Mini Atlas Series - Fundus Fluorescein Angiography

Jaypee Gold Standard Mini Atlas Series®
FUNDUS FLUORESCEIN
ANGIOGRAPHY
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FUNDUS FLUORESCEIN
ANGIOGRAPHY
Editors
Ashok Garg MS PhD FIAO(Bel) FRSM FAIMS ADM FICA
International and National Gold Medalist
Chairman and Medical Director
Garg Eye Institute and Research Center
235-Model Town, Dabra Chowk, Hisar-125005, India
José Maria Ruiz Moreno MD PhD T Mark Johnson MD FRCS

Professor of Ophthalmology Consultant, Vitreoretinal Surgeon
Albacete Medical School National Retina Institute, Suite 101
University of Castilla La Mancha 5530 Wisconsin Ave
Avendia de Almansa, 14 Chevy Chase 20815
02006, ALBACETE, Spain USA
Arturo Perez Arteaga MD PhD João J Nassaralla Jr MD FRCS

Medical Director Associate Professor of Ophthalmology
Centro Oftalmologico Tlelnepantla University of Brasilia, DF
Dr. Perez – Arteaga Vallarta No. 42 Consultant Ophthalmic Surgeon
Tlelnepantla, Centro, Estado de Mexico Department of Retina and
54000, Mexico Vitreous Goiania Eye Institute
Goiania GO, Brazil
Foreword
Fernando Oréfice
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

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Jaypee Gold Standard Mini Atlas Series®: Fundus Fluorescein Angiography
© 2010, Jaypee Brothers Medical Publishers
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Dedicated to
• My respected Param Pujya Guru Sant Gurmeet Ram Rahim
Singh Ji for his blessings and motivation.
• My respected parents, teachers, my wife Dr Aruna Garg,
son Abhishek and daughter Anshul for their constant
support and patience during all these days of hard work.
• My dear friend Dr Amar Agarwal, a renowned International
Ophthalmologist for his constant support, guidance and
expertise.
Ashok Garg
My family (Magali, my wife and Jorge, Guillermo and Magali,

my children) for the time, comprehension and patience that
they have had with me during all these years of hard work.
José Maria Ruiz Moreno
My wife Joanne and my son Connor for providing me with their

love, wisdom and support throughout the years.
T Mark Johnson
I dedicate my work to all the people in the world with

ophthalmic diseases, with the best wishes that we can improve
with this kind of material, our quality of care. I also dedicate
this opus to Prof Ashok Garg, because he has trusted in my
work many times.
Arturo Perez Arteaga
My wife Belquiz and our children, João Neto, Arthur and Anna
Paula, for providing me with their love, wisdom and support
throughout the years.
João J Nassaralla Jr
Contributors
Ashok Garg MS PhD FRSM CK Minija DO DNB

Chairman and Medical Shankara Eye Care
Director Institutions
Garg Eye Institute and Bangalore, India
Research Center
235-Model Town Dinesh Garg MD
Dabra Chowk Professor
Hisar-125005, India Department of
Ophthalmology
Arturo Perez Arteaga MD Dayanand Medical College
Ophthalmologist and Hospital
Anterior Segment Surgeon Ludhiana-141001, India
Medical Director and
Founder Javier A Montero MD PhD
Centro Oftalmologico Pio del Rio Hortega
Tlalnepantla, Mexico University Hospital
Vallarta No. 42, Tlalnepantla Valladolid, VISSUM
Centro, Mexico, 54000 Vitreoretinal Unit
Alicante, Spain
Belquiz A Nassaralla MD
Consultant Ophthalmic João J Nassaralla Jr MD
Surgeon Consultant Ophthalmic
Department of Cataract and Surgeon
Refractive Surgery Department of Retina
Goiania Eye Institute Goiania Eye Institute
Goiania, GO, Brazil Goiania, GO, Brazil
viii Fundus Fluorescein Angiography
José Maria Ruiz Moreno MD Pedro Amat-Peral MD

Professor Vitreoretinal Unit
Department of Alicante Institute of
Ophthalmology Ophthalmology
Albacete Medical School VISSUM, Alicante, Spain
Castilla La Macha University
Avendia de Almansa Rajesh MS
14, 02006, Albacete, Spain Shankara Eye Care
Institutions
Juan Jose Luis Parra Bangalore, India
Limon MD
Seema Gupta MD
Ophthalmologist
Assistant Professor
Posterior Segment Surgeon
Department of Anatomy
Retinal Consultant of Centro
Dayanand Medical College
Oftalmologico Tlalnepantla
and Hospital
Mexico, Vallarta No. 42
Ludhiana-141001, India
Tlalnepantla, Centro
Mexico, 54000
T Mark Johnson MD FRCSC
Consultant Vitreoretinal
Madhu Kumar R MS FICO FVR Surgeon
Shankara Eye Care National Retina Institute
Institutions Ste 101-5530 Wisconsin
Bangalore, India Ave Chevy Chase
MD 20815,USA
Mahesh P Shanmugam
DO FRCS PhD Yuri Axayacati Flores
Head Fuentes MD
VR and Oncology Services Consultant Vitreoretinal
Shankara Eye Care Surgeon
Institutions National Medical Center
Bangalore, India Century XXI, Mexico
Foreword
It gives me immense pleasure to write this

foreword for this Jaypee Gold Standard
Mini Atlas Series: Fundus Fluorescein
Angiography.
During the fourty-nine years of the
existence, the fundus fluorescein
angiography has become an indispens-
able toll in the clinical and experimental ophthalmology.
It is impossible to imagine ophthalmology today without
images, so ubiquitously and thoroughly do they dominate
the field. A rapid explosion of retinal angiography
techniques occurred in the late 1960s and early 1970s, and
during this time, digital retinography brought
revolutionary changes in retinal study. The improved
resolution power and the digitalization now enable the
documentation of individual retinal capillaries and
entitles the method to the denomination of microangio-
graphy of the ocular fundus.
Medicine has become far more complicated today.
Doctors are expected to perform at very high levels of skill
and consistency, in order to meet increasing patient
expectations, and to stand up to scrutiny amongst their
colleagues. An objective of the present volume is to offer
x Fundus Fluorescein Angiography
a guide for the interpretation of basic fluorescein findings.

Instead of listing itemized accounts of capillary
microaneurysms vs drusen or of differentiation of
background fluorescence from retinal one, we have
attempted to let the findings speak for themselves, as
recognition of typical, unequivocal instances is frequently
the best guide according to which interpretation in
ambiguous circumstances can be effected.
This text is an excellent compilation of lucid color
figures, an important contribution to contemporary
ophthalmic education.
I congratulate the authors and the editors on this
accomplishment.
Fernando Oréfice MD PhD

Head
Professor of Federal University de Minas Gerais
Brazil
Head of Department of Uveitis of
Centro Brasileiro de Ciências Visuais -
Belo Horizonte – MG - Brazil
Former President of Pan-American Society of
Intraocular Inflammatory Diseases
Address: Rua Esprito Santo 1634/102
Bairro de Lourdes
Belo Horizonte – MG – Brazil
Zip code: 30160-031
Tel: 55-31-3274—4001
Preface
Fundus Fluorescein Angiography (FFA) is an invasive

diagnostic test used commonly in posterior segment
diseases to aid in diagnosis of retinal conditions and to
identify fundal lesions. Sometimes FFA is also used in
anterior segment to investigate anterior vasculature.
There are very few quality Mini Atlas books on this
subject to be used by ophthalmologists as Ready Reckoner
in a concise and pocket format. Present book has been
designed to provide complete text and pictorial details
of FFA in various pathologies in a comprehensive manner.
Fifteen chapters of this Mini Atlas covers FFA procedure
and interpretations in all major posterior segment
diseases by leading International experts of this field.
Hats off to our publishers M/s Jaypee Brothers Medical
Publishers Pvt Ltd, specially Shri Jitendar P Vij (Chairman
and Managing Director), Mr Tarun Duneja (Director-
Publishing) and all staff members for publishing this
comprehensive Atlas in a short time.
We hope this Mini Atlas shall serve as quick look ready
reference companion to ophthalmologists worldwide.
Editors
Contents
1. Evolution of Fluorescein Angiography: 1

An Overview
Ashok Garg (India)
2. Investigation in Posterior Segment Diseases: 5
Fundus Fluorescein Angiography
CK Minija, Madhu Kumar,
Mahesh Shanmugam (India)
3. Diabetic Retinopathy 49
João J Nassaralla Jr, Belquiz A Nassaralla (Brazil)
4. FFA in Retinal Detachments 75
Arturo Perez Arteaga, Juan Jose Luis Parra Limon,
Yuri Axayacati Flores Fuentes (Mexico)
5. Fluorescein Angiography and Indocyanine 89
Green Angiography in Age-related
Macular Degeneration
T Mark Johnson (USA)
6. Fluorescein Angiography in 127
Retinal Vein Occlusion
Pedro Amat-Peral, Javier A Montero,
José Maria Ruiz Moreno (Spain)
7. Fluorescein Angiography in 143
Vitreous Diseases
Arturo Perez Arteaga,
Juan Jose Luis Parra Limon (Mexico)
xiv Fundus Fluorescein Angiography
8. Macular Diseases 151

Mahesh Shanmugam, CK Minija,
Madhu Kumar, Rajesh (India)
9. Choroidal Neovascularization in 165
High Myopia
José Maria Ruiz Moreno, Javier A Montero (Spain)
10. Fundus Fluorescein Angiography in 179
Posterior Uveitis
Dinesh Garg, Seema Gupta (India)
11. Drusen 211
João J Nassaralla Jr, Belquiz A Nassaralla (Brazil)
12. Central Serous Chorioretinopathy 229
Mahesh Shanmugam, CK Minija
13. Angiographic Diagnosis of Circumscribed 235
Choroidal Hemangioma
Javier A Montero, José Maria Ruiz Moreno (Spain)
14. Posterior Scleritis 251
15. Subhyaloid Hemorrhage 263
Index 267
Evolution of
Fluorescein
Angiography:
An Overview
1
Ashok Garg (India)

2 Fundus Fluorescein Angiography
Fluorescein Angiography is an important invasive

Diagnostic tool for posterior segment eye surgeons for the
evaluation of the retina and choroid.
A significant aspect in the retinal and choroidal study
is a good visualization of it that allows us in correct
interpretation of various pathologies for better medical,
surgical and laser management of the diseases of the
retina, choroid and optic nerve.
Fluorescein angiography with sodium fluorescein dye
is an indispensable diagnostic procedure of great clinical
significance. The specific physiochemical and the
absorption emission characteristics of sodium fluorescein
dye determines the features of fluorescein angiography.
Chemically, it is xanthene derivative with a molecular
weight of 376.27 which is large enough to prevent its
passage across the tight barriers and at the same time is
appropriate in allowing it to diffuse rapidly through fluid
departments. Sodium fluorescein dye has unique features
of ability to fluoresce (in visible spectrum), high solubility,
greater binding to plasma proteins and erythrocytes
enable it to be used in fluorescein angiography to evaluate
the functional integrity of the outer and inner blood
retinal barriers.
HISTORY OF EVOLUTION
Evaluation of fluorescein angiography has an unique and
interesting aspect. In terminal part of 1950, a medical
Evolution of Fluorescein Angiography: An Overview 3
student Harold Novotny and Dr David Alvis working
with Dr John Hickman (Head of Department of Internal
Medicine of Indiana University) determined the oxygen
saturation into the retinal arterioles for the first time.
Novotny struck with an idea of passing some kind of
the dye through the circulating system to determine the
oxygen saturation levels. He used sodium fluorescein for
fluoroscence observation. Meanwhile Dr David Alvis
used a mixed drop of its own blood with sodium fluore-
scein for fluorometric analysis. World’s first fluorescein
angiography was done on Dr David Alvis’s right eye.
Novotny and Alvis sent their research work to
American journal of ophthalmology in 1960 but the
journal rejected it as lack of originality of work.
Miller and Chao, collaborators of Dr Maumenae also
presented similar work. They presented their technique
of fluorescein imaging in the association for the
investigation in ophthalmology in April 1960. The first
description of the fluorescein angiography technique
appeared in the magazine officially in July 1961. In Spain
also first article on fluorescein angiography (FA) was
presented by Dr F Palomar Petit et al in 1969. It was
published in archives of American ophthalmogical society.
This landmark work by Novotny and Dr David Alvis
led to evolution of fluorescein angiography by several
other related clinically works in USA and Europe over the
time for the better refinement of FA technique alongwith
development of more sophisticated equipments used in
their technique for accurate and better assessment of

various ocular pathologies.
In the present era of greater ophthalmological
advances specially in last one decade, in the field of
diagnosis, surgical and laser management, fluorescein
angiography is an important diagnostic tool. Recent
advances in FA specially CUE wide field fluorescein
angiography, digital video angiography, high speed
fluorescein angiography and 3D color Doppler video
angiography have revolutionized the detection of
pathologies of retina and choroid tremendously.
In this introductory chapter, I shall not go into various
details of FA technique, procedures, indications, contra-
indications and adverse effects as they have been nicely
covered by International Masters of this field in the
following chapters.
In this Mini Atlas, fluorescein angiography techniques
have been shown in various posterior segment ocular
pathologies specially in diabetic retinopathy, age related
macular degeneration, retinal vascular occlusions,
vitreous diseases, macular diseases. Inflammatory
conditions and hemangiomas with short text and a large
number of clinical and investigative figures to serve as
Ready Reckoner for both anterior and posterior segment
ophthalmologists.
Investigation in
Posterior
Segment
Diseases:
2 Fundus
Fluorescein
Angiography
CK Minija, Madhu Kumar

Mahesh Shanmugam (India)
INTRODUCTION
Fundus fluorescein angiography involves photographic
imaging of the fundus to visualize the passage of
fluorescein through the retinal and choroidal circulation
following intravenous injection. Fluorescein angiography
is an invaluable tool in evaluation of retinal and choroidal
disorders.
CHEMICAL PROPERTIES OF FLUORESCEIN

Fluorescein is an orange brown crystalline substance with
a molecular weight of 376.27. It belongs to the group of
triphenylmethane dyes. Fluorescein is a product of a
reaction of phthalic acid anhydride and resorcinol in
which hot sulphuric acid is the catalyst. Chemical formula
of fluorescein is C20H10O5Na2.
PRINCIPLE
Fluorescein dye absorbs light energy from a lower wave
length and emits at a higher wave length with fluore-
scence properties.
The absorption spectrum of fluorescein lies between
465 and 490 nm (blue end of the visible spectrum). The
emission spectrum lies between 520 and 530 nm (green-
yellow area of the spectrum).
Fluorescein (500 mg) can be injected as 10 ml of 5%
solution, 5 ml of 10% solution or 3 ml of 25% solution
Investigation in Posterior Segment Diseases 7
(750 mg). On intravenous injection, 70-85% of fluorescein
molecules bind to serum proteins, the remaining unbound
component is responsible for fluorescence displayed
during angiography. The dye is excreted completely by
the kidneys in 24 hours.
FUNDUS CAMERA
A fundus camera consists of an optical system capable of
visualizing the fundus and an illumination system with
a flash strobe that allows photography of the fundus.
Various parts of the fundus camera are defined in
Figures 2.1 to 2.3.
Fig. 2.1
Fig. 2.2
Figs 2.1 to 2.3: Various parts of fundus camera

Filters of two types are used to ensure that blue light
enters the eye and only yellow green light enters the
camera to be captured on film or optical media. The blue
filter (exciter filter) allows passage of blue excitation light
(465-495 nm). Fluorescein absorbs the blue light and
fluoresces emitting green yellow light at 520- 530 nm. The
barrier filter built in within the camera allows only the
green-yellow fluorescent light to be reflected back into the
camera, which is captured on film or electronic media.
This filter system allows performing fluorescein
angiography.
CONTRAINDICATIONS FOR
FLUORESCEIN ANGIOGRAPHY
Known drug allergy to the dye, iodine, shell fish,
advanced renal failure and pregnancy.
TECHNIQUE
A good quality angiogram requires adequate pupillary
dilatation and clear media.
Patient is explained about the procedure and an
informed consent is taken.
Patient is seated in front of the camera comfortably
and the sequence is as follows:
• Color photograph of the fundus and red-free
photograph
• Securing an intravenous line
• Fundus photograph with the exciter and barrier filters

in place to look for auto or pseudo fluorescence
• Injection of fluorescein and switching on the timer
• Photographs are taken 8 seconds after the beginning
of the injection
• Photographs at intervals of 11/2 to 2seconds
• Late phase photographs at the end of 15 minutes.
SIDE EFFECTS AND COMPLICATIONS OF

• Extravasations of the dye and local tissue necrosis
• Nausea
• Vomiting
• Vasovagal attack (circulatory shock, myocardial
infarction)
• Allergic reaction
– Anaphylaxis
– Itching
– Hives
– Laryngeal edema
– Bronchospasm
NORMAL FLUORESCEIN ANGIOGRAM

Normal arm to retina time is 10 to 12 seconds. Fluorescein
enters the eye through the ophthalmic artery, passing into
the choroidal circulation through the short posterior
ciliary arteries and into the retinal circulation through the
central retinal artery. The inner blood retinal barrier is
formed by the tight junctions of the endothelium in the
retinal vessels and the outer blood retinal barrier by the
retinal pigment epithelium; these barriers keep the
fluorescein from diffusing in to the vitreous cavity or
subretinal space. The pigmented retinal pigment epi-
thelium masks the choroidal fluorescence during
fluorescein angiography.
Phases of the Angiogram

The Choroidal (Pre-arterial) Phase
One to two seconds before the dye appears in the central
retinal artery. Patchy filling of the choroid is obscured
almost immediately as the dye diffuse out of the chorio-
capillaries resulting in the choroidal flush (Fig. 2.4). A
cilioretinal artery, if present will fill at this time because
it is derived from the posterior ciliary circulation.
The Arterial Phase

Entry of the dye into the retinal arterioles (Fig. 2.5).
The Arteriovenous (Capillary) Phase

Dye enters the venules after passing through the retinal
capillaries. Early arteriovenous phase shows laminar flow
in the veins (Figs 2.6 to 2.8). In the late arteriovenous
phase, the veins are filled with the dye.
Fig. 2.4: Choroidal phase
Fig. 2.5: Arterial phase of FFA showing filling of the arterioles

Fig 2.6: Early arteriovenous phase of the

FFA showing laminar flow in the veins
Fig. 2.7: Arteriovenous phase showing more

pronounced laminar flow in the veins
The Venous Phase

Venous phase of the angiogram shows loss of laminar
flow and complete filling of the veins. In the late venous
phase the veins appear brighter than the arterioles as the
concentration of the dye is more in the venules than the
arterioles (Fig. 2.8).
The Late Phase

