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4 Retinal Hard Exudates
agrees with a two-hit model of the mutation
responsible for many ocular tumors [76]. If the
family history is positive, the diagnosis of VHL is
made even with a solitary tumor; in the absence
of family history, either more than one tumor or
one tumor with a visceral involvement is required
to make a diagnosis of VHL [76]. VHL disease is
often accompanied by multiple organ involvement, including the brain, kidneys, and others
with benign or malignant lesions that include cerebellar hemangioblastoma, renal cell cysts, renal
cell carcinoma, and pheochromocytoma. The
VHL gene is a tumor suppressor gene located on
chromosome 3p25.5.
The retinal angiomas may be located on or
near the optic disc or in the retinal periphery.
Most patients with VHL rst present to the ophthalmologists with massive hard exudates. The
hemangioblastoma/angiomas are small and continue to grow and leak profusely, leading to massive hard exudates in the macula, prompting them
to report vision loss (Fig. 4.13). The angiomas
have a feeder arteriole and a drainage vein that
are dilated. It may be difcult to tell the difference on a clinical exam, but it is readily identied
on fundus uorescein angiography.
Elevated levels of VEGF have been found in
80% of the aqueous humor of the eyes with retinal
angiomas [77]. On histopathological studies, loss
of heterozygosity of the VHL gene, co- localized
with VEGF gene overexpression in the vacuolated
stromal cells but not the vascular cells or the glial
cells in the angiomas, has been seen, suggesting
thereby that the true neoplastic component of the
retinal angiomas is the stromal cells and thus are
an ideal site for anti-VEGF therapy [78].
The treatment of retina capillary hemangiomas includes laser photocoagulation of tumors
up to two-disc size combined with anti-VEGF
agents. Photodynamic therapy has effectively
controlled retinal capillary hemangiomas, including the VHL and the sporadic forms [79]. For
advanced cases, cryopexy or pars plana vitreous
surgery can often be done with poorer results
than thermal laser photocoagulation.
4.13.4.1 Screening forVHL
Since VHL is a potentially lethal disease associated with benign lesions in several organs and
renal cell carcinoma, it is recommended that
patients with a positive family history or those at
risk should undergo screening by a multidisciplinary team. Essentially, it consists of offering a
DNA test to rule out mutation. A negative test
rules out a life-long vigilance for the VHL.Those
positive for the VHL mutation should undergo
annual ophthalmological, neurological, and
neuro-otological exams every 2–3years starting
in infancy. After 16 years, these examinations
should be done annually, including checking for
blood pressure, a plasma-free metanephrine test,
or a 24-hour urine metanephrine test to rule out
pheochromocytoma, and ultrasonography of the
abdomen. MRI should be done every 2–3years
[80]. The details of screening guidelines can be
seen on the website of the VHL Alliance. https://
vhl.org/professionals/screening- diagnosis/
importance- of- screening/ [80].
Fig. 4.13 Massive exudation with hard exudates seen
with retinal angiomas in a patient with von Hippel–Lindau
(VHL) disease
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Retinal Haemorrhages
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5
5.1 Introduction
The presence of retinal haemorrhages is one of
the most common intraocular signs physicians
encounter. Without exception, retinal haemorrhages indicate a breakdown of the retinal vascular homeostasis, which is critical for maintaining
retinal transparency and ensuring optimal visual
tasks assigned to the retina’s photoreceptors. The
central area of 500 μm of the retina, called the
fovea centralis, has the maximum concentration
of the cone photoreceptors and is responsible for
the detailed vision required in day-to-day activities like reading, recognition, colour vision, and
driving. This area is bereft of blood capillaries to
allow unrestricted passage of light to the photoreceptors. The haemorrhages in the retina may
remain asymptomatic so long as these do not
obscure the central fovea.
5.1.1 Blood Supply oftheRetina
andtheOcular Barriers
ply and is served by the choroid, one of the
human body’s highest blood ow tissues. Tight
endothelial junctions in the retinal blood vessels
constitute the inner blood-retinal barrier that does
not allow the movement of macromolecules and
cellular components into the extravascular space
in the neurosensory retina. Moreover, the retinal
arterial system is autoregulated to maintain a
constant blood ow to the inner retina. The retinal pigment epithelium (RPE) is the outermost
layer of the retina and separates the neurosensory
retina from the choroid. The blood supply in the
choroid is multilayered and is under autonomic
control. The choroid’s innermost layer of blood
vessels consists of fenestrated capillaries, known
as the choriocapillaris, which lie immediately
below the retinal pigment epithelium. The tight
gap junctions in the RPE provide the outer bloodretinal barrier and control the movement of
micronutrients into the retina.
