The Use of Fluorescein Angiography in Acquired Macular Diseases
ANTONIO P. CIARDELLA, STEPHEN R. KAUFMAN and LAWRENCE A. YANNUZZI
Table Of Contents
AGE-RELATED MACULAR DEGENERATION|
CENTRAL SEROUS CHORIORETINOPATHY
MACULAR CYSTS, HOLES, AND PSEUDOHOLES
CYSTOID MACULAR EDEMA
|Fluorescein angiography (FA) has been widely used clinically for more than 3 decades, and it has been valuable in the understanding, diagnosis, and treatment of acquired macular diseases. Extensive use of FA, combined with growing knowledge of the range of clinical presentations and natural histories of the acquired macular diseases, has helped clinicians obtain an appreciation of the indications for FA. Our aim in this chapter is to illustrate useful parameters of FA and to provide guidance for the optimal use of this technique. Comprehensive reviews of the interpretation of the fluorescein angiogram may be found elsewhere.1,2|
|AGE-RELATED MACULAR DEGENERATION|
Age-related macular degeneration (AMD) may be divided into two types. Nonexudative (“dry”) AMD has several morphologic forms, including “hard” discrete drusen, shallow retinal pigment epithelial detachments associated with thickened Bruch's membrane (“soft” drusen), and geographic atrophy (GA) of the retinal pigment epithelium (RPE).3 On FA the area of GA appears hyperfluorescent for window defect from the early frames of the angiogram, with late staining of the underlying sclera (Fig. 1). However, these pathologic changes can usually be assessed by clinical examination, and FA is generally not necessary to diagnose nonexudative AMD. An exception is cuticular drusen, which may appear clinically as a subtle disturbance of the RPE; FA reveals multitudes of small, discrete drusen described as “stars in the sky” (Fig. 2). The second type of AMD, which is associated with soft drusen, is known as exudative (“wet”) AMD. It is due to a choroidal neovascular membrane that has incompetent vessels resulting in detachments of the RPE and the neurosensory retina. Consequently, in patients with a large RPE and/or serous neurosensory detachment, FA is often necessary to rule out a choroidal neovascularization (CNV). In general, a small pigment epithelium detachment (PED) and a larger neurosensory detachment overlie CNV, while the opposite is generally the case in a nonexudative PED. Additionally, CNV often presents as a “notched” PED (Fig. 3).4 The presence of subretinal blood or pigment at the border of a PED strongly indicates that the detachment is exudative in origin (Fig. 4). Similarly, a rip in the RPE generally reflects subretinal fibrosis from a CNV (Fig. 5 and 6). The diagnosis is more difficult in patients who have a chronic, organized PED. Such a lesion may be due to either nonexudative AMD or to an organized, fibrotic CNV. Clinically and angiographically, it may be impossible to distinguish between these two conditions. In most cases, however, FA does assist in making the diagnosis.
In patients with a shallow neurosensory detachment, the Amsler grid test and visual acuity may be normal. If there is subtle elevation of the neurosensory retina on biomicroscopy examination, FA may demonstrate a CNV before it is symptomatic. It is often easier to evaluate both RPE and neurosensory detachments with good stereoscopic FA pictures than with direct examination.5 Consequently, FA can be helpful in determining the presence and extent of these processes. This is particularly important in patients with CNV due to AMD, because its aggressive course often requires prompt intervention to save central vision.6,7
Furthermore, FA helps in recognizing two types of CNV: classic and occult. Classic CNV consists of a well-defined neovascular membrane, which is apparent in the early phase of the angiogram and shows late leakage of dye beyond its boundaries (Fig. 7 and 8). Occult CNV is seen on by FA as an area of late hyperfluorescence of undefined origin or as a neovascularized PED (Fig. 9 and 10 ). Mixed-type CNV is predominately classic or minimally classic depending on whether the classic component is more or less than 50% of the entire lesion (Fig. 11).
