Jordi Monés,
David R. Guyer,
Sara Krupsky,
Ephraim Friedman,
Evangelos S. Gragoudas,
Antonio P. Ciardella
Fluorescein angioscopy[1] and angiography[2] were important technological advances in the study of retinal disorders. Although choroidal circulation patterns have been described with fluorescein angiography, the limitations of this technique for studying the choroid are well known.[3-6] The excitation and fluorescence of blue-green wavelengths (peak absorption 465nm peak fluorescence 525nm) are absorbed and scattered by the pigment layers of the fundus, including the macular xanthophyll. Thus, the choroidal layers cannot be well visualized.[7-10] In addition, sodium fluorescein, which is 60-80% bound to plasma albumin,[11] rapidly leaks from the fenestrated choriocapillaris[4] and produces a diffuse background fluorescence, which further obscures the details of the choroidal vessels.[12] Finally, the intricate branching of the choroidal vascular system[13] is difficult to study with fluorescein angiography.[12]
Because the choroid is the major blood supply of the eye[14] and the outer retinal layers, a better method of studying this important tissue was needed. Near-infrared absorption angiography, using indocyanine green (ICG) as an absorbing dye, was first studied in the canine brain by Kogure and Choromokos in 1969.[15] This study led to the development of ICG choroidal angiography.
HISTORY OF ICG ANGIOGRAPHY
In 1969, a qualitative method of studying choroidal blood flow using reflective densitometry with ICG was reported.[16] After using infrared absorption ICG angiography to study the circulation of the dog cerebral surface,[15] Kogure and associates first demonstrated choroidal absorption angiography using intraarterial ICG injection and false-color infrared film in monkeys.[17] These investigators demonstrated filling of the smaller choroidal veins and occasional laminar filling of the larger choroidal veins. A choroidal arterial phase was not noted. David was the first to perform ICG absorption choroidal angiography in human patients in 1969.[18] These patients underwent intraarterial ICG injections during carotid angiography. He described diffuse choriocapillaris filling and choroidal veins draining toward the vortex veins. In 1971, Hochheimer performed choroidal absorption angiography in cats using intravenous ICG injections and black-and-white infrared film.[19] This study solved two major problems. The first was the use of intraarterial injections and the second was the inconsistency of the false-color infrared film.
Intravenous ICG absorption angiography was first successfully performed in humans by Flower and Hochheimer in 1972.[20,21] With this method, the fundus is illuminated with infrared light and the reflected light exposes the photographic film. If larger vessels are filled with enough dye to absorb the incident light, the film will not be exposed.[21,22] In 1973, Flower and Hochheimer described a method of ICG fluorescence angiography.[23] With this technique, direct fluorescence of the vessels occurred, the resolution improved, and the arterial and capillary dye phases were evident. In 1974, Flower developed a multispectral fundus camera.[12] Simultaneous ICG fluorescence and absorption angiography with fluorescein angiography was performed. This combination allowed comparison of the various types of angiograms. Clinical reports of ICG angiographic imaging of choroidal neovascularization (CNV), choroidal tumors, choroideremia, choroidal hemangiomas, and the presumed ocular histoplasmosis syndrome were published.[24-31] Further technological improvements followed.[32-34] Visualization of the choriocapillaris filling pattern with ICG and study of the temporal differences of ICG and fluorescein choroidal filling were performed in monkeys.[33] Hyvärinen and Flower presented a case of CNV in which the feeding choroidal artery was identified and photocoagulated.[35]
In 1985, Bischoff and Flower reported their 10 years of experience with ICG choroidal angiography.[36] This series included 180 angiograms of normal volunteers and 500 angiograms of patients with various fundus diseases. Hayashi and colleagues in 1986 performed ICG angiography in patients with central serous chorioretinopathy using an infrared-sensitive video camera.[37] Videoangiography has also been used by other investigators to study CNV[38-40] and choroidal blood flow.[41,42] A digital computer system has also been used to study choroidal blood flow.[43,44] Preliminary results with ICG videoangiography with the scanning laser ophthalmoscope were reported by Scheider and Schroedel in 1989,[45] and Scheider and co-workers described their first experience with this technique and CNV.[46]
In 1992, Guyer and co-workers[47] and Yannuzzi and associates[48] introduced the use of a 1024-line digital imaging system to produce high-resolution enhanced ICG images. These systems have improved the resolution of ICG videoangiography such that this technique is now of practical clinical value.
DIGITAL IMAGING SYSTEMS
The coupling of a digital imaging system with an ICG camera allows production of enhanced high-resolution (1024-line) images, which are necessary for ICG angiography. These systems produce instantaneous images that decrease patient waiting time and expedite possible laser photocoagulation treatment. Digital imaging systems allow image archiving, hard-copy generation, and direct qualitative comparison between fluorescein and ICG angiography fidings. In addition, these systems are useful for planning preoperative laser treatment strategies and for monitoring the adequacy of treatment postoperatively.
Digital imaging systems contain film and video cameras with special antireflective coatings and appropriate excitatory and barrier filters. A video camera is mounted in the camera viewfider and is connected to a video monitor. The photographer selects the image and activates a trigger that sends the image to the video adapter. The digitally charged coupling device camera (mega-plus camera) then captures the images and transmits these digitized ('1024 line × 1024 line' resolution) images to a video board within a computer processing unit. Flash synchronization allows high-resolution image capture. These images are captured at one frame per second, stored in buffer memory, and displayed on a high-contrast, high-resolution video monitor. Optical discs are used to store images after editing. Hard-copy photographs can be obtained through a printer or slides can be produced directly from a slide-making device. Finally, via telecommunications, satellite stations can be placed in laser treatment areas and in other offices.
TECHNIQUES IN ICG ANGIOGRAPHY
Advances in ICG angiography were real-time angiography,[49] wide-angle angiography,[49] and digital subtraction ICG angiography.[50]
Real-time ICG angiography uses a modified fundus camera with a diode laser illumination system that has an output at 805nm that can produce images at 30 frames per second, and allows continuous recording. The images can be acquired either as a videotape or as a single image at a frequency of 30 images per second.
Wide-angle image of the fundus can be obtained by performing ICG angiography with the aid of wide-angle contact lenses. The contact lenses used are the Volk SuperQuad 160, the Volk Quadraspheric, or the Volk Transequator (Volk, Mentor, OH). Because the image formed by these lenses lies ?1 cm in front of the lens, the fundus camera is set on A or +, so that the camera is focused on the image plane of the contact lens.
This technique allows instantaneous imaging of a large area of the fundus. The combined use of the contact lens and of the laser illumination system allows real-time imaging of a wide field of the choroidal circulation up to 160° of field of view (Figs 129.1 and 129.2).
