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Made Easy
For Elsevier:
Commissioning Editor: Timothy Horne
Development Editor: Sheila Black
Project Manager: Nancy Arnott
Designer/Design Direction: Charles Gray
Illustration Manager: Bruce Hogarth
Illustrator: Andrew Bezear
Made Easy
Sujoy Ghosh MD DM MRCP(UK) MRCPS(Glas),
Clinical Teaching and Clinical Research Fellow,
The Ayr Hospital, Ayr, UK

Andrew Collier BSc(Hons) MBChB MD FRCP(Edin&Glas),

Honorary Senior Lecturer and Consultant Physician,
The Ayr Hospital, Ayr, UK

Mohan Varikkara MS FRCS(Edin),

Consultant Ophthalmologist, The Ayr Hospital, Ayr, UK

Stephen Palmer MIMI RMIP,

Head of Department, Medical Photography
and Audiovisual Services, NHS Ayrshire & Arran, UK

Foreword by
President, Royal College of Physicians, Edinburgh, UK

Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2010
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ISBN 978-0-7020-4297-3
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Knowledge and best practice in this field are constantly changing. As new research
and experience broaden our understanding, changes in research methods, professional
practices, or medical treatment may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge
in evaluating and using any information, methods, compounds, or experiments described
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With respect to any drug or pharmaceutical products identified, readers are advised
to check the most current information provided (i) on procedures featured or (ii) by
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Printed in China

Foreword vii
Preface ix
Acknowledgments xi
Digital retinal photography and the images in this book xiii

1. The basics: direct and indirect ophthalmoscopy 1

2. Specialised imaging techniques 11
3. The normal fundus and its variants 21
4. Diabetic retinopathy 31
5. Hypertensive retinopathy 53
6. Papilloedema 59
7. Optic atrophy 61
8. Glaucoma 65
9. Retinal vascular occlusions 67
10. Fundal haemorrhages 73
11. Age-related macular degeneration 77
12. Lipaemia retinalis 81
13. Angioid streaks 83
14. Retinitis pigmentosa 85
15. Choroidal naevus 89
16. Melanocytoma 91
17. Ocular inflammation 93
18. Roth spot 97
19. Retinal detachment 99

Index 103
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It is a pleasure to be invited to contribute a foreword for Fundoscopy

Made Easy. Acquiring knowledge and mastering clinical skills remain
core to training at both undergraduate and postgraduate level. Per-
fecting and maintaining the skills involved in ophthalmoscopy remain
challenging for most doctors in training. In this respect the introduc-
tory chapters on equipment, techniques and normal findings take the
reader in an orderly fashion through the basics. Over the years tech-
nology has advanced and the descriptions of the newer techniques for
visualising the retina are important even for the nonspecialist.
The sequence of the following chapters takes the reader through a
systematic and comprehensive review of the various retinal patholo-
gies. The layout is consistent between chapters and makes the whole
text highly readable with an appropriate level of detail related to not
only diagnosis but also treatment options for the various conditions.
I am sure all readers will be impressed by the quality of the image
reproduction. The authors are to be congratulated on producing a vol-
ume which is more than simply an atlas of pathology.
At a time when we all run the risk of becoming de-skilled in fun-
dal examination, this books publication is timely. It will be particularly
useful for all trainees in both primary and secondary care, especially
for those who may be studying for College examinations. It is a highly
readable text and I hope you enjoy it as much as I have.

Neil Dewhurst

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Examination of the fundus is an area where the non-specialist often has

limited knowledge. Medical students, junior doctors and physicians
(whatever grade) need to have a basic knowledge of fundal examina-
tion, irrespective of the speciality that they are working in. In todays
changing educational curriculum there is less opportunity for all con-
cerned to master this art. Although there are several textbooks on oph-
thalmology and fundoscopy, very few are targeted at the needs of
medical students and junior doctors.
This book has been specifically designed to fill that gap and make
fundoscopy and interpretation of fundal images as simple as possible.
Often making a diagnosis on fundoscopy is like matching wallpaper.
Once you have seen one you can identify it when you see it again. The
high-quality images provided in this book, together with concise write-
ups, should provide the core knowledge required not only for medical
students and junior doctors but also for doctors in training prepar-
ing for examinations (including the MRCP). It will also be useful for
optometrists and medical photographers.
This book in not meant to be an alternative to conventional textbooks
or the expert opinion of an ophthalmologist, but should be able to pro-
vide the reader with enough information to help identify/diagnose the
most common retinal abnormalities.

S. Ghosh
A. Collier
M. Varikarra
S. Palmer

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For valuable assistance preparing and sourcing the many Illustrations,

the authors would like to thank Sarah Syme, Valerie Wyllie, David
Dickie, Wendy Trainor and Emma Lehane from NHS Ayrshire & Arrans
Medical Photography department, John McCormick, Iain Smith and
Prof Gordon Dutton, from the Tennent Institute of Ophthalmology at
Gartnavel General Hospital, Glasgow, and Colin Clements from Kings
College Hospital, London.
We would like to thank Margaret McMurdo for her help preparing
the manuscript.

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Digital retinal
photography and the
images in this book

Most, if not all, of the photographs in this book were taken with Topcon
digital retinal cameras. Within the authors workplace these are predomi-
nantly the Topcon TRC-NW6 fitted with a Nikon D70 camera back. This
is a non-mydriatic camera which does not usually require the patients
eyes to be dilated; however, a much greater success rate can be achieved
if tropicamide or similar mydriatic eye drops are used. Non-mydriatic
cameras operate by using an infrared-sensitive video camera image to
position and focus the image of the
retina. As no visible light is used, the
patients pupil will not constrict, and
a photograph can then be taken using
the built-in flash. The flash duration
is so short that the exposure is made
before the pupil can react.
Mydriatic photographs taken within
the Ophthalmology Department were
produced using either a Topcon TRC-
50EX or a Canon CF-60 mydriatic cam-
era. In this way, a 45-degree area of the
retina can be covered by each photo-
graph. The Topcon TRC-NW6 incor-
porates one central and eight fixed
peripheral internal fixation points.
Using each of these fixation points will
Topcon Fundus Camera
cover 85 degrees of the retina. The cen-
tral fixation point allows a repeatable photograph of the posterior pole. This is
the basic image used for the Scottish Diabetic Retinal Screening Programme.

The Basics: Direct
and Indirect
Direct ophthalmoscopy

The direct ophthalmoscope is the instrument of choice for fundus

examination by medical students and physicians. It allows for a magni-
fied, monocular image of the retina and optic disc.

The instrument illuminates the subjects fundus by light reflected
off a mirror on the instrument head. A perforation in the centre of
the mirror helps the observer view the area illuminated. The ema-
nating rays from the subjects eyes are parallel, assuming the subject
is emmetropic (normal sighted). These rays are converged to a focus
(assuming the observer is also normal sighted) by the observers
cornea and crystalline lens onto the observers retina. The emanat-
ing rays from a myopic subjects eye would be convergent and there-
fore will require a concave lens to make it parallel before entering
1 Fundoscopy Made Easy

Viewing aperture

Filter control
Lens power wheel
Graticule control

On/off switch and brightness control

The ophthalmoscope.

the observers eye and the converse if the subject is hyperopic. These
lenses are mounted on a wheel on the ophthalmoscope head which
can be dialled appropriately.

If you are using an unfamiliar ophthalmoscope it would help to famil-
iarise yourself with the colour coding of the lens wheel and the vari-
ous apertures and filters. To undertake successful ophthalmoscopy
it is essential that both you and the patient are comfortable. Adjust
the height of the patient in such a way that you dont have to stoop
too much. Dim the main lights to allow for physiological mydriasis
if the pupil is not pharmacologically dilated. Tropicamide 1% is a

The Basics: Direct and Indirect Ophthalmoscopy 1
short-acting dilator which can be used safely unless contraindicated
by allergy or due to a shallow anterior chamber which may precipitate
an acute glaucoma on dilation of the pupil. A shallow chamber can be
reasonably assessed by using a pen light that is shone from the side of
the cornea, parallel to the iris. Normally the opposite half of the iris
beyond the pupil should be illuminated by your light. If it is shad-
owed, the configuration of the iris is considered convex, thus indicat-
ing a shallow anterior chamber.
Instruct the patient to look at a distant target. Let the patient know that
they can blink if required. Stand at the side of the patient. Ideally use
your left eye and left hand to examine the patients left eye. Rest your free
hand on the patients forehead, using your thumb to hold the upper lid
open if necessary. Use only the minimum required intensity of light. The
field of view of the fundus is increased the closer you are to the patients
eye. For low myopes and low hyperopes it is best to remove their spec-
tacles; however, for high myopes, hyperopes and for subjects with high
astigmatism it is advisable to keep the spectacles on in order to over-
come problems associated with magnification, minification or distortion,
respectively. The extra reflexes produced by the spectacle lenses may at
first prove distracting but can be overcome with practice.

1 Fundoscopy Made Easy

Examination by direct ophthalmoscope.

Examination of the red reflex

Start the examination by doing a distant direct ophthalmoscopy
from a distance of 30 cm using a plano lens in the aperture of the
ophthalmoscope. This technique is used to study the red reflex and
each eye should be compared. While examining the red reflex, ask the
patient to look up or down slightly. If, when the patient looks up, the
opacity appears to move in the same direction within the red reflex,
then it must lie anterior to the pupil plane (i.e. the cornea or the ante-
rior chamber). One that remains stationary must be in the plane of
the pupil and one that moves in the opposite direction to that of the
patients gaze must lie posterior to the pupil plane (i.e. the posterior
lens or vitreous). You may find it easier to move yourself slightly up
or down rather than ask the patient to move their eye to achieve the
same effect.

The Basics: Direct and Indirect Ophthalmoscopy 1
During ophthalmoscopy it is advisable to keep both eyes open and
suppress the image from the other eye. This reduces the effect of accom-
modation. It may take some practice to accomplish this.

Examination of the optic disc

Slowly move closer to the patient and at the same time gradually
increase the power of the lens in the wheel to focus on the retina.
The power necessary to focus on the fundus will depend on both
the patients and the observers uncompensated refractive error and
their accommodation. When the patient is looking straight ahead, the
optic disc should naturally come into the field of view. If not, try to
locate a blood vessel on the retina and then move along it and locate
the point at which it branches. Move your field of view in the direc-
tion in which the apex of the branch is pointing. By moving along a
blood vessel in this manner the optic disc will be located. You will
need to consider its colour, clear definition of its margins, cup (if
there is one) and the ratio of the size of the cup to the size of the optic
disc (cup disc ratio, denoted as, e.g., 0.3:1, meaning it occupies one-
third of the area of the optic disc). Note the capillaries on the optic
disc and look for the presence of a spontaneous venous pulsation.
Also note the presence of any pigment, choroidal or scleral crescents
around the disc.