FA is also useful in characterizing two other subgroups of CNV: retinal angiomatous proliferation (RAP)8–16 and polypoidal choroidal vasculopathy (PCV).17–50 RAP begins in the deep retinal complex, forming intraretinal neovascularization (IRN), which may subsequently progress to extend beneath the neurosensory retina, forming subretinal neovascularization (SRN), and a vascularized PED.8 In the later phases of the process there may be a retinal-choroidal anastomosis (RCA). Clinical features of RAP include intraretinal hemorrhages, cystoid macular edema, and associated vascularized PED. FA is useful in revealing the presence of the angiomatous intraretinal vascular complex and the extension of the associated PED (Figs. 12 and 13). However, other diagnostic techniques such as indocyanine green (ICG) angiography, and optical coherence tomography (OCT) may be able to better demonstrate the presence of the RAP lesion.
PCV is characterized by the presence of dilated, choroidal vascular channels ending in orange bulging polyp-like dilations in the peripapillary and macular area. Associated features are recurrent subretinal hemorrhage and vitreous hemorrhage, relatively minimal fibrous scarring, absence of retinal vascular disease, pathologic myopia, and signs of intraocular inflammation. FA demonstrates the presence of the dilated vascular channel (Fig. 14 and 15). However, the presence of blood and exudation may block the details of the choroidal circulation on the angiogram. In these cases, ICG angiography can better demonstrate the presence of a distinct network of vessels within the choroid because the larger choroidal vessels are filled with dye.
The FA can also distinguish CNV from simulating lesions. For example, a dark mound of blood due to hemorrhage from a CNV will block choroidal fluorescence, whereas vascular tumefactions such as choroidal hemangiomas leak fluorescein. Choroidal melanomas frequently block early choroidal fluorescence and then leak fluorescein from their intrinsic vascular network in later phases of FA.
FA is vital for the management of CNV.51–55 It can define the borders of the membrane and help localize the fovea. The final determination whether the CNV is subfoveal, juxtafoveal, or extrafoveal requires use of both FA to outline the membrane with respect to the retinal vasculature and clinical examination to define the precise location of the fovea (Fig. 16). Some patients, particularly those with high myopia, have an indistinct foveal avascular zone on FA. Other FA clues, such as the location of the macula lutea pigment, can be deceptive, because fixation does not necessarily correspond to the center of the macula lutea. The value of FA is also limited in cases of occult or poorly defined CNV, in which the exact location of the leaking CNV vessels cannot be angiographically determined (Fig. 17), and in patients with subretinal hemorrhage that obscures the membrane. In these patients, ICG angiography may be the most precise means of localization.
Conventional laser thermophotocoagulation is the treatment of choice for extrafoveal, well-defined, classic CNV. Photodynamic treatment (PDT) is the treatment of choice for subfoveal, predominantly classic CNV. FA is used to localize the lesion in relation to the fovea, classify the subtype, choose the type of procedure, and guide the treatment (Figs. 18, 19, and 20).56–73
FA is needed to assess response to laser photocoagulation of a CNV and to diagnose recurrent membranes.51,54 The authors generally obtain angiograms 2 weeks, 1 month, 3 months, and 6 months after treatment. The risk of recurrence is greatest during the first 3 months, and the patient, who often has decreased vision due to prior neurosensory detachment, may be asymptomatic. FA is also needed to evaluate the results of PDT. In the original protocol of the Verteporfin in Photodynamic Therapy (VIP) and Treatment of Age-Related Macular Degeneration with Photodynamic Therapy (TAP) studies, a fluorescein angiogram was obtained every 3 months, and if there was persistent leakage from the CNV PDT was applied again (see Fig. 18–20).60