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FIGURE 129.1 Wide-angle ICG angiography picture of a patient with a choroidal nevus. Note the typical butterfly distribution of the choroidal circulation. |
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FIGURE 129.2 A wide-angle ICG angiography picture of a patient with a subretinal hemorrhage secondary to idiopathic polypoidal choroidal vasculopathy. The image shows 160° of the fundus. |
Digital subtraction ICG angiography uses digital subtraction of sequentially acquired ICG angiographic frames to image the progression of the dye front in the choroidal circulation. A method of pseudocolor imaging of the choroid allows differentiation and identification of choroidal arteries and veins. Digital subtraction ICG angiography allows imaging of occult CNV with greater detail and in a shorter period of time than with conventional ICG angiography.
PHARMACOLOGY OF ICG
ICG was first used in 1957 to measure cardiac output.[51] It is a water-soluble tricarbocyanine dye, which is an anhydro-3,3,3',3'-tetramethyl-1,1'-di-(4-sulfobutyl)-4,5,4',5'-dibenzoindotricarbocyanine hydroxide sodium salt.
Its molecular weight is 775 Da, and its empirical formula is C43H47N2O6S2Na.[52] After intravenous injection, ICG is rapidly and almost completely bound to plasma proteins. It has been thought that ICG is bound to albumin in the blood.[53] However, 80% of ICG in human serum is actually bound to globulins, such as a-lipoproteins.[54]
The spectral absorption of ICG in aqueous solution with albumin is between 790 and 805nm.[54-56] ICG is eliminated from the blood almost exclusively by the liver and is excreted into the bile. Reabsorption of ICG from the intestine does not occur.[55-58] ICG is not detected in the cerebrospinal fluid,[58,59] nor does it cross the placental barrier.[60]
TOXICITY OF ICG
ICG is not very toxic in animals.[61-65] Only a few side effects have been reported with clinical use.[53,61,66,67] In 1978, 240000 cases of ICG use were reviewed.[68] In the early years, when the presence of 5% iodide in Cardio-Green was not appreciated, there were some side effects in patients with iodide allergies. In addition, one patient had urticaria and three patients had anaphylactic reactions. One of these patients died. Among 43 patients who underwent chronic hemodialysis, three patients with nausea and one patient with a reversible anaphylactoid reaction to ICG were reported.[69]
No side effects have been reported in the ophthalmic literature. There were no complications after intravenous doses of 150-200 mg of ICG in one study.[70] During 700 procedures in another study, no side effects were reported.[36] Thus, ICG is relatively nontoxic and appears to be safer than fluorescein dye. Between 5% and 20% of patients receiving fluorescein dye suffer from nausea, headache, or dizziness, and 5-10 in 1000 patients have allergic reactions.[11]
In a study that reported on ICG angiography performed on 1226 consecutive patients, there were three (0.15%) mild adverse reactions, four (0.2%) moderate reactions, and one (0.05%) severe adverse reaction. There were no deaths.[71]
Nevertheless, ICG may cause a severe anaphylactic reaction. ICG angiography should not be performed in patients who are allergic to iodide, in those who have a history of severe allergies, or in those who are uremic.[36] In addition, we would not recommend its use in patients with liver disease, as the dye is eliminated exclusively by this organ.
SPECIAL PROPERTIES OF ICG FOR CHOROIDAL ANGIOGRAPHY
ICG absorbs light in the near-infrared region of the spectrum (maximal absorption is approximately at 790nm)[17] and also fluoresces in the near-infrared region (maximal emission is approximately at 835nm).[72-75] Because of its activity at these longer wavelengths, ICG fluoresces through pigment and hemorrhage when it is excited by near-infrared light.
Approximately 98% of ICG is bound to plasma proteins,[53] and, therefore, the dye probably does not leak from the choriocapillaris.[72] This property allows better visualization of the choroidal vessels because ICG remains in the choroidal vasculature longer than fluorescein does. However, some authors believe that ICG can pass through the fenestrations of the choriocapillaris.[37,40] Bill stated that the choroidal blood vessels are permeable to substances with molecular weights of 17-156 kDa, such as myoglobin, albumin, and gamma globulin.[76] Thus, protein-bound ICG may pass through the fenestrations of the choriocapillaris to some extent.[36]
The liver rapidly removes ICG from the blood after intravenous injection.[53,57,77] Therefore, there is no significant ICG staining of normal ocular tissues.[17,78]
Another advantage of ICG is that its peak absorption coincides with the emission spectrum of the diode laser. This property may allow selective ablation of chorioretinal lesions using ICG dye-enhanced diode laser photocoagulation when a target tissue containing ICG is exposed to the diode laser beam.[49,50,75]
TECHNIQUE OF ICG INJECTION
A dye concentration of 0.03 mg/mL is required for maximal fluorescence of ICG in the choroidal vessels. The dye is diluted 600 times before it enters the choroidal circulation. Thus, ?20 mg of ICG in 1 mL of aqueous solvent has to be rapidly injected intracubitally. We currently inject ?50 mg of ICG for diagnostic studies. Rapid injection is essential in order to delineate various choroidal filling phases because the majority of the dye bolus must be in the choroidal vessels before reaching the retinal vasculature.[79] This injection should be immediately followed by a flush of 5 mL of normal saline solution. The timing of photography should be determined by arm to retina time,[36] since the fundus cannot be observed. This transit time is ?10s in young patients and ?12-18s in older patients.[11]
CHARACTERISTICS OF INFRARED WAVELENGTHS
Near-infrared light is used to perform choroidal angiography because it can penetrate pigmented layers[7-9] better than the shorter wavelengths of visible light. The percentage of absorption in human retinal pigment epithelium and choroid for equal intensities is between 59% and 75% for 500nm (blue-green visible light) and between 21% and 38% for 800nm (near-infrared light).[10] Near-infrared light causes ICG to fluoresce. Patients note that infrared light appears as barely visible red light. Therefore, photophobic patients may tolerate this procedure better than fluorescein angiography.[20]
Since longer wavelengths are less scattered than shorter wavelengths, near-infrared angiography may be performed in patients with diffuse opacities in the ocular media, such as cataract or vitreous hemorrhage.[24] Infrared light is less harmful than shorter-wavelength light to the retina; thus, a continuous light source may be used for high-speed angiography.[36] Thermal retinal damage, however, can be produced with the infrared light. With energies greater than 1W/cm2, the retinal temperature may rise by 10°C, and acute retinal damage can occur. The safe time exposure must be calculated.[80] The risk of near-infrared-induced lens damage is minimal with choroidal angiography.[36]
MORPHOLOGIC FEATURES OF THE CHOROIDAL VASCULATURE
NORMAL MORPHOLOGIC CHOROIDAL PATTERNS
Most of the short posterior ciliary arteries enter the eye near the macula. These choroidal arteries travel radially to the equator. After they have perforated the sclera and have entered the choroid, they divide into smaller branches. Interarterial anastomoses are common in the choroid,[81] but they cannot be distinguished with ICG angiography. The choroidal arteries do not fill at the same time. The earliest detectable filling of the arteries is usually nasal to the fovea. This region is the area of highest blood perfusion pressure in the eye.[21] The individual vessels of the choriocapillaris cannot be distinguished. The choriocapillaris filling pattern produces a faint and diffuse homogeneous fluorescence that prevents a clear visualization of the deeper choroidal layers (Fig. 129.3).[79] Choroidal veins run parallel to the periphery and eventually form the vortex veins (Fig. 129.4). Venous anastomoses occur between large vessels.[81] Veins are larger and more fluorescent than arteries, but these changes cannot be used to differentiate them. A horizontal watershed area between the superior and the inferior vessels is sometimes present (Fig. 129.5).[36] Choroidal arteries fill between 0.5 and 1s earlier than does the central retinal artery. Different phases of the ICG angiogram have been described.[36,82] The mean time values reported follow:
