=no
4.5 Signicance ofRetinal Hard
Exudates
In recent years there has been immense interest in
the automated detection of diabetic retinopathy
from 2-D retinal photographs using machine
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4.6 Formation ofRetinal Hard Exudates
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learning and articial intelligence algorithms.
While the microaneurysms and dot haemorrhages
are coloured red, the hard exudates, cotton wool
spots, and the drusen may look similar [3].
Contextual presence of the lesions, e.g., microaneurysms and hard exudates in the context of retinal vessels, may help differentiate them from
drusen, which are discrete without any context to
the retinal vessels. Semiautomatic algorithms
have also been attempted to detect and grade the
severity of hard exudates from colour fundus pictures [4].
4.6 Formation ofRetinal Hard
Exudates
Retinal hard exudates are formed when plasma
leaks from the microaneurysms (MAs) and the
retinal capillaries with a damaged endothelial
barrier. The retina is tightly packed with cells in
all its layers except the inner and outer plexiform
layers, which have a potential space for uid collection. Most leaking microaneurysms are located
in the inner nuclear layer (INL); hence, the uid
tends to collect in the outer plexiform layer. The
leaked uid can move back into the intravascular
compartment of the neighbouring, still normal,
capillaries leaving behind the macromolecules
consisting of the lipoprotein–cholesterol complex that is seen as yellow-white shiny hard exudates. The area of abnormal leaky MAs thus gets
surrounded by incomplete or complete rings of
hard exudates called circinate retinopathy
(Fig. 4.6). There may be one or many rings of
these deposits in the posterior pole of the retina.
This appears to be a dynamic process, and as the
new exudates are getting deposited, the older
ones are getting phagocytosed by the microglia,
the retinal macrophages carry these to the vessel
walls where their contents may be discharged
into the lumen or remain in the vessel walls.
Fig. 4.6 A complete ring of hard exudates, known as circinate retinopathy (black arrows), is seen in the right eye
(a) of a patient with moderate non-proliferative diabetic
retinopathy, The left eye (b) shows only microaneurysms
and dot haemorrhages. Optical coherence tomography
shows the leaked lipoproteins and uid in the outer plexiform layer as hyper-reective foci (yellow arrows) in the
right eye (c), while the left eye scan (d) appears normal
due to the absence of any leakage so far from the
microaneurysms
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