|CENTRAL SEROUS CHORIORETINOPATHY|
Central serous chorioretinopathy (CSC) is characterized by breakdown of the outer retinal barrier, with leakage of fluid through a defect in the retinal pigment epithelium into the subretinal space, resulting in a serous neurosensory detachment.78–205 The ophthalmologist can usually diagnose CSC based on the clinical examination and demographic information.93–95 Most patients with CSC are middle-aged men74 who often have type A personalities.75, 96–104 CSC has also been associated to the use of corticosteroids,105–118 pregnancy,119–126 increased adrenaline level and stress,127–132 hemodialysis,133,134 collagen vascular diseases,135–147 and hypertension.148–157 CSC typically presents as a large serous detachment in the posterior pole without an obvious source of the subretinal fluid.76 However, because a small CNV cannot be ruled out, FA is usually done to confirm the diagnosis. Characteristically, there is a small RPE defect, which hyperfluoresces early, and then there is slow filling of the overlying neurosensory detachment, which may have a classic “smokestack” (Fig. 21) or “ink blot” (Fig. 22) appearance.158–161 Occasionally, FA demonstrates multiple sites of leakage (Figs. 23, 24, and 25). FA sometimes fails to distinguish CSC from CNV readily because fibrinous subretinal precipitates can cause slow filling of the RPE detachment, which is suggestive of CNV (Fig. 26). Sometimes peripapillary PCV can cause a neurosensory macular detachment masquerading as CSC (Fig. 27).77
The diagnosis of CSC may be difficult if there is neither RPE detachment nor evidence of leakage into the subretinal space. Possible causes of a neurosensory elevation without evidence of leakage in the macula include CSC with the RPE detachment located outside the macular area (Fig. 28), CSC with a healed leak (in which case the neurosensory detachment should resolve soon), peripheral retinal hole, choroidal tumor, congenital optic nerve pit, and idiopathic uveal effusion syndrome. There are several other considerations in a patient who presents with a localized serous detachment of the macula, including age-related macular degeneration,162–164 a macular hole in a patient with high myopia, malignant hypertension, toxemia of pregnancy, collagen vascular disease, disseminated intravascular coagulation, choroidal inflammatory disease, Coat's disease (Fig. 29), and ocular contusion. Usually, these conditions are diagnosed based on clinical examination. ICG angiography may be helpful in differentiating CSC from AMD. On ICG studies there is often diffuse choroidal hyperpermeability in patients with CSC.165–181
The clinical course of CSC tends to be benign, with complete resolution within 3 to 4 months.74 Focal laser treatment of small RPE detachments has never been shown to improve the long-term vision of patients with CSC,78 but it does hasten resolution of the neurosensory detachment and it reduces the recurrence rate.79,182–203 The best candidates for treatment include those who have occupational needs and are strongly motivated to undergo treatment, and those with a chronic neurosensory detachment of 4 months or longer, particularly if there is evidence of loss of central or paracentral vision.55 Laser treatment to the point of RPE leakage is very effective in resolving the neurosensory detachment.80,81 In chronic CSC, grid treatment reduces macular edema and lipid and tends to stabilize vision.82,83
FA is rarely needed to follow the course of patients with CSC. As the subretinal fluid resolves, patients will have improved visual acuity, decreased metamorphopsia, and decreased induced hyperopia. Contact lens biomicroscopy reliably evaluates the amount of subretinal fluid. If the neurosensory detachment persists for several weeks after laser treatment, FA can be valuable in elucidating whether the RPE detachment has failed to resolve despite treatment, whether there have been unnoticed RPE defects that were not treated, whether there is recurrent CSC, or whether there is another cause of neurosensory detachment.