Examination of the retinal blood vessels

Retinal blood vessels should be examined by following the temporal
and nasal arcades from the optic disc. Veins are larger and dark red,
whereas arteries are relatively thinner and lighter (normal artery:vein
ratio is 2:3).

Examination of the macula

The macula is visualised by asking the patient to look at the light source
as this brings the fovea (fixation point) into view. The macula is the area
between the superior and inferior temporal arcades and its centre is

1 Fundoscopy Made Easy

the fovea. Since using an excessively bright light can make the macula
difficult to visualise, it may be useful to use a smaller aperture beam
and minimal required intensity.

Examination of the peripheral fundus

Finally, ask the patient to look in the eight cardinal directions to allow
you to view the peripheral fundus Look up, to see the superior
periphery and so on. You will need to adjust the lens in the wheel
slightly as the periphery is closer to you than the optic disc, requiring
more focusing power.

Indirect ophthalmoscopy

Binocular indirect ophthalmoscopy

This technique allows for viewing the fundus at a wider angle which
allows examination of the peripheral retina and also a better view
through lens opacities as well. Binocularity is achieved by the use of
mirrors in the instrument to reduce the pupillary distance of the observer
to about 15 mm. The instrument also carries a light source which is
attached to a headband or spectacle frame worn by the examiner.
The patients pupil may be dilated and background lights dimmed
as for direct ophthalmoscopy. The patient is examined either seated in
a reclining chair or lying on a couch. A condensing lens (varying from
+15 D to +30 D) is held in one hand of the examiner in front of the
patients eye. The image formed is magnified three-fold with a 20 D
lens and is inverted and laterally reversed (superior seen inferiorly and
temporal seen nasally).
Ensure that the patients and the observers eye are aligned before
placing the lens in front of the eye. Check for the red reflex first and
then bring the condensing lens in front of the patients eye. Now

The Basics: Direct and Indirect Ophthalmoscopy 1

Aerial image of fundus Condensing lens

Binocular indirect

The binocular indirect ophthalmoscope.

Examination by indirect ophthalmoscope.

1 Fundoscopy Made Easy

radually pull the lens towards you until the whole lens is filled with
the retinal image. Systematically view the patients fundus in primary
and all secondary positions of gaze. Also remember to compare the
two eyes. The ora serrata can be viewed by scleral indentation with
the free hand of the observer under local anaesthetic (proxymeta-
caine). It is important to remember that you are viewing the supe-
rior retina when the patient is looking up despite the image being
inverted and laterally reversed, and this relationship is maintained
for the other quadrants.

Slit lamp biomicroscopy

The fundus also can be viewed by using a non-contact Volk condensing
lens (+60 to +90 D) or a Goldmann contact lens (64 D) and the slit lamp.
This is the most common method of examination of the fundus dilated
or undilated at the ophthalmology clinic. The patients pupil may be
dilated and background lights dimmed as for direct ophthalmoscopy.
Once the patient is positioned comfortably at the slit lamp, the
patient is advised to look straight ahead and not into the light (ask
the patient to look at the examiners right ear with the left eye while
examining the patients right eye and vice versa). The slit lamp view-
ing piece and the light column are kept at an angle of 90 degrees.
Theintensity of the beam is kept to the minimum possible and the
magnification preferably set at 10 initially. The slit beam is set
around 1.52.5 mm wide and 510 mm long. The beam is focused
onto the patients pupil and the condensing lens aligned at around
1 cm from the patients eye. The slit lamp is then pulled backwards
gradually towards the examiner until it comes into focus with the
aerial image of the fundus between the condensing lens and the slit
lamp. Alternatively, the slit lamp could be drawn back completely
towards the examiner and then gradually moved forwards until the
image comes into focus.
As with indirect ophthalmoscopy, the image from a non-contact Volk
lens slit lamp biomicroscopic examination is inverted and laterally

The Basics: Direct and Indirect Ophthalmoscopy 1
reversed. The fundus is viewed systematically in primary and all
secondary positions of gaze. The ora serrata can be brought to view
using the Goldmann three-mirror lens.

Examination by slit lamp biomicroscopy.

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Lara Goldstein
In addition to binocular indirect ophthalmoscopy and slit lamp bio-
microscopy described in Chapter 1, the following specialised imaging
techniques are useful in diagnosing particular conditions.

Fundal fluorescein angiography (FFA)

Fluorescein angiography is a technique often used for examining the

circulation of the retina. It involves injection of sodium fluorescein dye
into the systemic circulation. A series of images are then obtained by
photographing the fluorescence emitted after illumination of the retina
with blue light.
Some staining of the skin is visible about 5 minutes after dye injec-
tion. The fluorescein dye is cleared by the kidney in 1224 hours. Some
patients experience nausea which is typically transient. Allergic reac-
tions are uncommon. The reaction can range from a minor annoy-
ance to a severe reaction. Anaphylactic shock following an injection of
sodium fluorescein dye is very rare. However, it is important to ensure
that a suitably equipped emergency trolley is available.
2 Fundoscopy Made Easy

Red free: Blood vessels are seen as dark against the background of normal fundus
reflectance with striations from the retinal nerve fibre layer.

11.1 sec: Choroidal filling which is the earliest, is seen as the grey background. The dye
has now filled the retinal arteries and is starting to show laminar flow in the retinal veins.

Specialised Imaging Techniques 2

133 sec: The next phase shows emptying of retinal arteries and full retinal veins. Note
the fine perifoveal capillary network.

342 sec: This is the late phase where the dye has already recirculated. Note the stain-
ing of the optic nerve head and extravasated dye in the choroidal spaces.

2 Fundoscopy Made Easy

Baseline colour and monochrome red-free (green filter) images
are taken prior to injection. This allows for the visualisation of
autofluorescence of the retinal tissues.
A bolus of approximately 5 cc of 10% sodium fluorescein is injected
into a suitable vein in the arm or the back of the hand.
A blue filter is placed before the photography light source. This has
the effect of exciting the fluorescein dye, which in turn produces
yellowgreen (530 nm) light.
A barrier filter is placed in front of the camera. This ensures that
only the yellowgreen fluorescence is recorded.
The fluorescein dye reaches the retinal circulation approximately
10 seconds after injection. A series of black and white digital
photographs are taken of the retina to capture the different phases
of the dye in the choroidal and retinal circulation. Late images are
obtained at 5 and 10 minutes.
Black and white photographs give a better contrast than colour
photographs, as only light of a very narrow wavelength is being
transmitted though the barrier filter.

Specialised Imaging Techniques 2

Indocyanine green (ICG) angiography

Indocyanine green is the second dye used in angiography. It fluoresces

less than fluorescein sodium and does so at 835 nm. It is also a relatively
larger molecule and is 98% bound to plasma proteins. As such, it does
not leak as easily as fluorescein sodium from the choroidal vessels and
therefore delineates them well. It is not metabolized and is filtered out
by the liver and excreted in the bile.
The images that follow illustrate the mid phase of an ICG angiogram
and show well-delineated choroidal vasculature of both eyes.

2 Fundoscopy Made Easy

Hyperfluorescent spots

ICG angiogram. Note the two hyperfluorescent spots (arrowed) responsible for the
exudative changes seen in the colour image above.

Specialised Imaging Techniques 2

ICG angiogram. Mid phase of angiogram delineating the choroidal vessels (colour
picture of the same eye seen above).

2 Fundoscopy Made Easy

Optical coherence tomography (OCT)

Optical coherence tomography is a medical diagnostic imaging tech-

nology that provides detailed cross-sectional or tomographic imaging
of biological tissues. Unlike ultrasound scans, this device relies on light
rather than sound waves. It permits simultaneous viewing of the posi-
tion on the ocular structure as well as its high-resolution transverse
cross-section/three-dimensional image. It allows for both anterior and
posterior segment high-resolution imaging.
The OCT signal from a particular tissue layer is a combination of its
reflectivity and absorption characteristics combined with the scattering
properties of its overlying layers. The nerve fibre layer forms the inner

Specialised Imaging Techniques 2
boundary and the retinal pigment epithelium forms the outer bound-
ary of the retina. High reflective layers are represented by red and white
colours while lower reflective layers are represented by blue and black
colours. OCT therefore helps in diagnosing minimal disturbances in
structural integrity. Its ability to quantify change combined with excel-
lent reproducibility makes it an invaluable tool to monitor changes.

Neuro-sensory retina Posterior vitreous face

Optic disc Fovea Choroid Retinal pigment layer

A normal OCT image.

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The Normal
Fundus and Its
The normal fundus

Anatomically the macula is the area centred within the temporal arcades
measuring about 5.5 mm (3.5 disc diameter, DD).

The fovea is a concavity in the centre of the macula measuring about
1.5 mm or 1.0 DD. It is the most sensitive part of the retina, serving
the function of high spatial resolution and colour vision. On fundos-
copy, due to its concavity, a fovea maintaining its normal architecture
shows a bright reflex known as the foveal reflex.

A central 0.35 mm of the fovea is known as the foveal avascular zone (FAZ)
of the retina as it is free of retinal capillaries. This area consists purely of
cone photoreceptors and no overlying inner layers of the retina.
3 Fundoscopy Made Easy








A normal fundus.

The Normal Fundus and Its Variants 3
Retinal arteries
The walls of the retinal blood vessels are transparent and therefore we
see the column of blood flowing in them. On fundoscopy, the arter-
ies appear lighter and narrower (arteriovenous ratio of 2:3) compared
to the retinal veins. The central retinal artery emerges at the optic
disc and divides into four branches (superotemporal, inferotemporal,
superonasal and inferonasal). In the retina they divide dichotomously
until third-order branches finally form a two-tier perivenular capillary
network. The superior branches respect the horizontal raphe and nor-
mally do not communicate with the inferior branches. The retinal capil-
lary wall is lined by endothelial cells and pericytes which form a tight
inner retinal barrier. The retinal blood vessels are autoregulated like
those of the brain.

Retinal veins
The perivenular capillaries ultimately form the four main branches
(superotemporal, inferotemporal, superonasal and inferonasal) before
forming the central retinal vein at the optic disc. The vessels cross over
one another in the retina.

The optic disc

Measuring about 1.5 mm, the optic disc lies about 3 mm nasal to the
fovea. The edge of the optic disc may be slightly elevated. The immedi-
ate peripapillary area may show hyperpigmentation or a scalloped pale
area representing the sclera, seen through the transparent retina. The
only neuroretinal elements at the optic disc are the axons of the gan-
glion cells which make up the neuroretinal rim. The central part, the
optic cup, occupying around 30% of the entire optic disc area, is paler
and appears depressed on binocular stereo fundoscopy. The central
retinal vessels enter and leave in this depression. Spontaneous venous
pulsations are often seen at the optic disc; however, they may be absent
in around 20% of normal individuals. The optic disc also has small cap-
illaries. Physiologically the optic disc represents the blind spot.