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FIGURE 129.3 The choroidal venous phase of ICG angiography of a normal fundus. A diffuse homogeneous fluorescence is noted in the macular area. Details of the deeper vessels in this area are not seen. Around the macular area, the choroidal veins are homogeneous in caliber and distributed uniformly to converge to form the vortex veins. |
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FIGURE 129.4 (a and b) The choroidal veins converge to form the vortex veins, with a large variability of patterns. |
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FIGURE 129.5 A horizontal watershed area between the superior and the inferior vessels found in a minority of patients. |
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Choroidal artery to choroidal vein |
1.8 s |
|
Central retinal artery to retinal vein (laminar) |
2.0 s |
|
Central retinal artery to retinal vein (full) |
6.2 s |
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Choroidal artery to vortex vein (initial) |
2.0 s |
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Choroidal artery to vortex vein (maximal) |
5.0 s |
MORPHOLOGIC FEATURES OF THE CHOROIDAL VASCULATURE
NORMAL MORPHOLOGIC CHOROIDAL PATTERNS
Most of the short posterior ciliary arteries enter the eye near the macula. These choroidal arteries travel radially to the equator. After they have perforated the sclera and have entered the choroid, they divide into smaller branches. Interarterial anastomoses are common in the choroid,[81] but they cannot be distinguished with ICG angiography. The choroidal arteries do not fill at the same time. The earliest detectable filling of the arteries is usually nasal to the fovea. This region is the area of highest blood perfusion pressure in the eye.[21] The individual vessels of the choriocapillaris cannot be distinguished. The choriocapillaris filling pattern produces a faint and diffuse homogeneous fluorescence that prevents a clear visualization of the deeper choroidal layers (Fig. 129.3).[79] Choroidal veins run parallel to the periphery and eventually form the vortex veins (Fig. 129.4). Venous anastomoses occur between large vessels.[81] Veins are larger and more fluorescent than arteries, but these changes cannot be used to differentiate them. A horizontal watershed area between the superior and the inferior vessels is sometimes present (Fig. 129.5).[36] Choroidal arteries fill between 0.5 and 1s earlier than does the central retinal artery. Different phases of the ICG angiogram have been described.[36,82] The mean time values reported follow:
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FIGURE 129.3 The choroidal venous phase of ICG angiography of a normal fundus. A diffuse homogeneous fluorescence is noted in the macular area. Details of the deeper vessels in this area are not seen. Around the macular area, the choroidal veins are homogeneous in caliber and distributed uniformly to converge to form the vortex veins. |
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FIGURE 129.4 (a and b) The choroidal veins converge to form the vortex veins, with a large variability of patterns. |
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FIGURE 129.5 A horizontal watershed area between the superior and the inferior vessels found in a minority of patients. |
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Choroidal artery to choroidal vein |
1.8 s |
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Central retinal artery to retinal vein (laminar) |
2.0 s |
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Central retinal artery to retinal vein (full) |
6.2 s |
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Choroidal artery to vortex vein (initial) |
2.0 s |
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Choroidal artery to vortex vein (maximal) |
5.0 s |
ICG ANGIOGRAPHY OF CHORIORETINAL DISORDERS
Age-Related Macular Degeneration
Macular disorders may occur secondary to specific choroidal vascular properties of this specialized area.[83] Only short arteries and arterioles are present between the ciliary arteries and the choriocapillaris in the macula. This cluster of arterial branches is greater in the macula than in any other region. These fidings may be responsible for the high pressure and rapid blood flow of the macula.[13,21,83] These pressure changes may cause choriocapillaris disease[83] and CNV.[84] The loss of contractility of the arterial wall that occurs with age may cause dilatation of the vessel.[85,86] Watershed areas of both arterial and venous circulations may be present in the macular area.[87,88,89] Hayashi and de Laey described a relationship between these choroidal 'watershed zones' and macular lesions and showed evidence of abnormal choroidal vessels. They suggested that chronic choroidal insufficiency may cause CNV.[88]
Bischoff and Flower[36] reviewed 100ICG angiograms of age-related macular degeneration (AMD) and described four abnormal fidings:
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1. |
Delayed or irregular choroidal filling, or both. In some patients, the interval between choroidal arterial and choroidal venous filling was 3-4 s. However, as these authors suggest, the significance of this fiding is uncertain because the investigators did not study an age-matched control group. |
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2. |
Generalized arterial changes. These authors describe 'wandering arteries' in some patients with AMD. |
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3. |
Localized arterial changes. Marked dilatation of macular choroidal arteries was observed in some patients. These arteries filled earlier than other vessels and often formed a loop close to the entrance site. These loops were anatomically related to overlying fundus lesions. The authors felt that a higher blood pressure in the choriocapillaris overlying vascular abnormalities may cause dilatation of the choriocapillaris and subsequent macular disease (Fig. 129.6).[84] |
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4. |
CNV. This fiding was observed by ICG angiography in only a small number of cases in Bischoff and Flower's series (Fig. 129.7). |
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FIGURE 129.6 The choroidal mid-transit phase of an ICG angiogram in a patient with age-related macular degeneration. Dilated tortuous arterial loops can be observed on the temporal side. |
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FIGURE 129.7 ((a) and (b)) Red-free photography and the late phase of the fluorescein angiogram of a poorly defied choroidal neovascular membrane. (c-e) In the ICG angiograms, the limits of the neovascular membrane can be better visualized. (f) Increased magnification shows some FVs. ((g) and (h)) With computer analysis, the membrane observed in the ICG angiogram can be traced and superimposed on the fluorescein angiogram. In some instances, ICG angiography improves the defiition of a choroidal neovascular membrane. |
Hayashi and co-workers reported that ICG angiography was particularly useful to detect occult CNV.[38] The same investigators showed that ICG leaks from CNV into the subretinal space. However, the leakage is slower and of lesser magnitude than fluorescein leakage of CNV. This slow ICG leakage is sometimes useful in defiing the borders of CNV and has delineated neovascularization not well identified with fluorescein angiography.[40] Destro and Puliafito[39] also found this technique very useful to study occult CNV, particularly those with overlying hemorrhage or those that had recurred on the edge of previously treated areas. CNV adjacent to chorioretinal scars showed greater contrast between the new vessels and the adjacent scar with ICG than with fluorescein angiography. Chorioretinal scars were hypofluorescent because of less ICG extravasation and the relative lack of choroidal vessels in those areas. ICG remained selectively in and around the CNV.[39] In addition, Scheider and colleagues described enhanced imaging of CNV by using the scanning laser ophthalmoscope with ICG angiography.[46]
High-resolution ICG images can now be produced by combining digital imaging systems and an ICG camera.[47,48] This technological advance now allows the theoretical advantage of ICG over fluorescein dye to fially be realized.