Although several authorities consider CSC to be a relatively benign disease,84 some patients develop recurrent, chronic neurosensory detachments that slowly cause photoreceptor degeneration. These patients often have a diffuse RPE “ooze,” reflecting generalized RPE dysfunction (Fig. 30). Their persistent neurosensory detachment can eventually lead to significant visual loss.85
Clinically discernible peripheral dependent bullous neurosensory detachments have been described in patients with chronic CSC.85–92 Yannuzzi and co-workers first characterized the presence of RPE atrophic tracts extending inferiorly in the fundus periphery secondary to antecedent retinal detachment in patients with CSC.85 Presumably, there is a particularly severe and/or longstanding leakage of fluid from an RPE defect in the subretinal space at the posterior pole. The subretinal fluid gravitates inferiorly to form a dependent neurosensory detachment in a “flask,” “teardrop,” “dumbbell,” or “hourglass” pattern (Fig. 31). Sometimes the tract of subretinal fluid connecting the macular detachment with the bullous neurosensory detachment in the inferior hemisphere is so shallow that it is very difficult to appreciate. The RPE under the chronic retinal detachment experiences atrophic changes that appear as atrophic RPE tracts connecting the posterior pole with the dependent retinal detachment. The retina itself develops secondary manifestations including pigment migration, capillary dilatation (telangiectasia) proximally and capillary nonperfusion (ischemia) distally to the area of detached retina (see Fig. 31). The changes in the RPE consist of both RPE atrophy and pigment clumping in the form of perivascular deposits or bone spicules, a condition described by Gass as a “pseudoretinitis pigmentosa–like atypical CSC presentation.”87
Other complications noted in these patients are cystoid macular edema or, more frequently, cystoid retinal changes in the areas of chronic detachment, subretinal lipid deposition, choriocapillaris atrophy secondary to the RPE damage in the areas of RPE tracts, and CNV.89,90,204–206 This severe variant of CSC appears to be more frequent in patients of Latin or Asian ancestry, and it is usually associated with frequent recurrences, permanent central vision loss, and significant superior visual field loss.
Epiretinal membrane (ERM) formation has been associated with retinal vascular occlusive disease, diabetes, uveitis, penetrating or blunt trauma with intraocular hemorrhage, ocular inflammation, ocular surgery, laser or cryotherapy for retinal breaks, telangiectasia, macular holes, retinal angiomas, retinal arteriolar macroaneurysms, intraocular tumors, and retinitis pigmentosa.207 A preretinal sheen, readily appreciated on direct ophthalmoscopy or contact lens biomicroscopy, provides a diagnosis. In more severe cases, a fibrous membrane and distortion of the retinal vessels can be seen (Fig. 32). Consequently, FA is generally not necessary to confirm the diagnosis of ERM. Nevertheless, FA can demonstrate leakage from vessels that have become relatively incompetent owing to traction from the membrane (Fig. 33).208,209 This often accounts, in part, for loss of vision in symptomatic patients. OCT examination is the gold standard for the study of the vitreoretinal interface. It nt only demonstrates the presence of an ERM,, but also helps in quantifying the degree of tractional neurosensory elevation and in differentiating an ERM from vitreomacular traction syndrome.
An ERM that causes severe loss of vision may warrant vitrectomy and membrane peeling. In these cases, the membrane is clinically obvious and FA is not necessary. Ultrasound is often useful to assess the degree of posterior vitreous separation from the posterior pole.210–212
FA plays no role in the chronic management of patients with ERMs. The clinical presentation, including visual acuity, Amsler grid, and fundus appearance, guides long-term care.
|MACULAR CYSTS, HOLES, AND PSEUDOHOLES|
In general, the diagnosis of a macular hole is readily made in patients who present clinically with a full-thickness retinal defect, yellow exudative deposits at the base, and, occasionally, an operculum. However, it is sometimes difficult, using contact lens biomicroscopy alone, to distinguish a full-thickness macular hole from simulating conditions. Visual acuity is often 20/200 to 20/400 in an eye with a full-thickness hole, whereas eyes with macular cysts or pseudoholes usually have better vision. Visual acuity, however, cannot rule in or rule out a full-thickness macular hole.213,214
The differentiation of a partial-thickness, or lamellar, macular hole from a full-thickness macular hole can be challenging, and FA is often helpful in assisting in the diagnosis.55 As in a full-thickness hole, a lamellar hole presents as an excavation of the retina, and the presence of drusen underneath the lamellar hole can simulate the yellow deposits seen at the base of full-thickness holes. Occasionally, there is a full-thickness hole at one side of a lesion, and the rest of the lesion consists of a lamellar defect. FA will show immediate hyperfluorescence from the choroidal circulation under a full-thickness hole (Fig. 34A), whereas a lamellar hole, with a relatively intact RPE, will block some of the normal fluorescence from the choriocapillaris (Fig. 34B).
