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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_103_библиотеки_им_акад_М_И_Перельмана
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Table 26.3 (continued)
FA appearance Category Mechanism Common examples
Hyperuorescence Pre-injection
uorescence
Transmitted
uorescence,
window defect
Abnormal
vessels
Leakage Fluorescein in the
Staining Physiological: Disc, sclera
Mismatched
monochromatic lters
Absent, atrophic, or
attenuated RPE, lack of
pigment in RPE
Fluorescence of the vessel
course
extravascular space
It is the continuous emission of uorescent
light in the abscence of uorescein dye in the
ocular structures.
Eg: Astrocytic hamartomas
Drusen of the optic nerve head
Geographic atrophy
RPE (retinal pigment epithelium) rip
Tortuosity and dilatation; anastomosis,
neovascularization, aneurysms, telangiectatic
vessels, tumor vessels
Physiological: Choriocapillaris around disc
margins, lamina cribrosa, peripapillary
atrophy
Pathological: Retinal or disc
neovascularization, intraocular inammation,
intraocular tumors, cystoid retinal edema,
non-cystoid retinal edema
Pooling: Central serous chorioretinopathy,
serous pigment epithelial detachment
Pathological: Fibrotic tissues, chorioretinal
scars, staphyloma, drusen
A. Kulkarni et al.
Fig. 26.6 Causes of hyperuorescence
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Fig. 26.7 Row 1. Proliferative diabetic retinopathy: multiple microaneurysms and neo vessels elsewhere (NVE)
(arrow) (Right-side image courtesy: Hitesh Agrawal,
MD). Row 2. (a) Right eye fundus photograph showing
microaneurysms, dot hemorrhage, and cystoid macular
edema in a patient with non-proliferative diabetic retinopathy with intermediate uveitis. (b) FA shows a petaloid
appearance corresponding to the cystoid edema. Row 3.
Classic macular new vessels (MNV): (a) Lacy pattern of
MNV in the early phase, (b) mid-phase, and (c) late phase
showing the lacy pattern increasing in size and intensity
with progressive leakage. Row 4. Acute central serous
chorioretinopathy (CSC): smokestack appearance on progressive phases of the angiogram (Image courtesy: Udit
Ajmani, MD, and Sameera Nayak, MD)
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Perecent transmission and
Wavelenght (nm)
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A. Kulkarni et al.
26.3 Indocyanine Green
Angiography
26.3.1 Technology
26.3.1.1 Properties ofIndocyanine
Green
Indocyanine green (ICG) has a molecular weight of
774.96 Daltons and is an anionic tricarbocyanine
dye [15]. To avoid recrystallization, the nished
product contains 5–9.5% sodium iodide [16]. Nearinfrared light is absorbed by ICG.The maximum
absorption occurs at 790 nm, and the maximum
emission occurs at 835nm (Fig.26.8) [17]. These
optical characteristics enable ICG imaging through
melanin, macular pigment, and blood. ICG is
mostly attached to plasma proteins, especially to
globulins like A1-lipoproteins. The liver metabolizes the dye actively and depends on hepatocellular function and liver blood ow. ICG is excreted
into the bile [3]. The kidneys, lungs, and placenta
do not show dye uptake [20]. The amount of dye
that leaks out of the fenestrations in the choroidal
arteries is low due to the high molecular weight of
ICG and because the dye usually remains bound to
plasma proteins. These properties make ICG ideal
for studying the choroidal vascular network.
26.3.1.2 Toxicity
ICG is a well-tolerated and safe dye.
Furthermore, subcutaneous extravasation of
the dye has no significant local effects [18,
21]. The incidence of side effects is usually
low, ranging from 0.15% for mild events (such
as nausea, vomiting, sneezing, and itching) to
0.2% for moderate events (such as urticaria,
syncope, pyrexia, and nerve palsy) to 0.05%
for severe events (such as bronchospasm,
laryngospasm, and anaphylaxis) [7, 21].
