**2.1 Cataract and pathologic myopia**

Three main studies have investigated the connection between cataract formation and high myopia: the Blue Mountains Eye Study and the Beaver Dam study. In the first one, researchers found that there may be a strong connection between the development of posterior polar cataract and myopia that appeared before 20 years. Furthermore, they found a correlation between the level of myopia and posterior subcapsular cataract. High myopia, however, was linked to the formation of all the three types of cataract known [4]. In the Beaver Dam study, researchers confirmed the connection highlighted in other studies between myopia and nuclear cataract [5]. Unlikely, the connection between myopia and age-related cataract is not fully confirmed, while the incidence of PSC and nuclear cataract in myopic eyes appears well established. Also, the distribution of the type of cataract in relation to the axial length

**69**

*Pathologic Myopia: Complications and Visual Rehabilitation*

compression, but also superior and medial rectus.

by limitation of abduction and elevation [11].

have an axial length that is more than 30 mm.

expansion of surrounding scleral tissue [13].

**3.1 Lacquer cracks**

**3. Posterior complications in pathologic myopia**

rior pole, and their peripheral formation is unusual [14].

of the eye has been investigated; some studies found no connection, while others found a significative direct correlation between AL and the severity of the lens opacity [6]. Eventually, the mechanism that underlies this condition is not fully understood.

**2.2 Motility and globe position alterations in high and pathologic myopic patients**

High myopia is one of the clinical entities that cause a unilateral proptosis [7], leading to poor cosmesis, motility alterations, and pain. Furthermore, chronic exposition of anterior surface may cause exposition keratopathy. The mechanics of the relationship between axial elongation and myopic proptosis is complex; in its elongation process, the eyeball tends to expand backward and proptosis forward [8]. There is also evidence of a linear correlation between sferic equivalent and proptosis grade. It has been observed that in patients that suffer from strabismus related to high myopia, there is a displacement of the globe from the muscle cone in the space that forms between superior and lateral rectus muscles [9]. Lateral rectus

Alterations in motility alterations can also be observed in high myopic eyes; the range of these alterations goes from small angle esotropia with mild reduction of abduction to strabismus fixus. Exotropia and hypotropia can also be seen in these patients. Exodeviations due to a lesser accommodative work are relatively common in myopes. Strabismus fixus is the latest stage of the abovementioned spectrum; the eye appears fixed in esotropic and hypotropic position; even passive movements in other positions of gaze are impossible. Many theories for that phenomenon have been proposed; one of them is that the displacement of the eyeball already described causes a compression of lateral rectus muscle against the orbital wall. According to other authors, not only lateral rectus muscle can experience this

To prove this hypothesis, many MRI studies of the orbit have been performed; some found a displacement of the abovementioned muscles, while others demonstrated a superotemporal prolapse of the elongated posterior portion of the globe, which displaces lateral and superior rectus [10]. High myopic patients with time can also develop diplopia, which is due to esotropia, and hypotropia that is accompanied

Patients that suffer from alterations in motility and position of the globe often

Lacquer cracks are linear breaks of the Bruch's membrane-choriocapillaris complex, which can be found in 4% of subjects with high myopia [12]. The main pathogenetic mechanism is the mechanical stretching of the chorioretinal structures due to scleral elongation [12]. However, according to other studies, their formation could be associated with near vessels perforating the sclera causing the

The first clinical presentation usually consists in subretinal hemorrhage, which is a potential sight-threatening condition. Fluoro angiography and indocyanine angiography are important for differential diagnosis with myopic choroidal neovascularization. At the fundus examination, lacquer cracks appear as yellowish-white linear lesions, rarely starry or mixed shapes. Usually, they are located at the poste-

*DOI: http://dx.doi.org/10.5772/intechopen.85871*

is also inferiorly displaced.