There are several causes of pseudoholes, including an area of sharply demarcated RPE atrophy, a dilated perifoveal capillary net, and an ERM with a clear center. Careful contact lens biomicroscopic examination will usually distinguish these conditions from a full-thickness macular hole, but FA can help. Both RPE atrophy and a full-thickness hole will exhibit window defects, but RPE atrophy tends to have more residual pigment and consequently a more mottled appearance of the transmitted choroidal fluorescence. A dilated perifoveal capillary net, which can be seen in diabetes or perifoveal telangiectasia, will leak fluorescein. A pseudohole will not have a window defect.
OCT examination is the most accurate test for differentiating full-thickness macular holes, lamellar holes, and pseudoholes.215–230
Autofluorescence imaging, a novel technique for diagnosis of macular holes, is based on the principle that the autofluorescence signal from the RPE is not blocked by the retinal pigments in the presence of a full-thickness macular hole; as a result, a full-thickness macular hole presents a bright autofluorescent signal, whereas pseudoholes and lamellar holes are not autofluorescent (Fig. 35). This technique has the advantage, compared with FA, of not requiring dye injection.
It is recommended to observe a stage 1 macular hole, since half of these will undergo spontaneous resolution. The treatment for stage-2 through stage-4 macular holes is surgical repair.231–238 The pseudohole itself is not visually disabling, but the condition may be clinically significant if there is considerable vitreoretinal traction such that the lesion threatens to develop into a full-thickness hole.
Just as the clinical findings of these conditions are most important for initial diagnosis and treatment, the findings on clinical examination guide long-term management.
|CYSTOID MACULAR EDEMA|
FA is generally not necessary to make the diagnosis of cystoid macular edema (CME). A history of recent cataract surgery, diabetes, uveitis, or other predisposing conditions is usually obtained. Clinically, the patient presents with retinal thickening, often with clinically evident cystic changes. FA reveals a characteristic petaloid collection of fluorescein that confirms the diagnosis, which has been shown histologically to reflect accumulation of fluid in the extravascular component of the outer plexiform layer.239 When FA demonstrates leakage from the optic nerve, this suggests an inflammatory etiology for the CME (Fig. 36). Although this sign is reliably present in CME associated with cataract surgery, penetrating keratoplasty, or posterior uveitis, it is not characteristically present in diabetics or in idiopathic CME. FA can also demonstrate dilated macular capillaries as a cause of CME in diabetes (Fig. 37). Different conditions that may cause CME include Irvine-Gass syndrome, previous penetrating keratoplasty, any inflammatory condition that involves the posterior segment, peripheral rhegmatogenous retinal detachment, peripheral cryotherapy, malignant melanoma, topical epinephrine, tapetoretinal degenerations, juxtafoveal telangiectasia, occult central retinal vein occlusion, nicotinic acid maculopathy, and idiopathic CME.
There are several conditions that may be confused with CME, including juvenile X-linked retinoschisis and Goldmann-Favre disease. FA can assist in making the diagnosis if it is not apparent on clinical examination.
FA does not help guide treatment of CME, which should address the underlying cause. For example, posterior uveitis is generally managed with corticosteroids, wherease aphakic CME may benefit from steroid, antiprostaglandin, and acetozolamide therapy.240–250
FA is often used to assess the response to therapy. Decreased fluorescein leakage can be a sensitive indicator of improvement, particularly when visual acuity is reduced to a level that makes subtle visual changes difficult to gauge. FA does not assist in prediction of the likely visual outcome. Although CME tends to resolve in some conditions, such as Irvine-Gass syndrome, patients with CME due to other causes such as diabetes generally suffer some irreversible loss of central vision.