Although the dye has no obvious association
with iodide or shellfish sensitivity, a dosedependent pseudoallergic mechanism may
occur in some people allergic to iodine and
shellfish [16]. However, due to concerns about
potential anaphylaxis, the dye should not be
administered to patients with a history of confirmed iodine allergy [21]. Since the incidence
of adverse events is 9.3% in dialysis patients,
caution is necessary; in patients with kidney
comorbidities [16] and liver diseases [19].
ICG is a pregnancy category C drug per the
US Food and Drug Administration (FDA)
classification, which means that optimal safety
studies for the dye on pregnant women have
not been carried out [20].
absorption
Fig. 26.8 Absorption (790nm) and emission (835nm) spectrum of ICG
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60
40
20
0
600 700
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26.3.1.3 Instrument
White light with excitation and barrier lters
(640–780 nm and 820–900 nm, respectively)
serves as the light source for digital cameras. In a
cSLO system, a laser monochromatic light is utilized for excitation (785–790nm), and the barrier
lter is set at 805nm.
A 5mL saline ush should follow the rapid injection of intravenous ICG.Infracyanine green, the
iodine-free version of ICG, is available for people with iodine allergies. The injection technique
is identical, but a glucose-based solvent is
required to prepare the bolus. Thus, combined FA
and infracyanine green angiography may not be
feasible [7].
26.3.2 Techniques
26.3.2.2 Normal Phases ofICGA
The ICG lling of the choroid at the posterior
26.3.2.1 Injection Technique
ICG (25mg) is dissolved in 5mL of solvent (for
ash-based fundus cameras) or 3mL (for cSLOs
cameras). For combined FA and ICG angiography, the solvent can be saline or a Sodium uorescein solution at 10, 20, or 25% concentrations.
Table 26.4 Phases of indocyanine green angiography
Time
ICG phases
Early phase
Prearterial and arterial-1
(Fig26.9a)
Early phase
Prearterial and arterial-2
Early phase
Prearterial and arterial-3
Middle phase (Fig.26.9b) 3–15min The uorescence in the choroidal vein fades; thus, the choroidal
Late phase (Fig.26.9c) 15–60min The optic disc becomes dark.
(normal eye) Appearance
First 2s The ICG dye enters the eye, lling the choriocapillaris rapidly; the
lling is completed in 2s. The choroidal veins commence to ll
concurrently with the choriocapillaris. The major retinal vessels
appear dark and block the choroidal uorescence underneath them
3–5s The choroidal veins are more noticeable.
The retinal arterioles begin to ll with ICG dye
6s–3min The watershed zone begins to get lled, and the larger choroidal
arteries and veins begin to fade
vascular characteristics are less distinct as they travel parallel to
the periphery. Large choroidal veins in myopic eyes occasionally
exhibit laminar ow, a layered blood ow pattern created by the
slower, nonturbulent travel of blood along the vessel wall
The major choroidal and retinal arteries are seen as dark structures
on a homogeneous, faintly uorescent background
pole shows the following stages, depending on
the passage of time (Table26.4, Fig.26.9) [22].
Dynamic ICGA refers to the simultaneous
videography of choroidal and retinal vessel- lling
patterns as the ICG dye is injected. It is possible
with cSLO.
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Fig. 26.9 Normal phases of ICGA. (a) Early phase: shows greater prominence of vessels. (b) Mid phase: shows fading
of choroidal vessels, but retinal vessels are still visible; diffuse tissue staining is also present. (c) Late phase
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Fig. 26.10 A hotspot (a) and a plaque (b) as seen on ICG angiography. (Image courtesy: Hardik Kiri, MD)
A. Kulkarni et al.
Hyperuorescence in ICGA: Generally,
there are two patterns of hyperuorescence in
ICGA: hot spot and plaque.
