Abstract
Polypoidal choroidal vasculopathy was initially described as a type of macula disorder presenting with recurrent subretinal pigment epithelial hemorrhage. Since then, more have been known about this particular disease. Current of the disease enables us to identify it as a separate entity to other macular disorders. It is characterized by the presence of subretinal hemorrhage, exudation, and reduction in central vision. Imaging characteristics include polypoidal lesions and branching vascular network seen on indocyanine-green angiography. Specific treatment has been devised, which includes antivascular endothelial growth factor injections into the vitreous, and also the combination of photodynamic therapy, in hope to induce regression of the polypoidal lesions. These will be discussed into detail in this chapter, with clear illustrations of the condition with clinical photos.
Keywords
Polypoidal choroidal vasculopathy, Age-related macular degeneration, Photodynamic therapy, Antivascular endothelial growth factor, Intravitreal injections, Indocyanine-green angiography, Fluorescein angiography, Branching vascular network
Introduction
Polypoidal choroidal vasculopathy (PCV) was first described as a type of macular disorder presenting with recurrent subretinal pigment epithelial hemorrhage by Yannuzzi et al . in 1982. Similar cases have then been described by Kleiner and Stern. Initial findings from these patients all displayed two main features, including dilated and branching inner choroidal vessels, together with terminal reddish-orange, spheroid aneurysmal-like polyps, which can be found at subfoveal, juxtafoveal, extrafoveal, peripapillary, or peripheral regions. These vascular abnormalities were associated with multiple, recurrent serosanguineous detachments of the retinal pigmentary epithelium and the neurosensory retina, with hemorrhage originating from the polypoidal components, as confirmed with fluorescein angiographies. With advances in imaging and clinical findings, it has now been accepted that PCV is a distinct form of choroidal neovascularization, with unique risk factors, clinical manifestations, natural course, treatment responses, and final outcomes.
Introduction
Polypoidal choroidal vasculopathy (PCV) was first described as a type of macular disorder presenting with recurrent subretinal pigment epithelial hemorrhage by Yannuzzi et al . in 1982. Similar cases have then been described by Kleiner and Stern. Initial findings from these patients all displayed two main features, including dilated and branching inner choroidal vessels, together with terminal reddish-orange, spheroid aneurysmal-like polyps, which can be found at subfoveal, juxtafoveal, extrafoveal, peripapillary, or peripheral regions. These vascular abnormalities were associated with multiple, recurrent serosanguineous detachments of the retinal pigmentary epithelium and the neurosensory retina, with hemorrhage originating from the polypoidal components, as confirmed with fluorescein angiographies. With advances in imaging and clinical findings, it has now been accepted that PCV is a distinct form of choroidal neovascularization, with unique risk factors, clinical manifestations, natural course, treatment responses, and final outcomes.
Epidemiology
PCV is more commonly found in pigmented race including black people and Asians. The prevalence can be up to 54.7% of patients suffering from presumed neovascular age-related macular degeneration (AMD) as described in one study from Japan but only accounting for only 5–10% of patients with AMD in Caucacians. Initially, it was believed that it would not occur in white people but now it has been found in Caucacians as well though with different clinical features like higher prevalence of peripapillary involvement and bilateral involvement.
Most of the patients suffering from PCV are over the age of 50, with a generally slightly younger presentation than wet AMD. Regarding sex predilection, studies from Japan showed a predominant involvement of male patients (71%), but for Europeans, females are more likely to be affected (75%).
Pathology
Histopathological findings from vitreoretinal surgeries and enucleation specimens have improved our understanding of the pathology of the disease. Large vascular channels have been identified from eyes with early vasculopathy. Degeneration of large dilated venules, small degenerated arterioles, and capillaries with thickened basement membranes were also found. In another study, hyalinization of choroidal vessels together with exudation of fibrin in plasma have been reported to be present in patients with PCV. Report of intra-Bruch membrane choroidal neovascularization has been identified which supported the idea that PCV is a variant of neovascular AMD. Interestingly, regarding the role of vascular endothelial growth factor (VEGF), different specimens showed conflicting immunostaining results, which may explain partly the refractory responses of PCV toward anti-VEGF treatment.
Risk Factors
Cardiovascular Diseases
As PCV is a vascular disease, it is not surprising to find its association with cardiovascular problems. It has been reported that as high as 42% of patients with PCV have hypertension. Smoking is also a risk factor for PCV with odds ratio reported ranging from 4.40 to 4.87.