The diagnosis of degenerative myopic maculopathy is clinically obvious. Patients with pathologic myopia are, however, at risk for development of CNV, and FA is helpful in their diagnosis and treatment.251–255 Patients with myopic degeneration have pigmentary changes that can be difficult to distinguish from small neovascular membranes. CNV in pathologic myopia tend to be smaller and less aggressive than the neovascular lesions of age-related macular degeneration.55 CNV in myopic eyes can often be strongly suspected on clinical grounds, using clues such as subretinal blood or lipid exudate, neurosensory elevation, and appearance of a gray membrane visible through atrophic RPE (Fig. 38). FA is sometimes helpful in distinguishing a neurosensory detachment due to a small macular hole from retinal elevation from leaking CNV. FA has been also valuable in demonstrating an association between Fuchs' spots and CNVs254 and in identifying disturbances of choroidal and retinal blood flow in pathologically myopic eyes.255
The value of treating CNV in highly myopic patients is controversial. The CNV generally does not grow extensively, there is considerable risk of rupturing Bruch's membrane, and the laser burn chorioretinal scar tends to enlarge substantially.251,252 Nevertheless, there is evidence that patients with pathologic myopia who receive treatment for CNV have better final visual acuity.243 FA often helps define the extent of CNV, but it has limited value in assisting the localization of the fovea. PDT has proved to be a useful option for the treatment of subfoveal CNV in myopia.256
FA is useful in evaluating the efficacy of treatment of CNV and in determining whether recurrent CNV has developed. Patients with subfoveal CNV are likely to lose central vision. The diagnosis and prognosis of atrophic myopic degeneration is best determined by clinical appearance.
Trauma can induce a wide spectrum of alterations of the retina, RPE, and choroid. Most types of traumatic maculopathy, such as Purtscher's retinopathy, Berlin's edema, retinal contusion, traumatic macular hole, and choroidal rupture, are readily apparent on clinical examination.257 Choroidal rupture, althoughe usually evident clinically, may be more obvious on FA (Fig. 39). Contusion necrosis of the RPE may present clinically with an associated RPE detachment, an overlying neurosensory detachment, and a subtle change in RPE pigmentation. FA can demonstrate the site of leakage into the subretinal space, unless the RPE defect has healed by the time of testing. FA is particularly helpful in differentiating retinal concussion (Berlin's edema), in which FA findings are normal, from retinal contusion, in which there is RPE damage and, consequently, increased transmission of choroidal fluorescence on FA.257 In Purtscher's retinopathy, FA can document vascular closure, which accounts for the retinal infarctions (Fig. 40).258
FA can define the locations of CNV in patients with choroidal rupture, which may be amenable to laser therapy.
Most trauma-related conditions are followed clinically with serial evaluations of clinical appearance and visual acuity. Routine FA to follow trauma-related maculopathies is not necessary.
Patients with choroidal rupture through the fovea, which is generally obvious clinically, lose central vision. In retinal contusion, a normal fluorescein angiogram indicates a good visual prognosis, wherease fluorescein leakage is associated with tissue damage, and nonperfusion carries a poor visual prognosis.257 The outcome of Purtscher's retinopathy and of RPE contusion largely depends on the location of macular involvement. Patients who suffer a macular hole are usually left with approximately 20/400 (6/120) vision.
Many drugs, metals, and inorganic compounds can induce maculopathy.259 Among the most clinically important macular toxins are chloroquine and hydroxychloroquine, which are commonly used in the U.S. to treat severe systemic lupus erythematosus and rheumatoid arthritis. Thhe ophthalmoscopic appearance of a ring of RPE alterations in the parafoveal area may be more sensitive than FA for detecting early chloroquine retinopathy.260 Also, self-administered Amsler grid testing is a simple and efficient means of detecting early retinopathy in many patients.261 As the maculopathy progresses, FA can readily detect RPE atrophy that extends peripherally and also advances centrally to involve the fovea (Fig. 41).
Oxalosis, which results from calcium oxalate deposition, can be due to an inborn metabolic disorder (primarily hyperoxaluria), ethylene glycol ingestion, or methoxyflurane general anesthesia.262–264 Clinically, patients have a crystalline retinopathy, and FA may show RPE hyperplasia, fibrous metaplasia, and choroidal neovascularization.55
Epinephrine induces CME that is generally diagnosed on clinical grounds. This condition occurs more commonly in aphakic patients. The maculopathy typically resolves with cessation of the drug, and FA can be useful to document resolution of the edema. Epinephrine-induced CME evidently increases retinal capillary permeability, but the pathophysiology of this process is poorly understood.265
Tamoxifen, an antiestrogen drug used in some cases of breast cancer, has a characteristic clinical picture.266 FA may reveal Tamoxifen-induced CME from capillary hyperpermeability and RPE alterations.