Yannuzzi and associates[48] showed that occult CNV could be converted into classic, well-defied CNV in 39% of the 129 patients in their series because of information obtained through digital ICG videoangiography. These authors found that digital ICG videoangiography is especially useful for patients with poorly defied CNV, pigment epithelial detachments (PEDs), and recurrent CNV. In many cases, the late ICG images reveal a hyperfluorescent area corresponding to an area of subretinal neovascularization that cannot be detected by fluorescein angiography. The fiding of a hyperfluorescent spot on the late ICG angiogram can separate the neovascularized portion from the serous portion of a PED.
Yannuzzi and co-workers used ICG angiography to study 235 consecutive AMD patients with occult CNV and associated vascularized PED. These eyes were divided into two groups, depending on the size and delineation of the CNV. Of the 235 eyes, 89 (38%) had a solitary area of neovascularization that was well delineated, no more than one disk diameter in size, and defied as focal CNV. The other 146 eyes (62%) had a larger area of neovascularization, with variable delineation defied as a plaque CNV.[90]
In a further report, 657 consecutive eyes with occult CNV by fluorescein angiography were studied with ICG angiography. Of 413 eyes with occult CNV without PEDs, focal areas of neovascularization were noted in 89 (22%). Overall, 142 eyes (34.3%) had lesions that were potentially treatable by laser photocoagulation based on additional information provided by ICG angiography. Of the 235 eyes with occult CNV and vascularized PEDs, 98 (42%) were eligible for laser therapy based on ICG angiography fidings. The authors calculated that ICG angiography enhances the treatment eligibility by approximately one-third.[91]
In an expanded series, the same authors reported their results on ICG angiography study of 1000 consecutive eyes with occult CNV by fluorescein angiography.[92] They recognized three morphologic types of CNV, which included focal spots (Figs 129.8 and 129.9), plaques (Fig. 129.10) (well-defied and poorly defied), and combination lesions (Fig. 129.11) (in which both focal spots and plaques are noted). Combination lesions were further subdivided into marginal spots (focal spots at the edge of a plaque of neovascularization), overlying spots (hot spots overlying plaques of neovascularization), or remote spots (a focal spot remote from a plaque of neovascularization).
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FIGURE 129.8 (a) Clinical photograph of a patient with exudative macular detachment. (b) Fluorescein angiography shows occult CNV and a serous PED. (c) ICG angiography study reveals a focal area, 'hot spot', of neovascularization at the superonasal edge of the serous PED. |
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FIGURE 129.9 (a) Clinical photograph of a patient with exudative macular detachment and subretinal hemorrhage. Note the presence of a blood level in the PED. (b) Fluorescein angiography shows blockage of fluorescence by the subretinal hemorrhage. By fluorescein angiography, there is probably occult CNV in the temporal macula. (c) ICG angiography of the same patient reveals a hot spot superior to the optic disk corresponding to a polypoidal choroidal vasculopathy. No active CNV is visible in the macular area. |
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FIGURE 129.10 (a) Clinical photograph of a patient who underwent multiple laser treatments for recurrent CNV. (b) Fluorescein angiography shows a large area of staining in the macula that may be interpreted as occult CNV. (c) Mid-phase ICG study reveals a plaque of CNV corresponding in morphology to the area of staining on fluorescein angiography.(d) Late-phase ICG study better shows the plaque lesion. |
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FIGURE 129.11 (a) Clinical photograph of a large serous PED surrounded by an exudative detachment of the neurosensory retina. (b) Mid-phase ICG study demonstrates a focal spot at the margin of the PED. (c) Late-phase ICG study reveals the presence of a plaque of inactive CNV that is not evident in the earlier phase of the study. This is an example of combination lesion: a hot spot at the margin of a plaque. As in this case, many hot spots evidenced by ICG angiography may correspond to the variant neovascularization secondary to polypoidal choroidal vasculopathy. |
The relative frequency of these lesions was as follows: focal spots 29%; plaques 61%, consisting 27% of well-defied plaques and 34% of poorly defied plaques; and combination lesions 8%, consisting of 3% of marginal spots, 4% of overlying spots, and 1% of remote spots (Table 129.1).[92] A follow-up study from the same authors of patients with newly diagnosed unilateral occult CNV secondary to AMD showed that the patients tended to develop the same morphologic type of CNV in the fellow eye.[93]
TABLE 129.1 -- Relative Frequency of Various Lesions Using Indocyanine Green Angiography in Eyes With Occult Choroidal Neovascularization
|
Lesion |
No. of Eyes (%) |
|
Focal spots |
283 (29) |
|
Plaques |
597 (61) |
|
Well-defined plaques |
265 (27) |
|
Poorly defined plaques |
332 (34) |
|
Combination lesions |
84 (8) |
|
Marginal spots |
35 (3) |
|
Overlying spots |
37 (4) |
|
Remote spots |
12 (1) |
|
Other lesions |
20 (2) |
|
Multiple spots |
7 (1) |
|
Null |
13 (1) |
From Guyer DR, Yannuzzi LA, Slakter JS, et al: Classification of choroidal neovascularization by indocyanine green angiography. Ophthalmology 1996; 103:2054, 1996.