Serum Biomarkers
High levels of C-reactive protein was shown to be associated with increased risk of PCV up to threefold after adjusting for age, sex, smoking status, alcohol use, body mass index, and use of antiinflammatory drugs, suggesting that inflammation and immune-related process takes part in the pathogenesis.
Elevated serum homocysteine level may result in endothelial injury, oxidative stress, and thrombosis and it is also related to various systemic vascular diseases such as ischemic heart disease and stroke. PCV, being a vasculopathy, has also been reported to be related to increased plasma homocysteine level with about 1.5-folds increased odds, and have been one of the pathogenic factors that causes arteriosclerosis and subsequent aneurysmal-like dilatation.
Matrix metalloproteinases (MMP) regulates extracellular metabolism, and hence, affects vascular remodeling. Extracellular matrix modeling derangement disorder has been observed in the Bruch’s membrane and the choroidal vasculature of PCV patients resulting in arteriosclerotic and aneurysmal changes. Increased in MMP-2 and MMP-9 levels have been observed in PCV patients that further support their role in the condition.
Genetic Factors
Down to genetic level, various genetic defects have been found to be related to PCV. A GG missense variant at rs5882 in the cholesteryl ester transfer protein locus was found to have a 3.53-fold increased risk of PCV compared with AA genotype, which may suggest the involvement of lipid metabolism in the pathogenesis.
Other genetic loci that have been found to be related to the pathogenesis include two single nucleotide polymorphisms in the complement factor H: rs1061170 and rs800292; and two in ARMS2/HTRA1: rs10490942 and rs11200638. Mutation of the complement family may lead to aberrant complement activation causing vasculopathies. In contrast, HTRA1 is a membrane serine peptidase and is thought to regulate degradation of extracellular matrix proteoglycan. Overexpression may affect the integrity of Bruch’s membrane that exerts a permissive effect on the expansion of abnormal choroidal capillaries.
Genetic factors determine treatment responses as well. A single-nucleotide polymorphism at rs 10490924 in ARMS 2 was found to be associated with visual prognosis after verteporfin photodynamic therapy (PDT). Among the various genotypes, the GG genotype is associated with better visual outcome when compared to the TT genotype. Another gene SERPINF1 is also associated with treatment outcome. AA genotype at rs12603825 in this gene was associated with shorter retreatment-free intervals after PDT among all identified genotypes.
Clinical Features and Course
Patient with PCV can be asymptomatic if there is no leakage from the lesions, whereas the less fortunate patients may suffer from acute or progressive visual loss. Acute visual loss is usually due to spontaneous rupture of the polypoidal lesions resulting in submacular hemorrhage ( Fig. 18.1 ) presenting with scotoma or even breakthrough vitreous hemorrhage causing profound visual loss. Polypoidal lesions may also result in exudative changes with accumulation of subretinal fluid and exudates, causing metamorphopsia and progressive blurring of vision.
On physical examination patients with PCV may have variable sized serous and serosanguinous detachments of neurosensory retina and/or pigmentary epithelium. Underlying vascular abnormalities may sometimes be visible especially when the overlying retina is flat and pigment epithelium is atrophic. Polyps’ size and number vary among patients. Microrips or tears of retinal pigment epithelium (RPE) may be present at margin of serosanguinous pigment epithelial detachments (PEDs). Complications may occur resulting in subretinal fibrosis, pigment epithelial hyperplasia, and atrophic degeneration. These lesions may appear in various parts of the retina and may be present bilaterally. Drusen may be present in the fellow eye, though less common than in cases of AMD.
The natural course of PCV can be highly variable, depending on the location, size, and associated complications including hemorrhages and exudates. It was previously thought that if PCV was left untreated, about 50% of patients will enjoy favorable outcome with spontaneous regression of lesions. However, it has been reflected from the results of longer term studies that PCV might not be as benign as ophthalmologists thought. Many PCV patients would instead suffer from repeated hemorrhage and leakage resulting in degeneration of photoreceptors and scarring of RPE, and subsequently leading to significant visual impairment. Microrips of RPE, though may present during the disease course, may resolve spontaneously afterward. A grape-like cluster of polyps have been identified to be associated with poorer visual outcomes due to their propensity to bleeding. A retrospective study in Chinese patients has revealed that there was a mean loss of 3.1 lines among PCV patients resulting in final visual outcome of 20/200 or worse in 68.2% of patients.