Clofazimine is an antimycobacterial agent that has been used since 1962 to treat dapsone-resistant leprosy and, more recently, to treat Mycobacterium avium-intracellulare complex infection in patients with acquired immunodeficiency syndrome (AIDS). There have been two reports of bull's eye maculopathy with multiple RPE defects demonstrated on FA (Fig. 42).267,268
Gentamicin and tobramicin toxicity, which often result from inadvertent injection into the vitreous during cataract surgery, cause devastating retinal damage. In areas where high concentrations of gentamicin reach the retina there is obliteration of the retinal vasculature and ischemic necrosis of the retina (Fig. 43).269,270
A number of other drugs, chemicals, and metals can induce retinopathy that manifests clinical and angiographic findings, including desferrioxamine, canthaxanthine, nicotinic acid, iron, and copper. Other texts deal with these conditions in greater detail.55,271
|Solar retinopathy272 is often evident clinically, and cooperative patients will provide a history
of sun gazing. Partial or complete recovery of central vision generally
occurs within 3 to 6 months.273,274 FA does not reveal vascular leakage or abnormal retinal vasculature, but
occasionally there are RPE defects (Fig. 44). RPE damage in photic retinopathy from the operating microscope
may be less obvious clinically, and FA illustrates RPE disruption better. Most
patients have good visual acuity despite some RPE damage; the
main role of FA in maculopathy from the operating microscope has been
investigational.275,276 One area of interest is the contribution of the operating microscope to
the development of CME following cataract surgery.277,278|
|The indications for FA will continue to be modified as knowledge of macular pathology grows and as experience with FA increases. FA can assist in the diagnosis of a wide range of macular conditions, and it can be most useful in guiding therapies and evaluating response to treatments. Although FA is not always necessary for clinical management, it remains a powerful investigative tool for virtually all of the acquired macular diseases.|
11. Axer-Siegel R, Bourla D, Priel E et al: Angiographic and flow patterns of retinal choroidal anastomoses in age-related macular degeneration with occult choroidal neovascularization. Ophthalmology 109:1726–1736, 2002.
52. Macular Photocoagulation Study Group: Persistent and recurrent neovascularization after krypton laser photocoagulation for neovascular lesions of age-related macular degeneration. Arch Ophthalmol 108:825, 1990.
57. Schmidt-Erfurth U, Miller JW, Sickenberg M et al: Photodynamic therapy with verteporfin for choroidal neovascularization caused by age-related macular degeneration: Results of retreatments in a phase 1 and 2 study. Arch Ophthalmol 117:1177–1187, 1999.
58. Miller JW, Schmidt-Erfurth U, Sickenberg M et al: Photodynamic therapy with verteporfin for choroidal neovascularization caused by age-related macular degeneration: Results of a single treatment in a phase 1 and 2 study. Arch Ophthalmol. 117:1161–1173, 1999.
59. Schmidt-Erfurth U, Miller J, Sickenberg M et al: Photodynamic therapy of subfoveal choroidal neovascularization: Clinical and angiographic examples. Graefes Arch Clin Exp Ophthalmol 236:365–374, 1998.
60. Treatment of Age-Related Macular Degeneration with Photodynamic Therapy (TAP) Study Group: Photodynamic therapy of subfoveal choroidal neovascularization in age-related macular degeneration with verteporfin: One-year results of 2 randomized clinical trials—TAP report. Arch Ophthalmol 117:1329–1345, 1999.
61. Bressler NM: Photodynamic therapy of subfoveal choroidal neovascularization in age-related macular degeneration with verteporfin: Two-year results of 2 randomized clinical trials—TAP report 2. Arch Ophthalmol. 119:198–207, 2001.
62. Bressler NM, Arnold J, Benchaboune M et al: Verteporfin therapy of subfoveal choroidal neovascularization in patients with age-related macular degeneration: Additional information regarding baseline lesion composition's impact on vision outcomes—TAP report No. 3. Arch Ophthalmol 120:1443–1454, 2002.