Finally, Chang and associates[94] reported on the clinicopathologic correlation of AMD with CNV detected by ICG angiography. Histopathologic examination of the lesion revealed a thick subretinal pigment epithelium CNV corresponding to the plaquelike lesion seen with ICG angiography.
The studies just discussed demonstrate that ICG videoangiography is an important adjunctive study to fluorescein angiography in the detection of CNV. Fluorescein angiography appears to be more sensitive than ICG videoangiography in imaging fie capillaries that connect larger vessels and capillaries at the proliferating edge of well-defied CNV. Although fluorescein angiography may image well-defied CNV better than ICG videoangiography in some cases, ICG videoangiography can convert occult CNV by fluorescein angiography into well-defied classic CNV eligible for ICG-guided laser treatment in ?30% of cases.[95,96] Thus, the best imaging strategy to detect CNV is to perform fluorescein angiography and ICG videoangiography.
ICG-Guided Laser Treatment of CNV in AMD
Slakter and associates performed ICG-guided laser photocoagulation in 79 eyes with occult CNV.[97] The occult CNV was successfully eliminated with stabilized or improved visual acuity in 29 (66%) of 44 eyes with occult CNV associated with neurosensory retinal elevations, and in 15 (43%) of 35 eyes with occult CNV associated with PED. This study demonstrated that in some cases, ICG videoangiography imaging can successfully guide laser photocoagulation of occult CNV.
In another pilot study of ICG-guided laser treatment of occult CNV, Regillo and colleagues had similar results.[98]
Guyer and co-workers reported on a pilot study of ICG-guided laser photocoagulation of 23 eyes that had untreatable occult CNV secondary to AMD with focal spots at the edge of a plaque of neovascularization on the ICG study.[99] ICG-guided laser photocoagulation was applied solely to the focal spot at the edge of the plaque. At 24 months of follow-up, anatomic success with resolution of the exudative fidings was obtained in six (37.5%) of 16 eyes.[99] Importantly, these studies set the foundation for future prospective studies of ICG-guided laser treatment. In addition, they proved that the presence of a PED is a poor prognostic factor in the treatment of exudative AMD.
A recent study prospectively evaluated 185 consecutive eyes with exudative AMD and a well-delineated area (hot spot or focal area) of hyperfluorescence by ICG angiography. All the patients were divided into two groups (with PED and without PED). Of the 185 eyes, 99 eyes without PED achieved a 71% rate of obliteration at 6 months and a 48% rate of obliteration at 12 months. Eyes with PED did significantly worse, with an obliteration rate of the CNV of 23% at 12 months. The overall success rate was 36% at 12 months.[96]
A possible explanation for the high recurrence rate of occult CNV after laser photocoagulation, particularly when a vascularized PED is present, may be found in the peculiar anatomy of the CNV in such cases. It has been observed that there is a variant of CNV where the neovascularization is fed both by a choroidal and by a retinal component to create a retinochoroidal anastomosis (RCA) (Figs 129.12 and 129.13) (JS Slakter, LA Yannuzzi, U Schneider, et al, personal communication, 1998).[100]
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FIGURE 129.12 (a) Clinical photograph of a patient with a serous PED and subretinal hemorrhage. (b) High-magnification early-phase ICG study reveals retina arterial and venous branches connecting to the intraretinal neovascularization of a retinal angiomatous proliferation. |
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FIGURE 129.13 (a) Clinical photograph demonstrates a serous PED and two focal subretinal hemorrhages at the site of two RAPs. (b) High-magnification red-free photograph better shows two small retinal vessels that appear to extend into each of intraretinal new vessels. (c) Mid-phase ICG study reveals two focal hot spots corresponding to the RAPs. (d)Clinical photograph after laser treatment. Note the persistence of an anastomotic red blood vessel at the center of the white laser burn. |
In a report by Kuhn and colleagues, RCAs were identified as occurring in 93% of patients with CNV associated with a serous PED. They reported a poor success rate from laser treatment as well.[100]
Slakter and co-workers followed prospectively 150 patients with newly diagnosed exudative AMD (JS Slakter, LA Yannuzzi, U Schneider, et al, personal communication, 1998). All had clinical and fluorescein angiographic evidence of occult CNV, and each demonstrated focal areas of hyperfluorescence on ICG angiography, believed to be representative of CNV. Thirty-one (21%) of the 150 eyes were found to have an RCA. In 82 eyes, the occult CNV was associated with a serous PED. Twenty-two (27%) of these patients were noted to have RCA. In the remaining 68 cases (occult CNV without serous PED), nine eyes (13%) were found to have an RCA. Associated clinical features of RCAs were identified in preretinal or intraretinal hemorrhages at the site of the lesion, dilated tortuous retinal vessels, sudden termination of a retinal vessel, and cystoid macular edema.
The same authors found that the success rate of laser photocoagulation of RCAs without serous PED was 66%, whereas with serous PED it dropped to 14% (JS Slakter, LA Yannuzzi, U Schneider, et al, personal communication, 1998). Thus, the presence of an RCA may well provide a key to understanding the poor outcome for laser treatment in this subgroup of patients.
Sorenson and associates reported on ICG-guided laser treatment of recurrent occult CNV secondary to AMD.[101] Of 66 eyes that entered in the study, only 29 (44%) were eligible for laser treatment, and of these 29 eyes, 18 (62%) had anatomic success with an average follow-up of 6 months. Interestingly, 56% of the patients remained untreatable by ICG angiography guidance, and even with treatment, 11 of 29 patients had incomplete resolution or worsening of the exudative manifestations.