Due to elimination of the dye on recirculation, fluo-
rescence within the retinal vessels is faint; disc staining
Fig. 2.8: Venous phase shows loss of laminar

flow and venules appear brighter than arterioles
Fig. 2.9: Late phase FFA shows minimal dye

in the retinal vessels and disc staining
may appear (Fig. 2.9). Scleral staining appears as a diffuse

background fluorescence.
Absence of blood vessels in the foveal avascular zone
and increased density of xanthophyl at the fovea and taller
retinal pigment epithelial cells at the fovea block the
choroidal fluorescence resulting in a dark fovea on FA
(Fig. 2.10).
ABNORMAL ANGIOGRAM
Abnormalities in the angiogram are classified essentially
as
• Hypofluorescence
• Hyperfluorescence
Fig. 2.10: Fundus fluorescein angiography of right

eye showing normal foveal avascular zone
HYPOFLUORESCENCE
Reduction or absence of normal fluorescence. This is
caused by
• Blocked fluorescence
• Hypoperfusion/vascular filling defect.
Blocked Fluorescence
Blood, pigment, exudates can block underlying fluo-
rescence. Area of blocked fluorescence corresponds to the
area of the lesion (Figs 2.11A and B).
Fig. 2.11A: Fundus photograph of left eye shows

preretinal hemorrhage (arrow) nasal to disc
Fig. 2.11B: Corresponding FFA shows blood blocking

(arrow) underlying retinal and choroidal fluorescence
Fig. 2.12: Hypofluorescence due to

loss of capillary bed (arrow)
Hypoperfusion/Vascular Filling Defect

Hypofluorescence due to non filling of the vasculature
due to vascular occlusion or loss of vascular bed
(Fig. 2.12).
HYPERFLUORESCENCE
• Pre-injection fluorescence—auto/pseudofluorescence
– Autofluorescence—fluorescent characteristic of an
abnormal fundus lesion
 Astrocytoma, optic nerve head drusen
– Pseudofluorescence—mismatched filters
Fig. 2.13: Early venous phase shows hyperfluorescent spots

temporal to macula (arrow) fading away in late phase suggestive
of retinal pigment epithelial window defect
• Transmitted fluorescence
– Due to transmission of the choroidal fluorescence
due to loss of RPE barrier (Fig. 2.13)
• Leakage
– Leakage of the dye in the vitreous (Fig. 2.15) or
subretinal space due to loss of blood retinal barrier
• Pooling
– Accumulation of the dye within a space (Fig. 2.14)
Fig. 2.14: Hyperfluorescence due to leakage: Fundus fluorescein

angiogram in idiopathic central serous retinopathy showing
leakage of the dye in to the subretinal space (arrow). The hyper-
fluorescent spot increases in intensity, size with fuzzy borders
Fig. 2.15: Hyperfluorescence due to leakage: Fundus fluorescein

angiogram showing increasing hyperfluorescence, size and fuzzy
margins indicative of leakage in to the vitreous from retinal
neovascularization
Fig. 2.16: Hyperfluorescence due to staining: late phase

angiogram showing staining of the disciform scar.
Hyperfluorescence occurs late and is confined to the area of the
scar as indicated by sharp lesion borders.
• Staining
– Accumulation of the dye into a tissue (Figs 2.16 and
2.17).
Window Defect
The well-defined subretinal hyperfluorescent spot
appears in choroidal phase, increasing in intensity with
pro-gression of the angiogram and fades in the late phase
with emptying of the choroidal vessels (Fig. 2.13). Size of
the lesion remains same and there are no fuzzy margins.
Fig. 2.17: Hyperfluorescence due to staining: Color fundus

photograph of right eye showing sclera in a high myope. Normal
scleral staining in the late phase is unmasked in this patient with
RPE atrophy due to myopia. Note borders of hyperfluorescence
corresponds to the area of RPE atrophy seen on fundus photo
FLUORESCEIN ANGIOGRAPHY IN
VARIOUS FUNDUS DISEASES
The fluorescein angiography in various fundus diseases
are shown in Figures 2.18 to 2.42.
• Inflammatory diseases
• Macular diseases—Dry ARMD
• Macular diseases—Mixed CNVM
• Macular disease—Myopic choroidal neovascular
membrane
• Macular diseases—Choroidal neovascularization
• Macular diseases—Cystoid macular edema
• Macular diseases—Idiopathic central serous
chorioretinopathy
Figs 2.18A to D: Inflammatory diseases (A) Color fundus

photograph of the right eye in a young patient shows hyperemic
disc, multiple subretinal placoid lesions involving the retinal
pigment epithelium (RPE) of the posterior pole with overlying
neurosensory retinal detachment. (B and C) Early and late
arteriovenous phase fundus fluorescein angiogram (FFA) shows
early hypofluorescence due to choroidal hypo-perfusion with late
hyperfluorescence typical of inflammatory choroidal lesions. (D)
Late phase FFA shows increasing hyper-fluorescence at the disc
due to leakage of the dye and pooling of the dye within areas of
neurosensory detachment as indicated by hyperfluorescence with
defined margins.
This is the FFA appearance of a patient with acute posterior
multifocal pigment epitheliopathy (APMPPE).
Figs 2.19A to D: Macular diseases—Dry ARMD (A) Color fundus

photograph of the right eye in this elderly patient shows a well
defined patch of retinal pigment epithelial atrophy at the macula
(arrow) and small to medium and some calcified drusen around
the geographic atrophy. (B) Early arteriovenous phase of
angiogram shows early hyperfluorescence along the borders of
the geographic atrophy. Variable fluorescence behavior of the
drusen can be seen—some exhibiting hyperfluorescence and
others blocked fluorescence. (C) Venous phase shows increased
intensity of hyperfluorescence at the geographic atrophy patch
but with well defined margins indicating this as transmitted choroidal
hyperfluorescence due to RPE atrophy (arrow). Some of the drusen
show more intense hyperfluorescence indicating slow filling, the
others transmitted fluorescence. (D) Late phase shows fading of
the fluorescence at the geographic atrophy patch and most
drusen area confirming this to be transmitted fluorescence. Some
drusen appear relatively hyperfluorescent due to staining.
This appearance is typical of a patient with dry age-related
macular degeneration and geographic atrophy.
Figs 2.20A to D: Macular disease—Mixed CNVM (A) Color

fundus photograph of right eye shows a grey subfoveal
membrane with subretinal fluid and specks of subretinal
hemorrhage. (B) Early arteriovenous phase of fluorescein
angiogram shows well demarcated early lacy subfoveal hyper–
fluorescence (arrow) suggestive of classic CNVM (C) Venous
phase of angiogram shows increased hyper fluorescence with
fuzzy margins at the classic CNVM. Note area of ill-defined
hyperfluorescence superotemporal to the classic CNVM(arrow).
(D) Late phase shows leakage from classic CNVM. Increased
area, intensity and fuzzy ill-defined leakage seen at the
superotemporal lesion, suggestive of occult component of CNVM.
The findings are suggestive of choroidal neovascular
membrane with predominantly classic component.
Figs 2.21A to D: Macular disease—Myopic choroidal neo-

vascular membrane (A) Color fundus photograph of left eye
shows myopic disc, peripapillary choroidal atrophy, tessellated
fundus and a grey, subfoveal choroidal neovascular membrane
with subretinal hemorrhage at the nasal border (arrow).
(B) Arteriovenous phase of angiogram shows lacy
hyperfluorescence in the membrane and blocked fluorescence
due to subretinal hemorrhage (C) Venous phase of angiogram
shows increased intensity and area of hyperfluorescence with
fuzzy borders indicating leakage (arrow). (D) Late phase of the
angiogram indicative of leakage.
The findings are suggestive myopic choroidal neovascular
membrane.
Figs 2.22A to D: Macular diseases—Choroidal neovascularization

(A) Color fundus photograph of the left eye in a young boy showing
a greyish subretinal membrane involving the peripapillary region
and extending beneath the inferotemporal arcade. Note subretinal
hemorrhage along the inferior borders of the lesion (arrow).
(B) Early arteriovenous phase shows hypofluorescence
corresponding to the subretinal hemorrhage (blocked fluore-
scence). A patch of pin point hyperfluorescence is seen superior
to the lesion. (C) Mid venous phase shows fuzzy hyperfluorescence
along the inferior part of the lesion indicative of active leakage. Sub
papillomacular component of the lesion has a well defined edge
with minimal fuzziness of the borders indicating predominant staining
of the lesion. The patch of pin-point hyperfluorescence appears
more hyperintense. (D) Late venous phase of the angiogram
increase in size and fuzziness of the borders of the hyperfluore-
scent lesion suggestive of leakage (predominantly along the inferior
arcade). Note fading of the patch of pin-point hyperfluorescence—
this is a characteristic of RPE defects (window-defects).
Figs 2.23A to D: Macular diseases—Cystoid macular edema

(A) Color fundus photograph of the left eye in this elderly diabetic
shows retinal hemorrhages, soft exudates (arrow), few hard
exudates (black arrow) and cystoid macula. (B) Early
arteriovenous phase FFA shows multiple hyperfluorescent spots
at the macula and blocked choroidal fluorescence due to retinal
hemorrhages. (C and D) Late venous phase of angiogram shows
increased intensity and area of hyper fluorescence of the spots
with fuzzy margins indicative of leakage from the micro
aneurysms. There is pooling of the dye in the cystoid spaces
around the fovea in a petalloid pattern suggestive of cystoid
macular edema in a patient with moderate nonproliferative
diabetic retinopathy.
Figs 2.24A to D: Macular diseases—Idiopathic central serous

chorioretinopathy (A) Color fundus photograph of the right eye
in a young male showing a well-defined pool of neurosensory
macular detachment (arrow). (B) Early arteriovenous phase of
FFA shows intense hyperfluorescent spot nasal to fovea (C and
D) The spot of hyperfluorescence increases in intensity and
extends superiorly in the form of a smoke stack. Late phase shows
the dye to pool beneath the retina after assuming a mushroom
cloud like appearance (arrow).
This appearance is typical of smoke-stack leak of idiopathic
central serous chorioretinopathy.

chorioretinopathy (A) Color fundus photograph of the right in
young male shows well defined ring-reflex around the fovea
suggestive of neurosensory foveal detachment (arrow).
(B) Arteriovenous phase of fluorescein angiogram pinpoint hyper-
fluorescent spot beneath the fovea (C) Venous phase of the
angiogram shows increased intensity and size of the
hyperfluorescence with fuzzy borders indicative of leakage
(arrow). (D) Late phase FFA shows increase in area of hyper-
fluorescence in an inkblot pattern.
This appearance is typical of ink-blot leak of idiopathic central
serous chorioretinopathy
• Macular diseases—Idiopathic central serous

chorioretinopathy
• Macular disease—Epiretinal membrane
Figs 2.26A to D: Macular disease—Epiretinal membrane

(A) Color fundus photograph of the right eye in an elderly patient
showing grayish reflex over the macula with increased tortuosity
of the underlying retinal vessels. Straightening of the vessels
nasal to the membrane is also seen. (B) Early arteriovenous
phase of the fluorescein angiogram showing increased tortuosity
(arrow) of the perifoveal vasculature with straightened vessels
over the papillomacular bundle. (C and D) Late arteriovenous
and recirculation phase pictures showing diffuse hyperfluore-
scence in the perifoveal region suggestive of perifoveal
intraretinal leak.
The findings are suggestive of epimacular membrane on the
underlying blood vessels.
Figs 2.27A to E: Macular disease—Bull’s eye maculopathy (A

and B) Color fundus photograph of both eyes shows pigmentation
at the fovea surrounded by well defined area of RPE atrophy
(arrow) (B and C) Mid venous phase of angiogram shows area
of hypofluorescence at the center surrounded by a circumscribed
area of hyperfluorescence, in turn surrounded by a ring of
hypofluorescence. (D and E) Late phase images show fading of
hyperfluorescence indicating the hyperfluorescent lesions to be
transmission defects (arrow).
The findings are suggestive of Bull's eye maculopathy
Figs 2.28A to D: Macular disease—Angioid streaks (A and B)

Color fundus photograph of left eye shows pigmented, irregular,
subretinal radiating streaks arising from the peripapillary region
suggestive of angioid streaks (arrow). (C and D) Late venous
phase of fluorescein angiogram shows hyperfluorescence within
the streaks that fades in the late phase suggestive of window
defects (arrow). The pigmented borders of the streaks block the
underlying choroidal fluorescence resulting in hypofluorescence.
This is the typical angiographic appearance of angioid streaks.
• Macular disease—Bull’s eye maculopathy

• Macular disease—Angioid streaks
• Vascular occlusion—Central retinal vein occlusion
• Vascular occlusion—Central retinal vein occlusion
• Vascular occlusion—Branch retinal vein occlusion
Figs 2.29A to I: Vascular occlusion—Central retinal vein

occlusion (A) Color fundus photograph of the left eye in a middle
aged lady shows disc edema, dilated tortuous central retinal vein,
superficial and deep intraretinal hemorrhages all quadrants. (B
to E) Blocked retinal and choroidal fluorescence due to retinal
hemorrhages in all quadrants with dilatation and tortuosity of the
retinal veins. Peripheral venular tree shows staining of the venous
walls. (F) Late phase FFA shows minimal staining of the disc
and minimal leak from the venular walls and macula. (G to I)
Shows normal right eye.
The right eye shows FFA appearance of acute ischemic central
retinal vein occlusion.
Figs 2.30A to D: Vascular occlusion—Central retinal vein

occlusion (A) Color fundus photograph of the left eye shows disc
pallor, new vessels involving the temporal optic disc margin
(arrow), dilated tortuous central retinal vein and its tributaries,
and featureless retina and macula. (B and C) Early and late
arteriovenous phase FFA shows an area of intense
hyperfluorescence involving the temporal part of the optic disc
with increasing intensity and area of hyperfluorescence with fuzzy
borders, suggestive of neovascularization of the optic disc.
Intense hypofluorescence in all quadrants due to capillary drop-
out make blunted, telangiectatic venular tributaries stand out in
relief. Gross distortion of the enlarged foveal avascular zone is
seen (arrow). (D) Late phase angiogram shows leakage of the
dye from the neovascularization at the disc and staining and
minimal leakage from the defunct venous walls.
This appearance is suggestive of the proliferative stage of
ischemic central retinal vein occlusion.
Figs 2.31A to D: Vascular occlusion—Branch retinal vein

occlusion (A) Color fundus photograph of right eye shows
sclerosed tributaries of the superotemporal with macular ischemia
as suggested by featureless superior macular retina. A
neovascular frond is seen at the arteriovenous crossing along
the superotemporal arcade (arrow). (B) Late arteriovenous phase
FFA shows well defined area of capillary nonperfusion along
superotemporal arcade, the apex of which corresponds to the
site of vein occlusion (arrow). Blunted tributaries of the vein border
the avascular zone. The neovascular frond shows hyper-
fluorescence with fuzzy margins suggestive of early leakage.
Superotemopral macular ischemia involves the foveal avascular
zone. (C) Late phase of angiogram shows increased hyper-
fluorescence and leakage at the neovascular frond. (D) Color
fundus photograph shows appearance immediately after sectorial
laser photocoagulation.
This is suggestive of proliferative stage of branch retinal vein
occlusion where in laser photocoagulation is indicate.
Figs 2.32A to D: Vascular occlusion (A) Color fundus photograph

of the right eye in a middle-aged male showing sheathed supero-
temporal branch retinal venule, a collateral vessel superior to
the disc (arrow), macular ischemia as seen by the sclerosed
vessel at the superior macula. (B and C) Early and mid phase of
FFA shows distorted foveal avascular zone that is grossly
enlarged suggesting macular ischemia, staining of the venous
walls, capillary telangiectasia and capillary non perfusion in the
area of occlusion. (D) Late phase of the angiogram shows diffuse
intraretinal leakage of the dye from venous walls and
telangiectasia. No new vessels at the disc or elsewhere are seen.
Collateral vessels do not leak or leak minimally in contrast to
new vessels.
This is the appearance of a patient with branch retinal vein
occlusion that is resolving and macular edema.
Figs 2.33A to D: Vascular disease—Retinal artery macro-

aneurysm (A) Color fundus photograph of right eye shows spindle
shaped aneurysm (arrow) along the second order arteriole of
the inferotemporal arcade with circinate and hard exudate clump
at the fovea (B) Arteriovenous phase of FFA shows fusiform
dilatation of the retinal arteriole with telangiectatic vessels around
the macroaneurysm. Note blocked fluorescence due to hard
exudates clump involving the fovea. (C and D) Venous phase of
angiogram shows diffuse leak in to the retinal tissue with macular
edema. The macroaneurysm walls retain the dye in the late phase
(arrow).
The findings are suggestive of Retinal artery macroaneurysm
with macular exudation.
Figs 2.34A to D: Vascular disease—Periphlebitis (A) Color

fundus photograph of right eye showing hyperemia of the optic
disc, dilatation and tortousity of the veins with sheathing.
(B) Venous phase of fluorescein angiogram shows staining of
the disc, staining of the vein walls and patchy hyperfluorescence
along superior part of the macula. (C) Nasal quadrant of the same
eye shows patchy hyperflourescence with intense leak suggestive
of neovascularization elsewhere and staining of the venous walls
(arrow). (D) Late venous phase of angiogram staining of the disk,
venular walls, perivascular leakage of the dye into the retina and
increased fluorescence superior part of the macula.
The findings are suggestive of periphlebitis and RPE level
inflammation in a young male patient.
Figs 2.35A to D: Vascular retinopathy—Coat’s disease (A and

B) Color fundus photograph of the right eye in a 12-year-old boy
showing dense subretinal exudates inferior and temporal to
the fovea and retinal aneurysmal vascular malformations. (C and
D) Fluorescein angiogram shows hyperfluorescent bulb like
vascular malformations that leak in the late phase. Note areas of
hypofluorescence due to capillary nonperfusion.
The findings are indicative of vascular malformations in Coat’s
disease.
• Vascular occlusion
• Vascular disease—Retinal artery macroaneurysm
• Vascular disease—Periphlebitis
• Vascular retinopathy—Coat’s disease
Figs 2.36A to D: Tumors—Choroidal melanoma (A) Color fundus

photograph of the left eye shows large dark brown/gray dome-
shaped mass arising from the temporal choroid (B) Early
arteriovenous phase FFA shows multiple pin-point hyper-
fluorescent spots within the tumor. (C and D) Mid phase angiogram
high lights the intrinsic tumor vessels and overlying retinal vessels
suggestive of “double circulation” in a melanoma. Mid to late venous
phase of angiogram shows increased intensity and area of
hyperfluorescent spots with fuzzy borders suggestive of leakage.
The color, shape along with the fluorescein angiographic
features suggests a diagnosis of choroidal melanoma.
• Tumors—Choroidal melanoma
• Tumors—Choroidal hemangioma
• Tumors—Retinal capillary angioma
Figs 2.37A to D: Tumors—Choroidal hemangioma (A) Color

fundus photograph of the left eye in a young male shows reddish
orange well-circumscribed choroidal lesion along the
superotemporal arcade. Note pigmentation along the borders of
the lesion. (B) Arterial phase of fluorescein angiogram shows
early hyperfluorescence within the lesion indicating the choroidal
origin and intense vascularity of the lesion. (C) Early venous
phase FFA shows increase in hyperfluorescence with fuzziness
indicative of early leakage. An area of pinpoint hyperfluorescence
around the tumor extending towards the macula, suggestive of
RPE atrophy along the track of subretinal fluid leakage towards
the macula (arrow). (D) Late phase FFA shows leakage of the
dye from the tumor and fading of the transmission defects due to
RPE atrophic patch.
The red orange color of the choroidal lesion, early filling and
late profuse leakage suggest a diagnosis of solitary,
circumscribed choroidal hemangioma.
Figs 2.38A to I: Tumors—Retinal capillary angioma (A to C)