A Hotspot (Fig.26.10a) is an area of abnor-
mal intense hyperuorescence of more than
1-disc diameter seen during the mid to late phases
of ICGA.It is usually seen in retinal angiomatous
proliferation (RAP) and polypoidal chorial vasculopathy (PCV).
A Plaque (Fig.26.10b) is an area of abnormal
intense hyperuorescence of more than 1-disc
diameter in size seen during the mid to late phases
of ICGA.It is seen in occult macular neovascularization (MNV) and central serous chorioretinopathy (CSC).
26.3.3 Clinical Application
andInterpretation
ofIndocyanine Green
Angiography
26.3.3.1 Age-Related Macular
Degeneration (AMD)
This section will use the “Consensus on
Neovascular Age-Related Macular
Degeneration Nomenclature (CONAN)” study
group- recommended new consensus nomenclature [23]. According to the Macular
Photocoagulation Study, type 1 MNV tends to
correlate with “occult” CNV on FA, and type 2
MNV is typically seen to correspond with
“classic” CNV [24].
Type 1 MNV.A dynamic ICGA can identify
the neovascular network (Fig.26.11) in brovascular PED (pigment epithelial detachment)
type of occult MNV, feeder vessels, and distinguish between a type 1 MNV and a type 3 MNV
[5, 7, 26].
Type 2 MNV. ICGA shows a discrete hyperuorescent neovascular network in the early
phase and a dark rim at the MNV boundary that
correlates to a hyperreective ring on nearinfrared reectance imaging [27].
Type 3 MNV.ICGA demonstrates the vascularity of the brovascular PED or late leakage of
an undetermined source (LLUS). When the PED
is present, type 3 MNV is typically seen within
the PED area rather than at the margin. These
lesions also exhibit increasing leakage in the late
stage; this is not seen in the other MNV lesions.
Dynamic ICGA can capture the progressive lling of the lesion, enabling the location of very
small type 3 MNV lesions of recent onset [25,
27]. The diagnosis of type 3 MNV has been typi-
cally based on the temporal evidence of the dye
lling into at least one retinal arteriole that
descends into the deep retinal space to a vascular
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Fig. 26.11 ICGA showing the vascular network in the
early phases. (a) Choroidal vessels are beginning to ll,
but no network is seen in the early phase. (b) The neovascular network can be discerned, mixed in a background of
hyperuorescent choroidal vessels. (c) Choroidal vessels
connection and with at least one draining retinal
vein, as visualized on dynamic ICG [7].
are beginning to empty, and the network is becoming
more well dened. (d) Choroidal vessels become less distinct, but the neovascular network is visible. (Image courtesy: Rajeev K Reddy Pappuru, MD)
vascular networks (BNNs), a form of aberrant
vascular networks (AVNs), can be detected in
the rst 30s, especially in the feeder vessels. In
26.3.3.2 Polypoidal Choroidal
Vasculopathy (PCV) or
Aneurysmal Type 1 MNV
Polypoidal choroidal vasculopathy (PCV) or
aneurysmal type 1 MNV can be identied and
characterized with improved sensitivity and
specicity using ICGA [15]. In the initial stages
of the ICGA, the various morphological traits of
the vascular lesion are apparent. Branched neo-
the rst minute, interconnecting channels, a type
of AVN, can be detected, which show a lack of
feeder vessels. Early hyperuorescence originating from the choroid (observed in the rst 6min)
can be used to identify polypoidal lesions
(Fig.26.12). Additional features include pulsatile lling of the polypoidal lesion (seen on
dynamic ICGA) and a hypouorescent halo surrounding the hyperuorescent nodule. After
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Fig. 26.12 (a) Right eye color fundus photo showing
massive macular hemorrhage. (b) Blocked hypouorescence due to subretinal hemorrhage in early phase ICGA.
(c–e) Polypoidal lesion lling up progressively on ICGA
10 min of ICG dye injection, late geographic
hyperuorescence (LGH) is visible as a hyperuorescent, well-delineated lesion with a rosette
pattern [28]. After 20min of ICG dye injection,
i.e., in the late phase, dye washout is seen from
these bulging dilated lesions [7].