The spectrum of neovascular AMD expanded over the past decade, and entities such as retinal angiomatous proliferation (RAP) and polypoidal choroidal vasculopathy (PCV) emerged.[102-107] After retina specialists became aware of these variants of neovascular AMD, many of the previously described 'hot spots' appeared to be RAP or polypoidal lesions. That might explain the variability in the response of ICG guided treated CNV, especially regarding the 'hot spots'. Fernandes et al described the nature of focal areas of hyperfluorescence or hot spots imaged with ICG from a total of 190 patients (220 eyes) with exudative ARMD. Thirty patients and 34 eyes (16%) with hot spots were identified. Hot spots were noted to be of three distinct patterns: polypoidal choroidal neovascularization (polypoidal CNV) in 21 of 34 eyes, or 62%; retinal angiomatous proliferation (RAP) in 11 of 34 eyes, or 30%; and focal occult CNV in two of 34 eyes, or 8%. The authors concluded that focal area of intense hyperfluorescence or so-called hot spot seen on ICG angiography in exudative ARMD was due to one of three possible forms of neovascularization: most frequently polypoidal CNV, less commonly RAP, and infrequently nonspecific, focal occult CNV.[108]
Central Serous Chorioretinopathy
ICG angiography of patients with central serous chorioretinopathy may show, in the early phase of the study, diffuse or multifocal areas of choroidal hyperpermeability not associated with abnormalities detectable by fluorescein angiography or clinical examination (Fig. 129.14); in the late phase of the ICG study, there is dispersion of the fluorescence and a distinctive silhouetting of the larger choroidal vessels.[47,127-129]
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FIGURE 129.14 (a) Fluorescein angiography of a patient with central serous chorioretinopathy demonstrates multifocal pinpoint areas of leakage at the posterior pole. (b) Wide-angle ICG study reveals diffuse choroid hyperpermeability and scattered areas of hyperfluorescence. (c) Late-phase ICG study shows multifocal areas of leakage throughout the fundus. |
Diabetic Retinopathy
The choroidal angiography fidings of 60 patients with diabetic retinopathy were reported by Bischoff and Flower.[36] Most of the patients with proliferative diabetic retinopathy showed irregular and delayed choroidal filling. Approximately 50% of patients with background diabetic retinopathy showed such changes.
Choroidal Tumors
Choroidal ICG absorption angiography and ICG fluorescence angiography have been used to study choroidal tumors.[24,25,27,29,36,70,112-115] This technique can visualize the vascularization and filling patterns of nonpigmented and lightly pigmented tumors. The near-infrared light is absorbed by melanin of heavily pigmented tumors, such as choroidal melanomas, and thus blocks ICG fluorescence (Fig. 129.15). Nevertheless, the borders of the pigmented tumors may be better delineated by ICG angiography than by fluorescein angiography, and therefore ICG angiography may serve as a more accurate tool for assessment of tumor growth.[24,25,36] Bischoff and Flower reported that in some lightly pigmented tumors, ICG angiography was able to resolve some of the larger vessels of the tumor with staining of their walls and leakage into the mass.[34]
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FIGURE 129.15 Late-phase ICG angiogram of a patient with a juxtapapillary choroidal melanoma. No intratumoral vessels can be noted because the heavy pigmentation of the tumor absorbs the near-infrared wavelengths. |
In contrast to pigmented choroidal melanomas, choroidal hemangiomas show progressive hyperfluorescence because they are composed of vascular channels[29,112-114]; thus, ICG angiography may be useful in distinguishing choroidal hemangiomas from some choroidal melanomas. Choroidal metastasis originating from different primary tumors will show different angiographic characteristics, depending on the vascularity and pigmentation of the mass: Metastasis of breast carcinoma blocks choroidal fluorescence,[115] whereas metastasis of thyroid carcinoma[70] and metastatic bronchial carcinoid tumors[115] are hyperfluorescent on ICG angiography. However, intense late hyperfluorescence may be more characteristically observed with choroidal hemangiomas than with choroidal metastasis.
Choroiditis
In patients with birdshot choroiditis, ICG angiography was found to be superior to fluorescein angiography in defiing the typical patches. Multiple hypofluorescent lesions radiating to the periphery are observed between the choroidal veins.[115] These lesions are consistent with choriocapillary dropout and sometimes are more evident on later stages of the angiogram (Fig. 129.16). In patients with serpiginous choroiditis, actively inflamed areas within the lesion block choroidal fluorescence (Fig. 129.17).[114] With resolution, the fluorescence of choroidal vessels can be seen in the previously hypofluorescent areas. Late hyperfluorescence can be seen at sites at which CNV has evolved. Overt leakage from choroidal vessels was observed on ICG angiography in a patient with acute choroiditis.[115]Complete clinical angiographic resolution was noted after treatment.
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FIGURE 129.16 Multiple hypofluorescent lesions straddle the choroidal veins in birdshot choroiditis. |
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FIGURE 129.17 (a and b) Late-phase fluorescein angiograms of an eye with a recurrence of serpiginous choroidopathy. (c and d) Late-phase ICG angiograms show marked hypofluorescence in the areas of active inflammation. |
Slakter and associates reported on the ICG angiography fidings in a series of 14 patients with multifocal choroiditis. Fourteen (50%) of the 28 eyes were found to have large hypofluorescent spots in the posterior pole on ICG angiography, which, in most cases, did not correspond to clinically or fluorescein angiographically detectable lesions. In seven eyes exhibiting enlarged blind spots on visual-field testing, ICG angiography showed confluent hypofluorescence surrounding the optic nerve (Fig. 129.18). The ICG angiogram was found useful in evaluating the natural course in two patients with multifocal choroiditis as well as a response to oral prednisone therapy in four others. The ICG angiography performed in these patients showed changes correlating with the clinical course. After administration of the oral prednisone, the patients were noted to have decreased symptoms and less vitreitis on clinical examination. The ICG angiography showed a reduction in the size and number of the hypofluorescent spots in three patients, with complete resolution of these angiographic lesions noted in the fourth patient.[116]
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FIGURE 129.18 (a) Fluorescein angiography of a patient with multifocal choroiditis. Note the presence of an atrophic ring around the optic disk. (b) Late-phase ICG angiography reveals the presence of multifocal hyperfluorescent lesions that do not have a clinical or fluorescein angiography correspondence. (c) Wide-angle ICG shows scattered hypofluorescent spots around the optic disk and around the superotemporal vortex vein. |
Acute multifocal posterior placoid pigment epitheliopathy (AMPPPE) lesions are hypofluorescent by ICG angiography in both the early and the late phases of the study (Fig. 129.19). The ICG choroidal hypofluorescence in this condition may be due to a partial choroidal vascular occlusion secondary to occlusive vasculitis.[117,118]
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FIGURE 129.19 (a) Clinical photograph of a patient with acute multifocal posterior placoid pigment epitheliopathy demonstrates the pale, flat, and the placoid lesions involving the pigment epithelium. (b) Late-phase fluorescein angiography demonstrates the optic nerve staining and mottled hyperfluorescence at the periphery of the lesion. (c) Early-phase ICG study shows uniform hypofluorescence of the lesion. (d) Late-phase ICG study demonstrates a well-demarcated hypofluorescent lesion. |
Multiple evanescent white dot syndrome presents with a characteristic ICG angiography picture in the acute phase of the disease (Fig. 129.20).[119] Unlike the subtle white dots seen clinically or the indistinct punctate hyperfluorescence seen with fluorescein angiography, ICG angiography shows a pattern of hypofluorescent spots throughout the posterior pole and peripheral retina. These hypofluorescent spots appear ?10 min after the dye injection in the mid-ICG phase and persist throughout the remainder of the study. These spots appear larger than the white dots seen clinically, varying in diameter from less than 50 to ?500 ?m. Many more lesions can easily be identified on ICG angiography than on fundus examination or fluorescein angiography.