3 Fundoscopy Made Easy

Normal fundus variants

In a tigroid fundus there are lesser amounts of pigment in the reti-
nal pigment epithelium, allowing streaks of underlying normal chor-
oidal pigmentation to become visible and give the characteristic

Tigroid fundus: larger choroidal vessels with interspersed choroidal pigment showing

The Normal Fundus and Its Variants 3
Myelinated nerve fibres
Myelinated nerve fibres are relatively common and may follow several
Isolated peripheral patch of myelination.
Pericapillary myelination may be mistaken for papilloedema on
The myelinated nerve fibres follow the pattern of normal fibres
and extend as regular, feather-like patches, which may or may not
obscure the retinal blood vessel. Although myelination usually
remains stationary, it may very well disappear in optic atrophy
following either optic neuritis or ischaemia. It may be associated
with neurofibromatosis-1.

3 Fundoscopy Made Easy

Myelinated nerve fibres

Myelinated nerve fibres. Note the pale appearance adjacent to the optic disc
corresponding to arrangement or pattern of retinal nerve fibres.

The Normal Fundus and Its Variants 3
Albino fundus
Melanocytes normally synthesise melanin in the retinal pigment
epithelium. Absence of melanin due to any defect in its synthesis allows
the choroidal vasculature to be seen under the retinal vessels.
Ocular albinism is a rare X-linked disorder, affecting the eyes only.
Oculocutaneous albinism is an autosomal recessive condition, char-
acterised by hypopigmentation of skin, hair, fundus and irides. It is
often associated with a decrease in visual acuity, photophobia and
Such patients may be classified as tyrosinase positive or negative,
with the degree of pigmentation usually being greater in tyrosinase-
positive patients.

Albino fundus: note the lighter fundal reflex with large choroidal vessels showing
through. Absence of normal macular pigmentation and loss of foveal reflex represents
macular hypoplasia.

3 Fundoscopy Made Easy

Artefacts in the normal fundus

Note eye lash artefact inferior to the optic disc.

The Normal Fundus and Its Variants 3

Blurred fundus image due to media opacity caused by cataract.

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Diabetic retinopathy is more likely to occur in patients who have
poorly controlled diabetes and its prevalence increases with the dura-
tion of the diabetes. In type 1 diabetic patients, 50% will have some
form of retinopathy after 10 years. Approximately 510% of type 2
diabetic patients will have retinopathy at the time of diagnosis of
diabetes. Other risk factors for diabetic retinopathy include hyper-
tension, renal disease, obesity, dyslipidaemia, pregnancy, smoking
and anaemia. Microvascular leakage and non-perfusion are the main
aetiopathogenic processes. The tight junction of the endothelial cells
constitutes the inner bloodretinal barrier. Pericytes wrapped round
the capillaries are thought to be responsible for the structural integrity
of the blood vessels. In diabetic patients there is a reduction in pericytes
and endothelial cells, leading to a breakdown of this barrier.

Classification of diabetic retinopathy

Conventionally, involvement of the retina in patients with diabetes has

been classified as non-proliferative (background) retinopathy, pre-
proliferative retinopathy and proliferative retinopathy. The macula may
be involved (maculopathy) with any of the above forms of retinopathy.
4 Fundoscopy Made Easy

A commonly used grading system is that of the Early Treatment

Diabetic Retinopathy Study (ETDRS) (Table 4.1).

Table 4.1 Early treatment diabetic retinopathy study system

Grade Features
Non-proliferative diabetic retinopathy (NPDR)
None Normal retina
Early Microaneurysms only
Mild Microaneurysms plus:
Retinal haemorrhages, and/or
Hard exudates (> 2 DD from fovea)
Moderate Mild; NPDR plus:
Haemorrhage and/or cotton wool spots (< 5), and/or
Minimal venous beading/looping or IRMAs in one
Severe Moderate; NPDR plus
4/2/1 rule Microaneurysms/haemorrhages in four quadrants, or
Venous beading/looping in two or more quadrants, or
IRMAs in one quadrant
Very severe Any two or more of the severe categories

Proliferative diabetic retinopathy (PDR)

PDR without high-risk changes NVE or NVD < DD
PDR with high-risk changes NVE or NVD > DD plus pre-retinal and/or vitreous

IRMAs, intraretinal microvascular abnormalities; NVD, neovascularisation of the disc;

NVE, neovascularisation elsewhere.

Diabetic Retinopathy 4

Table 4.1 Early treatment diabetic retinopathy study


Disease severity Findings observable on dilated

level ophthalmoscopy
Diabetic macular oedema No apparent retinal thickening or hard exudates
apparently absent in posterior pole
Diabetic macular oedema Some apparent retinal thickening or hard
apparently present exudates in posterior pole
Mild diabetic macular Some retinal thickening or hard exudates in poste-
oedema rior pole but distant from the centre of the macula
Moderate diabetic Retinal thickening or hard exudates approaching
macular oedema the centre of the macula but not involving the centre
Severe diabetic macular Retinal thickening or hard exudates involving the
oedema centre of the macula

Non-proliferative (background) diabetic retinopathy

Microaneurysms are the first clinically detectable lesions and repre-
sent a dilated part of the perivenular capillaries. They occur due to
a reduction in the number of endothelial cells and pericytes, appear-
ing as tiny round dots anywhere in the retina. Intraretinal haemor-
rhages can be dot or blot if they lie in the deeper compact layers of the
retina, or flame shaped if they lie in the nerve fibre layer (obeying the
arrangement of the nerve fibres). Hard exudates appear yellow and
waxy with relatively distinct margins and represent intraretinal depo-
sition of serum lipids. They usually border the normal and oedema-
tous retina, are usually found in the posterior pole and can often be
seen in a circinate pattern around a cluster of microaneurysms. Retinal
oedema represents leaky capillaries and is often difficult to delineate
with direct ophthalmoscopy. It should always be suspected in the
presence of hard exudates. Visual acuity declines if the retinal oedema
involves the fovea.

4 Fundoscopy Made Easy


Blot haemorrhages

Dot haemorrhages

Hard exudates

Cotton wool spot

There are numerous hard exudates, microaneurysms and dot and blot haemorrhages
which are characteristic of background diabetic retinopathy.

Pre-proliferative diabetic retinopathy

Pre-proliferative diabetic retinopathy develops in eyes that initially
may only show simple background retinopathy; it is caused by retinal
ischaemia. Pre-proliferative diabetic retinopathy is characterised by:
Vascular changes consisting of venous changes in the form of
beading, looping and sausage-like segmentation. The arterioles
may also be narrowed and even obliterated, resembling a branch
retinal artery occlusion.
Cotton wool spots caused by interruption of axoplasmic flow caused
by the ischaemia, and subsequent build-up of transported material
within the nerve axons, is responsible for the white appearance of
these lesions.

Diabetic Retinopathy 4
Dark blot haemorrhages represent haemorrhagic retinal infarcts.
Intraretinal microvascular abnormalities (IRMAs) represent either
dilated pre-existing vessels or early intraretinal new vessels. They
are found within an area of capillary non-perfusion.
As pre-proliferative changes suggest increasing retinal ischaemia and
precede proliferative retinopathy, the patient should be informed of the
worsening of their retinopathy and the likely need for laser photoco-
agulation in the future. The presence of ischaemic maculopathy should
be assessed as it could lead to irreversible loss of vision.
A grading system for screening for diabetic retinopathy, and guidelines
for specialist assessment, are outlined in Tables 4.2 and 4.3, respectively.

Venous beading

Cotton wool spots

The abnormalities are suggestive of retinal ischaemia and diagnostic of pre-

proliferative diabetic retinopathy, the forerunner of neovascularisation. These patients
should be referred for specialist assessment and close follow-up.

4 Fundoscopy Made Easy


Blot haemorrhages

Pre-proliferative diabetic retinopathy suggested by the presence of intraretinal microvascular

abnormalities (IRMAs) and dark blot haemorrhages suggestive of retinal ischaemia.

Diabetic Retinopathy 4

Table 4.2 Grading system used for screening for

diabetic retinopathy (UK National Guidelines)

Retinopathy (R)
Level R0: (no visible retinopathy)
Level R1: Background diabetic retinopathy (BDR) mild
The presence of at least one of any of the following features anywhere:
Dot haemorrhages
Hard exudates
Cotton wool spots
Blot haemorrhages
Superficial/flame shaped haemorrhages
Level R2: Background diabetic retinopathy (BDR) observable
Four or more blot haemorrhages in one hemi-field only (inferior and superior hemi-
fields delineated by a line passing through the centre of the fovea and optic disc)
Level R3: Background diabetic retinopathy (BDR) referable
Any of the following features:
Four or more blot haemorrhages in both inferior and superior hemi-fields
Venous beading
Intraretinal microvascular abnormalities
Level R4: Proliferative diabetic retinopathy (PDR) referable
Any of the following features:
Active new vessels
Vitreous haemorrhage
Level R5: Blind or phthisical eye
Level R6: Not adequately visualised
Retina not sufficiently visible for assessment technical failure


4 Fundoscopy Made Easy

Table 4.2 Grading system used for screening for

diabetic retinopathy (UK National Guidelines)Contd

Maculopathy (M)
Level M0: No maculopathy
No features 2 disc diameters (DD) from the centre of the fovea sufficient to qual-
ify for M1 or M2 as defined below
Level M1: Lesions as specified below within a radius of > 1 but 2 DD from the
centre of the fovea
Level M2: Lesions as specified below within a radius of 1 DD of the centre of
the fovea
Blot haemorrhages
Hard exudates

Photocoagulation (P)
Laser photocoagulation scars present

Other lesions (OL)

Other non-diabetic lesions present:
Pigmented lesion (naevus)
Age-related macular degeneration
Drusen maculopathy
Myelinated nerve fibres
Asteroid hyalosis
Retinal vein thrombosis

Diabetic Retinopathy 4

Table 4.3 Guidelines for referral for specialist

assessment of diabetic retinopathy

Clinical problem Urgency

There is sudden loss of vision Within 1 day
There is evidence of retinal detachment Within 1 day
There is new vessel formation (on the disc or elsewhere) Within 1 week
There is vitreous or pre-retinal haemorrhage Within 1 week
Rubeosis iridis is present Within 1 week
There are hard exudates within 1 DD of the fovea or Within 4 weeks
clinically significant macular oedema
There is an unexplained drop in visual acuity Within 4 weeks
There are unexplained retinal findings Within 4 weeks
Severe or very severe non-proliferative retinopathy is Within 4 weeks

General principles of management of diabetic retinopathy

Glycaemic control
Improvement of glycaemic control has been shown to reduce the risk
of development and progression of diabetic retinopathy. The Diabetes
Control and Complications Study (DCCT) demonstrated that inten-
sive glycaemic control reduces the risk of onset of diabetic retinopathy,
progression of pre-existing retinopathy, and the need for laser photo
coagulation of patients with type 1 diabetes. The United Kingdom
Prospective Diabetes Study (UKPDS) demonstrated a similar reduction
in the risk of onset and progression in diabetic retinopathy in patients
with type 2 diabetes.