26.3.3.3 Pachychoroid Disease
Spectrum
In ICG, pachychoroid spectrum disease is characterized by dilated submacular vessels
(pachyvessels). The pachyvessels are dilated and
relatively straight choroidal vessels without
attenuation. This contrasts with normal choroidal
vessels that typically taper in caliber as they
approach the macula. Central serous chorioretinopathy (CSC) is one of the pachychoroid diseases. In the mid to late phases of ICGA, CSC
shows multiple areas of choroidal hyperpermeability (Fig.26.13) [29]. The localized RPE leak
evident on FA may have an underlying region of
images. (f) Late phase ICGA: empty choroidal and retinal
vessels are seen, and polypoidal hyperuorescence is seen
to be reduced. (Image courtesy: Hardik Kiri, MD)
choroidal hyperpermeability. In conditions
caused by severe and chronic CSC, areas of choroidal hyperpermeability often persist and help
differentiate CSC from AMD in elderly people
with signs of type 1 MNV detected by OCT
(optical coherence tomography). The
management of CSC relies on identifying choroidal hyperpermeability on ICGA, as the verteporn photodynamic therapy (PDT) is targeted to
these regions [7].
Numerous serous PED, choroidal lling
defects, focal or punctate hyperuorescent areas
that may indicate choroidal ischemia, punctate
hyperuorescent spots, delays in the arterial lling of the choroidal arteries and choriocapillaris,
and venous congestion are other ICGA ndings
in the pachychoroid disease spectrum [21].
Pachychoroid neovascularization exhibits
type 1 MNV without aneurysmal dilations (polypoidal lesions). In eyes with pachychoroid neovascularization, type 1 MNV uorescence may
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Fig. 26.13 Focal leaking points on FFA (a) and choroidal vessel hyperpermeability and hot spots on ICG (b) in CSC
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be masked by diffuse leakage from underlying
dilated choroidal vessels during ICG angiography. These type 1 MNV lesions are detected better with OCT angiography, which frequently
demonstrates a well-dened “tangled network”
of ow signals [7].
dye. A late “washout” phenomenon is seen
as the dye fades out, and the tumor appears
hypouorescent with a hyperuorescent rim
(Fig. 26.14). This washout pattern occurs
due to the tumor’s high ow and lowresistance properties, leading to the rapid
outow of dye and tumor emptying earlier
26.3.3.4 Choroidal Tumors
FA and ICGA are used to evaluate tumor size,
location, and proximity to surrounding anatomical structures and to establish a baseline for
assessing treatment response and adverse effects.
It is a useful tool for identifying the nature of
choroidal tumors [7].
(a) Choroidal hemangioma: FA for choroidal
hemangioma is barely useful as it appears
normal if the lesions do not have exudative
complications. The ICGA ndings of choroidal hemangioma are distinct and pathognomonic; a lobular, uniform, and well-dened
pattern of hyperuorescence is seen soon
after dye administration. Intrinsic vascular
patterns in the tumor are visible within 30s
of dye injection, and by 1 min, choroidal
hemangiomas appear well-dened and
hyperuorescent as they ll completely with
than the surrounding choroidal tissue [30,
31].
(b) Choroidal melanoma: When outer retinal
atrophy is present, along with the lling of
the choroidal capillaries, an irregular
hyperuorescence in the tumor may be seen
in the early transit phase of FA [5]. In the late
phases, varying amounts of leakage can be
seen. Clumps of orange pigment appear
hypouorescent. The near-infrared light used
in ICGA offers better penetration of the pigmented layers of the fundus than the shortwavelength light used for FA. Therefore,
ICGA reveals the intrinsic microvascular
structures of the tumor, which are seen as
hyperuorescent vessels on a hypouorescent background (Fig.26.15) [7].