5.1.2 Role ofPhysicians
The blood supply of the retina is multitier. The
supercial and deep capillary plexus and the
interconnecting capillaries arise from the
branches of the central retinal artery and supply
oxygen and micronutrients to the inner neurosensory retina [from the retinal nerve bre layer
(RNFL) to the inner nuclear layer]. In contrast,
the outer neurosensory retina has no blood sup-
© 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_5
Many systemic and ocular disorders may cause
haemorrhages in the eye and, specically, in the
retina. Unless the haemorrhages obscure the
macula, patients may remain asymptomatic,
thereby delaying the diagnosis of both sightthreatening and life-threatening diseases. Using
deep learning algorithms, ultrawide colour fundus photographs taken through an undilated pupil
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5 Retinal Haemorrhages
have shown potential for automated general population screening with remarkably high sensitivity and specicity in diagnosing retinal
haemorrhages. The automated detection of retinal haemorrhages was more sensitive than the
detection of these haemorrhages by general ophthalmologists. The retinal haemorrhages occupying the macular area call for an immediate referral
to a retinal specialist [1]. The physician needs to
identify the location and distribution of the haemorrhage, the extent, the shape, the number and
specic characteristics, and other accompanying
eye signs that help narrow the etiological
diagnosis.
5.2 Location ofHaemorrhages
intheEye
Haemorrhage may be localized in the anterior
chamber (hyphema), vitreous cavity (vitreous
haemorrhage), under the post hyaloid membrane
(subhyaloid haemorrhage), under the internal
limiting membrane but in front of the RNFL
(sub-ILM haemorrhage), in the RNFL (supercial, linear or ame-shaped), in the ganglion cell
layer, inner plexiform and the inner nuclear layer
(dot and blot haemorrhages), in the Henle’s layer
(petaloid haemorrhage), under the neurosensory
retina (sub-retinal haemorrhage), under the RPE
(sub-RPE haemorrhage), in the choroid, or in the
suprachoroidal space that lies between the sclera
and the choroid (suprachoroidal haemorrhage).
Clarity of the visual media permitting crossectional line scans on the spectral domain optical
coherence tomography can determine the location of the haemorrhages, whether in front of the
retina, within, or below the retina.
anterior and posterior chambers, which gets clotted and is dark coloured. Less commonly, RBCs
red or grey coloured may move into the anterior
chamber from a dissolving blood clot in the vitreous cavity or erosion of the ciliary blood vessels
by a misplaced haptic of an intraocular lens
implant. It is called microhyphema, is not visible
to the naked eye, and requires careful biomicroscopy. In all cases of hyphema, it is mandatory to
monitor the intraocular pressure, which is often
increased.
5.2.2 Vitreous Haemorrhage
Several ocular or systemic disorders or trauma
may result in haemorrhage in the vitreous cavity.
Visual symptoms may vary from the sudden
onset of cobwebs (oaters) to the complete
obscuration of vision, depending upon the severity of the haemorrhage (Figs.5.1 and 5.2). If it
prevents a satisfactory examination of the entire
retina, ocular ultrasonography must be done.
5.2.3 Subhyaloid andSub-ILM
Haemorrhages
A characteristic boat shape can recognize these
due to the gravitational settling of the RBCs and
a horizontal level (Fig.5.3). The boat shape indicates that there is no blood clot formation. The
5.2.1 Haemorrhage intheAnterior
Chamber
Hyphema often follows trauma to the eye and is a
red-coloured layered collection of RBCs in the
anterior chamber. If it covers the pupillary area,
vision is obscured. Severe blunt trauma may
cause haemorrhage to ll the anterior segment’s
Fig. 5.1 A patient with proliferative diabetic retinopathy
(PDR) presented with oaters in the right eye due to vitreous haemorrhage (green arrow) and subhyaloid haemorrhage (red arrows)
ab
ab
5.2 Location ofHaemorrhages intheEye
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Fig. 5.2 A patient with hypertension presented with sudden onset dimness of vision due to vitreous haemorrhage (a).
Three months later, there was spontaneous and complete resolution of vitreous haemorrhage (b)
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Fig. 5.3 Subhyaloid haemorrhage (boat-shaped) in a 55-year-old male (a) and 61-year-old female (b) with prolifera-
tive diabetic retinopathy
most common cause of subhyaloid haemorrhage
is proliferative diabetic retinopathy. The subhyaloid haemorrhage may break into the vitreous
cavity obscuring the retina’s details and preventing pan-retinal laser photocoagulation (Fig.5.4).
A dense subhyaloid haemorrhage does not
resolve spontaneously and may facilitate intense
brovascular proliferation. Such patients require
If it obscures the fovea, a simple puncturing of
the posterior hyaloid membrane or ILM with a
neodymium:YAG laser can release the trapped
RBCs from these spaces and trickle into the
lower periphery of the retina. Sub-ILM haemorrhage (Fig.5.6) may unmask underlying pancytopenia due to COVID-19 [2] or megaloblastic
anaemia [3].
pars plana vitreous surgery to remove the haemorrhage and also do a pan-retinal laser photocoagulation (Fig.5.5).
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5 Retinal Haemorrhages
Fig. 5.4 A patient with proliferative diabetic retinopathy
(Note new vessels on the optic disc and brovascular proliferation along the lower temporal vessels. Laser photocoagulation scars can be seen temporal to the fovea (a).
a
c
While waiting for spontaneous resolution of the subhyaloid haemorrhage, it broke into the vitreous cavity obscuring all details of the retina (b)
b
Fig. 5.5 A 22-year-old type 1 diabetic presented with
sudden visual loss from the right eye due to a dense subhyaloid haemorrhage over the macula (a). Three months
later, there was a massive brovascular proliferation on
the optic disc, and the haemorrhage over the macula persisted (b). Six months following pars plana vitreous surgery, the media has cleared, but he required treatment for
macular oedema (c)
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