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FIGURE 129.20 (a) Color photograph of a patient with acute onset of multiple evanescent white dot syndrome. Only a few yellowish spots are visible temporally. (b) The spots are better seen with a red-free light. (c) Mid-phase fluorescein angiography demonstrates a few hyperfluorescent spots and staining of the disk margin. (d) Late-phase fluorescein angiography shows marked staining of the optic nerve. (e) Late-phase ICG study shows a hypofluorescent ring around the optic nerve. ((f) and (g)) There is also evidence of multiple hypofluorescent spots at the posterior pole and in the mid-periphery. (h) Goldmann visual field demonstrates an enlarged blind spot. (i) Late-phase ICG study 4 months later demonstrates resolution of the hypofluorescent ring around the optic nerve. (j) Goldmann visual field of the same day shows resolution of the enlarged blind spot. |
In a few cases, there is also a ring of hypofluorescence surrounding the optic nerve. In these patients, a blind spot enlargement on visual-field examination is always present. The resolution of the hypofluorescent ring around the optic nerve is accompanied by a normalization of the visual field.
During the convalescent phase, there is resolution of the hypofluorescent spots seen on ICG angiography with return of visual function and normalization of the clinical examination.
Digital ICG videoangiography is thus valuable in the diagnosis and monitoring of patients with choroiditis. Further investigation is warranted in this area.
Polypoidal Choroidal Vasculopathy
ICG angiography has been used to detect and characterize the abnormality of polypoidal choroidal vasculopathy with enhanced sensitivity and specificity.[120-122] In the initial phases of the ICG study, a distinct network of vessels within the choroid becomes visible.
Early in the course of the ICG study, the larger vessels of the polypoidal choroidal vasculopathy network start to fill before the retinal vessels, but the area within and surrounding the network is relatively hypofluorescent compared with the uninvolved choroid. Shortly after the network can be identified on the ICG angiogram, small hyperfluorescent 'polyps' become visible within the choroid.
These polypoidal structures correspond to the reddish orange choroidal excrescence seen on clinical examination. In the later phase of the angiogram, there is a uniform disappearance of the dye ('washout') from the bulging polypoidal lesions. The late ICG staining characteristic of occult CNV is not seen in the polypoidal choroidal vasculopathy vascular abnormality.
Retinal Angiomatous Proliferation
ICG angiography is useful in determining the characteristics of the variant of exudative AMD, retinal angiomatous proliferation, better than fluorescein angiography.[102-107] At stage I, the neovascularization appears as a focal area of usually very intense hyperfluorescence (hot spot). There is also some late extension of leakage within the retina from the intraretinal neovascularization (IRN) which is quite characteristic for RAP. In some cases, a retinal-retinal anastomosis can be visualized. In stage II, the ICG angiogram, besides the hot spot of the IRN, reveals a serous PED that remains hypofluorescent. In stage III, ICG angiography differentiates the serous component of the PED that remains dark, from the vascularized component which becomes hyperfluorescent. At this stage, ICG angiography may sometimes reveal RCA.
OTHER CONDITIONS
Choroidal involvement in the presumed ocular histoplasmosis syndrome has been described with ICG angiography.[31,36] Bischoff and Flower reported no significant abnormality in ICG angiograms of patients with Best's disease.[36] In these eyes, it is our experience that a hypofluorescent lesion in the macula can be found, which most likely corresponds to a blocking effect of the abnormal material, although choroidal nonperfusion at that area cannot be ruled out.
Reduced filling of the choriocapillaris in cases of myopia has been noted with ICG angiography.[36] ICG angiography is also particularly useful in patients with mild vitreous hemorrhage, which prevents evaluation by fluorescein angiography.[36]
CHOROIDAL BLOOD FLOW STUDIES
ICG angiography has also been used to investigate ocular hemodynamics. This technique is enhanced by the low affiity of ICG to ocular tissue structures as shown with 123I ICG measurements.[76] Flower, Bischoff, Prünte and their associates[41-44] have used choroidal filling times to assess the velocity of the choroidal circulation with some success. These techniques have yet to demonstrate clinical usefulness. In 1979, Ernest and Goldstick estimated choroidal blood flow in monkeys by determining the rate of clearance of ICG from the choroidal circulation.[117] Several authors have attempted to quantify morphologic and dynamic parameters in the choroidal circulation. Quantification of effective nutrient choroidal blood flow is difficult, however. Fluorescence is a superficial phenomenon. It is not proportional to the quantity of dye in the blood vessel,[79,124] and it depends on multiple variables such as vessel size, the cardiovascular system, and the injection technique.[125]
FEEDER VESSEL TREATMENT OF CHOROIDAL NEOVASCULARIZATION
Photocoagulation of the feeder vessels (FVs) has been investigated for the treatment of the CNV, especially when the neovascular membranes are under the fovea in which direct treatment with laser would cause a large and irreversible scotoma. Before the availability of antiangiogenic therapy, many cases of subfoveal CNV had a poor visual prognosis, both with laser photocoagulation and with photodynamic therapy, due to the size or angiographic subtype of the lesion.
Feeder vessel treatment (FVT) is an attractive combination since it is not drug-based and acts directly on the source of CNV blood flow, rather than the membrane itself.[126] The rationale of treatment of the FVs of the choroidal neovascular membranes arose from the initial concept of laser photocoagulation of the FVs in diabetic retinopathy.[109]
Early attempts of FVT failed due to lack of optimal technology in the imaging of the fundus as well as in delivery of laser with precision.[126] New equipment in the late 1990s demonstrated the feasibility of FVT of subfoveal and juxtafoveal CNV with efficacy.[110,111,130]
Shiraga et al[110] and Staurenghi et al[111] reported improved or stabilized visual acuity between 70% and 75% of the cases following FV photocoagulation. In many cases, the resolution of CNV and associated edema resolved dramatically and within hours of the FVT.
FVT is a two-step process, including identification and location of FVs with high-speed ICG angiography, and FV photocoagulation delivery of laser energy through a slit-lamp delivery system. It is necessary, therefore, to transfer information regarding FV location from the ICG image of the angiograms to the slit-lamp view of the fundus of the eye to be treated. Since the landmarks between the angiograms and the fundus are different, their reinterpretation is needed, with potential minor deviations and thus lack of precision. This may result in a larger area being treated than really necessary, which limits how close the treatment can be applied to the fovea.