Color fundus photograph of left eye shows dilated, tortuous paired
vessels feeding an orange red tumor mass elevated in to the
vitreous. (D to F) FA shows early filling of the dilated arteriole
(arrow), intense hyperfluorescence of the tumor and the draining
venule (block arrow) fills earlier than other retinal vessels,
demonstrating the rapid blood flow within the tumor (G to I) Late
venous phase shows profuse leakage from the angioma.
The findings are suggestive of capillary angioma of the retina
• Macular diseases—Diabetic macular edema

• Macular disease—Diffuse diabetic macular edema
with cystoid macular edema
• Vascular Retinopathy—Proliferative diabetic retinopathy.
Figs 2.39A to D: Macular diseases—Diabetic macular edema

(A) Color fundus photograph of the right eye in this diabetic patient
shows circinate of hard exudates temporal to the fovea extending
within 500 microns of the same. Multiple circumscribed dots
suggestive of microaneurysms are seen within and out of the
circinate. A few deep and superficial retinal hemorrhages and
scattered hard exudates are also seen. (B) Early venous phase
FFA shows multiple hyperfluorescent spots corresponding to the
microaneurysms are seen within the circinate and elsewhere.
Blocked intraretinal and choroidal fluorescence due to retinal
hemorrhages and hard exudates can be seen. (C) Mid phase
FFA shows increasing leakage from the microaneurysms and
an area of patchy hyperfluorescence along the superotemporal
arcade suggestive of neovascularization elsewhere. (D) Late
phase FFA shows pooling of the dye within the Henle's layer in a
petalloid pattern suggestive of clinically significant diabetic
macular edema with cystoid macular edema.
Figs 2.40A to D: Macular disease—Diffuse diabetic macular

edema with cystoid macular edema (A) Color fundus photograph
of left eye shows deep retinal hemorrhages at the temporal
macula with retinal thickening. Note paucity of hard exudates
(B) Early venous phase of fluorescein angiogram shows areas
capillary nonperfusion (arrow), hyperfluorescent patches
suggestive of neovascularization at the disc and elsewhere (block
arrow). In addition, there is generalized ill-defined leakage of the
dye at the macula from retinal capillaries (unlike the pinpoint
leakage from microaneurysms). (C and D) The mid and late phase
angiogram shows profuse leakage of the dye into the retina, also
showing a petalloid appearance.
The findings are suggestive of diffuse diabetic macular edema
with cystoid changes along with proliferative diabetic retinopathy.
Figs 2.41A to D: Vascular retinopathy—Proliferative diabetic

retinopathy (A) Color fundus photograph of the right eye in a
diabetic shows preretinal hemorrhage nasal to disc (B) Nasal
fundus of the left eye shows areas of hypofluorescence due to
capillary nonperfusion, patches of intense hyperfluorescence with
fuzzy margins suggestive of neovascularization elsewhere and
pinpoint hyperfluorescence from microvascular anomalies. Note
venous beading in the nasal quadrant (arrow). (C and D) Venous
phase FFA shows hyperfluorescent patches nasal and
inferotemporally with fuzzy borders suggestive of neovasculari-
zation elsewhere. Note blocked retinal fluorescence due to pre-
retinal hemorrhage and hyperfluorescence at the macula due to
leaking microaneurysms.
This appearance in a diabetic is suggestive of proliferative
Figs 2.42A to D: (A) Color fundus photograph of right eye shows

numerous small to medium sized serous pigment epithelial
detachments (arrow). (B) Early venous phase of fluorescein
angiogram shows early hyperfluorescence due its connection to
the choroidal circulation. The hyperfluorescence increases but
the lesion borders remain well defined. (C and D) Mid-to-late
venous phase of angiogram shows increase in intensity of the
fluorescence but with well-defined borders indicating pooling of
the dye in the sub RPE space.
This appearance on FFA is suggestive of serous pigment
epithelial detachment.
Diabetic
Retinopathy
Belquiz A Nassaralla (Brazil)
DIABETIC RETINOPATHY
Diabetic retinopathy is a complication of diabetes that
results from damage to the blood vessels of the light-
sensitive tissue at the retina. It is an ocular manifestation
of systemic disease which affects up to 80% of all patients
who have had diabetes for 10 years or more.1 Despite
these intimidating statistics, research indicates that at least
90% of these new cases could be reduced if there was
proper and vigilant treatment and monitoring of the eyes.2
There are two stages of diabetic retinopathy: non-
proliferative and proliferative. Nonproliferative is the
earlier of the two stages and is more common. In this stage,
there may be bleeding inside the retina (hemorrhages) and
leakage of serum into the retina causing a “wet retina” or
protein deposits in the retina (exudates). One of the
consequences of this change is that the retina does not
receive enough oxygen which can cause a progression to
the next stage. This early stage usually produces no visual
symptoms but if there is fluid in the central portion of the
eye then vision may drop. Proliferative is the next stage.
New abnormal vessels can develop in the retina and grow
towards the center of the eye. These vessels frequently
bleed into the clear jelly in the center of the eye (vitreous
hemorrhage). Such bleeding episodes usually cause severe
visual difficulties in patients. Small bleeds may clear up
on their own but larger bleeds may need surgery. These
abnormal vessels may also produce large scars in the retina
Diabetic Retinopathy 51
that may cause the underlying retina to detach producing
a retinal detachment.1,3,4
NONPROLIFERATIVE RETINOPATHY
This is graded into one of four categories, which predict
the likelihood of progressing to proliferative retinopathy.
In particular, the 4-2-1 rules were developed to define
severe and very severe diabetic retinopathy (Table 3.1).
Fig. 3.1: Diabetic proliferative retinopathy neovascularization

elsewhere (NVE), microhemorrhages (H), cotton wool spots (E)
and intraretinal microvascular abnormalities (IRMA). (Courtesy:
Prof Miguel H Amaro and Prof Aaron Brock Roller)
Table 3.1: The 4-2-1 classification of diabetic retinopathy

Classification Features
Mild >1 microaneurysm
Moderate Severe retinal hemorrhages in 1-3 quadrants or
venous beading or IRMA definitely present.
Severe Any one of: 4 quadrants of severe retinal
hemorrhages, 2 quadrants of venous beading, 1
quadrant of moderately-severe IRMA
Very Severe Any two of the severe features
Fig. 3.2: Diabetic retinopathy angiogram, showing hemorrhage

(black dots). The diabetic retinopathy is bilateral and asymmetric.
It can be appreciated when comparing both eyes of the same
patient
Fig. 3.3: Nonproliferative diabetic retinopathy with microhemor-

rhages (black dots) in both eyes, typical of mild types
Fig. 3.4: Nonproliferative diabetic retinopathy in both eyes. The

bleeding into the retina and cotton-wool spots typical of mild to
moderate types
Fig. 3.5: Diabetic retinopathy fluorescein angiogram showing

intraretinal microvascular abnormalities, microaneurysms (white
dots) and hemorrhage (black dots). Retinal microaneurysms are
focal dilatations of retinal capillaries, 10 to 100 microns in
diameter, and appear as red dots. They are usually seen at the
posterior pole, especially temporal to the fovea. They may
apparently disappear while new lesions appear at the edge of
areas of widening capillary nonperfusion. Microaneurysms are
the first ophthalmoscopically detectable change in diabetic
retinopathy
Fig. 3.6: Nonproliferative diabetic retinopathy. Macular cotton-

wool spots in left eye and retinal photocoagulation in posterior
pole. Laser grid photocoagulation reduces the risk of visual loss
by 50% at 2 years
Diabetic macular edema was defined as the

appearance of retinal thickening at the macula caused by
the presence of fluid outside cells (extracellular edema)
or inside cells (intracellular edema). Diabetic macular
edema is categorized2,3 into:
Fig. 3.7: A fundus photo of nonproliferative diabetic retinopathy

showing numerous hemorrhages, hard and soft exudates with
macular edema
• Circinate
• Diffuse
• Ischemic
• Mixed
Fig. 3.8: Circinate macular edema refers to the presence of focal

areas of macular edema (retinal thickening) with surrounding
hard exudates formation and is the result of focal leakage
Fig. 3.9: Circinate macular edema refers to the presence of focal

areas of macular edema (retinal thickening) with surrounding
hard exudates formation and is the result of focal leakage. Hard
exudates (intraretinal lipid exudates) are yellow deposits of lipid
and protein within the sensory retina. Accumulations of lipids
leak from surrounding capillaries and microaneurysms, they may
form a circinate pattern. Hyperlipidemia may correlate with the
development of hard exudates
Fig. 3.10: Ischemic macular edema can only be identified by

fluorescein angiography
Fig. 3.11: Mixed edema (circinate macular and ischemic) refers

to the presence of focal areas of macular edema (retinal
thickening) with surrounding hard exudates formation and is the
result of focal leakage. Accumulations of lipids leak from
surrounding capillaries and microaneurysms; they may form a
circinate pattern
Fig. 3.12: A fundus photo and fluorescein angiography of non-

proliferative diabetic retinopathy showing hemorrhages and
yellowish hard exudates
Fig. 3.13: Fundus photograph of nonproliferative diabetic

retinopathy with clinically significant macular edema. Fluorescein
angiogram reveals diffuse macular edema and leakage from
microaneurysms in diabetic retinopathy
Fig. 3.14: Color retinal photograph and fluorescein angiogram

of the same patient. The retinal vessels are filled with the
fluorescent dye. Hemorrhages appear as dark spots in the
angiogram and correspond to those seen in the color photo. There
is damage to retinal blood vessels which no longer fill with the
dye. This is called an area of nonperfusion, also called retinal
ischemia
Fig. 3.15: To treat the abnormal growth of tiny blood vessels

and bleeding that often result from diabetic retinopathy, frequently
use a type of laser surgery called pan-retinal photocoagulation
(PRP)
Fig. 3.16: When performing pan-retinal photocoagulation (PRP)

for diabetic retinopathy treatment, the surgeon uses a laser to
destroy oxygen-deprived retinal tissue outside of a patient’s
central vision. This prevents further growth of fragile blood vessels
and seals leaking ones, helping to stop the disease from
progressing. The tradeoff of this treatment is that it creates some
blind spots in the patient’s peripheral vision
PROLIFERATIVE RETINOPATHY
Proliferative retinopathy is defined by the presence of
new vessels. These were defined by their location as being
either present at the disc or within one disc diameter of
the disc (NVD) or elsewhere (NVE). The distinction is
important as the presence of NVD signifies a far greater
risk of visual loss than NVE.2,3,5
Proliferative retinopathy was categorized into early
proliferative diabetic retinopathy or high-risk
proliferative diabetic retinopathy. To be categorized as
having high risk proliferative diabetic retinopathy, three
of the following four features have to be present:
1. Presence of new vessels.
2. Location of new vessels on or within one disc diameter
of the optic disc (NVD).
3. Severity of new vessels—
• NVD equal or greater than one-fourth to one-third
disc area
• NVE equal or greater than one-half disc area
4. Vitreous or preretinal hemorrhage.
Fig. 3.17: This picture is the classic image of diabetic retinopathy.

This patient has new blood vessels, neovascularization on the
disc that is causing bleeding. There is also some other
neovascularization and the blood vessels are leaking resulting
in diabetic macular edema. It is considered a microvascular
disease. We see the blood vessel changes because the blood
vessels contain hemoglobin, which is a pigment. But the retina,
which actually does the seeing, is transparent like a window.
From our clinical examination and on angiography, it is
transparent to our view in right eye, but in the left eye, we can
see intense vitreous hemorrhage. Preretinal hemorrhages are
often associated with retinal neovascularization, they may
dramatically reduce vision within a few minutes
B
Figs 3.18A and B
D
Figs 3.18A to D: This picture is the classic image of diabetic
proliferative retinopathy. New blood vessels, neovascularization,
the blood vessels and microvascular disease (Courtesy:
Prof Jayme)
Fig. 3.19: A fundus photo of proliferative diabetic retinopathy

with fibrovascular bands and retinal detachment in the left eye.
Tractional retinal detachment occurs when fibrous membranes
(essentially scarring processes) in the vitreous humor and retina
produce mechanical traction on the retina, literally pulling the
retina from the underlying layer, known as the retinal pigment
epithelium (RPE). This type of retinal detachment is most common
in the advanced stages of diabetic retinopathy, known as
proliferative diabetic retinopathy
Fig. 3.20: A fundus photo of proliferative diabetic retinopathy

with pan-retinal photocoagulation (PRP) scars and fibrovascular
bands
REFERENCES
1. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. The
Wisconsin Epidemiologic Study of Diabetic Retinopathy. II.
Prevalence and risk of diabetic retinopathy when age at
diagnosis is less than 30 years. Arch Ophthalmol 1984;102:
520-26.
2. UK Prospective Diabetes Study Group. Tight blood pressure
control and risk of macrovascular and microvascular
complications in type 2 diabetes: UKPDS 38. BMJ 1998;317:
708-13.
3. Estacio RO, Jeffers BW, Gifford N, Schrier RW. Effect of
blood pressure control on diabetic microvascular complica-
tions in patients with hypertension and type 2 diabetes.
Diabetes Care 2000;23(Suppl. 2):B54-B64.
4. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. The
Wisconsin Epidemiologic Study of Diabetic Retinopathy. III.
Prevalence and risk of diabetic retinopathy when age at
diagnosis is 30 or more years. Arch Ophthalmol 1984;102:
527-32.
5. Batchelder T, Barricks M. The Wisconsin Epidemiologic
Study of Diabetic Retinopathy (Letter) Arch Ophthalmol
1995;113:702-03.
FFA in Retinal
Detachments

Juan Jose Luis Parra Limon
Yuri Axayacati Flores Fuentes (Mexico)
TRACTIONAL RETINAL DETACHMENT
General Aspects
A tractional retinal detachment (TRD) is produced when
the adherences between the vitreous and the retina are
able to mechanically separate the retina from the
pigmentary epithelium.
The features of the TRD are vitreous strands or
epiretinal tissue that elevates the retina from the
pigmentary epithelium. These detachments are not
associated with a retinal rupture. They are frequently
observed in the Diabetic Retinopathy (RD), the
Proliferative Vitreoretinopathy (VRP), the penetrating
trauma, the occlusive disease of the retinal vein and in
the retinopathy of prematurity.
The traction forces can be produced inside the vitreous
body, at the retinal surface or even below the retina, like
in the subretinal fibrosis. The traction is associated to a
membrane, that in most of the cases, becomes clinically
apparent. The hystologic components of these membranes
are fibroblast and Glial cells from the pigmentary
epithelium. The traction forces are transmitted to the
retina itself, through direct bridges of tissue or through
vitreous strands.
The contraction of the vitreous body is frequently
produced in the eyes with proliferative diabetes
FFA in Retinal Detachments 77
Fig. 4.1: Tractional RD with intense fibrous proliferation and

temporal traction
retinopathy. As the vitreous becomes thicker, the retina

is pulled to the center of the eye, through the vitreous
base.
At the beginning, the only one zone of retinal
detachment is the temporal one (most frequent), but later
on, the detachment increases and the macula can be
involved.
Fig. 4.2: Intense temporal traction with

local retinal detachment
Clinical Features
These detachments are not associated to a retinal brake.
They usually have a concave appearance, are localized to
a specific zone and frequently have not extension to the
ora serrata.
The biomicroscopy with contact lens is very useful in
the definition of the anatomy of the detachment and the
vitreous strands. The progressive tractional elevation of
Fig. 4.3: Initial picture from FAR showing the edges of

the fibrotic reaction
the retina can cause a defect of total thickness, leading so

to a rhegmatogenous retinal detachment, it means, a
mixed pattern.
Fluorescein Angiography
The FAR can show important details regarding the
ischemia and the neovascularization. Frequently, the
neovascularization leakage appears like white spots at the
Fig. 4.4: Middle A-V phase showing hyperfluorescence at the

site of fibrotic prliferation
posterior vitreous, over the retinal vessels. Also it is very

useful in the follow-up, in cases of photocoagulation or
vitrectomy.
Treatment
Since the arrival of the posterior vitrectomy in 1970,
important advances in the treatment of these cases have
Fig. 4.5: Late FAR phase. The hyperfluorescence

hides the tractional proliferation
been noticed. The indications for surgery, mostly in the

diabetic group, keep on evolving. The surgical objectives
include the cleaning of opacities and the liberation of the
traction, the cause of the retinal detachment.
The epiretinal membranes and the fibrous tissue are
dissected from the retinal surface in a bimanual fashion.
Avoiding bleeding is very important during the surgical
care. If there is not a retinal rupture during or before the

surgery and if the macular zone is not involved, the
prognosis is good.
Currently, with the antiangiogenic medication, the
prognosis is becoming better. The injection is performed
some days before the surgery. It produces a neovascular
retraction helping the surgeon to the liberation of the
membranes and decreasing the bleeding.
CENTRAL SEROUS CHORIORETINOPATHY
General Aspects
The Central Serous Chorioretinopathy (CSC) is characteri-
zed by the accumulation of translucent fluid at the
posterior pole of the eye (fundus). There are two main
kinds of this disease as is described as follows. The typical
or classic form occurs in young patients, and causes a
localized retinal detachment; there is an acute decrease
in the visual acuity with one or various points of leakage.
The second form is characterized by a diffuse disturbance
in the pigmentation of the retinal pigmentary epithelium,
associated with the chronic presence of a small amount
of subretinal fluid; this type of the disease has been named
also like pigmentary diffuse epitheliopathy of the retina;
it corresponds to the chronic form of the CSC.
The pathophysiology has not been clearly understood.
The fluorangiography (FAR) shows one or various spots
Fig. 4.6: FAR showing hyperfluorescence dots

in the center of the macula
of leakage able to produce a detachment of the

pigmentary epithelium and also of the neurosensory
retina in cases of active CSC. When this leakage is solved,
the retinal detachment solves also.
The typical clinical presentation corresponds to a
patient with Type “A” personality that has had a stressful
event. Also elevated levels of cortisol have been found is
Fig. 4.7: FAR showing a neurosensory detachment

of the macula before the entering of fluorescein
frequent in Cushing’s disease and in pregnant women,

because of the increase in the endogenous cortisol. A
severe form of CSC is found in patients treated with high
dose of steroids, like some forms of transplantation.
The global incidence is by far more frequent in men,
being the relation 8 to 1. Nevertheless, there is a women
shift between the ages of 30 to 40.
Fig. 4.8: Acute central serous chorioretinopathy with a

neurosensory macular detachment
Clinical Features
The symptoms in the typical form are decrease in the
visual acuity, metamorphopsia, dyschromatopsia and
central scotoma. The physician can find some degree of
hyperopia and with the refraction, the visual acuity can

improve. The visual acuity can be found in a range
between 20/25 to 20/200. Amsler‘s test is very useful in
these cases.
At the fundus exploration there is visible a neurosensory
retinal detachment at the macular zone; it seams like an
ampule, well defined and translucent; frequently presents
a reflex that defines the elevated zone. Yellow deposits over
the retinal detachment can also be found.
With the Coherent Tomography, we can see the
detachment of the pigmentary epithelium under the
elevation of the retina.
Fluorescein Angiography Findings