Clinical Imaging of Polypoidal Choroidal Vasculopathy
In this era of multimodal imagings for retinal diseases, there are reports on the use of various imaging modalities to visualize PCV. The use of these imaging techniques is useful not only in making the diagnosis but also has treatment implications. Moreover, it could be used to monitor treatment progress. In this section, we shall look into detail how different imaging modalities can be of use.
Clinical Diagnosis
The diagnosis, or at least suspicion of PCV, can be picked up at slit-lamp biomicroscopy. At times, PCV appears as an orange-red nodule ( Fig. 18.2 ). This is when there is elevation of the RPE overlying the polyp. Although this is highly indicative of PCV, it can sometimes be just a small PED.
However, when PCV presents in other ways, such as massive subretinal hemorrhage ( Fig. 18.1 ), or presents with subretinal fluid only, making a diagnosis at the slit-lamp may be difficult. In any case, any clinical suspicion should lead to indocyanine-green angiography (ICGA), for better delineation of the lesion.
Fluorescein Angiogram
The use of fluorescein angiogram (FA) is useful in making a diagnosis of neovascular AMD. However, in the case of PCV, as the lesion lies beneath the RPE, signal from the lesions would be blocked off. Moreover, tendency of fluorescein molecules to leak out of the choriocapillaries would lead to blurriness of the lesions on FA and would make diagnosis difficult.
On FA, PCV appears like an occult choroidal neovascular membrane (CNV), or a minimally classic CNV. On many instances, it could lead to the diagnosis of CNV instead of PCV in a real PCV case, if ICGA was not being performed. As ICGA is not routinely done in all patients in many clinics, most often PCV patients would present as intravitreal anti-VEGF treatment nonresponders, and only to find out later that the underlying cause was PCV, when ICGA was eventually performed due to clinical suspicion.
Indocyanine-Green Angiography
While being a disease with heterogeneous presentations, there is no doubt that at this current stage of imaging era, indocyanine green (ICG) angiogram (ICGA) remains the gold standard in making a diagnosis of PCV. It was being used to distinguish PCV from other types of AMD, such as retinal angiomatous proliferation, and typical neovascular AMDs. The lesion of PCV primarily arises from the inner choroidal vasculature. Hence, if fluorescein angiography (FA) is used, fluorescent signal would be blocked off by the RPE. In the case of ICGA, the dye absorbs and emits near-infrared light, which readily penetrates the RPE and even thin hemorrhages. Hence, the vasculature could be visualized even if the lesion is located beneath the RPE. Moreover, the higher binding affinity of the ICG dye to plasma proteins retains it within the choriocapillaries. This is in contrast to how fluorescein leaks out of the choriocapillaries.
Timing of Image Acquisition on ICGA
The EVEREST trial panel published a guideline on the diagnosis and treatment of PCV in 2013 and decided that frames taken roughly 6 min after injection of the ICG dye are best to make a diagnosis of PCV. Although some would argue that polyps usually light up earlier on ICGA, the reason why the EVEREST trial group decided that 6 min was preferable was that it allowed time for most of the commercially available angiogram cameras to capture what should be seen. Although polyps or lesions often appear in the early frames (i.e., on or before 6 min), mid or late frames should also be used to assist the diagnosis of PCV, especially when polyps may change from hyperfluorescent to hypofluorescent nodules with surrounding halos in the ICGA washout phase and branching vascular network (BVN) may present with mid-to-late staining in ICGA. In addition, to visualize pulsations of the polyp, dynamic ICGA should ideally be used. This also requires the images be captured in very early frames of the ICGA, that is, <1 min after injection of the dye.
Polyp
The Japanese Study Group of PCV has written a diagnostic criterion for PCV on ICGA and described its appearance as “masses” or “grape-like clusters” on ICGA ( Fig. 18.2 ). The original description by this group referred to the appearance of the polyp as a hyperfluorescent nodule in the early phase, which expands gradually and remains stable in the late phase on ICGA.
Presence of pulsation in the polyp is not a must when making a diagnosis of PCV. A dynamic ICGA has to be used in order to capture the pulsation in the very early frames of ICGA, preferably within the first minute after injection of the dye (often seconds after injection). If available, stereoscopic ICGA photographs can be used to appreciate the three-dimensional structures of polyps in PCV.