63. Blumenkranz MS, Bressler NM, Bressler SB et al: Verteporfin therapy for subfoveal choroidal neovascularization in age-related macular degeneration: Three-year results of an open-label extension of 2 randomized clinical trials—TAP Report No. 5. Arch Ophthalmol 120:1307–1314, 2002.
68. Guidelines for using verteporfin (visudyne) in photodynamic therapy to treat choroidal neovascularization due to age-related macular degeneration and other causes. Retina . 2002 Feb;22(1):6–18. Review.
70. Bressler NM. Verteporfin therapy of subfoveal choroidal neovascularization in age-related macular degeneration: two-year results of a randomized clinical trial including lesions with occult with no classic choroidal neovascularization-verteporfin in photodynamic therapy report 2. Am J Ophthalmol . 2002 Jan;133(1):168–9
71. Verteporfin in Photodynamic Therapy Report 2: Verteporfin therapy of subfoveal choroidal neovascularization in age-related macular degeneration: Two-year results of a randomized clinical trial including lesions with occult with no classic choroidal neovascularization— Am J Ophthalmol 131:541–560, 2001.
85. Yannuzzi LA, Shakin JL, Fisher YL et al: Peripheral retinal detachments and retinal pigment epithelial atrophic tracts secondary to central serous pigment epitheliopathy. Ophthalmology 91:1554, 1984.
112. Gass JDM, Little HL: Bilateral bullous exudative retinal detachment complicating idiopathic central serous chorioretinopathy during systemic corticosteroid therapy. Ophthalmology 102:737–747, 1995.
132. Yasuzumi T, Miki T, Sugimoto K: Electron microscopic studies of epinephrine choroiditis in rabbits. I. Pigment epithelium and Bruch's membrane in the healed stage. Acta Soc Ophthalmol Jpn 78:588–598, 1974.
149. Klien BA: Ischemic infarcts of the choroid (Elshing's spots): A cause of retinal separation in hypertensive disease with renal insufficiency: A clinical an histopathological study. Am J Ophthalmol 66:1069–1088, 1968.
177. Giovannini A, Scasellati Sforzolini B, D'Altobrando E: Choroidal findings in the course of idiopathic serous pigment epithelium detachment detected by indocyanine green videoangiography. Retina 17:286–293, 1997.
203. Schatz H, Yannuzzi LA, Gitter KA: Subretinal neovascularization following argon laser photocoagulation treatment for central serous chorioretinopathy; complication or misdiagnosis? Trans Am Acad Ophthalmol Otolaryngol 83:893–906, 1977.
206. Weiler W, Foerester MH, Wessing A: Exudative retinal detachment, pigment epithelium tear and subretinal exudate in a case of central serous chorioretinopathy. Klin Monatsbl Augenheilkd 199:450–453, 1991.
217. Apostolopoulos MN, Koutsandrea CN, Moschos MN et al: Evaluation of successful macular hole surgery by optical coherence tomography and multifocal electroretinography. Am J Ophthalmol 134:667–674, 2002.
218. Uemoto R, Yamamoto S, Aoki T et al: Macular configuration determined by optical coherence tomography after idiopathic macular hole surgery with or without internal limiting membrane peeling. Br J Ophthalmo. 86:1240–1242, 2002.
226. Akasaka Y, Nishikawa S, Tamai M: Analysis of the retinal edema of full-thickness macular holes by scanning laser ophthalmoscopy and optical coherence tomography. Tohoku J Exp Med 189:233–238, 1999.
246. Moldow B, Sander B, Larsen M et al: The effect of acetazolamide on passive and active transport of fluorescein across the blood-retina barrier in retinitis pigmentosa complicated by macular oedema. Graefes Arch Clin Exp Ophthalmol 236:881–889, 1998.
256. VIP Report No. 1: Photodynamic therapy of subfoveal choroidal neovascularization in pathologic myopia with verteporfin. 1-year results of a randomized clinical trial.— Ophthalmology 108:841–852, 2001.