The main advantages of FVT are: (1) Even when the CNV is large only a small fundus area is photocoagulated; (2) the photocoagulation is away from the CNV, thus sparing the fovea and the presumably damaged RPE associated with the CNV; (3) there are no adverse events due to the laser burn even after multiple laser treatments; (4) there are no untoward side effects to the treatment, even when administered multiple times; and (5) the worst adverse event reported to date is failure of treatment, in which case other treatments can be applied. FVT does not cause irreversible damage or adverse events that might impede other therapies.[126] The main disadvantages are: (1) the difficulty in precisely aiming the laser beam to the FV since the location needs be transferred from the angiogram to the fundus view; (2) reopening of the successfully treated FVs; (3) damage to the overlying RPE producing a paracentral scotoma that can be seen bt the patient; (4) changes in fundus pigmentation may cause a large variability in the efficiency of the photocoagulation; and (5) limitations in getting the treatment close to the fovea.[126]
Characterizing and defiing FVs is not an easy task; the same can be stated about understanding the angiographic-anatomic correlation, epecially when often the anatomic and functional relationships are also difficult to interpret. To solve this problem Flower proposed a theoretical anthropomorphic model of the CNV and the FVs.[130] The model implies that FVs are not the small abnormal capillary-like vessels that arise from the choriocapillaris and feed directly the CNV, but vessels of the inner layer of medium-sized choroidal arterioles and venules that supply the region of the choriocapillaris that feeds the CNV. Thus, it is not necessary that there is a direct anatomic connection between the FVs identified in the ICG angiogram and the CNV. The close proximity of these FVs in the inner layer of the medium-sized choroidal arterioles and the associated CNV vessel penetrating Bruch's membrane may result in the FV and CNV appearing to be contiguous in an ICG angiogram image. In the model system, the choriocapillaris acts like a relief valve inserted in the afferent vessel pathway, proximal to the CNV membrane.
In some classic lesions, the capillary-like segments connecting the CNV to the choriocapillaris (i.e., the penetrating vessels) actually can be long enough to be detectable as FVs in angiogram images and, therefore, directly treatable by photocoagulation, instead of photocoagulating the associated Sattler's layer vessel as in the case of occult CNV lesions (Fig. 129.21).
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FIGURE 129.21 Treatment of a 'mixed' CNV lesion. (a) Pretreatment angiogram. (b) The penetrating vessel (yellow arrow) leading to the 'classic' component was photocoagulated, resulting in closure of only the 'classic' component, as demonstrated on subsequent ICGA. (c) About 2 weeks later, the photocoagulated penetrating vessel reopened. Rather than re-treating the penetrating vessel, the FV (green arrow) that supplied blood to both the 'classic' and 'occult' components was photocoagulated. (d) Subsequent ICGA showed that both lesion components had been closed, demonstrating that closure of the Sattler's layer FV supplying blood to the area of choriocapillaris (CC) from which the lesion's penetrating vessels originated resulted in stopping blood flow through both CNV components. The mixed lesion is shown schematically in the cartoon to the left of the angiogram images showing the penetrating vessels in yellow and the FVs in green. |
Since the submacular choriocapillaris is a true vascular plexus, based on available histologic and hemodynamic data, a more sophisticated model was developed to simulate changes in blood flow through larger choriocapillaris areas after FV photocoagulation.[131] This model can explain why partial closure of the FV is enough to reduce the blood flow through the CNV achieving its functional closure. If reduced choriocapillaris blood flow is a hemodynamic mechanism of successful CNV treatment, the endpoint of any modality of laser treatment is not total obliteration of the CNV, which may result frequently in recurrence, but reduction of the CNV blood flow.[131,132]
Dye-enhanced photocoagulation of FVs using ICG had been demonstrated in animal studies,[130] and in human eyes.[133] In previous studies, dye-enhanced photocoagulation with ICG consisted of intravenous injection of large amounts of ICG dye in order to accumulate the dye in the CNV and thus theoretically enhancing the uptake of laser energy during confluent photocoagulation.[134,135]
Flower has described a technique by which FV can be identified and treated at the same time with ICG dye-enhanced photocoagulation with an adapted fundus camera that can deliver a diode laser beam.[136,137] With this modality, the laser burns can be more accurately placed and it is possible to get closer to the fovea. On the other hand, the thermal energy is more selectively confied in the vessel, making its closure more efficient and thus avoiding unnecessary thermal energy absorption by the surrounding tissues (Fig. 129.22). Immediately following FV closure, the presence of incarcerated ICG dye in the vessel adjacent to the burn proves that the blood flow has stooped in the treated vessel. (Fig. 129.23)
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FIGURE 129.22 The effects of FVT by conventional photocoagulation compared to ICG-dye enhanced photocoagulation (ICG-DEP). The cartoons suggest the differences in location for the epicenter of light to heat transduction and the volume of fundus tissue involved in the two methods of photocoagulation. With ICG-DEP the tissue volume in which transduction takes place is shifted away from the RPE to the target vessel, and it becomes more focused, thereby reducing the volume of surrounding tissue damaged. The left-hand image is from a late phase ICGA of an eye in which FVT was by conventional photocoagulation; the thermal damage was great enough that the nerve fiber layers overlying the laser spot were sufficiently damaged to produce a scotoma, and the associated dark arcuate area presumably was due to atrophic nerve fibers. The right-hand image is from a posttreatment ICGA that demonstrates an additional advantage to ICG-DEP, namely that immediately following successful FV closure, incarcerated ICG dye often can be detected at the laser burn site, which provides immediate proof that blood flow in the target vessel had stopped. |
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FIGURE 129.23 Results of ICG-DEP FVT of a classic CNV. The circles indicate the location of the CNV area in each ICGA image, and the arrow in the pretreatment image identifies the FV. In this case, immediately posttreatment, ICG-stained blood was incarcerated in the CNV as well as in the short FV segment distal to the photocoagulation site. Shortly thereafter, a posttreatment angiogram demonstrated no filling of the CNV's FV, although fluorescence from the dye-stained blood incarcerated in the CNV persisted - less intensely, however, than in the immediate posttreatment angiogram. Subsequent angiograms demonstrated that blood flow to the CNV had been successfully stopped by the treatment. |
Compared to some of the current treatments for CNV, FVT has some advantages for the patient, if ICG is not contraindicated: it is minimally invasive, safe, inexpensive, has no cumulative effect, and its failure does not preclude use of other therapies since it does not leave an irreversible damage. These attributes make FVT another attractive first-line option to treat exudative AMD.[126]
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