Even that the clinical features can lead easily to the
diagnosis, the FAR is very helpful in these cases. The
typical lesion in the FAR shows one or more points of
leakage; they are hyperfluorescent and are at the level of
the pigmentary epithelium. The contrast is running in
slow motion but showing a uniform pattern; this is called
“chymney pattern”. Later on, there is an expansion in a
typical pattern called “umbrella”. It runs until the
superior boundary of the lesion presenting one or many
points of leakage. This is finally seen as a diffuse
hyperfluorescense; these points of leakage are more
frequently seen at the upper-nasal quadrant, the second
place is the lower-nasal quadrant, the third the upper-
temporal and finally the lower-temporal.
Treatment
Most of the cases are solved in a spontaneous way in few
months; it is frequently a self-limited disease. A typical
case recovers until the 20/20 of visual acuity, but there can
be some cases of less visual recovery.
In many cases, the argon laser photocoagulation can
decrease the time of evolution of the disease but also the
rate of retinal detachment. Some reports have shown a
decrease of the recurrences of the disease with the use of
photocoagulation. It is indicated if the retinal detachment
has been present for more than 3 months and if the
leakage point is not over the foveal zone. In no complica-
ted cases, after two weeks, after the photocoagulation, the
point of leakage should disappear; in some cases it can
last until 6 months to solve.
The laser therapy can induce a secondary neovascu-
larization in particular when a high power is utilized
during the treatment.
RHEGMATOGENOUS RETINAL DETACHMENT
Description of the Fluorangiography Correspondent

to a Rhegmatogenous Retinal Detachment
At the clinical picture we are able to see the optic disc
with an oblique insertion; this finding is very
characteristic of a myopic eye. We can see an antique
retinal detachment; it is complete, and involving the
Fig. 4.9: Rhegmatogenous retinal detachment FFA
macula. The retinal detachment is complicated with a

proliferative vitreoretinopathy, because of the long time
of the disease.
At the fluorangiography we can see the blood vessels
with increased hyperfluorescence with alteration in its
trajectory. We can also see the hyperfluorescence of the
proliferative membranes.
Fluorescein
Angiography
and Indocyanine
Green
5 Angiography in
Age-related
Macular
Degeneration
T Mark Johnson (USA)

INTRODUCTION
Age-related macular degeneration is an important cause
of visual disability worldwide. Retinal imaging is critical
for the diagnosis, classification and management of AMD.
Multiple imaging techniques are employed including
fluorescein angiography, autofluorescence and indocyanine
green angiography.
Fluorescein angiography has assumed an important role
in the ancillary testing of retinal disease. It provides
valuable information on the anatomy, physiology and
pathology of the retina. 10 % sodium fluorescein is injected
intravenously. Blue light is used to excited fluorecein at its
absorption peak of 465 to 490 nm. Return of the fluorescein
molecules to ground state results in emission of light at
520 to 530 nm light. The emitted light is captured to
produce the image. The results of fluorescein angiography
can be classified as pseudofluorescence, hyperfluorescence
and hypofluorescence. All of the fluorescein features are
observed in cases of age-related macular degeneration.
Autofluorescence is observed with the barrier filter
prior to the injection of fluorescein dye. Fundus auto-
fluorescence (FAF) is the result of lipofuscin accumulation
within the retinal pigment epithelium (RPE) and may
reflect altered structure and function.1 Autofluorescence
Fluorescein Angiography in ARMD 91
images have been recorded with traditional fundus
cameras using barrier or with confocal scanning laser
systems. Near infrared autofluorescence can also be
recorded using confocal scanning laser systems with
excitation at 787 nm and emission > 800 nm. Near infrared
autofluorescence (NIA) may provide information on
melanin distribution and function in the fundus. Scanning
laser images may be superior to FAF images obtained with
a fundus camera due to superior signal to noise ratios.2
Differing patterns of FAF and NIA in AMD may provide
insights into the pathophysiology of macular degene-
ration.3 Increased autofluorescence is observed in areas of
drusen and lipofuscin deposits. Decreased autofluore-
scence is observed in areas of geographic atrophy (Fig. 5.1).
The FAF patterns in the areas bordering areas of geographic
atrophy may be predictive of progression.4 FAF will likely
play an increasingly important role in the evaluation of
therapies for geographic atrophy in the future.
Hyperfluorescence may result from leakage of dye,
staining or pooling of dye or transmission (window)
defects. Leakage of dye results from extravasation of dye
from disruption of endothelial cell tight junctions.
Leakage is characterized by hyperfluorescence that
increases in intensity and area over the course of the
study. In the context of AMD leakage is indicative of
choroidal neovascularization, usually in the subretinal
space (Figs 5.2A and B). In cases of retinal angiomatous
proliferation neovascularization begins in the retina and
Fig. 5.1: Confocal scanning laser autofluoresence image of

patient with geographic atrophy. Atrophic areas appear as areas
of decreased autofluorescence. Drusen appear as areas of
increased autofluorescence
B
Figs 5.2A and B
D
Figs 5.2C and D
E
Fig. 5.2E
Figs 5.2A to E: Classic choroidal neovascular membrane. Well
defined early hyperfluorescence (A) with late leakage (B). Note
the increasing intensity and area of hyperfluorescence
characteristic of leakage. Blocked fluorescence is present
superior and inferior to the lesion due to blood. (C) Patient with
recurrent CNVM 5 years postfocal laser ablation of extrafoveal
CNVM. Color photo shows atrophy at prior laser site with
subretinal hemorrhage superonasal. (D) Early phase FA shows
well-defined, lacy early hyperfluorescence that leaks in the late
phases of the FA (E) typical of a classic CNVM
thus leakage is observed as a primary intraretinal process

(Fig. 5.3). Pooling of dye results when fluorescein
accumulates in a potential anatomic space. In AMD this
most typically occurs within a pigment epithelial detach-
ment. Staining results from a progressive accumulation
of fluorescein within a tissue and thus becomes brighter
in the later phases of the angiogram. Staining may be
observed with late hyperfluorescence of drusen or
Fig. 5.3: Ill-defined (occult) leakage with pooling in cystoids

spaces in patient with a stage I RAP lesion
accumulation of dye within areas of subretinal fibrosis
and scarring (Fig. 5.4). Transmission (window) defects are
observed in areas of focal loss of RPE (Fig. 5.4). These
areas appear bright in the early phase of the angiogram
and fade later in the study. The configuration and area of
the brightness does not change throughout the study.
Hypofluorescence is defined as a lack of fluorescence
during the angiogram study. It may result from a blockage
of fluorescence or an absence of perfusion. In AMD
patients hypofluorescence is typically the result of
blockage of fluorescence due to hemorrhage, fluid or
pigment accumulation (Fig. 5.5). Perfusion defects can
sometimes be observed following laser therapies
including focal coagulation and photodynamic therapy
(Fig. 5.6D).
Fluorescein angiography is most commonly utilized
in the evaluation of AMD patients when examining for
the presence of choroidal neovascularization. CNVM may
be described on the basis of the fluorescein angiogram
appearance. A classic CNVM appears as an early area of
well defined hyperfluorescence that leaks in the later
frames of the angiogram (Figs 5.6A to D). During the
conduct of the Macular Photocoagulation Study it became
evident that some patients with AMD had other, less
defined areas of choroidal neovascularization that are
now referred to as occult CNVM (Figs 5.6A to D). These
areas are typically punctuate areas of hyperfluorescence
that progressively leak in the late frames of the
B
Figs 5.4A and B
C
Fig. 5.4C
Figs 5.4A to C: (A) Fluorescein angiogram corresponding to
patient in Figure 5.1. Late FA shows well-defined hyper-
fluorescence in areas of geographic atrophy. Note that the
margins of the hyperfluorescence are clearly demarcated
indicating an absence of leakage. (B) Patient with fibrovascular
pigment epithelial detachment developed RPE rip postinjection
of anti VEGF drug. The late FA shows staining of the fibrovascular
tissue nasally and staining of the geographic atrophy temporally.
(C) Corresponding autofluorescence image shows decreased
autoflourescence in the area of geographic atrophy
B
Figs 5.5A and B: (A) Patient with sudden decrease in vision.
Extensive submacular hemorrhage is demonstrated as blocked
fluorescence. Temporal leakage is evident, however, the FA does
not allow complete visualization of the neovascular complex.
(B) Patient presenting with acute decrease in vision. Clinical exam
showed extensive subretinal hemorrhage. FA shows blockage
secondary to blood without obvious leakage source
B
Figs 5.6A and B
C
Fig. 5.6C
D
Fig. 5.6D
Figs 5.6A to D: Early well-defined hyperfluorescence (A) that
leaks profusely in the late frames of the angiogram
(B) characterizing classic CNVM. Color photo post-MPS type
photocoagulation of the classic CNVM shows whitening of the
lesion (C). 1 week posttreatment angiogram shows hypo-
fluorescence due to nonperfusion of the neovascular complex
(D). Note that superior to the treatment area there is persistent,
stippled late hyperfluorescence indicative of a larger occult
choroidal neovascular membrane. The presence of occult CNVM
was not well-understood prior to the conduct of the MPS study
B
Figs 5.7A and B
C
Fig. 5.7C
Figs 5.7A to C: (A) Patient with ill-defined late leakage (occult
CNV). Note blocked fluorescence due to subretinal hemorrhage.
(B and C) Patient with ill-defined late leakage inferior to prior
superior PDT site indicative of recurrent occult CNVM (B). 1 year
postserial injections of anti-VEGF therapy there is near complete
regression of leakage with mild staining of the prior scar and
blocked fluorescence secondary to pigmentary clumping (B)
E
Figs 5.7D and E
F
Fig. 5.7F
Figs 5.7D to F: Patient presenting with decreased vision and
new subretinal hemorrhage. Early FA shows blockage secondary
to subretinal hemorrhage (D) with late stippled leakage (E) typical
of occult CNVM. Patient received serial injections of anti-VEGF
medication with resolution of subretinal hemorrhage. Late FA
shows staining of a fibrovascular pigment epithelial detachment
(F)
angiogram. The margins are typically ill defined (Fig. 5.7).

Patients with exudative AMD may have features of
both classic and occult CNVM simultaneously (Figs 5.8A
and B).
B
Figs 5.8A and B: Patient with mixed CNV. Early phase FA (A)
shows well-defined early hyperfluorescence nasally that leaks
in late phase (B) Late phase FA shows larger area of ill-defined
leakage temporally
INDOCYANINE GREEN ANGIOGRAPHY

Although fluorescein angiography has been proven to be
useful in establishing the extent of leakage of neovascular
lesions in ARMD, in many instances, it has its limitations,
particularly in the identification of the details of the
vascular structures. In situations where choroidal
neovascular membranes (CNVM) are obscured by
overlying hemorrhage, edema or retinal pigment
epithelial (RPE) hyperplasia, fluorescein angiography
provides very little useful information with regards to
choroidal vascular supply. Indocyanine green allows for
visualization of the choroidal vasculature due to the high
protein binding of the dye reducing leakage from the
vasculature of the choroid. ICG absorbs and emits in the
near infrared spectrum and thus transmits through areas
of blood and edema.
ICG has proven to be useful in the diagnosis and
management of choroidal disorders such as ARMD. Since
the reports of human ICG angiograms were first published
in 1970, there has been a continuous refinement of the
technique leading to increased spatial and temporal
resolution of the images. Subsequently with the advent of
the ICG video angiogram in 1976, feeder vessel treatment
of CNVM became a possibility. ICG angiography, and in
particular “High speed ICG” (HSICG) video angiography
can provide useful information with regard to the
underlying vascular source to the neovascular complex.
ICG angiography was first utilized to study occult

neovascularization. At the conclusion of the macular
photocoagulation study focal laser was demonstrated to
be superior to observation in the treatment of well-defined
(classic) CNVM, however no benefit was observed in cases
of mixed classic and occult CNVM and the study did not
enroll patients with occult disease.5 A review of 67 cases
of new CNVM demonstrated that only 13% had lesions
amenable to MPS laser. 6 Thus, the initial goal of ICG
imaging was to identify lesions that would amenable to
focal laser ablation in the management of CNVM. Initial
ICG angiograms were conducted as static imaging
techniques obtained with injections of 25 to 50 mg of ICG
and images recorded over a 20 to 60 minute period. In
one case series of 1000 patients with occult CNVM imaged
with static ICG several patterns were described. The most
commonly observed pattern (61%) was a subfoveal plaque
of late hyperfluorescence. The second most common
pattern was a focal hot spot occurring in 29% of cases.
The remained of cases had mixed lesions.7 Several case
series suggested that focal laser ablation of hot spots
successfully reduced exudation with stabilization of
visual loss, however, few cases of visual improvement
were noted.8 In retrospect many of these hot spots likely
represented areas in retinal angiomatous proliferation.9
Subsequent case series have confirmed that focal ablation
of these lesions, particularly at early stages, can stabilize
visual loss.10
The more recently developed scanning laser
ophthalmoscope (SLO) allows real-time image capture at
very low illumination levels. The typical exciter light
source in such systems uses a small spot size
(approximately 10 micron) diode laser. This “dynamic”
scanning system measures the reflectance of the retina as
it is scanned by the laser beam. Confocal SLO systems are
also capable of performing both fluorescein and ICG
angiography. Selection of light reflected from different
focal planes in the retina is performed by moving the
pinhole. The imaging capabilities of the SLO system has
in many instances provides added information to
classifications such as “classic”, “occult”, or “mixed”
types of the neovascular membrane. HSICGA also allows
for a more precise determination of reduction in vascular
perfusion postoperatively than is achievable with either
FA or conventional ICGA. Currently, the most commonly
employed imaging system for FVT is the digital “High
speed ICG” (HSICG) video angiogram. This SLO-based
imaging technique allows for the a capture rate of ICGA
images to the level where directional flow through
choroidal vessels can be identified. This approach to
delineating the feeder vessels is superior to older
techniques of “dye accumulation” methods where later
phases of the ICGA are examined for hyperfluorescence.
ICG angiography was initially used to identify areas
of CNVM potentially amenable to direct focal laser
ablation in patients with occult neovascularization.
Currently, ICG can be a valuable ancillary test in the

classification of patients with exudative AMD. In
particular ICG is useful for identifying patients with AMD
variants such as retinal angiomatous proliferation (RAP)
and polypoidal choroidal vasculopathy (PCV). Patients
with RAP lesions are typically elderly females. Patients
have predominately intraretinal edema and intraretinal
hemorrhage rather than the more typical subretinal
exudation (Fig. 5.9A). Fluorescein angiography reveals
diffuse, occult intraretinal leakage with cystoids macular
edema. Static ICG images show a clearly defined hot spot
(Figs 5.9B to D, Fig. 5.10). High speed ICG clearly defines
the intraretinal neovascular lesion with frequent retinal
to retinal anastomoses. More advanced lesions develop
subretinal neovascularization that can be differentiated
from the intraretinal component of the neovascular
complex on the high speed ICG (Fig. 5.11). Patients with
PCV present with large subretinal or sub-RPE
hemorrhages that are often centered on the disk rather
than the macula. It is a more common form of CNVM in
non-Caucasian patients. Leakage on FA is often blocked
by hemorrhage or fluid and when present appears as
occult leakage. On ICG the polypoidal lesions are well-
defined grape-like structures (Figs 5.12A to E). On high
speed ICG a feeding arteriole can often be identified.
While the advent of pharmacotherapy directed against
vascular endothelial growth factor has largely replaced
laser in the management of AMD there may still be some
B
Figs 5.9A and B
D
Figs 5.9C and D
Figs 5.9A to D: (A) Patient with RAP lesion with cystoid macular
edema and intraretinal hemorrhage. Early (B) and mid phase
(C) of high speed ICG angiogram shows a clear area of intraretinal
neovascularization with a retinal to retinal anastamoses. Postfocal
laser ICG shows obliteration of the RAP lesions (D)
B
Figs 5.10A and B
C
Fig. 5.10C
Figs 5.10A to C: Late FA images (A) show ill-defined late
intraretinal leakage with CME. Window defect secondary to
geographic atrophy is present superiorly. Frame of high speed
ICG shows well-defined intraretinal neovascularization (B).
Postfocal laser ICG shows complete obliteration of lesion (C)
B
Figs 5.11A and B
C
Fig. 5.11C
D
Fig. 5.11D
Figs 5.11A to D: Patient with stage 2 RAP lesion. FA shows occult

leakage with CME (A). Early phase of high speed ICG shows a
retinal vessel (long arrow) feeding into deeper vessel (arrowhead)
diving posterior to supply subretinal component of the CNVM
complex (B). Late phase of the high speed ICG shows the
subretinal component of the RAP lesions (arrowheads) (C).
Postablation of the feeding retinal arteriole produces complete
closure of the entire intraretinal and subretinal complex on the
high speed ICG (D)
B
Figs 5.12A and B
D
Figs 5.12C and D
E
Figs 5.12A to E: Patient with occult leakage on the late phase FA
(A). Centered on the optic nerve. Frame from ICG shows polypoidal
dilations typical of PCV (B). Patient presenting with subretinal
hemorrhage in the peripapillary region that blocks early
fluorescence (C). Late frame angiogram shows ill-defined late
leakage (D). Frame from high speed ICG shows polypoidal dilation
in the papillomacular bundle. Note additional polypoidal lesions
inferiorly (E)
role for combination therapy in the future. One laser
technique dependent on high speed ICG is the direct
photocoagulation of feeder vessels. Detection of FVs in
exudative ARMD has been reported to be from 22–86%
depending on the case series. Early studies of eyes with
“classic” CNVMs showed that FVs can be identified in at
Fig. 5.13: Single frame from high speed ICG of classic CNVM
shows a well defined feeder vessel. The lacy brush border is
well demonstrated
Fig. 5.14: FA pre- and post-feeder vessel ablation shows