(c) Choroidal metastases: In the early stages,
blocking of the background uorescence is
seen on FA with mottled hyperuorescence
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Fig. 26.14 Choroidal hemangioma. (a) Right eye color
fundus photo showing a reddish, well-circumscribed choroidal mass. (b–e) A lobular, uniform, and well-dened
pattern of hyperuorescence is seen soon after dye admin-
due to the RPE defects. Irregular areas of
hyperuorescence are seen in the late phases
of FA corresponding with the tumor, a variable amount of hyperuorescent leakage,
and pooling in the subretinal space. Choroidal
metastases can be seen with ICGA as clearly
dened patches of hypouorescence without
any intrinsic microvascular networks.
Hypouorescence is typically noted throughout all the phases of the ICGA, with progressive attenuation in the late stages that lead to
a giraffe or leopard skin pattern [32].
26.3.3.5 Varix oftheVortex Vein
Ampulla
A varix of the vortex vein ampulla is an exceptionally large dilation of the vortex vein seen as a
single, smooth, red-brown elevation [33]. ICG
angiography exhibits the typical early and consistent uorescence with uniform lling [34].
istration. (f) Choroidal hemangiomas appear well-dened
and hyperuorescent in 1 min. (Image courtesy: Vishal
Ramesh Raval, MD)
26.3.3.6 Choroidal Inammation
(a) Multiple evanescent white dot syndrome
(MEWDS): At the posterior pole and peripheral retina, ICGA reveals a pattern of many
hypouorescent regions with a distinctive
lobulated form. These spots are larger on
ICGA images than on fundus examination
and FA [15], become detectable in the mid-to
late phases, and range in size from 50 to
1000 μm. Additionally, hypouorescence
can be seen in the peripapillary region [35].
The hypouorescent patches in the ICGA
vanish over time when the inammation subsides [7].
(b) Multifocal choroiditis: Active lesions are vis-
ible as uniform hypouorescent patches on
ICGA [36]. These lesions could disappear or,
more often, turn into chorioretinal scarring.
After successful therapy, the hypouorescent
patches are smaller and fewer in number. On
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Fig. 26.15 Choroidal melanoma: (a) right eye wide eld
color fundus photograph showing a well-dened, optic
disc mass; (b) enlarged view. (c, d) Early phase ICGA:
blocked uorescence due to the tumor is seen as the reti-
ICGA, the scars appear more hypouorescent than the surrounding tissue, and a window defect enables one to see the massive
choroidal vessels [7].
(c) Birdshot chorioretinopathy: On ICGA, these
lesions appear as round or oval hypouorescent spots of similar size dispersed across the
fundus, predominantly in the nasal quadrant,
followed by dye leakage in the late phases,
making the choroidal vessels appear hazy
[37]. ICGA angiography is the gold standard
for diagnosing and monitoring the activity of
birdshot lesions as this method allows these
lesions to be better visualized than on FA.In
the chronic phase of the disease, the hypouorescent spots corresponding to chorioretinal scars are evident in the late stages of
the angiography [7, 15].
nal vessels are lling gradually. (e) In the mid-phase, ne
vessels are seen within the tumor- “double circulation.”
(Image courtesy: Vishal Ramesh Raval, MD)
(d) Acute posterior multifocal placoid pigment
epitheliopathy (APMPPE). In the early
stages of ICGA, APMPPE lesions appear as
numerous placoid/ameboid hypouorescent
patches larger than those observed clinically
or with FA. The lesions are progressively
more prominent and darker than the surrounding unaffected areas in the late stages
of ICGA. Some of these lesions are gone
after therapy and become barely detectable
during clinical examinations and with
ICGA.Other lesions may turn into scars with
the loss of RPE, the choriocapillaris, and the
outer retinal layer [7]. On ICGA, these inactive lesions generally exhibit a window
defect. ICGA is also helpful in monitoring
the course of the disease and response to
treatment [38].
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