*Intraocular Lens*

complications that will be discussed in this chapter. Corneal modifications in high myopic patients are still under debate; some studies reported modifications in corneal biomechanical properties in high myopic patients, such as lower hysteresis. According to some studies [1], highly myopic patients had flatter curvature, modifications in corneal thickness, and decreased endothelial density, while other studies did not report any statistical difference in central corneal thickness (CCT) in various ranges of myopia [2]. Choroid's thickness is significantly reduced in highly elongated eyes; its thickness in foveal and parafoveal portions showed to be inversely proportional to parameters such as patient's age, myopic sferic equivalent, and axial length of the globe, with this last parameter showing to be the most consistently related. Also, distribution of choroidal thickness is altered in these eyes, with temporal and superior regions far from the fovea that show to be thicker than foveal region. Another strong predictor for choroidal thinning in high myopic patients is the presence of a posterior scleral staphyloma [3]. Furthermore, this thinning in choroidal tissue has a negative impact on retinal trophism. With regard to choroidal flow in highly myopic eyes, studies are controversial; for some of them, blood flow in choriocapillaris is augmented, while for others not. It is possible to find differences between high myopic patients and emmetropic ones even in retinal blood flow. Density of the superficial and deep plexus is significatively reduced in high myopic subjects, and the magnitude of this phenomenon is negatively related to axial length and myopic refraction. It is possible to postulate that increasing of the axial length on this eyes can lead to mechanical stretching of ocular structures, leading to damage to retinal pigmented epithelium (RPE), retinal microvascular network, and endothelial cells. Furthermore, in highly myopic eyes, excessive elongation of the globe and tilting of the optic disc can lead to posterior staphylomas formation and the tilting of the optic disc could lead to alterations in macular and foveal morphology, leading to a change in foveal position that can be found moved mainly in the vertical direction. High axial length is associated with many morphologic changes in the optic nerve and peripapillary region. The axial elongation is associated with the enlargement of the optic nerve head and of the peripapillary scleral tissue. The scleral flange is strongly adherent to the lamina cribrosa and axial-elongation-induced scleral enlargement during eye movements. This condition may lead to thinning of the lamina cribrosa, and it may also be associated with the formation of peripapillary choroidal cavitation. Thinning of lamina cribrosa leads to an alteration between intraocular pressure (optic nerve tissue pressure and cerebrospinal fluid pressure) with a steepening of the translamina cribrosa pressure gradient; this may play a role in the development of the glaucomatous

**68**

optic neuropathy.

**2. Anterior complications in pathologic myopia**

Three main studies have investigated the connection between cataract formation and high myopia: the Blue Mountains Eye Study and the Beaver Dam study. In the first one, researchers found that there may be a strong connection between the development of posterior polar cataract and myopia that appeared before 20 years. Furthermore, they found a correlation between the level of myopia and posterior subcapsular cataract. High myopia, however, was linked to the formation of all the three types of cataract known [4]. In the Beaver Dam study, researchers confirmed the connection highlighted in other studies between myopia and nuclear cataract [5]. Unlikely, the connection between myopia and age-related cataract is not fully confirmed, while the incidence of PSC and nuclear cataract in myopic eyes appears well established. Also, the distribution of the type of cataract in relation to the axial length

**2.1 Cataract and pathologic myopia**

of the eye has been investigated; some studies found no connection, while others found a significative direct correlation between AL and the severity of the lens opacity [6]. Eventually, the mechanism that underlies this condition is not fully understood.

#### **2.2 Motility and globe position alterations in high and pathologic myopic patients**

High myopia is one of the clinical entities that cause a unilateral proptosis [7], leading to poor cosmesis, motility alterations, and pain. Furthermore, chronic exposition of anterior surface may cause exposition keratopathy. The mechanics of the relationship between axial elongation and myopic proptosis is complex; in its elongation process, the eyeball tends to expand backward and proptosis forward [8].

There is also evidence of a linear correlation between sferic equivalent and proptosis grade. It has been observed that in patients that suffer from strabismus related to high myopia, there is a displacement of the globe from the muscle cone in the space that forms between superior and lateral rectus muscles [9]. Lateral rectus is also inferiorly displaced.

Alterations in motility alterations can also be observed in high myopic eyes; the range of these alterations goes from small angle esotropia with mild reduction of abduction to strabismus fixus. Exotropia and hypotropia can also be seen in these patients. Exodeviations due to a lesser accommodative work are relatively common in myopes.

Strabismus fixus is the latest stage of the abovementioned spectrum; the eye appears fixed in esotropic and hypotropic position; even passive movements in other positions of gaze are impossible. Many theories for that phenomenon have been proposed; one of them is that the displacement of the eyeball already described causes a compression of lateral rectus muscle against the orbital wall. According to other authors, not only lateral rectus muscle can experience this compression, but also superior and medial rectus.

To prove this hypothesis, many MRI studies of the orbit have been performed; some found a displacement of the abovementioned muscles, while others demonstrated a superotemporal prolapse of the elongated posterior portion of the globe, which displaces lateral and superior rectus [10]. High myopic patients with time can also develop diplopia, which is due to esotropia, and hypotropia that is accompanied by limitation of abduction and elevation [11].

Patients that suffer from alterations in motility and position of the globe often have an axial length that is more than 30 mm.

## **3. Posterior complications in pathologic myopia**

#### **3.1 Lacquer cracks**

Lacquer cracks are linear breaks of the Bruch's membrane-choriocapillaris complex, which can be found in 4% of subjects with high myopia [12]. The main pathogenetic mechanism is the mechanical stretching of the chorioretinal structures due to scleral elongation [12]. However, according to other studies, their formation could be associated with near vessels perforating the sclera causing the expansion of surrounding scleral tissue [13].

The first clinical presentation usually consists in subretinal hemorrhage, which is a potential sight-threatening condition. Fluoro angiography and indocyanine angiography are important for differential diagnosis with myopic choroidal neovascularization. At the fundus examination, lacquer cracks appear as yellowish-white linear lesions, rarely starry or mixed shapes. Usually, they are located at the posterior pole, and their peripheral formation is unusual [14].