4 Fundoscopy Made Easy

Control of blood pressure

The UKPDS demonstrated that the risk of progression of diabetic retin-
opathy was decreased with tight control of blood pressure (with either
captopril or atenolol) and led to an almost 35% relative reduction in the
need for retinal photocoagulation. The EURODIAB Controlled Trial of
Lisinopril in Insulin-dependent Diabetes (EUCLID) study (using lisino-
pril), and the Diabetic Retinopathy Candesartan Trials (DIRECT trial)
demonstrated delay in the progression of retinopathy using drugs that
act on the reninangiotensinaldosterone axis.

Management of dyslipidaemia
The Early Treatment Diabetic Retinopathy Study (ETDRS) and the
DCCT revealed that an elevated serum cholesterol level was related
to development and progression of diabetic retinopathy, especially
diabetic maculopathy. Recent studies suggest that aggressive lipid
lowering is beneficial in the prevention of progression and also in the
management of diabetic retinopathy, especially maculopathy.

Multifactorial risk reduction

The Steno 2 trial showed benefit of multiple interventions, which
included behavioural therapy (dietary intervention, exercise and
smoking cessation) and pharmacological intervention (reduction
of blood pressure, improvement in glycaemic control and lipid

Diabetic Retinopathy 4
Proliferative diabetic retinopathy
Proliferative diabetic retinopathy (PDR) affects about 510% of the
diabetic population and is more common in type 1 diabetes.
Neovascularisation is the hallmark of PDR. New vessels are com-
monly seen along the retinal arcades but can occur at the optic disc or
elsewhere in the retina. As a general rule, the retina distal to the neovas-
cularisation should be considered as ischaemic. It has been estimated
that over one-quarter of the retina has to be non-perfused before neo-
vascularisation occurs. Ischaemia upregulates the vascular endothelial
growth factor (VEGF) in the retina, which in turn stimulates neovas-
cularisation. New vessels start as endothelial proliferations, and pass
through the internal limiting membrane to lie in the potential plane
between the retina and the posterior vitreous face.
PDR can result in visual deterioration from ischaemia, haem-
orrhage and tractional retinal detachment involving the macula.
New vessels can break through the internal limiting membrane
and grow into the vitreous gel using the posterior face of the vit-
reous as a scaffold. This invariably leads to a pre-retinal or vitre-
ous haemorrhage and also increases the risk of tractional retinal
Basic principles of management of diabetic retinopathy have already
been discussed in previous sections. Patients with proliferative diabetic
retinopathy have to be assessed and managed by specialists and are
treated with panretinal photocoagulation (discussed in the following
sections in detail).

4 Fundoscopy Made Easy

New vessels

Neovascularisation at the optic disc, if present, is diagnostic of proliferative diabetic


Diabetic Retinopathy 4
Diabetic maculopathy

Involvement of the macula with exudative or ischaemic changes has a

potential to involve the fovea, thus threatening vision. Exudative mac-
ulopathy may be amenable to treatment but ischaemic changes are not.
Diabetic maculopathy can present in the following patterns:
Focal: Focal leakage, characterised usually by the presence of a
cluster of microaneurysms surrounded by retinal thickening and a
complete or incomplete ring of hard exudates.

Circinate pattern
of hard exudates

Focal diabetic maculopathy showing areas of hard exudates at the macula.

4 Fundoscopy Made Easy

Diffuse: Diffuse retinal thickening and exudation from capillaries,

often involving the fovea. Cystoid changes suggest chronicity of the

Diffuse diabetic maculopathy showing widespread hard exudates at the macula; note
the paler appearance of the macula suggesting retinal thickening.

Ischaemic: Diagnosed ideally by fluorescein angiography,

representing an enlarged or irregular foveal avascular zone.
Clinically it may lack features; however the hallmarks are reduced
visual acuity, deep blot haemorrhages and IRMAs.

Diabetic Retinopathy 4

Ischaemic maculopathy. Note the disruption of the perifoveal capillary network

resulting in an irregular and widened foveal avascular zone (FAZ) and adjoining
areas of capillary non-perfusion.

Optical coherence tomographic image showing cystoid macular oedema.

4 Fundoscopy Made Easy



Fundus fluorescein angiographic (FFA) image showing retinal nerve fibre layer
haemorrhage and deep blot haemorrhage. Temporal to the macula there are areas of
capillary drop-out, intraretinal microvascular abnormalities (IRMA) representing ischaemia.
The foveal avascular zone (FAZ) is enlarged and irregular, showing loss of the perifoveal
capillary network.

Capillary drop-out
with IRMA


FFA image showing proliferative changes such as neovascularisation elsewhere (NVE)

in the retina. Intraretinal microvascular abnormalities (IRMA).

Diabetic Retinopathy 4

Laser photocoagulation

The efficacy of photocoagulation has been demonstrated in the ETDRS

study. It is believed that the regression of neovascularisation is due to
the destruction of the ischaemic and hypoxic retina with the reduction
in angiogenic factors.
Panretinal photocoagulation is now the main modality of treatment
for proliferative diabetic retinopathy and severe non-proliferative dia-
betic retinopathy. Clinically significant macular oedema (CSMO) can be
treated with focal or grid photocoagulation.
Panretinal laser involves the application of 500 m of Argon laser
photocoagulation spots, each separated by an interval of a similar spot
size to the mid-peripheral retina. A row of laser burns is initially placed
approximately three disc diameters temporal to the fovea to avoid get-
ting too close to the fovea. About 1500 burns are usually required (in
two or three sessions). Severe cases may require further photocoagu-
lation. The aim is to cover the ischaemic areas, and regression of new
vessels occurs in almost 80% of cases. Fundus fluorescein angiography
(FFA) could be done initially to delineate the ischaemic areas; however,
it should be done to ensure coverage of ischaemic areas with the laser if
good regression of neovascularisation is not achieved with initial retinal
Laser treatment can be associated with pain, transient visual loss,
loss of visual field (inevitable) and sometimes reduced visual acuity
and choroidal damage.
In very aggressive cases of PDR, an intravitreal injection of an anti-
VEGF can give a valuable window period while waiting for laser pho-
tocoagulation to take effect which can take up to 2 weeks.

4 Fundoscopy Made Easy

Examples of newer and older types of laser treatment

Fresh laser burns applied as part of panretinal photocoagulation.

Fresh laser burns appear greyish white. Laser energy is taken up by the
pigment in the retinal pigment epithelium, resulting in photocoagula-
tion or a thermal burn of the retina. Within a period of about 2 weeks
the laser burns appear hyperpigmented. The above image shows fresh
laser burns applied as part of a panretinal photocoagulation.

Diabetic Retinopathy 4

Older laser burns (larger spot size) appear more intense due to the larger and
stronger thermal reaction caused by the application.

Regression of neovascularisation following panretinal photocoagulation. Note the

much smaller spot sizes of newer laser burns.

4 Fundoscopy Made Easy

Macular laser
Laser photocoagulation is considered primarily for clinically signifi-
cant macular oedema. This could be applied focally to leaking micro
aneurysms or in a grid pattern over the macula in cases of diffuse
macular oedema. The spot sizes used vary from 50 to 100 and power
just enough to cause a very minimal blanch. Using higher power by
itself can result in reduction of visual acuity. Utmost care should be
taken to avoid the foveal avascular zone (FAZ). Ideally a macular laser
should be done only after angiographically assessing the macula.
Other modalities in the local management of macular oedema
are intravitreal injections of triamcinolone acetonide or anti-VEGF.
However, the effect of these is only short-lived.

Grid laser burns are applied in a grid fashion to the macula, avoiding the foveal
avascular zone.

Diabetic Retinopathy 4
Grid laser burns are applied in a grid fashion to the macula, avoiding
the FAZ. These mild laser burns help to stimulate the retinal pigment
epithelium to dry the macular oedema by actively pumping the fluid
out of the retina.
Focal laser burns are targeted at the leaky microaneurysm within a
circinate area of hard exudate.

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The primary response of retinal arterioles to systemic hypertension is
narrowing. The degree of narrowing is dependent upon the amount of
pre-existing arteriosclerosis (see Box 5.1). For this reason hypertensive
narrowing is seen in its pure form only in young individuals.
Hypertensive retinopathy is characterised by:
Vasoconstriction, which can be generalised or focal with arteriolar
narrowing. However, ophthalmoscopic diagnosis of generalised
narrowing may be difficult.
Leakage, which is caused by abnormal vascular permeability leading
to the development of flame-shaped haemorrhages, hard exudates
and a retinal oedema. Swelling of the optic nerve is the hallmark of
malignant phase hypertension.
Arteriosclerosis, which is caused by thickening of the vessel wall,
which consists of intimal hyalinization and medial hypertrophy.
With increased thickening of arterial wall and narrowing of lumen,
the light diffuses giving rise to a copper wire reflex. When this
process continues it assumes a silver wire appearance when the
blood is no longer visualised. Arteriosclerosis also leads to changes
at the arteriovenous crossing termed as AV nipping. This can vary
from tapering of vein (venous compression Gunns sign on either
side of the crossing to interruption of visible column of blood.
5 Fundoscopy Made Easy

Box 5.1 KeithWagenerBarker classification of

hypertensive retinopathy

Grade 1

Mild to moderate narrowing or sclerosis of the arteries

Grade 2

Moderate to marked narrowing of the arterioles

Local and/or generalised narrowing of arterioles
Exaggeration of the light reflex
Arteriovenous crossing changes

Grade 3

Retinal arteriolar narrowing and focal constriction

Retinal oedema
Cotton wool patches

Grade 4

As for Grade 3, plus papilloedema

Hypertensive Retinopathy 5

Arteriovenous nipping secondary to hypertensive retinopathy. At the arteriovenous

crossing the vessels share a common sheath within which the hardened artery,
secondary to arteriosclerotic changes, compresses the retinal vein.

5 Fundoscopy Made Easy

Cotton wool

Nerve fibre layer


Hypertensive retinopathy showing nerve fibre layer (pre-retinal) haemorrhage and

cotton wool spot secondary to interruption of axoplasmic flow representing nerve fibre
layer infarcts.

Hypertensive Retinopathy 5
Management of hypertension

Non-pharmacological treatment of high blood pressure

The following lifestyle measures should be recommended for all
patients with high blood pressure:
Reduce salt intake.
Limit alcohol consumption: less than 21 units/week for men and 14
units/week for women is recommended.
Lose weight: people with hypertension who are overweight (body
mass index [BMI] 2530) or obese (BMI > 30) should be encouraged
to lose weight.
Increase physical exercise.
Follow a healthy diet: a randomized trial found that patients
who increased fruit and vegetable consumption to at least five
portions a day showed a significant reduction in blood pressure
of approximately 4/1.5 mmHg. Other healthy eating suggestions
include replacing saturated fat with polyunsaturated and
monounsaturated fats, eating oily fish and reducing total fat intake.
Stop smoking.