complete cessation of leakage from neovascular membrane
Fig. 5.15: High speed ICG pre- and post-feeder vessel treatment.
In the pre-treatment images the central feeder vessel is visible
along with the lacy brush border of the neovascular complex.
Post-treatment ICG shows complete closure of the complex
least 29% of cases using HSICGA. The advent of newer
imaging devices and software has allowed the
identification of FVs in more than 90% or eyes with CNV
regardless of the type of leakage. There are several
configurations of subretinal neovascular complexes in
AMD that have been identified in HSICGA. Delineation
of a particular complex type can often be of assistance in
locating the point of entry of the FV. For example, a “sea
fan” or “kidney bean” configuration, which is often seen
in “classic” CNVMs, will more commonly have the FV
located at the hilus of the complex. Similarly, a
neovascular complex with a “Medusa Head” or
“cartwheel” configuration will often have the FV entering
centrally at the “hub”.
REFERENCES
1. Delori FC, Dorey CK, Staurenghi G, Arend O, Goger DG,
Weiter JJ. In vivo fluorescence of the ocular fundus exhibits
retinal pigment epithelium lipofuscin characteristics. Invest
Ophthalmol Vis Sci 1995;36(3):718-29.
2. Schmitz-Valckenberg S, Fleckenstein M, Gobel AP, et al.
Evaluation of autofluorescence imaging with the scanning
laser ophthalmoscope and the fundus camera in age-
related geographic atrophy. American Journal of
Ophthalmology 2008;146:183-92.
3. Kellner U, Kellner S, Weinitz S. Fundus autofluorescence
(488 NM) and near-infrared autofluorescence (787 NM)
visualize different retinal pigment epithelium alterations

in patients with age-related macular degeneration. Retina
2010;30:6-15.
4. Holz FG, Bindewald-Wittich A, Fleckenstein M, et al.
Progression of geographic atrophy and impact of fundus
autofluorescence patterns in age-related macular
degeneration. American Journal of Ophthalmology
2007;143:463-72.
5. Macular Photocoagulation Study. Occult choroidal
neovascularization. Arch Ophth 1996:114;400-12.
6. Freund BK, Yannuzzi LE, et al. Age-related macular
degeneration and choroidal neovascularization. Am J
Ophth 1993:115;786-91.
7. Guyer DR, Yannuzzi LA, et al. Classification of choroidal
neovascularization by digital indocyanine green video
angiography. Ophth 1996;103;2054-60.
8. Slakter JS, Yannuzzi LA, et al. A pilot study of indocyanine
green video angiography laser photocoagulation of occult
choroidal neovascularization in age-related macular
degeneration. Arch Ophth 1994;112;465-72.
9. Yannuzzi LA, Negrao S, Iida T, et al. Retinal angiomatous
proliferation in age-related macular degeneration. Retina
2001;21:416-34.
10. Johnson TM, Glaser BM. Focal laser ablation of retinal
angiomatous proliferation. Retina 2007;26:765-72.
Fluorescein
Angiography in
Retinal Vein
Occlusion
6
Pedro Amat-Peral, Javier A Montero

INTRODUCTION
Retinal vein occlusion (RVO) is a common eye condition,
second only to diabetic retinopathy as a cause of visual
loss due to retinal vascular disease.1-7 The two main forms
of retinal vein occlusion are central retinal vein occlusion
(CRVO) (Fig. 6.1) and branch retinal vein occlusion
(BRVO) (Fig. 6.2). There is a third, intermediate form,
hemi-central retinal vein occlusion which may be
considered a variant of CRVO. FA differentiates ischemic
vein occlusion from nonischemic forms. Determines the
extent of ischemia and macular edema and differentiates
telangiectasias from the new vessels. It may have some
prognostic value. Not performed during the acute phase
of the RVO by blocking effect of hemorrhage.
Fluorescein Angiography (FA) Findings in CRVO

Fluorescein angiography (FA) shows changes in vascular
caliber and permeability, and closure of the retinal
capillaries. It is helpful in making the diagnosis of CRVO,
identifying complications, and selecting patients for
treatment. Retinal arteries fluorescence may be delayed
and the arteriovenous transit time is typically prolonged,
with small areas of non-perfusion meaning risk for
neovascularization. Prolongation beyond 20 seconds and
staining of the walls of the retinal veins are usually
associated with a greater risk of rubeosis iridis.6
Fluorescein Angiography in Retinal Vein Occlusion 129
Fig. 6.1: Central retinal vein occlusion, with multiple flame shaped
retinal hemorrhages, papilledema, thickened and tortuous veins,
and macular edema
Fig. 6.2: Branch retinal vein occlusion affecting the superior

temporal vein. Initial macular edema can be appreciated in
fluorescein angiography. Notice the flame shape hemorrhages
following the lines of the nerve fiber layer
B
Figs 6.3A and B: Nonischemic central retinal vein occlusion:
(A) Central retinal vein occlusion with peripapillary retinal
hemorrhages; (B) Fluorescein angiography of same patient
shows blocked fluorescence corresponding to hemorrhages
Fig. 6.4: OCT of a branch retinal vein occlusion

with macular edema
Fig. 6.5: OCT of a central retinal vein occlusion

with macular edema
B
Figs 6.6A and B: Ischemic central retinal vein occlusion (A)
Ischemic CRVO with peripapillary retinal hemorrhgaes; (B)
Fluorescein angiography shows leaks corresponding to NVD and
areas of capillary nonperfusion
B
Figs 6.7A and B
B
Figs 6.8A and B
B
Figs 6.9A and B
Figs 6.7 to 6.9: Branch retinal vein occlusion: (A) Cases of
ischemic type of BRVO with retinal hemorrhages; (B) Fluorescein
angiography shows blocked fluorescence corresponding to
hemorrhages
FA is the most important criteria to differentiate
ischemic CRVO, with arterial circulation damage and
extensive areas of capillary nonperfusion from non-
ischemic CRVO without significant arterial damage and
with good capillary perfusion. FA has demonstrated that
even though retinal blood circulation may be slower, there
is not a complete stop and blood flows beyond the point
of the occlusion.
Changes in Arterial Circulation

• Generalized delay in the arterial phase compared to
the other eye.
• Reduced or absence of arterial ramification. Arterial
branches can be seen crossing “black”, ischemic areas.
Changes in Venous Circulation

• Delay in venous filling, more severe in ischemic forms
(10 to 25 s) than in nonischemic forms (7 to14 s), as
compared with the healthy eye.
• Increased permeability, especially in edematous (non
ischemic) forms, affecting mainly the postcapillary
veins.
• Vein wall stain, affecting more frequently ischemic
forms. It is caused by retinal ischemia. It may reduce
and disappear with the resolution of the occlusion.
• Occasionally some veins may appear completely
occluded, especially in ischemic forms. It is frequent
to find blood flow discontinuation in some retinal

branches, in a thorn-like pattern.
Changes in the Capillary Bed

• Occasionally the capillary bed background
fluorescence may disappear. This is more frequent in
ischemic forms.
• The capillary bed may appear hyperfluorescent in
edematous forms.
Optic Disk Changes

• Optic disk edema may appear in all edematous cases.
Ischemic forms may develop optic disk edema in 20%
of cases.
Macular Changes
• Erosion of the perifoveal anastomotic capillary arcade,
often causing decrease in visual acuity. The foveal
avascular zone may appear enlarged in all ischemic
forms. Nonischemic forms may show sectorial defects
of the anastomotic capillary arcade.
• Diffuse macular edema or ischemia—Macular edema
is more frequent in nonischemic forms and often
appears as a cystoid edema. Macular ischemia is more
frequent in ischemic forms.
Irideal Hyperfluorescence
• May appear as part of the anterior segment neovascu-
larization, more frequently in extensive ischemic
CRVO.
Collateral Circulation
Shunts may form in the deep retinal circulation in order
to provide an alternative for the occluded vessels. There
is almost no leakage from them, and filling is slowly and
takes place during the venous phase. They may appear
joining one vein of the occluded area to one healthy vein
(the most frequent), or joining one vein to an artery. The
most frequent are the veno-venous anastomoses which
take place in the retina, joining the upper and the lower
retina, the nasal and the temporal retina, or two different
segments of the same vessel. Occasionally they may
appear in the optic disk, such as those that follow
decompression surgery; they are usually associated to
CRVO occurring behind the lamina cribrosa and involve
the ciliary vessels.
Arteriovenous anastomosis usually point out areas of
nonperfusion, and are more frequent in ischemic CRVO
and BRVO. They may show increased permeability. Focal
vessel dilatations may appear in these anastomoses.
New Vessels
New vessels are part of the attempt to create anew
capillary net after extent capillary occlusions, and usually
develop in the limit of nonperfusion areas, though
occasionally they may appear in well perfused areas.
There is a fast filling, usually in the arterial phase and they
leak masking the limits of the new vessel. They make
appear as hyperfluorescent leaking dots in an ischemic
area. New vessels usually appear in all ischemic CRVO,
and may appear in the retina, over the retina, on the optic
disk or in the anterior segment.
Retinal and optic disk new vessels may cause vitreous
hemorrhages. Anterior segment new vessels are
associated to the apparition of neovascular glaucoma.
Fluorescein Angiography Findings in BRVO

FA usually shows filling delay in the affected area. The
fluorescein column may be narrowed in the site of the
occlusion and early hyperfluorescence may appear
proximal to the occlusion. Retinal edema is common
surrounding the area of the occluded vein, usually
affecting the macula in the form of a cystoid macular
edema. Retinal hemorrhages may block fluorescence and
disturb retinal evaluation and persist for months after the
onset of the occlusion.
As in CRVO, FA is the most important criteria to
differentiate ischemic BRVO from nonischemic BRVO.
Changes in Arterial Circulation
• Local delay in the arterial phase, affecting the retina
dependant from the occluded branch, while the
circulation of the rest of the retina behaves normally.
• Reduced or absence of arterial ramification.
Changes in Venous Circulation

• Delay in venous filling, more severe in ischemic forms,
affecting only the occluded branch.
• Increased permeability and vein wall stain.
• Completely occluded branches.
Changes in the Capillary Bed

• Occultation of the background fluorescence in the
occluded area, more frequent in ischemic forms.
Macular Changes
• Sectorial defects of the anastomotic capillary arcade.
• Diffuse macular edema or ischemia in the occluded
area, may appear both in ischemic and nonischemic
forms.
New Vessels
New vessels in BRVO are similar to those of CRVO,
though less frequent. The may appear in 50% of ischemic
BRVO, depending on the extent of ischemia. The

appearance of new vessels indicates that more than one
retinal quadrant is ischemic. Irideal new vessels appear
only in BRVO affecting one half of the retina.
REFERENCES
1. Hayreh SS, Rojas P, Podhajsky P, Montague P, Woolson RF.
Ocular neovascularization with retinal vascular occlusion
III. Incidence of ocular neovascularization with retinal vein
occlusion. Ophthalmology 1983;90:488-506.
2. David R, Zangwill L, Badarna M, Yassur Y. Epidemiology
of retinal vein occlusion and its association with glaucoma
and increased intraocular pressure. Ophthalmologica.
1988;197:69-74.
3. Priluck IA, Robertson DM, Hollenhorst RW. Long-term
follow up of occlusion of the central retinal vein in young
adults. Am J Ophthalmol 1980;90:190-202.
4. Risk factors for central retinal vein occlusion. The Eye
Disease Case-Control Study Group. Arch Ophthalmol
1996;114:545-54.
5. Minturn J, Brown GC. Progression of nonischemic central
retinal vein obstruction to the ischemic variant.
Ophthalmology. 1986;93:1158-62.
6. Sinclair SH, Gragoudas ES. Prognosis for rubeosis iridis
following central retinal vein occlusion. Br J Ophthalmol
1979;63:735-43.
7. Christoffersen NLB, Larsen M. Pathophysiology and
hemodynamics of branch retinal vein occlusion.
Ophthalmology 1999;106:2054-62.
Fluorescein
Angiography in
Vitreous
Diseases
7

OCULAR TOXOPLASMOSIS (VITREITIS)
General Aspects
The infection by Toxoplasma gondii, a strict intra-cell
parasite, is a common cause of retinal disease. Thin
infection affects not only human beings, but some other
animal species. The human infection caused by this
parasite can be congenital or acquire. In children and in
patients with some compromise of the immune system,
this disease can be severe. In these cases, the ophthalmic
compromise can become a necrotic retinitis, able to cause
blindness with a prolonged evolution and recurrences.
The infection is a zoonosis where the cats are the
definitive host. The humans can be infected by eating
meat, chicken or eggs not well cooked. In some countries,
between 20 to 70% of the general population can be
positive for toxoplasma antibodies.
Some other forms of transmission include aside from
the direct ingestion of the contaminated food, milk
ingestion, inoculation through a skin lesion, blood
transfusion and through the placenta from mother to child.
Clinical Features
The characteristic lesion consist in a zone of necrotizing
retinitis, white-yellowish colored, in the edge, or near an
scar, which is identified as a zone of choroid-retinal
atrophy with different degrees of pigmentation. It can be
Fluorescein Angiography in Vitreous Diseases 145
found accompanied of vitreous body inflammation,
frequently more severe near the lesion, which originates
the term “lighthouse in the fog”. Less frequent signs of
the disease can include zones of retinal swelling without
scars, multifocal infiltrates without vitreous reaction, and
severe forms with swelling of the optic nerve, sometimes
with macular involvement and vitreitis. Some
perivascular infiltrate is frequently seen. The reaction in
the anterior chamber can exist or not; in some cases,
endothelial deposits and other signs of anterior uveitis,
are easily seen. In some patients, we can see retinal
detachment and obstruction of the retinal vessels near the
main lesion.
The diagnosis should be suspected because of the
clinical features of the lesions. The initial investigation
should be demonstration of the IgG antibodies for
toxoplasma, at any dilution. We can perform the
determination by indirect fluorescence or the enzymatic
immunologic test (ELISA). New methods, like the
polymerase chain reaction, can be very sensitive and
specific in the determination of toxoplasma.
Fluorescein Angiography
The FAR is not mandatory for the diagnosis of
toxoplasma; it is used to make the differential diagnosis
with some other pathologies. At the initial phases, we can
observe some zones delineating a hypofluorescent area,
so that we are unable to see the choroid fluorescence;
Fig. 7.1: At this fundus photo is seen a white lesion with

cotton-like infiltrate showing the inflammatory area
Fig. 7.2: At the early phase, there is hypofluorescent area,

that blocks the view of the choroidal fluorescence
Fig. 7.3: At the artery-vein phase, the previously

hypofluorescent area starts to become hyperfluorescent
Fig. 7.4: At the late phase, the hyperfluorescence

becomes very apparent at the affected zones
Fig. 7.5: In a very late phase,

the hyperfluorescence continues
taking care of the observation we can see the retinal

vessels through a “fog-like” layer.
At the late artery-vein phase, this area that previously
was hypofluorescent, start to “turn on”, becoming
hyperfluorescent, remaining so, until the very late phases.
The blocking material (retinal exudate) visible at the
retinography, is the responsible of the hypofluorescence
in the early stages. The late hyperfluorescense is because
the fluorescein passes to the retinal tissue.
Treatment
The toxoplasmosis, in the form of a systemic and acquired
disease, is a benign one, and frequently no treatment has
to be established. But in a patient with deficiencies in the
performance of the immune system, or in the cases of the
congenital form of the disease, the treatment is mandatory.
Nevertheless, in every case of ocular toxoplasmosis, the
decision of treat, will be taken depending upon the nature
of the disease and the localization of the lesion. Some
small peripheral lesions, cannot be treated, and have
spontaneous remission, frequently without sequel. But the
big lesions of the posterior pole, and the big destructive
lesions, can cause significant visual loss without
treatment.
The classical treatment is based upon the use of
pirimetamide, sulphadiazine and steroids. This is known
as the triple pharmacologic treatment. Sometimes
clindamicine can be added with good results.
Macular
Diseases
Mahesh Shanmugam, CK Minija,

A B
C D
Figs 8.1A to D: Macular diseases—Cystoid macular edema: (A)

Color fundus photograph of the left eye in this elderly diabetic
shows retinal hemorrhages, soft exudates (arrow), few hard
exudates (arrow) and cystoid macula; (B) Early arteriovenous
phase FFA shows multiple hyperfluorescent spots at the macula
and blocked choroidal fluorescence due to retinal hemorrhages
(arrow); (C and D) Late venous phase of angiogram shows
increased intensity and area of hyperfluorescence of the spots
with fuzzy margins indicative of leakage from the micro-
aneurysms. There is pooling of the dye, the cystoid spaces around
the fovea in a petalloid pattern suggestive of cystoid macular
edema in a patient with moderate nonproliferative diabetic
retinopathy
Macular Diseases 153
A B
C D
E F
Figs 8.2A to F: (A and B) Color fundus photograph of both eyes
shows pigmentation at the fovea surrounded by retinal pigment
epithelial changes with a halo around this; (C and D) Mid venous
phase of angiogram shows area of hypoflourescence in the center
surrounded by hyperfluorescence with hypofluorescence
surrounding it; (E and F) Transition phase showing hypofluore-
scence in the center with decrease in hyperfluorescence
surrounding it suggestive of retinal pigment epithelial window
defects. This findings suggestive of Bull’s eye maculopathy
A B
C D
Figs 8.3A to D: Epiretinal membrane: (A) Color fundus

photograph of the right eye in a elderly patient showing grayish
reflex over the macula of 2 disc diameter along with the increased
tortuosity of the underlying vessels. The straightening of the
vessels nasal to the membrane is also seen; (B) Early arterio-
venous phase of the fluorescein angiogram showing increased
tortuosity (arrow) of the perifoveal capillaries with straightened
vessels over the papillomacular bundle; (C and D) Late
arteriovenous and the recirculation phase pictures showing
hyperfluorescent spots in the perifoveal region suggestive of
perifoveal leak. Impression: Findings suggestive of epiretinal
membrane with traction on the underlying blood vessels
A B
C D
Figs 8.4A to D: Stargardt’s disease: (A) Color fundus photograph
of the right eye showing chorioretinal atrophy at macula with
choroidal vessels suggestive of advanced stage of Stargardt’s
disease. Yellowish flecks distributed in all quadrants; (B) Colour
fundus photograph of left eye showing central area of beaten
bronze appearance surrounded by yellowish flecks; (C and D)
Late arteriovenous and the recirculation phase showing “Bull’s
eye” due to a “window effect” at the level of the perifoveolar
depigmentation. Other areas of hyperfluorescent spots
(transmitted fluorescence) corresponding to the lesions seen in
the color photos are well appreciable. Impression: Findings
suggestive of Stargardt’s disease
Figs 8.5A to I: Best Vitelliform dystrophy: (A) Color fundus

photograph of the right eye showing scrambled egg-yolk
appearance of the macular area; (B to D) Fluorescein
angiography showing speckled hyperfluorescence at the macula
which does not increase in intensity in the late phase of the
angiogram; (E) Color fundus photograph of the left eye showing
yellowish lesion at the fovea with hemorrhage surrounding it;
(F to I) Fluorescein angiography showing early hypofluorescence
with increase in intensity in late phase associated with fuzzy
borders suggestive of choroidal neovascular membrane.
Impression: Findings suggestive of best Vitelliform dystrophy
Figs 8.6A to D: Choroideremia: (A and B) Color fundus

photograph of the both eyes showing degeneration of the choroid
beginning with peripheral pigmentary retinopathy, followed by
atrophy of the choriocapillaris. Central patchy area of preserved
RPE can be noted; (C and D) Late arteriovenous phase pictures
showing loss of choroidal fluorescence due to atrophy of the
choroidal vessels
Figs 8.7A to D: (A) Color fundus photograph of the right eye

showing macular hole; (B to D) Early and late arteriovenous and
the recirculation phase pictures showing transmitted fluorescence
s/o window defect in foveal region. Impression: Findings
suggestive of macular hole
Figs 8.8A to D: Myopic fundus with Foster Fuchs’ spots:

(A) Color fundus photograph of the right eye in this young myopic
girl showed myopic changes with 2 spots of subretinal
hemorrhages; (B) Early arteriovenous phase FFA shows two
spots of blocked choroidal fluorescence due to subretinal
hemorrhage just temporal to the macula; (C and D) Late venous
phase of angiogram shows similar features of the early phases.
No area of underlying hyperfluorescence was noted. Impression:
Findings suggestive of Foster Fuchs’ spots
Figs 8.9A to D: Myopic choroidal neovascular membrane:

(A) Color fundus photograph of the left eye showing circumscribed
grayish lesion in the juxta foveal (inferior) region with subretinal
hemorrhage surrounding it; (B to D) Early and late arteriovenous
and the recirculation phase pictures showing a well defined hyper-
fluorescent lesion with increase in intensity in the later phases
Figs 8.10A to D: Ampiginous choroiditis: (A) Color fundus

photograph of right eye of a 35-year-old male showing creamy
yellow lesions in the posterior pole (juxtafoveal region). Periphery
showed confluent lesions with RPE atrophy and scarring; (B)
Early phase shows hypofluorescent lesions, both at and away
from the macula; (C and D) Late arteriovenous and the recircu-
lation phase pictures showing a well defined hyperfluorescent
lesion adjacent to the FAZ increasing in area and intensity s/o
active leakage at fovea. Adjacent areas of staining are seen
corresponding to the scar region
Figs 8.11A to D: Inflammatory diseases: (A) Color fundus

photograph of the right eye in a young patient shows hyperemic
disc, multiple subretinal placoid lesions involving the retinal
pigment epithelium (RPE) of the posterior pole with overlying
neurosensory retinal detachment; (B and C) Early and late
areteriovenous phase fundus fluorescein angiogram (FFA) shows
early hypofluorescence due to choroidal hypoperfusion with late
hyperfluorescence typical of inflammatory choroidal lesions; (D)
Late phase FFA shows increasing hyperfluorescence at the disc
due to leakage of the dye and pooling of the dye within areas of
neurosensory detachment as indicated by hyperfluorescence with
defined margins. This is the FFA appearance of a patient with
acute posterior multifocal pigment epitheliopathy (APMPPE)
Figs 8.12A to D: Para-foveal telangiectasia: (A) Color fundus

photograph of left eye of a 40-year-old female showing RPE
changes temporal to the foveal avascular zone with right angled
venule. (B) Early phase shows hyperfluorescent lesions, caused
by the actively leaking telangiectatic vessels; (C and D) Late
arteriovenous and the recirculation phase pictures showing late
leakage with increase in the intensity and size as compared to
the early phases
Choroidal
Neovasculari-
zation in High
Myopia
9
José Maria Ruiz Moreno

Javier A Montero (Spain)
INTRODUCTION
High myopia (HM) is a potentially disabling condition
and one of the main causes of legal blindness, as well as
the main cause of choroidal neovascularization (CNV)
among patients under 50 years of age (up to 60% of the
cases in Western Europe).1
High myopia is anatomically defined by a distention
of the posterior segment of the eyeball associated with
scleral and choroidal thinning and deviation of the optic
nerve insertion. These changes induce characteristic
myopic features such as the peripapillary crescent, the
albinoid pallor of the posterior pole and the oval and
tilted optic disk. The natural history of high myopia is
complicated by the posterior pole distention with the
appearance of hemorrhages, choroidal neovascularization
(CNV) and Fuchs’ spot.
Pathogenesis
Mechanical stress may induce choroidal ischemia
followed by atrophy of the retinal pigment epithelium
(RPE) and overlying retina and subsequent growth factor
release.2 These changes may lead to the formation of
breaks in Bruch’s membrane (lacquer cracks), RPE
atrophy, and subsequent CNV formation. Lacquer cracks
and chorioretinal atrophic areas are predictive of an
unfavorable course in pathologic myopia and are
Choroidal Neovascularization in High Myopia 167
Fig. 9.1: Color retinography (CR) and Fluorescein angiography

(FA) (medium and late phases) of a myopic patient with sub-
foveolar CNV and intraretinal hemorrhage. The leakage of the
dye is low as it is typical from these lesions. OCT study shows
CNV
associated with macular atrophy and CNV.3 Blood vessels

from the underlying choriocapillaris may grow through
the ruptured Bruch´s membrane and under the retina.
The appearance of lacquer cracks and the presence of
high levels of vascular endothelial growth factor (VEGF)
Fig. 9.2: Red free photography and FA in medium and late phases
of a patient with myopic CNV juxtafoveolar. As in previous case
the leakage of the dye is low. Horizontal OCT study shows CNV
and low levels of pigment epithelium-derived factor

(PEDF),4 are probably involved in the development of
myopic CNV. These findings have given way to new
theories and approaches to the treatment of myopic CNV.
Clinical Signs and Fluorescein Angiography

Myopic maculopathy may appear in the form of different
pathologies, though many of them are not specific of high
Fig. 9.3: FA in early, medium and late phases of a myopic

subfoveolar CNV with hemorrhages in the edge of the lesion
and leakage of the dye in late phase
myopia. Subfoveolar CNV usually leads to a decreased

central visual acuity associated with central scotoma and
metamorphopsia. Myopic CNV usually appear at an
earlier age than those associated with age-related macular
degeneration (AMD) and the diameter of the lesions is
usually smaller; however, myopic CNV are subfoveal in
up to 89% of the cases. The presence of serous retinal
detachment is usually more limited and less elevated than
in AMD, and the associated hemorrhages are smaller.
Fig. 9.4: Natural evolution of a subfoveolar myopic CNV towards

fibrosis. The FA study from May, August and November shows
the spontaneous evolution towards fibrotic scar. OCT study
confirms the fibrosis
It has been estimated that 36 to 82% of the eyes with

CNV show lacquer cracks,5 though their frequency among
highly myopic eyes without CNV is considerably lower
(0.6% for lacquer cracks, 3.2% for Fuchs’ spots).
Curtin proved the presence of a maintained defect in
the Bruch’s membrane in myopic patients, 6 and
considered that these defects are necessary to permit the
development of CNV. The low blood flow to the thinned
Fig. 9.5: CR and FA in medium and late phases of myopic CNV

with low activity characteristics (superior). Inferior, we can see
the inactivation of a myopic CNV after intravitreal injection of
bevacizumab. In the middle area we can see the change in the
OCT study before (left) and after treatment (right)
choriocapillaris and the reduced metabolic needs of the

myopic retina caused by its reduced volume would not
favor the appearance of new vessels, as is proved by the
lower frequency of ischemic obstructive and proliferative
conditions in myopic eyes.6 Since CNV is derived from
choroidal vascularization, a very low fluorescein leakage
Fig. 9.6: CR and FA study of a myopic eye with retinal hemor-

rhage and lacquer crack without CNV (superior). New FA study
one month later confirms the absence of CNV
should be expected in extreme forms of myopic

degeneration, as has been reported by Avila et al who
described fluorescein leakage limited to the border of the
chorioretinal atrophy. A better visual prognosis was found
in 91% of the cases with severe myopic degeneration, with
smaller, atrophic and quiescent CNV, compared with
CNV showing marked fluorescein leakage in cases with
moderate chorioretinal atrophy forming more severe
exudative fibrovascular scars.7 It has been postulated that
these two types of CNV may be two different stages of
the same condition, or related to age: the forms with small
Fig. 9.7: CR of a myopic eye with macular hemorrhage.

FA study confirms the absence of CNV
new vessels and little fluorescein leakage in late frames

appearing in younger patients, and the extensive
neuroepithelial detachments with marked CNV leakage
appearing among patients older than 55 years of age,
possibly associated with AMD.
Myopic CNV can be classified into two groups:
Type 1 is formed by well delimited lesions with early
Fig. 9.8: CR and FA study of a myopic eye with retinal hemor-

rhage. FA does not allow the detection of CNV. However, due to
thickness we decided to carry out an indocyanine study which
confirms the absence of CNV (inferior). Retinography of the
patient one month later without hemorrhage and no CNV
hyperfluorescence and little leakage in late phases of the

angiogram. Type 2 is formed by lesions with early
hyperfluorescence and leakage causing a neuroepithelial
detachment.
Clinically, patients report metamorphopsia caused by
the retinal deformation induced by the presence of the
new vessels and the leaking fluid, which will increase and
evolve into a relative scotoma in the central visual field
secondary to the appearance of a serous detachment or
hemorrhage. As the scotoma increases its intensity and
Fig. 9.9: CR and FA study of a myopic eye with retinal

hemorrhage. The thickness of the blood does not permit the
detection of the presence of an incipient CNV which was
confirmed with a new study with FA 15 days later (in this case
indocyanine could not be performed due to iodine allergy)
size, the perception of metamorphopsia will decrease due

to the progressive damage to the photoreceptors.
Decreased visual acuity tends to be progressive though
it may appear suddenly, especially when associated with
an intraretinal or vitreous hemorrhage.
Fluorescein angiography (FA) may show a small
hyperfluorescent area of new vessels in the early frames
and very rarely the feeding vessel can be identified. This
hyperfluorescent area is usually surrounded by a
hyperpigmented ring.
Differential Diagnosis
When we found a retinal hemorrhage in a myopic patient,
we must always to confirm the absence/presence of a
CNV. Indocyanine green angiography (ICGA) permits the
identification of CNV through hemorrhagic areas, though
it is less sensitive than FA in the detection of myopic CNV.
CNV hyperfluorescence as detected by ICGA is less
evident and shorter than by FA.
The Förster-Fuchs’ spot is a dark spot in the macula
that can be associated with a choroidal hemorrhage. Its
color, size and form may be highly variable and be related
to the amount of blood, exudates and pigment changes.
FA may show a serous or hemorrhagic pattern with a
subretinal neovascular network, which will ultimately
evolve to a macular scar. The size of the spot usually
increases with the age of the patient.
Acknowledgments
The authors have no economical interests in the devices
and procedures described.
REFERENCES
1. Cohen SY, Laroche A, Leguen Y, Soubrane G, Coscas GJ.
Ophthalmology 1996;103(8):1241-4.
2. Grossniklaus HE, Green WR. Retina 1992;12(2):127-33.
3. Ohno-Matsui K, Tokoro T. Retina 1996;16(1):29-37.
4. Tong JP, Chan WM, Liu DT, Lai TY, Choy KW, Pang CP,
Lam DS. Am J Ophthalmol 2006;141(3):456-62.
5. Rabb MF, Garoon I, LaFranco FP. Int Ophthalmol Clin
1981;21(3):51-69.
6. Curtin BJ. Trans Am Ophthalmol Soc 1977;75:67-86.
7. Avila MP, Weiter JJ, Jalkh AE, Trempe CL, Pruett RC,
Schepens CL. Ophthalmology 1984;91(12):1573-81.
Fundus
Fluorescein
Angiography
in Posterior
10 Uveitis
Dinesh Garg, Seema Gupta (India)

INTRODUCTION
Posterior uveitic entities have very characteristic clinical
features and diagnosis is mainly on clinical examination.
Differentiating infective from noninfective conditions is
important for their treatment. Macular or optic disc
involvement can cause irreversible visual impairment in
these cases and hence, early diagnosis and prompt
management is important to save vision.
Investigations such as fundus fluorescein angiography
(FFA), indocyanine green angiography (ICG), ultrasono-
graphy (USG), optical coherence tomography (OCT) and
selective laboratory investigations help in confirming the
diagnosis. Fundus fluorescein angiography is an
important diagnostic tool in cases of posterior uveitis.
It has following advantages:
1. To confirm and document the findings of clinical
examination.
2. Grading of inflammatory lesions depending upon
the level and degree of inflammation.
3. Good baseline record of inflammatory lesion to be
regularly used for follow-up.
4. To monitor the disease intensity, recurrence and
impact of therapy.
In choroiditis, there is associated inflammation of
retina and the barrier effect of retinal pigment epithelium
is lost. Fluorescein angiography therefore demonstrates
the leak. This property of fluorescein angiography is used
in all clinical cases of choroiditis to study the—
Fundus Fluorescein Angiography in Posterior Uveitis 181
a. Activity of the lesion
b. To know the extent of lesion
c. To differentiate cases of macular edema due to
choroiditis or peripheral uveitis from cases of typical
central serous retinopathy.
In uveitis, hyperfluorescence can be due to:
i. Leakage producing, pooling or staining.
ii. Increased transmission of fluorescence due to
fundus atrophy or due to small window defects.
iii. Presence of abnormal vessels (NVD, NVE, CNVM).
In uveitis, hypofluorescence can be due to:
i. Transmission reverse (Blockage)
ii. Filling defect (Vascular delayed perfusion or non-
perfusion).
FFA is useful in confirming the activity of choroiditis
characterized by early hypofluorescence and late
hyperfluorescence in case of active choroiditis. It can also
be used to detect disease sequelae such as neovascularization
and capillary nonperfusion areas. It can reveal a typical
flower petal pattern in cystoid macular edema (CME) or
pooling of dye in late phase in VKH. FFA is most useful to
detect the presence, type, and activity of choroidal
neovascularization (CNV), which is a vision-threatening
complication associated with many cases of posterior uveitis.
In patients with posterior uveitis, FFA is helpful even
after the resolution of lesions for complications related
to the disease, such as CNVM, vitreous hemorrhage or
retinal breaks.
Fig. 10.1
Fig. 10.2
Fig. 10.3
Fig. 10.4
Figs 10.1 to 10.4: A 24-year-old female presented with sudden

diminision of vision in right eye since 3 days. Her best corrected
visual acuity was 6/18 in the right eye. Patient was diagnosed as
a case of posterior uveitis right eye. Colored fundus and red free
photographs show multiple yellowish lesions in the macula
involving the fovea extending inferiorly. On FA, multiple
hyperfluorescent lesions are seen in mid and late phase with
fuzzy borders suggestive of active lesions. Patient was advised
systemic steroids
Fig. 10.5
Fig. 10.6
Fig. 10.7
Fig. 10.8
Fig. 10.9
Figs 10.5 to 10.9: A 23-year-old female presented with decrease

in vision in right eye since 2 days. Her presenting visual acuity
was finger counting at 1 meter. Patient was diagnosed as a case
of posterior uveitis right eye. Colored fundus photograph of the
patient shows multiple yellowish areas in the macula. Red free
photograph of the patient was showing whitish areas in the
macula. On FA, early phase was showing hypofluorescent lesions
in the macular area, mid phase and late phase was showing
multiple hyperfluorescent areas with blurred margins suggesting
active choroiditis. Patient was advised systemic steroids
Fig. 10.10
Fig. 10.11
Fig. 10.12
Fig. 10.13
Fig. 10.14
Figs 10.10 to 10.14: A 34-year-old female presented with sudden

decrease in vision since 15 days. Her presenting visual acuity
was 6/24 in the right eye. The patient was diagnosed as a case
of posterior uveitis. Right eye colored fundus photograph was
showing a yellowish lesion along the superior arcade with ill-
defined margins. FA was showing hypofluorescent lesion in the
early phase. Mid phase was showing leakage of the dye and
late phase was showing a hyperfluorescent lesion along the
superior arcade with ill-defined margins suggesting an active
lesion. Patient was advised intravenous methylprednisolone for
3 days followed by oral steroids
Fig. 10.15
Fig. 10.16
Fig. 10.17
Fig. 10.18
Figs 10.15 to 10.18: A 21-year-old male patient was diagnosed
as a case of posterior uveitis ( AMPPE) both eyes with history of
laser photocoagulation right eye 3 years back. Right eye coloured
fundus photograph is showing multiple yellowish lesions with
pigmentation in the centre involving the posterior pole including
the fovea and whitish lesions on red free photograph. On FA,
multiple hypofluorescent lesions are seen in early phase
becoming hyperfluorescent in late phase with well defined borders
suggesting healed posterior uveitis
Fig. 10.19
Fig. 10.20
Fig. 10.21
Fig. 10.22
Fig. 10.23
Figs 10.19 to 10.23: A 21-year-male presented to us with sudden

loss of vision in right eye since 1 day. His present visual acuity in
the right eye was 6/36. Patient was diagnosed as a case of
multifocal choroiditis involving the macula. Colored fundus
photograph is showing yellowish lesions involving the macula
extending upto the superior arcade and lesions corresponding
to that are seen on red free photograph. The lesions appear
hypofluorescent in the early phase of FA which become
hyperfluorescent in the mid phase. Late phase is showing
hyperfluorescent lesion in the macula with fuzzy margins
suggesting an active lesion. He was advised intravenous
methylprednisolone
Fig. 10.24
Fig. 10.25
Fig. 10.26
Figs 10.24 to 10.26: 16-year-old male presented with decreased

vision in the right eye since 3 days. His present visual acuity was
6/24 in the right eye. Patient was diagnosed as a case of
intermediate uveitis with cystoid macular edema (CME). Right
eye colored fundus photograph was normal but slit lamp
biomicroscopy was showing retinal thickening in the macular area.
On FA, there was accumulation of the dye in the cystoid spaces
at the fovea giving a typical petaloid appearance. Patient was
advised posterior subtenon injection of triamcinolone
Fig. 10.27
Fig. 10.28
Fig. 10.29
Fig. 10.30
Figs 10.27 to 10.30: A 46-year-old female patient presented