Spaide et al . reported the appearance of “polypoidal structures” at the terminals or edges of an abnormal vascular network (BVN), which appeared in the early phase of ICGA. The authors described an initial rim of hypofluorescence surrounding a hyperfluorescent core within the polypoidal structure, and in later phase, the reverse was observed, that is, a hyperfluorescent rim surrounding a hypofluorescent center ( Fig. 18.3 ). This was agreed by many reports that followed. However, it must be pointed out that BVNs are not necessarily present on the ICG in all cases of PCV.
Branching Vascular Network
The presence of an interconnected choroidal vascular network, referred to as the BVN, is another characteristic feature of PCV. Polyps usually appear at the edge of the BVN ( Fig. 18.4 ). In the initial description by Yannuzzi et al ., this network of vessels appears early on ICGA. This was agreed by many subsequent reports. However, as mentioned above, in a certain proportion of patients with PCV, especially those with smaller lesions, BVN may not be present, or at least, not visible on ICGA.
The Clinical Use of ICGA in Patients With PCV
In patients with PCV, imaging with ICG is as important in making a diagnosis, as it is in following up the progress after treatment. The importance in making a diagnosis has been explained above. After treatment, repeating ICGA can allow the treating physician to know whether the lesion has regressed. However, it must be stressed that even when the original lesion has regressed on follow-up ICGAs, recurrence can appear as reappearing of a previously regressed polyp. Moreover, new lesions can arise elsewhere. This highlights the importance of repeating ICGA when suspicion of clinical progression is present.
Optical Coherence Tomography
The use of optical coherence tomography (OCT) in retinal imaging is now widely adopted as the standard of care in many retinal diseases, such as AMD, central serous chorioretinopathy (CSC), diabetic retinopathy, just to name a few. Its application has also been extended to rare retinal diseases such as viral retinitis, inherited retinal diseases, and uveitic retinal diseases. It is also used widely in other ocular diseases such as glaucoma, and even in pediatric patients. The main advantage of it lies in the noninvasiveness, feasibility of repeated scanning in the same location with eye-tracking features in some OCT machines, and the high resolution achieved with the latest versions of spectral-domain or swept-source OCTs.
In recent years, there have been major advances in the technology of OCT imaging. Conventional spectral-domain OCT using an 840-nm light source is met with significant light scattering at the level of the RPE, thereby limiting its ability to visualize structures beneath RPE. Enhanced-depth imaging OCT (by software modification in spectral-domain OCT) or swept-source OCT have greatly improved the penetration of OCT imaging to deeper layers underneath the RPE, that is, the choroid. This enabled visualization of the choroidal vasculature, and many reports have since then been published. In typical cases of PCV where polyps protrude upward upon the RPE, the lesions can sometimes be seen on OCT ( Fig. 18.5 ). Recent advancement in the technology of en-face OCT and OCT angiogram (OCTA) have took this further to enable visualization of the vasculature in a head-on view without the need to inject any dye invasively.
Application of OCT in the Management of PCV
Conventional Cross-Sectional Approach
The use of OCT is useful in many aspects in the management of PCV. It can assist making the diagnosis of PCV. Typically, an orange-red nodule representing a polyp protruding up upon the RPE would appear as a small upward protrusion of the RPE on a cross-sectional OCT scan ( Fig. 18.5 ). In other phenotypic presentations of PCV such as massive subretinal hemorrhage in the macula, although visualizations of the polyp on OCT scans are usually difficult, OCT scans can provide baselines for future comparison.
In a report by Ueno et al ., it was reported that some lesions in PCV were not being seen on ICGA but were being detected by OCT instead. However, this cannot be generalized to all cases, and at the current moment, ICGA still remains the gold standard in making a definitive diagnosis of PCV.
Choroidal OCT Imaging in PCV
It was reported that PCV eyes demonstrated significantly greater mean subfoveal choroidal thickness than typical neovascular AMD eyes. Therefore, choroidal vascular lesion seen in PCV may not be just the CNV accompanied by saccular capillary dilations at the border but may have a significant structural difference in the choroid compared to typical neovascular AMD. The reason may be partially attributed to the dilation of middle or large choroidal vessels or choroidal vascular hyperpermeability (CVH) revealed by ICGA. CVH, which is visualized as multifocal hyperfluorescence in the middle and late phases of ICGA, usually bilaterally, was originally described as a characteristic finding in CSC. PCV eyes with CVH showed greater mean subfoveal choroidal thickness than those without CVH, probably due to the increased hydrostatic pressure within the choroid.