Pharmacological treatment of high blood pressure

If the lifestyle measures outlined above are ineffective in reduc-
ing a patients high blood pressure to acceptable levels, the British
Hypertension Society recommends a four-step treatment programme
as outlined in the following algorithm.

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55 years or black patient

< 55 years
of any age

A C or D Step 1

A+C or A+D Step 2

A+C+D Step 3

further diuretic therapy
alpha blocker or Step 4
beta blocker
Consider seeking specialist advice

A = ACE inhibitor
C = Calcium channel blocker
D = Diuretic

The British Hypertension Society (BHS) A/CD algorithm for the treatment of high blood
pressure. A, angiotensin converting enzyme inhibitor; C, calcium channel blocker; D,
diuretic. Redrawn from BHS IV Summary. BMJ 2004; 328: 634640.

Papilloedema is defined as the swelling of the optic nerve head second
ary to raised intracranial pressure. It is bilateral, although it may be
asymmetrical. As the term papilloedema is reserved for raised intra
cranial pressure all other causes of a swollen optic disc are referred to
as disc swelling.
Patients with papilloedema should be suspected of having an
intracranial mass until proved to the contrary. However, if anatomi
cal variation at the optic nerve exists, papilloedema may not develop
even if the intracranial pressure is raised. Since chronic papilloedema
results in glial scarring of the optic nerve head, patients who have
had a subsequent rise in intracranial pressure need not develop fresh

Causes of raised intracranial pressure

Space-occupying lesion.
Blockage of the ventricular system (by congenital or acquired
Obstruction of cerebrospinal fluid (CSF) absorption (via arachnoid
villi, previously damaged by meningitis).
6 Fundoscopy Made Easy

Subarachnoid haemorrhage or cerebral trauma.

Idiopathic intracranial hypertension.
Diffuse cerebral oedema (possibly from blunt head trauma).
Severe hypertension.
Very rarely by hypersecretion of CSF by a choroidal plexus tumour.

Grossly swollen optic disc with dilated vessels and flame haemorrhage. The normal
cup is totally obliterated and cotton wool spots are present at the peripapillary region
due to interruption of axoplasmic flow in the retinal nerve axons. Although there may
be transient loss of vision, permanent visual deterioration only occurs late with an
enlarged blind spot.

Optic Atrophy
Optic atrophy is a hallmark of damage to the retinal ganglion cells.
Clinically it is seen as pallor of the optic disc. This change usually takes
weeks to develop after the insult has occurred. It is associated with loss
of vision.
Classically, optic atrophy has been classified as primary, secondary
and consecutive:
In primary optic atrophy pallor occurs without prior optic disc
swelling and is seen as a consequence of retrobulbar damage to the
optic nerve up to the lateral geniculate body. The optic disc appears
whiter than usual with well-defined margins.
In secondary optic atrophy, optic disc swelling is seen prior to
pallor. The optic disc margins may appear less defined and the
colour appears dirty white to grey.
Consecutive optic atrophy is a consequence of diffuse retinal disease
and, in addition to the findings as described in secondary optic
atrophy, the retina appears abnormal.


Hereditary autosomal dominant or autosomal recessive optic atrophy.

Leber heriditary optic neuropathy.
Retinal dystrophy including retinitis pigmentosa.
7 Fundoscopy Made Easy

Vascular causes include central retinal artery occlusion which is

often associated with other evidence of vascular disease.
Nutritional causes include vitamin B12 deficiency.
Other causes include tobacco, alcohol and drugs (e.g. ethambutol).
Inflammatory causes include sarcoidosis and polyarteritis nodosa.
In patients with demyelination there is often a history of attacks of
optic neuritis and other neurological symptoms.
Compressive causes include optic nerve glioma, meningioma or
other intracranial tumours.

Primary optic atrophy. The disc appears pale, almost chalky white, with well-defined

Optic Atrophy 7

Secondary optic atrophy. Note the dirty white appearance of the optic disc with
poorly defined margins, thready retinal vessels and diffuse retinal atrophy.

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Glaucoma is a disease which results in progressive optic neuropathy
due to a variety of risk factors. It is classified into open angle, angle
closure and glaucoma due to developmental anomalies. It can be
further divided into primary open or primary angle closure glaucoma
or secondary causes resulting in either.
Three features that are the hallmark of glaucoma are:
1. Raised intraocular pressure (normal range 1021 mmHg),
2. Progressive optic neuropathy represented by an enlargement of the
optic cup, and
3. A corresponding progressive visual field defect as a consequence of
the above.
If untreated, glaucoma results in irreversible blindness.
The only proven effective treatment is reduction of intraocular pres-
sure, initially medically and later, if required, surgically. The definitive
treatment for acute primary angle closure glaucoma following medical
reduction of intraocular pressure is to create a hole in the peripheral iris
(iridotomy) usually by laser, which prevents an angle closure in the
8 Fundoscopy Made Easy

Glaucoma. Note enlargement of the optic cup due to thinning of the neuroretinal rim
caused by loss of retinal nerve fibres.

Retinal Vascular
Retinal artery occlusion

Embolisation is a common cause for retinal arterial obstruction how-

ever it may also be caused by inflammation. The task of the clinician is
to find the cause and in the case of emboli, the source.

Emboli from the heart may be from:
Thrombus originating from the left side of the heart as a
consequence of a mural thrombus secondary to myocardial
infarction or atrial fibrillation.
Calcific emboli from the mitral or aortic valve
Vegetations from valves due to bacterial endocarditis
Cardiac myxoma in rare cases

Internal carotid artery

The bifurcation of the common carotid artery into the external and
internal carotid arteries is vulnerable to atherosclerosis. Emboli from
the carotid artery or the heart may be of the following types:
Cholesterol emboli appear as minute refractile gold into yellow
crystals. They often appear at arteriolar bifurcations and as they
rarely cause significant obstruction are generally asymptomatic.
9 Fundoscopy Made Easy

Fibrin-platelet emboli are dull and plaque like in appearance. They

may be the cause of retinal transient ischaemic attack (TIA
amaurosis fugax) and occasionally complete obstruction. The
patient will complain of painless unilateral loss of vision, often
described as a curtain coming down. The visual loss usually lasts
for a few minutes and spontaneous recovery follows. Frequency
may range from several times a day to one every few months.
Calcific emboli appear as a larger, white, non-refractile, usually single
embolus near the optic nerve. They may cause complete obstruction
of the artery resulting in loss of vision.
Other causes of embolus are from intravenous drug abuse or lipid
embolus due to pancreatitis.
Inflammatory diseases such as Systemic lupus erythematosus, Poly
arteritis nodosa, Wageners granulomatosis, Behcets disease and Giant
cell arteritis can cause retinal arterial obstruction.

Central retinal artery occlusion. Note the multiple retinal artery emboli and ischaemic
retina suggested by diffuse pallor of the posterior pole.

Retinal Vascular Occlusions 9

Branch retinal artery occlusion. Note the occluding plaque in the inferotemporal retinal
artery. The artery beyond appears narrowed with a broken column of blood. The affected
retina appears pale, suggesting ischaemia, whereas the normal colour of the fundus is
preserved in the unaffected retina.

Central retinal artery occlusion with cherry red spot. Note the diffuse retinal ischaemia
represented by the pale retina. The fovea retains its normal red reflex (cherry red spot)
since it has only photoreceptors and is devoid of any overlying inner retinal layers.

9 Fundoscopy Made Easy

Retinal venous occlusion

The retinal artery and vein share a common sheath at the optic nerve
head and at the site of arteriovenous crossing. The retinal artery which
hardens with age tends to compress the vein beside it at the optic nerve
head or at the crossing sites especially if the arteriole crosses over the
vein. Narrowing of the vein eventually leads to the formation of a
thrombus and occlusion. This results in raised capillary pressure and
rupture causing haemorrhages and retinal oedema. Stagnation of blood
results in secondary retinal ischaemia.

Central retinal vein occlusion

This presents clinically as an acute unilateral impairment of vision, the
profoundness depending on the amount of ischaemia.
Features seen are:
Extensive nerve fibre layer and dot and blot haemorrhages
Tortuous, enlarged retinal veins
Optic disc swelling
Cotton wool spots
Macular oedema.
Risk factors including hypertension, diabetes mellitus, hyperviscosity
and glaucoma must be identified and treated if present. If the retina
becomes ischaemic it stimulates the formation of new vessels on the
iris (rubeosis) and subsequent neovascularisation of the angle may lead
to secondary glaucoma. Fluorescein angiography may be useful. Laser
treatment may be used to ablate the ischaemic retina in an attempt to
prevent new vessel formation.

Retinal Vascular Occlusions 9

Central retinal vein occlusion. Note the scattered, flame-shaped, nerve fibre layer and
deeper blot haemorrhages all over the retina with tortuous, dilated retinal veins. The
normal appearance of the macula is lost due to oedema.

Branch retinal vein occlusion

Significant visual loss usually accompanies occlusion of temporal reti-
nal veins which also drain the macula. Haemorrhage occurs along the
area of retina drained by the occluded vein.
Chronic signs include cystoid macular oedema which may be accom-
panied by underlying retinal pigment epithelial atrophy. Veins show
sheathing and arterioles are often narrowed.
Visual recovery depends on the formation of collateral vessels which
re-route the drainage of blood to normalise capillary pressure.
Poor vision results due to chronic macular oedema, macular ischae-
mia and neovascularisation secondary to ischaemia.
Prompt laser photocoagulation to the ischaemic retina is required to
prevent vitreous haemorrhage and neovascular glaucoma.

9 Fundoscopy Made Easy

Branch retinal vein occlusion. The colour image shows a dilated tortuous
superotemporal vein with cotton wool spots and haemorrhages in the affected
retina. Note the site of occlusion is where the artery crosses over the retinal vein
(arrowhead). The fluorescein angiographic image shows the darker ischaemic retina.
The haemorrhage at the macula masks the fluorescence.

Vitreous haemorrhage

Haemorrhage into the vitreous can result in painless loss of vision. The
extent of the visual loss will depend on the degree of haemorrhage.
Small haemorrhages may be asymptomatic or present with floaters
and/or a slight reduction in visual acuity.
Haemorrhage may be due to traction on the fragile new vessels, usu-
ally due to proliferative diabetic retinopathy, a retinal tear avulsing a
retinal blood vessel, traumatic or breakthrough of a subretinal haemor-
rhage into the vitreous.
Urgent referral to an ophthalmologist is important to determine the
cause and manage any complications.
10 Fundoscopy Made Easy

Vitreous haemorrhage. Note the haemorrhage masking the underlying retinal vessels.