with sudden decrease in vision in the right eye since 1 week.
Her present visual acuity was 6/18 in the right eye. Patient was
diagnosed as a case of posterior uveitis. Right eye colored fundus
photograph was showing a yellowish lesion just temporal to the
fovea and a whitish lesion on red free photograph. FA shows a
hyperfluorescent lesion in mid phase and late phase with fuzzy
borders suggestive of active lesion. Patient was advised
intravenous methylprednisolone
Fig. 10.31
Fig. 10.32
Fig. 10.33
Fig. 10.34
Figs 10.31 to 10.34: A 40-year-female had blurring of vision in
the left eye 4 years back which had deteriorated further in last 2
months. Her present visual acuity was 6/60 in left eye. Patient
was diagnosed as a case of healed posterior uveitis in left eye.
Fundus photograph of left eye was showing a yellowish lesion
(toxoplasma scar) in the peripappillary area extending temporally
upto fovea and whitish lesion on red free photograph in the
corresponding region. FA was showing hypofluorescent lesion
in early phase becoming hyperfluorescent in the late phase with
indistinct margins suggesting reactivation of toxoplasma scar.
Patient was advised systemic steroids
Fig. 10.35
Fig. 10.36
Fig. 10.37
Fig. 10.38
Fig. 10.39
Fig. 10.40
Figs 10.35 to 10.40: A 41-year-female presented with decrease

in vision in both eyes since 4 months. Her present visual acuity
was 6/36 in both eyes. Patient was diagnosed as a case of
panuveitis in both eyes. Colored fundus photograph of right eye
shows multiple yellowish lesions involving posterior pole including
macula and whitish lesion on red free photograph in the
corresponding region. FA shows hyperfluorescent lesions in the
posterior pole in mid phase and late phase with fuzzy borders
suggesting active lesions. Left eye also shows multiple yellowish
areas in the posterior pole but not that obvious on color
photograph due to media haze. FA shows multiple hyperfluore-
scent areas involving the macula with indistinct borders. Patient
was advised systemic steroids
Fig. 10.41
Fig. 10.42
Fig. 10.43
Fig. 10.44
Figs 10.41 to 10.44: A 23-year-old male diagnosed as a case of
posterior uveitis in right eye and on treatment (oral steroids) for
last 3 months. Colored photograph of the patient shows multiple
golden yellow lesions, one involving the fovea, one along the
superior arcade and another one involving the inferior arcade in
right eye. Red free photograph shows whitish lesions in the
corresponding areas. FA early phase shows hypofluorescent
areas which on late phase are hyperfluorescent with fuzzy borders
suggesting activity (Healing posterior uveitis). Patient was
advised to continue with oral steroids
Fig. 10.45
Fig. 10.46
Fig. 10.47
Figs 10.45 to 10.47: A 14-year-female presented with redness

and foreign body sensation in right eye. Her presenting visual
acuity was 6/9 in both eyes. Patient was diagnosed as a case of
panuveitis in right eye. Fundus photograph of right eye was
showing yellowish lesions in the peripappillary area not involving
the fovea and whitish lesions on red free photograph in the
corresponding region. FA shows hyperfluorescent lesions in the
peripappillary area with fuzzy borders suggesting active lesions.
Patient was advised oral steroids
Fig. 10.48
Fig. 10.49
Fig. 10.50
Figs 10.48 to 10.50: 32-year-old male diagnosed as a case of

central serpiginous choroiditis in the right eye 2 years back. At
that time his visual acuity was 6/18. Patient again presented with
loss of vision in the right eye with presenting visual acuity of
hand movements only. Right eye colored fundus photograph was
showing multiple pigmented lesions in posterior pole suggestive
of healed geographic helicoid peripapillary choroidopathy
(GHPC). FA showed multiple hyperfluorescent areas with
indistinct borders involving macular area suggestive of activity.
Patient was advised systemic steroids
Drusen
11
Belquiz A Nassaralla (Brazil)
Drusen (singular, “druse”) are tiny yellow or white

accumulations of extracellular material that build up in
Bruch's membrane of the eye. The presence of a few small
(“hard”) drusen is normal with advancing age, and most
people over 40 have some hard drusen. However, the
presence of larger and more numerous drusen in the
macula is a common early sign of age-related macular
degeneration (AMD).1
Drusen associated with aging and macular degene-
ration are distinct from another clinical entity, optic disc
drusen, which is present on the optic nerve head.1,2 Both
age-related drusen and optic disc drusen can be observed
by ophthalmoscopy.
Through fluorescein studies, the drusen are seen as
discrete fluorescent spot which becomes manifest from
the initial arterial stage on. The intensity in fluorescence
remains almost stationary throughout the venous phase
and usually persists long after the retinal vessels have
ceased to fluoresce. The drusen do fluoresce not only
because the pigment in the pigment epithelium is absent,
but mainly because active immigration of fluorescein
takes place into the degenerated colloid body from the
choroidal space.1-4
Drusen 213
Fig. 11.1: Presence of a few small (“hard”) drusen. Fluorescein

angiogram in both eyes shows pooling noted in the pigment
epithelial detachment, as well as staining associated with the
drusen
Fig. 11.2: Soft drusen with auto-fluorescence and hyper-

fluorescence in the macular area. In this case, marked asymmetry
of the drusen can be appreciated when comparing both eyes of
the same patient
Drusen 215
Fig. 11.3: Soft drusen, are usually bilateral and symmetric,

with auto-fluorescence and hyperfluorescence in the posterior
pole
Fig. 11.4: Retina of left eye with age-related macular degene-

ration (AMD) with associated drusen with auto-fluorescence and
hyperfluorescence in the posterior pole. In the right eye, small
yellow-white spots are hard drusen. Fluorescein angiogram
shows pooling with staining of drusen
Drusen 217
Fig. 11.5: These pictures revealed bilateral and symmetric drusen

with hyperfluorescence in the eye fundus (posterior pole and middle
periphery)
Fig. 11.6: The small yellow-white spots are drusen. Temporal

multiple hard drusen with auto-fluorescence and hyperfluore-
scence
Drusen 219
Fig. 11.7: Multiple drusen bilateral and symmetric with

hyperfluorescence in the eye fundus (posterior pole and mid-
periphery)
Fig. 11.8: Mild nonexudative age-related macular degeneration

is shown with the presence of drusen (yellow deposits) in the
macular region. Macular drusen are usually symmetric and
bilateral. An angiogram, showing the staining of drusen. Drusen
absorb dye and, in the late frames of the angiogram, show
hyperfluorescence. This staining is distinguished from the
leakage that occurs when the dye spreads outside the boundary
of the lesion
Drusen 221
Fig. 11.9: The small yellow-white spots are drusen. There are
many in this eye, with auto-fluorescence and hyper-fluorescence
in the eye fundus (posterior pole and mid-periphery)
Fig. 11.10: Left eye—advanced case of nonexudative age-

related macular degeneration (AMD). This image shows drusen
that are larger, more confluent, and soft. Soft drusen are defined
as drusen that have indistinct borders. Such drusen are more likely
to convert to wet AMD. There are few areas of atrophy, where the
retinal pigment epithelium (RPE) has lost pigmentation. The retinal
cells overlying atrophic RPE are generally nonfunctional and result
in a scotoma. An angiogram with atrophic retinal pigment epithelium
(RPE) demonstrates staining of the underlying choroidal
vasculature. Normally, the intact RPE masks the presence of
choroidal fluorescence. However, when the RPE atrophies, the
underlying dye appears as an area of hyperfluorescence in the
early stages of angiography. In the late stages, the drusen lose
fluorescence in concert with (or with a small time lag) the rest of
the retinal layers. AMD scar can be noted in the right eye of the
same patient
Drusen 223
Optic disc drusen are globules of mucoproteins and
mucopolysaccharides that progressively calcify in the optic
disc.1,2 They are thought to be the remnants of the axonal
transport system of degenerated retinal ganglion cells.3-5
Optic disc drusen have also been referred to as congenitally
elevated or anomalous discs, pseudopapilledema,
pseudoneuritis, buried disc drusen, optic nerve head
drusen and disc hyaline bodies.6 They may be associated
with vision loss of varying degree occa-sionally resulting
in blindness.
Fig. 11.11: Optic disc drusen with hyperfluorescence may

appear as yellowish glistening globular masses at the optic disc.
Auto-fluorescence occurs when a highly reflective structure, such
as optic nerve head drusen, is seen when photographed prior to
the injection of fluorescein.
B
Figs 11.12A and B: Auto-fluorescence is sometimes mentioned
as a diagnostic sign of optic nerve head drusen, but some doctors
think it is of little diagnostic usefulness. If the drusen is reflective
enough to demonstrate auto-fluorescence, then it is on the
surface of the optic nerve head and it can easily be seen with an
ophthalmoscope. If the drusen is deeper in the optic nerve head,
then it will not be reflective and it will not demonstrate auto-
fluorescence (Courtesy: Prof Jayme Arana)
Drusen 225
Fig. 11.13: Optic disc drusen with hyperfluorescence

(Courtesy: Prof Jayme Arana)
Fig. 11.14: Bilateral optic disc drusen (Courtesy:

Prof Miguel H Amaro and Prof Aaron Brock Roller)
Drusen 227
REFERENCES
1. Davis PL, Jay WM. “Optic nerve head drusen”. Semin
Ophthalmol 2003;18(4):222-42.
2. “Age-Related Macular Degeneration”. National Eye
Institute. Retrieved 2008;05-21.
3. Donders FC. "Beitrage zur pathologischen Anatomie des
Auges”. Graefes Arch Clin Exp Ophthalmol 1855;1(2):
106-18.
4. Shikano S, Shimizu K. Atlas of Fluorescence Fundus
Angiography Igaku Shoin Ltd. Tokyo Japan, 1968.
5. Friedman AH, Henkind P, Gartner S. “Drusen of the optic
disc. A histopathological study”. Trans Ophthalmol Soc
UK 1975;95(1):4-9.
6. Purvin V, King R, Kawasaki A, Yee R. “Anterior ischemic
optic neuropathy in eyes with optic disc drusen”. Arch
Ophthalmol 2004;122(1):48-53.
Central Serous
Chorioretinopathy
12
Mahesh Shanmugam, CK Minija


chorioretinopathy: (A) Color fundus photograph of the right eye
in a young male showing a well defined area of neurosensory
macular detachment, (B) Early arteriovenous phase shows
intense hyperfluorescent spot nasal to fovea showing early smoke
stack appearance, (C and D) The spot of hyperfluorescence
increases in intensity and extends superiorly in the form of a
smoke stack. Late phase shows the dye to pool beneath the
retina after assuming a mushroom cloud like appearance. This
appearance is typical of smoke-stack leak of idiopathic central
serous chorioretinopathy
Central Serous Chorioretinopathy 231
Figs 12.2A to D: (A) Color fundus photograph of the right eye in

young male shows well defined ring-reflex around the fovea
suggestive of neurosensory foveal detachment, (B) Arteriovenous
phase of fluorescein angiogram shows pinpoint hyperfluorescent
spot beneath the fovea, (C) Venous phase of the angiogram
shows increased intensity and size of the hyperfluorescence with
fuzzy borders indicative of leakage, (D) Late phase FFA shows
increase in area of hyperfluorescence in an inkblot pattern. This
appearance is typical of ink-blot leak of idiopathic central serous
chorioretinopathy

a 48 years old male areas of RPE atrophy/hypertrophy in the
macular region, (B) Arteriovenous phase of fluorescein angiogram
shows multiple pinpoint hyperfluorescent spots of variable
intensity throughout the macular region. Note RPE atrophic tract
inferiorly (arrow), (C) Venous phase of the angiogram shows
increased intensity and size of the hyperfluorescence with fuzzy
borders indicative of ill-defined leakage, (D) Late phase FFA
shows increase in area of hyperfluorescence with leakage in the
subretinal space. Window defects due to RPE atrophy show less
intense fluorescence. All features suggestive of multi-focal CSR
Central Serous Chorioretinopathy 233

a middle aged male on chronic steroid therapy for post renal
transplant shows vast areas of RPE atrophy/hypertrophy in the
entire posterior pole with subretinal fibrosis in the peripapillary
region and subretinal fibrin superotemporal macula,
(B) Arteriovenous phase of fluorescein angiogram shows multiple
pinpoint hyperfluorescent spots distributed throughout the
macular region with large hypo-fluorescence patch in the temporal
peripapillary region, (C) Venous phase of the angiogram shows
increased intensity and size of the hyperfluorescence with fuzzy
borders indicative of leakage, (D) Late phase FFA shows increase
in area of hyperfluorescence indicating leakage into the subretinal
space. The peripapillary gliosis that was hypofluorescencent is
well defined in the late phase due to staining
Angiographic
Diagnosis of
Circumscribed
Choroidal
13 Hemangioma
Javier A Montero
Circumscribed choroidal hemangioma (CCH) is an

uncommon benign vascular tumor of the choroid that is
usually diagnosed between the second to the fourth
decade of life when it causes visual disturbance due to
exudative retinal detachment. The diagnosis of CCH is a
challenge for most clinicians and it is frequently
misdiagnosed for suspected choroidal melanoma or
choroidal metastasis. The occurrence of CCH is 15 to 50
times lower than that of malignant melanoma.1,2
CCH is generally a solitary finding without systemic
associations. These tumors are usually round or oval in
shape, slightly elevated, ill-defined orange red colored
lesions which frequently occur behind the equator of the
eyeball. Mushroom appearance is extremely rare. The
tumor is frequently surrounded by a pigmented rim
which has been attributed to compression of adjacent
choroid or elevation of the retinal pigment epithelium
(RPE).
These lesions are usually diagnosed when they cause
an exudative retinal detachment which extends beyond
the inferior limit of the tumor and may induce thickening
of the overlying retina with cystic degeneration. Other
symptoms of this condition are visual field defect,
metamorphopsia, flashes and floaters, and progressive
hypermetropia.
Color retinography usually shows a mottled yellow-
orange elevated lesion (Figs 13.1 and 13.2) located in the
Angiographic Diagnosis of CCH 237
proximity of the optic disk or the macula. Small, round
yellow deposits of lipid exudates may appear in the outer
cystic spaces of the retina (Fig. 13.1B). The borders of the
Fig. 13.1: Color fundus retinographies from different cases of

circumscribed choroidal hemangioma (CCH). Notice the orange-
yellow elevated lesion in the proximity of the macula. The borders
of the lesion are ill-defined and at times cannot be differentiated
from the normal choroid. Notice the blurred inferior border of the
lesion caused by exudative retinal detachment. Yellow lipid
exudates can be seen as in cases of long standing exudative
activity of the CCH
Fig. 13.2: Composite color fundus retinography in a case of an

exudative retinal detachment associated with a massive CCH in
the macula. Visual acuity was hand movements
lesion are typically blurred. Transillumination of CCH is

highly characteristic. The lesion becomes completely
illuminated when the light from the slit-lamp hits an
extreme of the tumor, what is described as the “Japanese
Lamp” phenomenon. Hyperpigmentation secondary to
RPE hyperplasia can be found which may cause a
misdiagnosis with malignant melanoma. Areas of RPE
atrophy and a bone corpuscular pattern of pigmentation
are indicative of long standing exudative retinal
detachment. Choroidal detachment may seldom occur.
Fluorescein angiography is useful to determine the
extension and degree of activity of CCH, and may aid in
the diagnosis, though the findings are not pathognomo-
nic. Meyer and Augsburger performed a comparative
study on the reliability of fluorescein angiography in the
differential diagnosis of choroidal tumors. The average
success ratio for 10 examiners was 45.4% for the different
choroidal tumors, which was similar to that of CCH, and
lower than for choroidal melanoma (55%).3 Actually, CHH
clinical picture is most similar to that seen with malignant
melanoma.4
Early choroidal frames show a pattern of hetero-
geneous hyperfluorescence which usually increases
irregularly.
The early arteriovenous phase shows multiple blood
vessels within the tumor with a lacy hyperfluorescence
pattern (Figs 13.3 to 13.11). Later frames show diffuse,
intense, hyperfluorescence with staining of the surface of
the tumor.
Venous phase angiogram shows staining of the tumor
surface, with small hypofluorescent plaques which are
probably related to melanocytes.
Late venous angiogram (30 minutes) shows a
multiloculated pattern of dye and subretinal fluorescein
Fig. 13.3: Fluorescein angiography (FA) showing the typical

image of CCH with early heterogeneous hyperfluorescence and
multiple blood vessels within the tumor with a lacy
hyperfluorescence pattern. Late frame shows diffuse, intense,
hyperfluorescence with staining of the surface of the tumor
accumulation causing retinal detachment (Figs 13.9 and

13.10).
Indocyanine green angiography (ICGA) demonstrates
an early, well-defined area of intense hyperfluorescence,
Fig. 13.4: Fluorescein angiography (FA) showing an image of

CCH similar to Figure 13.3, with a lower degree of exudation.
The macula can be involved in case of increased exudation
often followed by a characteristic “dye washout” in late

frames (Figs 13.12 and 13.13). Shields et al5 reported on the
differential diagnose of choroidal tumors by ICGA. All
CCH showed similar findings with little variability. The
onset of fluorescence occurred at 33 seconds on average
and achieved a maximum by an average of 72 seconds as
Fig. 13.5: Fluorescein angiography (FA) shows early filling of

the CCH in the choroidal phase, with progressive and irregular
staining of the tumor
a lacy diffuse hyperintense pattern first of the peripheral

portion of the tumor followed by the central portion. The
normal choroidal pattern was obscured in all cases by the
tumor vessels. The fluorescence clears at variable rates
leaving traces of fluorescence in the vessels. In all cases, a
rim of hyperfluorescence surrounding the tumor persisted
in the late frames.5
Fig. 13.6: Fluorescein angiography (FA) in a case of CCH shows

staining of the tumor surface, with small hypofluorescent plaques
Following treatment to the CCH funduscopy shows

regression of the tumor with areas of retinal pigment
epithelial stippling and atrophy are present in the treated
areas. Lipid exudates usually decrease though complete
resolution may take a longer time. Fluorescein
angiography reveals resolution of exudative retinal
detachment (Figs 13.10 and 13.11). Post-treatment ICGA
Fig. 13.7: Fluorescein angiography (FA) in a case of a massive

CCH (as in Figure 13.2) showing staining of the tumor surface
and multiple small hypofluorescent plaques, as well as pigmented
borders and inferior exudative retinal detachment
demonstrates an area of a hypovascular choroid in the

area of the CCH.
Fluorescein angiography is useful to determine the
extension and degree of activity of CCH, and may aid in
the diagnosis and follow-up after treatment. However, the
Fig. 13.8: Fluorescein angiography (FA) in a case of a massive