OCT Angiogram
OCTA is a recent advancement. This is made possible by exploiting the flow properties of regional circulations to reconstruct the vascular tree in both the en-face and cross-sectional planes. This enables visualization of the vasculature noninvasively without the need for dye injection. This can easily be repeated at each follow-up visit as it is noninvasive.
In a report by Inoue et al ., comparison between en-face approach and the cross-sectional approach on the OCTA was studied. On the en face view, the BVN could be seen to a certain clarity, and the topographical correlation of the BVN with surrounding structures could be identified ( Figs. 18.6 and 18.7 ). That is, the layering of the lesions could be assessed by altering the plane of interest, from the inner retina to deeper layer through the various choroidal layers. On the other hand, polyps were being better seen on cross-sectional planes. Despite the advantages mentioned, OCTA still lack information regarding vascular leakage and activity of the lesion, which is offered by ICGA.
Introduction
Polypoidal choroidal vasculopathy (PCV) was first described as a type of macular disorder presenting with recurrent subretinal pigment epithelial hemorrhage by Yannuzzi et al . in 1982. Similar cases have then been described by Kleiner and Stern. Initial findings from these patients all displayed two main features, including dilated and branching inner choroidal vessels, together with terminal reddish-orange, spheroid aneurysmal-like polyps, which can be found at subfoveal, juxtafoveal, extrafoveal, peripapillary, or peripheral regions. These vascular abnormalities were associated with multiple, recurrent serosanguineous detachments of the retinal pigmentary epithelium and the neurosensory retina, with hemorrhage originating from the polypoidal components, as confirmed with fluorescein angiographies. With advances in imaging and clinical findings, it has now been accepted that PCV is a distinct form of choroidal neovascularization, with unique risk factors, clinical manifestations, natural course, treatment responses, and final outcomes.
Epidemiology
PCV is more commonly found in pigmented race including black people and Asians. The prevalence can be up to 54.7% of patients suffering from presumed neovascular age-related macular degeneration (AMD) as described in one study from Japan but only accounting for only 5–10% of patients with AMD in Caucacians. Initially, it was believed that it would not occur in white people but now it has been found in Caucacians as well though with different clinical features like higher prevalence of peripapillary involvement and bilateral involvement.
Most of the patients suffering from PCV are over the age of 50, with a generally slightly younger presentation than wet AMD. Regarding sex predilection, studies from Japan showed a predominant involvement of male patients (71%), but for Europeans, females are more likely to be affected (75%).
Pathology
Histopathological findings from vitreoretinal surgeries and enucleation specimens have improved our understanding of the pathology of the disease. Large vascular channels have been identified from eyes with early vasculopathy. Degeneration of large dilated venules, small degenerated arterioles, and capillaries with thickened basement membranes were also found. In another study, hyalinization of choroidal vessels together with exudation of fibrin in plasma have been reported to be present in patients with PCV. Report of intra-Bruch membrane choroidal neovascularization has been identified which supported the idea that PCV is a variant of neovascular AMD. Interestingly, regarding the role of vascular endothelial growth factor (VEGF), different specimens showed conflicting immunostaining results, which may explain partly the refractory responses of PCV toward anti-VEGF treatment.
Risk Factors
Cardiovascular Diseases
As PCV is a vascular disease, it is not surprising to find its association with cardiovascular problems. It has been reported that as high as 42% of patients with PCV have hypertension. Smoking is also a risk factor for PCV with odds ratio reported ranging from 4.40 to 4.87.
Serum Biomarkers
High levels of C-reactive protein was shown to be associated with increased risk of PCV up to threefold after adjusting for age, sex, smoking status, alcohol use, body mass index, and use of antiinflammatory drugs, suggesting that inflammation and immune-related process takes part in the pathogenesis.
Elevated serum homocysteine level may result in endothelial injury, oxidative stress, and thrombosis and it is also related to various systemic vascular diseases such as ischemic heart disease and stroke. PCV, being a vasculopathy, has also been reported to be related to increased plasma homocysteine level with about 1.5-folds increased odds, and have been one of the pathogenic factors that causes arteriosclerosis and subsequent aneurysmal-like dilatation.