Subhyaloid haemorrhage

This haemorrhage settles behind the posterior face of the vitreous gel
but in front of the retina. It usually takes a boat shape with a flat supe-
rior border and a crescent-shaped inferior border. It occludes the retinal
details as it lies in front of it. It usually arises from neovascularisation
secondary to proliferative diabetic retinopathy but may also result from
trauma or rupture of a retinal artery macroaneurysm. It usually takes
much longer to absorb than an intragel vitreous haemorrhage and may
require surgical clearance if it lies in front of the macula.

Fundal Haemorrhages 10

Subhyaloid haemorrhage. Note the haemorrhage masking the underlying features.

It usually takes a boat shape with a straight superior border and a curved inferior
border. Note neovascularisation at optic disc.

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Age-related macular degeneration (ARMD) is the result of a spectrum
of changes that occur at the macula seen in individuals over the age of
50 years. The incidence increases from 3.9% in those aged 4354 years
to 22.8% in those aged 75 years and over (Beaver Dam Eye Study).


Early changes are seen as deposits under the retinal pigment epithe-
lium (RPE) called drusen. These appear as yellow excrescences in the
posterior pole. They may vary in number, size, shape, degree of eleva-
tion and extent of associated changes in the RPE. Drusen are rarely
clinically visible before the age of 45 years but are fairly common
between the ages of 45 and 60 years and almost always thereafter.

Types of ARMD

There are two main types of ARMD: non-exudative and exudative.

11 Fundoscopy Made Easy

Non-exudative ARMD
Non-exudative ARMD is slowly progressive with mild to moderate
impairment of central vision developing over several months or years.
It accounts for 90% of cases.
It usually presents with focal hyperpigmentation of the RPE fol-
lowed by development of the sharply circumscribed circular areas of
RPE atrophy (geographic atrophy) associated with varying degrees of
loss of choriocapillaris. Subsequently, the larger choroidal vessels may
become prominent within the atrophic areas and pre-existing drusen
may disappear.

Hallmarks of dry ARMD. Small hard and larger soft and confluent drusen are seen at
the macula along with hyperpigmentation of RPE.

Age-Related Macular Degeneration 11
One or both eyes may be affected; when bilateral, the lesions are fre-
quently symmetrical. Unfortunately, treatment is not available although
the provision of low vision aids is useful in many patients. AREDS (Age
Related Eye Disease Study) is looking into effects of supplementing
Leutein 10mg, Zeaxanthin 2mg and Omega 3 fatty acids on the risk of
progression of ARMD. Risk factors such as smoking and exposure to
ultraviolet light should be addressed.

Exudative ARMD
Exudative ARMD is much less common and is rapidly progressive. In
some cases vision may be lost within a few days. It may occur in iso-
lation or in association with dry ARMD. Features of exudative ARMD
are detachment of RPE and those secondary to choroidal neovasculari-
sation such as sub-retinal haemorrhage, sub retinal fluid and hard exu-
dates. Treatment with intravitreal injections of anti vascular endothelial
growth factors (Ranibizumab) is advised to stop progression.

Advanced non-exudative ARMD showing geographic atrophy at the macula with

larger choroidal vessels showing through. Note the surrounding calcified drusen.

11 Fundoscopy Made Easy

Exudative ARMD showing hyperpigmentation representing a choroidal neovascular

membrane surrounded by subretinal haemorrhage.

Lipaemia Retinalis
Lipaemia retinalis is a rare disorder characterized by the creamy white
appearance of retinal blood vessels and occurs in patients with severe
hypertriglyceridaemia. High levels of circulating chylomicrons account
for the appearance. Normally this is not associated with visual loss and
the appearance disappears when serum triglyceride returns to normal

Lipaemia retinalis. Note the creamy white appearance of the retinal blood vessels due
to hypertriglyceridaemia.
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Angioid Streaks
Angioid streaks appear as dark red or brown irregular lines radiat-
ing from the optic disc. They represent cracks or dehiscence in Bruchs
membrane which is thickened and calcified. There is a risk of secondary
choroidal neovascularisation developing through these cracks, which
can result in visual loss if it involves the fovea. Neovascularisation can
be treated with anti-vascular endothelial growth factor (anti-VEGF)
agents although the risks of scarring and recurrence are high.
The systemic disease with which this is most commonly associated
is pseudoxanthoma elasticum. An associated fundus finding of peau
dorange is seen as a fine stippled appearance at the interface of the
lighter orange colour at the area of the crack with the darker orange
colour of the normal fundus.
Other systemic conditions associated with angioid streaks are
Pagets disease, sickle cell anaemia and EhlersDanlos syndrome.
EhlersDanlos syndrome is a rare, usually dominantly inherited,
disorder of collagen. Systemic features include thin skin which is
hyperelastic and heals poorly. Joints are hyperextensible. Bleeding
diatheses and dissecting aneurysms may occur. Other lesions include
diaphragmatic hernias, diverticula of the upper gastrointestinal and
respiratory tracts, as well as epicanthic folds, high myopia and retinal
13 Fundoscopy Made Easy

Angloid streaks

Angioid streaks. Note the radiating dark, irregular streaks from the optic disc.

Retinitis pigmentosa is a term used for a group of hereditary disorders
that are characterised by a progressive loss of photoreceptor and retinal
pigment epithelium function. The prevalence is approximately 1:5000.


Approximately 23% are sporadic without any family history.

Approximately 45% are autosomal dominant and have the best
Approximately 20% are autosomal recessive. X-linked recessive is
uncommon and has the worst prognosis.
In 6% of cases there is an uncertain family history.

Clinical signs

Retinitis pigmentosa is associated with bilateral loss of peripheral

vision, caused by predominantly rod dysfunction, followed by progres-
sive loss of cone photoreceptor function. Presentation is usually with
defective dark adaptation (night blindness). By the third decade over
14 Fundoscopy Made Easy

75% of patients are symptomatic. The age of onset, clinical progression,

visual loss and the presence of clinical features are usually related to
the form of inheritance.
Progressive constriction of the peripheral visual field ultimately
leads to tunnel vision which may eventually be lost. Classic clinical fea-
tures are represented by arteriolar narrowing, perivascular bone spicule
pigmentation and a waxy optic disc pallor. Advanced feature suggest-
ing atrophy may present as unmasking of larger choroidal vessels.
Other associations commonly are cataract, open-angle glaucoma,
cystoid macular oedema, keratoconus and myopia. Systemic associa-
tions are Refsum syndrome, Barder-Biedl syndrome, Kearns-Sayre
syndrome and Bassen-Kornzweig syndrome.

Retinitis Pigmentosa 14

Retinitis pigmentosa. Note the dark, perivascular bone spicules. The optic disc
appears pale with thready retinal blood vessels. The upper image shows loss of
the foveal reflex at the macula; the lower image shows advanced changes with
hyperpigmentation, macular atrophy and unmasking of larger choroidal vessels.

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Choroidal Naevus
Choroidal naevi are benign single or occasionally multiple grey or blu-
ish lesions. They are round or oval and are usually less than 5 mm in
diameter. They are usually present at birth and tend to grow until the
end of puberty. If there is any increase in size or pigmentation in adult-
hood, then the possibility of malignant change should be considered.
The benign lesions are asymptomatic, except rarely when a macular
lesion can lead to a serous retinal detachment (see overleaf). Presence
of drusen is a favourable sign to stay benign whereas haemorrhage,
fluid or lipofuscin are not.
15 Fundoscopy Made Easy

Choroidal naevus. Note the bluish-grey area of discoloration with indistinct margins.
The overlying retina appears normal.

Melanocytomas may arise anywhere in the uveal tract. In the anterior
segment acute necrosis of the tumour may cause inflammation, pigment
dispersion and secondary glaucoma. Most frequently melanocytomas
affect the optic nerve head. They typically affect dark-skinned indi-
viduals but may also occur in whites. Detection is usually by chance,
although occasionally a deep-seated tumour causes optic nerve dys-
function as a result of necrosis.

Clinical signs

Melanocytoma presents as a black lesion with feathery edges, most fre-

quently occupying the inferior part of the optic nerve head. Occasionally
the tumour is elevated and occupies the entire disc surface, and a small
proportion develop into melanomas. It is uncertain whether these rep-
resent melanomas in the first place or whether they are initially mel-
anocytomas that undergo malignant transformation.


Treatment is not required except in the very rare event of malignant

16 Fundoscopy Made Easy

Melanocytoma. Note the dark raised lesion bordering the superonasal part of the
optic disc with feathery margins.


Although the term choroiditis signifies inflammation of the choroid,

it often involves the overlying retina resulting in chorioretinitis. The
causes are either infectious or inflammatory.

Infectious causes
Ocular histoplasmosis

Inflammatory causes
Birdshot choroidopathy
Punctate inner choroidopathy
Sympathetic ophthalmia
17 Fundoscopy Made Easy

Clinical signs
Clinically the lesions may be single or multiple, varying from 1 disc
diameter to less in size. Inactive lesions appear as well-delineated,
hypopigmented patches with hyperpigmented clumps and borders.
Active lesions appear poorly delineated, with fuzzy margins and
overlying inflammation; oedema gives a pale white cloudy appear-
ance. In toxoplasmosis an active lesion is usually seen adjacent to an
old inactive one. Inflammatory cells may also be seen in the vitreous,
making the media hazy. If a lesion affects the fovea, it can result in sig-
nificant loss of central vision.

Choroiditis. Well-defined inactive lesions with clear areas showing the sclera
interspersed with dark areas of choroidal pigment.

Ocular Inflammation 17
Cytomegalovirus retinitis

Cytomegalovirus resides in the body, usually as a commensal. However,

in an immunocompromised state (AIDS, severe immunosuppression in
inflammatory disease, aplastic anaemia) it can result in infections of the

Clinical signs
Retinitis is seen typically along the blood vessels and looks like white
cottage cheese (representing a necrotic retina) with ketchup (retinal
haemorrhage). It may be seen at the optic disc or in the peripheral ret-
ina. The vitreous is usually clear due to the individual being unable to

Cytomegalovirus retinitis. Cottage cheese appearance of the superonasal perivascular

retina representing areas of active retinitis. These areas later become atrophic. At this
stage they are prone to developing retinal tears.

17 Fundoscopy Made Easy

host an immunological response. It can spread rapidly and can result

in loss of vision due to involvement of the fovea, vascular occlusion or
secondary retinal detachment.

Treatment is in the form of either systemic administration or intravit-
real injection of ganciclovir.

Roth Spot
Roth spots are retinal haemorrhages with a pale white centre and rarely
involve the macula. Histologically, they consist of platelet and fibrin
thrombus in the centre surrounded by haemorrhage from a ruptured
retinal capillary.
Although initially described in subacute bacterial endocarditis, they
are non-specific and can occur in other conditions such as blood dys-
crasias, diabetic and hypertensive retinopathy, severe anaemia, shaken
baby syndrome and anoxia. They are asymptomatic and usually resolve
when the cause is treated.
18 Fundoscopy Made Easy

Roth spot

Roth spot. Note the pale white centre of this lesion nasal to the optic disc.