CCH showing staining of the tumor surface and multiple small
hypofluorescent plaques, as well as pigmented borders and
exudative retinal detachment. The massive leakage blurs the
choroidal pattern and hypofluorescent plaques in the late frames
findings are not pathognomonic, and differential

diagnosis with malignant melanoma may be difficult on
the basis of this procedure solely.4
Fig. 13.9
Fig. 13.10
Fig. 13.11
Figs 13.9 to 13.11: Fluorescein angiography (FA) in a case of

suprapapillary CCH with subretinal exudation detaching the
macula, before treatment (Figure 13.9) and following two sessions
of photodynamic therapy (Figures 13.10 and 13.11). Notice the
progressive reduction of subretinal fluid. Frames in 13.9, 13.10
and 13.11 were taken 30 minutes after the injection of fluorescein
Fig. 13.12
Fig. 13.13
Figs 13.12 and 13.13: Indocyanine green angiography (ICGA)

demonstrates an early, well-defined area of intense
hyperfluorescence. The normal choroidal pattern is obscured in
all cases by the tumor vessels. A rim of hyperfluorescence
surrounding the tumor persisted in the late frames.
REFERENCES
1. Cohen SY, Quentel G. Diagnostic angiographique des
maladies rétiniennes. Paris: Elsevier 1997.
2. Mashayekhi A, Shields CL. Circumscribed choroidal
hemangioma. Curr Opin Ophthalmol 2003;14(3):142-9.
3. Meyer K, Augsburger JJ. Independent diagnostic value of
fluorescein angiography in the evaluation of intraocular
tumors. Graefes Arch Clin Exp Ophthalmol 1999;237(6):
489-94.
4. Lemke L, Jutte A, Scheibe A. [Differential diagnosis of
malignant melanoma of the choroid with fluorescein].
Albrecht Von Graefes Arch Klin Exp Ophthalmol 1968;
175(1):58-67.
5. Shields CL, Shields JA, De Potter P. Patterns of indocyanine
green videoangiography of choroidal tumors. Br J
Ophthalmol 1995;79(3):237-45.
Posterior
Scleritis
14

GENERAL ASPECTS
The Posterior Scleritis (PS) is defined as the inflammatory
process that involves the posterior sclera; this includes the
sclera from the optic nerve until the level of the ora
serrata. Unfortunately this inflammatory process is
expanded through the ocular structures beside the sclera
itself, affecting tissues like orbit, extraocular muscles,
optic nerve, retina and choroid.
The PS is frequently associated to inflammatory
systemic diseases. Examples of these can be the
Erythematosus Lupus, the Wegener‘s disease and the
Rheumatoid Arthritis. As these inflammatory diseases, the
PE is more frequent in women.
It is classified in different forms: diffuse, nodular and
necrotizing. It can be associated with Anterior Scleritis or
can have a presentation as an isolated process. It can be
affecting both eyes, it can be recurrent, and sometimes it
can be even bilateral (in particular in women). PS is not
a disease of the childhood but it can be present in isolated
cases.
CLINICAL FEATURES
The main form of presentation is with intense ocular pain
often with reference to the periocular tissues. Some other
painless forms are rare but able to develop. Decreased
visual acuity is also a frequent symptom; sometimes a
Posterior Scleritis 253
Fig. 14.1: Picture of the fundus showing serous

retinal detachment because of PS
hyperopic shift is present and can even have an

improvement in the visual acuity at the refractive test.
This hyperopia is induced by the decreased visual axis
secondary to the increase of thickness of the posterior
Fig. 14.2: Picture of the same eye with a better view of the
inferior serous retinal detachment
sclera wall. The lost of best corrected visual acuity can be

due to the retinal involvement tan may cause
corrugations. Some other features can include choroid
folds, serous retinal detachment, macular edema and optic
disc swelling.
The diagnosis of PS is performed at the observation
of the fundus when finding changes in the retina, choroid
or optic nerve. High suspect should be observed when
some risk factors are present in the particular patient.
Fig. 14.3: Picture of the contralateral eye of the same patient

showing macular folds
The echography is an essential investigation. It shows

an increase in the retinal and choroid thickness. It can also
show edema at the Tenon‘s space; it is called the “T” sign.
The computed tomography is essential for the
diagnosis of exclusion regarding orbit inflammatory
disease, tumors, thyroid disease or inflammatory
pseudotumor. It can also be helpful to identify the
extension of the inflammatory process at the posterior
sclera and its extension to some other structures.
Fig. 14.4: FAR in artery phase showing slow

filling of the vessels and choroid swelling
Fig. 14.5: Artery phase showing mild attenuation of the vessels

Fig. 14.6: Artery-vein phase showing normal

venous circulation and choroid folds
Fig. 14.7: Middle phase artery-vein. Pattern of

choroid folds without block in the choroid filling
Fig. 14.8: Artery-vein phase, showing the inferior

serous retinal detachment
Fig. 14.9: Late phase showing choroid

hyperfluorescence with persistent folds
The magnetic resonance is able to identify the
increased thickness of the sclera and choroid. It has value
in a case of choroid detachment.
This study can show the choroid folds, the detachment
of the neurosensory retina and the pigmentary
epithelium, optic disc swelling and the presence of
macular cyst. It can also be helpful for the differential
diagnosis. We can observe a decrease speed in the choroid
perfusion, with prolonged choroid hyperfluorescence.
Less frequent are other findings like spots of leakage at
the retinal pigmentary epithelium.
TREATMENT
The PS needs, in almost every case, systemic medication.
Nonsteroid anti-inflammatory agents, are very useful, but
according the severity of the case, steroids and even
suppressors of the immune system, may be utilized. We
should always remember that the control of the systemic
disease, cause of the inflammatory process, must be
performed.
Important considerations regarding the treatment
should be done. There must exist a precise classification
about the type of scleritis and the identification of the
systemic disease. The treatment should be evaluated in
its duration according the evolution. Possible interactions
of the utilized medications should be taken in count.
Subhyaloid
Hemorrhage
15

GENERAL ASPECTS
Very often, the diabetic retinopathy remains asympto-
matic until the appearance of hemorrhages in the sub-
retinal space or in the vitreous body. The bleeding is
frequently caused by the new formation vessels but also
of the fibrotic and glial intraocular tissue.
The blood remains trapped between the retina and the
posterior hyaloid face that has been detached; this is called
subhyaloid space, preretinal or behind the posterior
hyaloid.
The hemorrhages can be product of the bleeding of
the new formation vessels in sites of localized vitreous,
with or without previous detachment. Sometimes the
hemorrhage itself can be the cause of the detachment.
CLINICAL FEATURES
Very often they have a “ship” aspect (like a boat). At the
superior portion they are horizontal while at the inferior
portion they are curved, delineating the vitreousretinal
adherence.
The hemorrhages can also be round, oval or lineal.
Those situated at the anterior retinal surface are also
included in this group. They can have spontaneous
remission over weeks or months.
Subhyaloid Hemorrhage 263
The fluorescein angiography (FAR) is a diagnostic
technique which is very helpful in the study of the
different manifestations of the diabetic retinopathy; it is
useful to locate lesions and to perform a differential
diagnosis.
In the FAR, we can observe hypofluorescent areas,
caused by the blockage of the hemorrhages. The photo-
graphic picture is not able to observe the layers beneath
the hyaloids hemorrhage.
We need to obtain color pictures previous to the
filtered ones in order to observe the hemorrhages and be
sure that they are the cause of the hypofluorescence.
TREATMENT
The subhyaloid hemorrhage occurs frequently in an area
of neovascularization without previous vitreous
detachment. Most of them have a spontaneous solution.
The treatment of choice is the extensive photocoagulation.
It is not possible for the laser to go through the hemorrhage,
but with the photocoagulation of the visible areas of retina,
there is a remission of the hemorrhage. Sometimes the
hyaloids face brakes down, dealing to a vitreous
hemorrhage that is treated with conservative measures.
Maybe the worst scenario can be the one with dense
and extensive hemorrhages over the macula inside an
incomplete vitreous detachment. The damage over the

photoreceptors in this area can be important causing some
degree of visual loss.
Without treatment there can be fibrovascular prolife-
ration from the limitant membrane and the posterior
cortical hyaloids; this can cause macular detachment or
foveal displacement because of the contraction of the
epiretinal membrane.
If photocoagulation is not enough to induce the
involution of the hemorrhage and the vascular prolife-
ration, a vitrectomy should be considered. Also if the
hemorrhage is anterior to the macula, the vitrectomy must
be performed. To perform the surgery within the first
months, allows to an easier surgical dissection, because
the plane is anatomically stablished; better visual results
can be obtained with less rate of complications. With the
early vitrectomy, the surgical success can be about 85%.
Later surgery performance can lead to more tissue
damage because of the attached tissues.
The surgical objectives are the elimination of the
posterior hyaloid face, the drainage of the hemorrhage
and the complete photocoagulation.
Subhyaloid Hemorrhage 265
Fig. 15.1: Subhyaloid hemorrhage

in a severe diabetic retinopathy
Fig. 15.2: Middle A-V phase. Big hypofluorescent zone

because of the hemorrhage blockage
Fig. 15.3: Middle A-V phase. The hypofluorescent

zones are also because of vascular obliteration
Fig. 15.4: Late phase. Notice the hypofluorescent

area over the inferotemporal arcade ischemic retina
Index
A C
Abnormal angiogram 15 Central retinal vein 131, 132
Acute central serous occlusion 33, 128, 129
chorioretinopathy 85 Central serous chorioretino-
Age-related macular pathy 82, 229
degeneration 212, 216 Changes in
Allergic reaction 10 arterial circulation 137, 141
Ampiginous choroiditis 161 capillary bed 138, 141
Anaphylaxis 10 venous circulation 137, 141
Angioid streaks 33 Choroid 4, 252
Anterior scleritis 252 hyperfluorescence 258
Arterial phase 11 Choroidal
Arteriovenous phase 11 fluorescence 146
hemangioma 41, 237
melanoma 41, 236
B metastasis 236
neovascular membranes 109
Bilateral optic disc drusen 226 neovascularization 22, 166,
Blocked fluorescence 16 181
Branch retinal vein 130 in high myopia 165
occlusion 33, 132, 136 phase 11
Bronchospasm 10 Choroideremia 157
Bruch’s membrane 166 Circinate 57
Bull’s eye 155 macular 61
maculopathy 33 edema 59
Circulatory shock 10 Diffuse

Circumscribed choroidal diabetic macular edema 43
hemangioma 236 macular edema 138
Classic choroidal neovascular Digital video angiography 4
membrane 95 Drusen 211
Classification of diabetic Dry ARMD 22
retinopathy 52
Clinical signs and fluorescein E
angiography 168
Coat’s disease 40 Enzymatic immunologic test 145
Collateral circulation 139 Epiretinal membrane 30, 154
Color Erythematosus lupus 252
fundus 152 Evolution of fluorescein
retinography 167, 236 angiography 1
Contraindications for fluore- Extracellular edema 56
scein angiography 9 Extraocular muscles 252
Contralateral eye 255 Exudative retinal detachment
Cotton wool spots 51, 146 237
Cystoid macula 152
edema 22, 43, 152, 181, 196 F
Few hard exudates 152
D
FFA in retinal detachments 75
Description of fluorangiogra- Filling defect 181
phy correspondent 87 Fluorangiography 82
Diabetic Fluorescein angiogram 55, 213
macular edema 43, 56 Fluorescein angiography 2-4,
proliferative retinopathy 51 79, 90, 128, 131, 136,
retinopathy 49, 50, 52, 55, 145, 167, 175, 239, 263
76, 262 Fluorescein angiography in
angiogram 52 retinal vein occlusion 127
Index 269
various fundus diseases 22 I
vitreous diseases 143
Fluoroscence 3 Idiopathic central serous chorio-
Fuchs’ spot 166 retinopathy 22, 30, 230
Fundus 82 Indocyanine green angiography
autofluorescence 90 89, 109, 176, 180, 240,
camera 7 249
fluorescein angiography Inflammatory diseases 22, 162
179, 180 Injection of fluorescein 90
Intense temporal traction 78
Intracellular edema 56
G
Intraretinal
Geographic helicoid peripapil- lipid exudates 59
lary choroidopathy 209 microvascular abnormalities
Glial cells 76 51, 55
Investigation in posterior
H segment diseases 5
Irideal hyperfluorescence 139
Hard Ischemic
drusen 213 central retinal vein occlusion
exudates 59 133
High macular edema 60
myopia 166 Itching 10
speed
fluorescein angiography 4 K
ICG 111
Hyperfluorescence 18, 80 Kidney bean 125
dots 83
Hyperfluorescent 147 L
Hypofluorescent 147
area 146, 266 Lacquer cracks 166
zones 266 Laryngeal edema 10
M Normal fluorescein angiogram

10
Macular
changes 138, 141
O
cotton-wool spots 56
diseases 22, 43, 151, 152, 230 Ocular toxoplasmosis 144
edema 129, 130, 132 Optic disc 67
Microaneurysms 55 changes 138
Microhemorrhages 51 drusen 223
Mixed swelling 259
CNVM 22 Optic nerve 252
edema 61 Optical coherence tomography
Myocardial infarction 10 180
Myopic choroidal neovascular Orbit 252
membrane 22, 160
P
N
Pan-retinal photocoagulation
Nausea 10 65, 66
Near infrared autofluorescence Papilledema 129
91 Para-foveal telangiectasia 163
Neovascularization elsewhere Peripapillary retinal hemor-
51 rhages 131, 133
Nerve fiber layer 130 Periphlebitis 40
Neurosensory Phases of angiogram 11
detachment of macula 84 Pigmentary epithelium 259
retina 259 Polypoidal choroidal
Nonischemic central retinal vasculopathy 112
vein occlusion 131 Posterior
Nonproliferative pole 219
diabetic retinopathy 56 scleritis 251, 252
retinopathy 51 uveitis 191
Index 271
Pre-injection fluorescence 18 Sodium fluorescein dye 2
Proliferative Soft
retinopathy 67 drusen 214
vitreoretinopathy 76 exudates 152
Stargardt’s disease 155
R Subhyaloid hemorrhage 261,
265
Retina 4, 52 Superior temporal vein 130
Retinal Systemic disease 50
arterioles 3
artery macroaneurysm 40 T
capillaries 55
capillary angioma 41 Tenon‘s space 255
exudate 148 Tortuous veins 129
hemorrhages 129, 36, 52 Toxoplasma gondii 144
microaneurysms 55 Tractional
photocoagulation 56 RD with intense fibrous
pigment epithelium 71, 90, proliferation 77
162, 166, 222, 236 retinal detachment 76, 81
thickening 58 Transmitted fluorescence 19
tissue 148 Tumors 41
vein occlusion 128
Rhegmatogenous retinal U
detachment 87, 88
Rheumatoid arthritis 252 Ultrasonography 180
S V
Scanning laser ophthalmoscope Various parts of fundus camera
111 8
Serous retinal detachment 253 Vascular
Severe diabetic retinopathy 265 disease 40
endothelial growth factor Vitelliform dystrophy 156

167 Vitreitis 144
filling defect 16, 18 Vomiting 10
occlusion 33, 40
retinopathy 40, 43 W
Vasovagal attack 10
Venous phase 14 Wegener‘s disease 252
Video angiogram 111 Window defect 21

Mini Atlas Series - Fundus Fluorescein Angiography

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Mini Atlas Series - Fundus Fluorescein Angiography

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Jaypee Gold Standard Mini Atlas Series®

Accompanying Photo CD ROM is playable only in Computer and not in DVD

José Maria Ruiz Moreno MD PhD T Mark Johnson MD FRCS

Arturo Perez Arteaga MD PhD João J Nassaralla Jr MD FRCS

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Jaypee Gold Standard Mini Atlas Series®: Fundus Fluorescein Angiography

© 2010, Jaypee Brothers Medical Publishers

First Edition: 2010

Typeset at JPBMP typesetting unit

My family (Magali, my wife and Jorge, Guillermo and Magali,

My wife Joanne and my son Connor for providing me with their

I dedicate my work to all the people in the world with

Ashok Garg MS PhD FRSM CK Minija DO DNB

José Maria Ruiz Moreno MD Pedro Amat-Peral MD

It gives me immense pleasure to write this

a guide for the interpretation of basic fluorescein findings.

Fernando Oréfice MD PhD

Fundus Fluorescein Angiography (FFA) is an invasive

1. Evolution of Fluorescein Angiography: 1

8. Macular Diseases 151

Ashok Garg (India)

Fluorescein Angiography is an important invasive

their technique for accurate and better assessment of

CK Minija, Madhu Kumar

CHEMICAL PROPERTIES OF FLUORESCEIN

Figs 2.1 to 2.3: Various parts of fundus camera

• Fundus photograph with the exciter and barrier filters

SIDE EFFECTS AND COMPLICATIONS OF

NORMAL FLUORESCEIN ANGIOGRAM

Phases of the Angiogram

The Arterial Phase

The Arteriovenous (Capillary) Phase

Fig. 2.4: Choroidal phase

Fig. 2.5: Arterial phase of FFA showing filling of the arterioles

Fig 2.6: Early arteriovenous phase of the

Fig. 2.7: Arteriovenous phase showing more

The Venous Phase

The Late Phase

Fig. 2.8: Venous phase shows loss of laminar

Fig. 2.9: Late phase FFA shows minimal dye

may appear (Fig. 2.9). Scleral staining appears as a diffuse

Fig. 2.10: Fundus fluorescein angiography of right

Fig. 2.11A: Fundus photograph of left eye shows

Fig. 2.11B: Corresponding FFA shows blood blocking

Fig. 2.12: Hypofluorescence due to

Hypoperfusion/Vascular Filling Defect

Fig. 2.13: Early venous phase shows hyperfluorescent spots

Fig. 2.14: Hyperfluorescence due to leakage: Fundus fluorescein

Fig. 2.15: Hyperfluorescence due to leakage: Fundus fluorescein

Fig. 2.16: Hyperfluorescence due to staining: late phase

Fig. 2.17: Hyperfluorescence due to staining: Color fundus

Figs 2.18A to D: Inflammatory diseases (A) Color fundus

Figs 2.19A to D: Macular diseases—Dry ARMD (A) Color fundus

Figs 2.20A to D: Macular disease—Mixed CNVM (A) Color

Figs 2.21A to D: Macular disease—Myopic choroidal neo-

Figs 2.22A to D: Macular diseases—Choroidal neovascularization

Figs 2.23A to D: Macular diseases—Cystoid macular edema

Figs 2.24A to D: Macular diseases—Idiopathic central serous

Figs 2.25A to D: Macular diseases—Idiopathic central serous

• Macular diseases—Idiopathic central serous

Figs 2.26A to D: Macular disease—Epiretinal membrane

Figs 2.27A to E: Macular disease—Bull’s eye maculopathy (A