Matrix metalloproteinases (MMP) regulates extracellular metabolism, and hence, affects vascular remodeling. Extracellular matrix modeling derangement disorder has been observed in the Bruch’s membrane and the choroidal vasculature of PCV patients resulting in arteriosclerotic and aneurysmal changes. Increased in MMP-2 and MMP-9 levels have been observed in PCV patients that further support their role in the condition.
Genetic Factors
Down to genetic level, various genetic defects have been found to be related to PCV. A GG missense variant at rs5882 in the cholesteryl ester transfer protein locus was found to have a 3.53-fold increased risk of PCV compared with AA genotype, which may suggest the involvement of lipid metabolism in the pathogenesis.
Other genetic loci that have been found to be related to the pathogenesis include two single nucleotide polymorphisms in the complement factor H: rs1061170 and rs800292; and two in ARMS2/HTRA1: rs10490942 and rs11200638. Mutation of the complement family may lead to aberrant complement activation causing vasculopathies. In contrast, HTRA1 is a membrane serine peptidase and is thought to regulate degradation of extracellular matrix proteoglycan. Overexpression may affect the integrity of Bruch’s membrane that exerts a permissive effect on the expansion of abnormal choroidal capillaries.
Genetic factors determine treatment responses as well. A single-nucleotide polymorphism at rs 10490924 in ARMS 2 was found to be associated with visual prognosis after verteporfin photodynamic therapy (PDT). Among the various genotypes, the GG genotype is associated with better visual outcome when compared to the TT genotype. Another gene SERPINF1 is also associated with treatment outcome. AA genotype at rs12603825 in this gene was associated with shorter retreatment-free intervals after PDT among all identified genotypes.
Clinical Features and Course
Patient with PCV can be asymptomatic if there is no leakage from the lesions, whereas the less fortunate patients may suffer from acute or progressive visual loss. Acute visual loss is usually due to spontaneous rupture of the polypoidal lesions resulting in submacular hemorrhage ( Fig. 18.1 ) presenting with scotoma or even breakthrough vitreous hemorrhage causing profound visual loss. Polypoidal lesions may also result in exudative changes with accumulation of subretinal fluid and exudates, causing metamorphopsia and progressive blurring of vision.
On physical examination patients with PCV may have variable sized serous and serosanguinous detachments of neurosensory retina and/or pigmentary epithelium. Underlying vascular abnormalities may sometimes be visible especially when the overlying retina is flat and pigment epithelium is atrophic. Polyps’ size and number vary among patients. Microrips or tears of retinal pigment epithelium (RPE) may be present at margin of serosanguinous pigment epithelial detachments (PEDs). Complications may occur resulting in subretinal fibrosis, pigment epithelial hyperplasia, and atrophic degeneration. These lesions may appear in various parts of the retina and may be present bilaterally. Drusen may be present in the fellow eye, though less common than in cases of AMD.
The natural course of PCV can be highly variable, depending on the location, size, and associated complications including hemorrhages and exudates. It was previously thought that if PCV was left untreated, about 50% of patients will enjoy favorable outcome with spontaneous regression of lesions. However, it has been reflected from the results of longer term studies that PCV might not be as benign as ophthalmologists thought. Many PCV patients would instead suffer from repeated hemorrhage and leakage resulting in degeneration of photoreceptors and scarring of RPE, and subsequently leading to significant visual impairment. Microrips of RPE, though may present during the disease course, may resolve spontaneously afterward. A grape-like cluster of polyps have been identified to be associated with poorer visual outcomes due to their propensity to bleeding. A retrospective study in Chinese patients has revealed that there was a mean loss of 3.1 lines among PCV patients resulting in final visual outcome of 20/200 or worse in 68.2% of patients.
Clinical Imaging of Polypoidal Choroidal Vasculopathy
In this era of multimodal imagings for retinal diseases, there are reports on the use of various imaging modalities to visualize PCV. The use of these imaging techniques is useful not only in making the diagnosis but also has treatment implications. Moreover, it could be used to monitor treatment progress. In this section, we shall look into detail how different imaging modalities can be of use.
Clinical Diagnosis
The diagnosis, or at least suspicion of PCV, can be picked up at slit-lamp biomicroscopy. At times, PCV appears as an orange-red nodule ( Fig. 18.2 ). This is when there is elevation of the RPE overlying the polyp. Although this is highly indicative of PCV, it can sometimes be just a small PED.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