Separation of the neurosensory retina from the retinal pigment epithe-
lium is termed retinal detachment (RD). It is classified into three types:
rhegmatogenous, exudative and tractional.

Rhegmatogenous retinal detachment

Rhegmatogenous RD is caused by a retinal tear that allows the vitre-

ous gel to access the subretinal space and detach the retina. Presenting
symptoms are floaters, flashes and visual field defect.
If very small and isolated, argon laser retinopexy could be done to
create a scar around the tear to prevent further progression.
Choices of surgery are either in the form of an external procedure of
cryotherapy to the tear to create a scar and scleral buckle to indent the
globe so as to close the tear and prevent further traction from the vitre-
ous gel, or an intraocular procedure with vitrectomy and laser around
the retinal tear.
19 Fundoscopy Made Easy

Horseshoe retinal tear

Rhegmatogenous retinal detachment. Note the horseshoe retinal tear with surrounding
detached retina. The detached retina appears grey and thrown into folds.

Exudative retinal detachment

Exudative RD is due to the accumulation of serous fluid in the sub-

retinal space without a retinal tear. The retinal pigment epithelial cell
pump is damaged, usually due to inflammation (Harada disease, pos-
terior scleritis). Management is by treating the cause.

Tractional retinal detachment

Tractional RD is due to pre-retinal tractional bands pulling the

neurosensory retina away from the retinal pigment epithelium. The
most common cause is fibrovascular proliferation due to proliferative
diabetic retinopathy or trauma. If the detachment involves the macula,
it can result in loss of vision.

Retinal Detachment 19

Traumatic retinal detachment. Note the large tear nasal to the optic disc involving the
retina and choroid. There are pre-retinal and subretinal haemorrhages. The peripheral
nasal retina is detached, represented by the bluish area.

Tractional retinal detachment. Note the fibrovascular complex elevating the retina
around the optic disc.

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Note: Page numbers followed by f indicate figures; t indicate tables; b indicate boxes.

A Arteriosclerosis, hypertensive
Accommodation, direct retinopathy, 53
ophthalmoscopy, 5 Arteriovenous nipping, hypertensive
Age-related macular degeneration retinopathy, 53, 55f
(ARMD), 7779 Astigmatism, 3
bilateral, 79
drusen, 77, 78, 79f B
dry, 78f, 79 Bacterial endocarditis, 97
exudative, 79, 80f Beaver Dam Eye Study, age-related
non-exudative, 7879, 79f macular degeneration, 77
and RPE, 77, 78, 79 Behavioural therapy, diabetic
types, 7779 retinopathy, 40
see also Macula Binocular indirect ophthalmoscopy,
Albino fundus, 27, 27f 68, 7f
Amaurosis fugax (TIA), 68 Blind spot, optic disc, 23
Anaphylactic shock, sodium Blindness
fluorescein dye injection, 11 glaucoma, untreated, 65
Angioid streaks, 83, 84f night, in retinitis pigmentosa,
Angle closure glaucoma, 65 8586
Anti-vascular endothelial growth Blood pressure, high
factor (anti-VEGF) central retinal vein occlusion, risk
angioid streaks, 83 factor for, 70
laser photocoagulation, 47, 50 control of in diabetic retinopathy,
Aperture beam, macula examination, 40
56 lifestyle measures, 57
Argon laser retinopexy, pharmacological treatment,
rhegmatogenous retinal 57
detachment, 99 seealso Hypertensive retinopathy
ARMD see Age-related macular Branch retinal artery occlusion,
degeneration 69f

Branch retinal vein occlusion, Condensing lens

71, 72f binocular indirect
British Hypertension Society (BHS) ophthalmoscopy, 68
algorithm, 57, 58f slit lamp biomicroscopy, 89
Bruchs membrane, cracks/ Cornea, direct ophthalmoscopy,
dehiscence in, 83 13
Cotton wool spot, 56f
C Cross-sectional imaging, optical
coherence tomography, 18
Calcific emboli, retinal artery
Cryotherapy, rhegmatogenous
occlusion, 68
retinal detachment, 99
Carotid artery disease, retinal artery
Crystalline lens, direct
occlusion, 67
ophthalmoscopy, 12
Cataracts, media opacity
CSMO see Clinically significant
causingblurred fundus
macular oedema (CSMO)
image, 29f
Cystoid macular oedema, 45f, 71
Central retinal artery, anatomy,
Cytomegalovirus retinitis, 9596, 95f
clinical signs, 9596
Central retinal vascular occlusions
treatment, 96
with cherry red spot, 69f
optic atrophy, 62
retinal artery occlusion, D
68f, 69f Demyelination, optic atrophy, 62
retinal vein occlusion, 70, 71f Developmental anomalies,
Cerebrospinal fluid (CSF), glaucoma, 65
obstruction in papilloedema, Diabetes
59 central retinal vein occlusion, risk
Cholesterol control, diabetic factor for, 70
retinopathy, 40 poorly controlled, 31
Cholesterol emboli, retinal artery type 1, 31, 39, 41
occlusion, 68 type 2, 31, 39
Choroidal naevus, 89, 90f see also Diabetic maculopathy;
Choroiditis/chorioretinitis, Diabetic retinopathy
9394, 94f Diabetes Control and
clinical signs, 94 Complications Study (DCCT),
infectious causes, 93 39, 40
inflammatory causes, 93 laser photocoagulation, 47
Chylomicrons, lipaemia Diabetic maculopathy, 4344
retinalis, 81 cystoid macular oedema, 45f
Clinically significant macular diffuse, 44, 44f
oedema (CSMO), laser dyslipidaemia management, 40
photocoagulation, 47, 50 exudative, 43
Concave lens, direct focal, 43, 43f
ophthalmoscopy, 12 ischaemic, 44, 45f


Diabetic retinopathy, 3151 Diverticula, angioid streaks, 83

blood pressure control, 40 Dot or blot haemorrhages
classification, 3141 diabetic maculopathy, 46f
dyslipidaemia, management, 40 non-proliferative diabetic
Early Treatment Diabetic retinopathy, 33, 34f
Retinopathy Study, 32, 32t Drusen, age-related macular
fundus fluorescein angiographic degeneration, 77, 78, 79f
image, 46f Dyslipidaemia, management, 40
general management principles,
3940 E
glycaemic control, 39
Early Treatment Diabetic
grading system used for screening
Retinopathy Study (ETDRS),
(UK National Guidelines),
32, 32t, 40
35, 37t
laser photocoagulation, 47
guidelines for referral for
EhlersDanlos syndrome, angioid
specialist assessment, 39t
streaks, 83
laser photocoagulation, 4751
Embolisation, retinal artery
multifactorial risk reduction, 40
occlusion, 67, 68
non-proliferative (background),
Endothelial cells
31, 33, 47
diabetic retinopathy, 31, 33
pre-proliferative, 31, 3440, 36f
retinal arteries, 23
proliferative, 31, 41, 42f
Epicanthic folds, angioid streaks, 83
laser photocoagulation, 47
EURODIAB Controlled Trial
subhyaloid haemorrhage, 74
of Lisinopril in Insulin-
risk factors, 31
dependent Diabetes
Diabetic Retinopathy Candesartan
(EUCLID) study, 40
Trials (DIRECT trial), 40
Exudates, diabetic retinopathy, 33,
Direct ophthalmoscopy, 6
accommodation, 5
Exudative age-related macular
distant direct, 4
degeneration, 79, 80f
examination, 4f
Exudative diabetic maculopathy, 43
examination of macula, 56
Exudative rhegmatogenous
examination of optic disc, 5
detachment, 100
examination of peripheral fundus, 6
Eye lash artefact, 28f
examination of red reflex, 45
examination of retinal blood
vessels, 5 F
methods, 23 FFA see Fundal fluorescein
myopic person, 12 angiography (FFA)
normal sighted person, 12 Fibrin-platelet emboli, retinal artery
principle, 12 occlusion, 68
pupil dilation, 23 Fibrovascular proliferation, tractional
and retinal oedema, 33 retinal detachment, 100


Flashes, rhegmatogenous RD, 99 macula, 21

Floaters myelinated nerve fibres, 25, 26f
haemorrhage, 73 normal, with variants, 2128, 22f
rhegmatogenous RD, 99 optic disc, 23
Fluorescein angiography see Fundal peripheral, examination, 6
fluorescein angiography retinal arteries, 23
(FFA) retinal veins, 23
Fovea (fixation point) slit lamp biomicroscopy, 89
anatomy, 21 tigroid, 24, 24f
central retinal artery occlusion, 69f
cytomegalovirus retinitis, 9596 G
in diffuse maculopathy, 44
Ganciclovir, 96
macula examination, 56
Ganglion cell axons, optic disc, 23
ocular inflammation, 94
Genetic factors
Foveal avascular zone (FAZ)
optic atrophy, 61
avoiding in macular laser
retinitis pigmentosa, 85
treatment, 50, 50f
Geographic atrophy, age-related
diabetic maculopathy, ischaemic,
macular degeneration, 78
44, 45f, 46f
Glaucoma, 65
retina, 21
central retinal vein occlusion, risk
Foveal reflex, 21
factor for, 70
Foveola, anatomy, 21
direct ophthalmoscopy, 23
Fundal fluorescein angiography
haemorrhage, 73
(FFA), 1114, 12f
neovascular, prevention, 71
diabetic maculopathy, 44, 46f
Glycaemic control, diabetic
diabetic retinopathy, 46f
retinopathy, 39
and laser photocoagulation, 47
Goldmann contact lens, slit lamp
retinal vein occlusion, 70
biomicroscopy, 89
technique, 14
yellow-green fluorescence, 14
Fundal haemorrhage see H
Haemorrhage Haemorrhage, 7374
Fundus dark blot, 35, 36f, 44, 46f
albino, 27, 27f fundal, 7374
artefacts, 28, 28f intraretinal, 33
binocular indirect pre-retinal, 41, 56f
ophthalmoscopy, 68 retinal, 9596, 97
blurred image, cataract, 29f retinal venous occlusion, 70
direct ophthalmoscopy subhyaloid, 74, 75f
methods, 3 vitreous, 3141, 71, 73, 74f
optic disc examination, 5 Harada disease, exudative retinal
fovea, 21 detachment, 100
foveola, 21 Heart, emboli from, 67


Hernias, angioid streaks, 83 Intraretinal microvascular anomalies

Horizontal raphe, retinal arteries, 23 (IRMAs)
Hyperfluorescent spots, ICG diabetic maculopathy, 44, 46f
angiogram, 16f diabetic retinopathy, 35, 36f
Hyperpigmentation, optic disc, 23 Iris, direct ophthalmoscopy, 23
Hypertension see Blood pressure, Iritis, 91
high Ischaemia
Hypertensive retinopathy, 5357 diabetic maculopathy, 44
arteriosclerosis, 53 macular, 71
arteriovenous nipping, 53, 55f and myelination, 25
British Hypertension Society pre-proliferative diabetic
algorithm, 57, 58f retinopathy, 34, 35, 35f, 36f
cotton wool spot, 56f
KeithWagenerBarker K
classification, 54b
KeithWagenerBarker classification,
leakage, 53
hypertensive retinopathy, 54b
management, 57
nerve fibre layer haemorrhage, 56f
vasoconstriction, 53 L
Hypertriglyceridaemia, lipaemia Laser photocoagulation see
retinalis, 81, 81f Photocoagulation, laser
Hyperviscosity, central retinal vein Leakage, hypertensive
occlusion, 70 retinopathy, 53
Lens wheel, ophthalmoscope, 13
I Lipaemia retinalis, 81
Lisinopril, 40
Imaging techniques, 1119
fundal fluorescein angiography,
1114, 12f M
indocyanine green angiography, Macula
15, 16f anatomy, 21
optical coherence tomography, diabetic retinopathy, 31
1819, 19f proliferative, 41
Immunosuppression, examination by direct
cytomegalovirus retinitis, 95 ophthalmoscopy, 56
Indirect ophthalmoscopy, 69, 7f retinal detachment, 100
binocular, 68, 7f subhyaloid haemorrhage lying in
slit lamp biomicroscopy, 89, 9f front of, 74
Indocyanine green (ICG) see also Age-related macular
angiography, 15, 16f degeneration (ARMD)
Intracranial pressure, raised in Macular laser, 5051
papilloedema, 5960 Maculopathy see Diabetic
Intraretinal haemorrhages, 33 maculopathy


Medications Nystagmus, oculocutaneous

diabetic retinopathy, 40 albinism, 27
high blood pressure, 57
Melanin, albino fundus, 27 O
Melanocytes, albino fundus, 27
Ocular albinism, 27
Melanocytoma, 91, 92f
Ocular inflammation, 9396
Melanomas, 91
choroiditis/chorioretinitis, 9394, 94f
Meningioma, optic atrophy, 62
cytomegalovirus retinitis, 9596, 95f
Oculocutaneous albinism, 27
macular laser, 50
non-proliferative diabetic
clinically significant macular, 47
retinopathy, 33, 34f
cystoid macular, 45f, 71
Microvascular leakage, diabetic
macular, 71
retinopathy, 31
retinal, 33
Myelinated nerve fibres, 25, 26f
Open angle glaucoma, 65
Ophthalmoscopy, 19
angioid streaks, 83
direct see Direct ophthalmoscopy
direct ophthalmoscopy, 12
indirect see Indirect ophthalmoscopy
lens wheel, 13
N open eyes recommendation, 5
National Guidelines (UK), diabetic ophthalmoscope, 2f
retinopathy grading system, successful, 23
35, 37t Optic atrophy, 6162
Necrosis, melanocytomas, 91 aetiology, 6162
Neovascularisation classification, 61
angioid streaks, 83 and myelination, 25
branch retinal vein occlusion, 71 primary, 62f
diabetic maculopathy, 46f secondary, 63f
proliferative diabetic retinopathy, Optic cup
41, 42f anatomy of optic disc, 23
regression, 47, 49f enlargement in glaucoma, 66f
subhyaloid haemorrhage, 74 Optic disc
Nerve fibre layer (pre-retinal) anatomy, 23
haemorrhage, 41 angioid streaks, 84f
diabetic maculopathy, 46f examination by direct
hypertensive retinopathy, 56f ophthalmoscopy, 5
Night blindness, 8586 eye lash artefact inferior to, 28f
Non-perfusion, diabetic retinopathy, 31 neovascularisation near, 42f
Non-proliferative diabetic pallor
retinopathy (NPDR), 31, in optic atrophy, 61
33,34f in retinitis pigmentosa, 86
laser photocoagulation, 47 swelling in papilloedema, 60f


Optic nerve pre-proliferative diabetic

glioma, 62 retinopathy, 35
melanocytomas affecting head, 91 retinal vein occlusion, 70, 71
pallor, in retinitis pigmentosa, 86 Photophobia, oculocutaneous
swelling of nerve head in albinism, 27
papilloedema, 59 Photoreceptor function, progressive loss
Optic neuritis, and myelination, 25 in retinitis pigmentosa, 8586
Optical coherence tomography Pigment dispersion,
(OCT), 1819, 19f melanocytomas, 91
cystoid macular oedema, 45f Plano lens, red reflex examination, 4
Ora serrata Plaques, atheromatous, 68, 69f
binocular indirect Polyarteritis nodosa, optic atrophy, 62
ophthalmoscopy, 68 Pre-proliferative diabetic
slit lamp biomicroscopy, 89 retinopathy, 31, 3440, 36f
Pre-retinal haemorrhage, 41, 56f
P Proliferative diabetic retinopathy
(PDR), 31, 41, 42f
Pagets disease, angioid streaks, 83
laser photocoagulation, 47
Panretinal laser treatment, diabetic
subhyaloid haemorrhage, 74
retinopathy, 41, 47, 48f
Pseudoxanthoma elasticum, angioid
Papilloedema, 5960
streaks, 83
pericapillary myelination
Pupil dilation
mistaken for, 25
binocular indirect
Peau dorange, angioid streaks, 83
ophthalmoscopy, 6
Pericapillary myelination, mistaken
direct ophthalmoscopy, 23
for papilloedema, 25
slit lamp biomicroscopy, 8
Pupil plane, red reflex examination, 4
diabetic retinopathy, 31, 33
retinal arteries, 23
Perivenular capillaries R
non-proliferative diabetic RD see Retinal detachment (RD)
retinopathy, 33 Red reflex examination
retinal arteries and veins, 23 binocular indirect
Photocoagulation, laser, 4751, 50f ophthalmoscopy, 68
effects, 47 direct ophthalmoscopy, 45
focal, 47, 51 Refractive error, uncompensated, 5
fresh burns, 48, 48f Renin-angiotensin-aldosterone axis, 40
grid, 47, 50f, 51 Retina
macular laser, 5051 binocular indirect
newer and older types of ophthalmoscopy, 68
treatment, 48, 49f direct ophthalmoscopy
panretinal, diabetic retinopathy, optic disc examination, 5
41, 47, 48f principle, 12


Retina (Continued) Retinal tear

fovea, 21 haemorrhage, 73
foveal avascular zone, 21 rhegmatogenous retinal
fundal fluorescein angiography, 11 detachment, 99
infections, 95 Retinal vascular occlusions, 6771
intraretinal haemorrhages, 33 branch
necrotic, 9596 retinal artery occlusion, 69f
optical coherence tomography, 19f retinal vein occlusion, 71, 72f
pale, in retinal artery occlusion, 69f central
see also Intraretinal microvascular with cherry red spot, 69f
anomalies (IRMAs) optic atrophy, 62
Retinal arteries retinal artery occlusion, 68f, 69f
anatomy, 23 retinal vein occlusion, 70, 71f
occlusions, 67 cholesterol emboli, 68
and retinal venous occlusion, 70 cytomegalovirus retinitis, 9596
Retinal blood vessels, examination, 5 fibrinoplatelet emboli, 68
Retinal detachment (RD), 99100 retinal arteries, 67
angioid streaks, 83 retinal venous, 7071
choroidal naevus, 89 Retinal veins
cytomegalovirus retinitis, 9596 anatomy, 23
exudative, 100 retinal arteries compared, 23
rhegmatogenous, 99, 100f Retinitis pigmentosa, 8586, 87f
secondary, 9596 clinical signs, 8586
tractional, 41, 100, 101f inheritance, 85
traumatic, 101f and optic atrophy, 61
types, 99 prevalence, 85
Retinal dystrophy, 61 Retinopathy
Retinal ganglion cells, damage to in diabetic see Diabetic retinopathy
optic atrophy, 61 hypertensive see Hypertensive
Retinal ischaemia retinopathy
branch retinal artery occlusion, 69f Rhegmatogenous retinal
branch retinal vein occlusion, 71 detachment, 99, 100f
central retinal artery occlusion, 69f Rod dysfunction, in retinitis
diabetic retinopathy, 34, 35, pigmentosa, 8586
35f, 36f Roth spot, 97, 98f
proliferative, 41
secondary, in retinal venous
occlusion, 70 S
Retinal oedema, 33 Sarcoidosis, optic atrophy, 62
Retinal pigment epithelium (RPE) Sclera, optic disc, 23
age-related macular degeneration, Short-sightedness see Myopia
77, 78, 79 Sickle cell anaemia, angioid
tractional retinal detachment, 100 streaks, 83


Slit lamp biomicroscopy, 89, 9f V

Sodium fluorescein dye Vascular changes, pre-proliferative
fundal fluorescein angiography, diabetic retinopathy, 34
11, 14 Vascular endothelial growth factor
indocyanine green dye compared, 15 (VEGF), 41
Spectacles, 3 anti-VEGF treatment, 47, 50, 83
Steno 2 trial, diabetic retinopathy, 40 Vasoconstriction, hypertensive
Subhyaloid haemorrhage, 74, 75f retinopathy, 53
Ventricular system, blockage in
T papilloedema, 59
Tigroid fundus, 24f Visual acuity, reduction in
Tomographic imaging, optical diabetic maculopathy, 44
coherence tomography, 18 diabetic retinopathy, 33
Toxoplasmosis, 94 oculocutaneous albinism, 27
Tractional retinal detachment, 41, vitreous haemorrhage, 73
100, 101f Visual field defect,
Transient ischaemic attack (TIA), rhegmatogenous RD, 99
fibrinoplatelet emboli, 68 Visual loss
Traumatic retinal detachment, 101f cytomegalovirus retinitis, 9596
Triamcinolone acetonide, 50 haemorrhage, 73
Tropicamide 1%, direct ocular inflammation, 94
ophthalmoscopy, 23 peripheral, bilateral loss in retinitis
Tumours pigmentosa, 8586
melanocytomas, 91 retinal detachment, 100
optic atrophy, 62 retinal vascular occlusions,
papilloedema, 59 68, 71
Type 1 diabetes, 31, 39, 41 Vitamin B12 deficiency, optic atrophy,
Type 2 diabetes, 31, 39 62
Tyrosinase-positive patients, albino Vitrectomy, rhegmatogenous retinal
fundus, 27 detachment, 99
Vitreous haemorrhage, 3141,
U 74f
prevention, 71
United Kingdom Prospective Diabetes
Volk (non-contact) condensing lens
Study (UKPDS), 39, 40
slit lamp biomicroscopy, 8
Uveal tract, melanocytomas, 91