#### *Intraocular Lens*

In autofluorescence exam, they appear ipoautofluorescent. Spectral domain optical coherence tomography (SD-OCT) allows studying RPE and Bruch's membrane breaks; "en face" OCT angiography shows avascular bands in choriocapillaris segmentation [12].

Break of Bruch's-choriocapillaris complex leads to near RPE atrophy and fibrotic degeneration. Thus, fluoro angiography shows window-effect hyperfluorescence with no leakage; staining can appear during late phases, especially in fibrotic-evoluted breaks. In those cases, indocyanine angiography shows linear ipocyanescent lesions, which extension results longer than the one appreciable in fluoro angiography exam. Therefore, indocyanine angiography results in a most accurate examination in lacquer crack detection. Breaks on Bruch's-choriocapillaris complex lead to RPE damage and subsequent retina-epithelial "patchy atrophies" and, in 30% of cases, choroidal neovascularization (CNV) [19].

#### **3.2 Chorioretinal atrophy (tessellation, patchy, diffuse)**

Choroid thinning and subsequent retinal involvement are typical findings in pathologic myopia. Retinal remodellation seems to be associated with choroidal hypoperfusion due to vascular axial stretching. There are three main atrophy morphologies.

Tessellated fundus is the most common. It consists in multiple linear choroid-RPE thinning, making fundus appear as tiger streaked. Tessellated fundus is a very early manifestation of myopic retinal changes, and it can evolve in other more severe lesions. In fact, it is associated to lacquer crack formation and myopic chorioretinal atrophies.

Patchy atrophy appears as a gray-white lesion with well-defined edges; they can be found on staphyloma edges, near lacquer cracks, or as CNV evolution [15]. Coalescent patchy atrophies can lead to diffuse atrophy; furthermore, they have been described as very important risk factor in CNV formation (20%).

Diffuse atrophy, instead, is a large yellowish-white lesion with no well-defined edges. Usually, it is located in peripapillary zone and its correlation with CNV formation is rare (3.7%). RPE atrophy, patchy ore diffuse, leads to photoreceptor atrophy and their loss of function. Thus, macular or foveal atrophy is responsible of important and irreversible central vision loss. Fluorescein and indocyanine angiographies show hyperfluorescence and hypercyanescence due to window effect. In autofluorescence, atrophy is hypoautofluorescent with mild hyperautofluorescent edges, especially in patchy atrophy.

SD-OCT allows the operator to study the retinal structures involved, measuring progression of lesions over time (**Figure 1**).

The process that can lead to complications due to myopic chorioretinal atrophies is resumed in **Figure 2**.

**71**

*Pathologic Myopia: Complications and Visual Rehabilitation*

Fuchs' spots are patch-like whitish retinal lesions characterized by a dark pigmented central formation. They are the result of previous myopic CNV and their atrophic evolution with subretinal and intraretinal pigment dispersion. As for patchy atrophies, multiple Fuchs' spots can coalesce forming macular atrophy. Presence of Fuchs' spots in a myopic eye is very important to understand the history

Myopic CNV (mCNV) is found in 5–10% of high myopic eyes. Over time, many environmental and genetic risk factors have been detected. Among the main ones, lacquer cracks (29%), patchy atrophy (20%), female gender, and genetic proinflammatory protein expression are important to remember. However, the most important one is history of myopic CNV in the other eye (34%). Very often, mCNVs grow between RPE and neuroepithelium (CNV type 2 or "classic CNV") [17] in the macular region and precisely: 58% foveal and 23% juxtafoveal. Only 19% of mCNVs have extramacular location on the edges of a peripapillary diffuse atrophy

The pathogenesis of mCNVs is still controversial. Their subretinal growth associated to underlying RPE atrophy (75–94% of mCNVs occur on lacquer cracks), together with strong association of choroidal thinning, suggests that an angiogenic stimulus due to choroidal hypoxia could be a plausible pathogenic mechanism, when RPE barrier breaks are present (patchy atrophies and lacquer cracks). Axial length and refractive error, if considered by themselves, do not represent risk factors for mCNVs development [18]. mCNVs growth is asymptomatic until the activation, which leads to rapid reduction of visual acuity with metamorphopsia

On the funduscopic examination, they appear as small grayish spots with pigmented edges; subretinal hemorrhages' and intraretinal exudation are modest. Fluoro angiography remains the benchmark test for early diagnosis of myopic CNVs, presenting a higher sensitivity than SD-OCT in the detection of early active forms [19]. These lesions appear as hyperfluorescence in the early phases. When active, they show late fluorescein leakage, which is modest when compared to CNV in

*DOI: http://dx.doi.org/10.5772/intechopen.85871*

of the pathology and its future prognosis [16].

*Myopic chorioretinal atrophies and complications.*

**3.3 Fuchs' spots**

**Figure 2.**

**3.4 Myopic CNV**

(periconus-CNV).

and scotoma.

**Figure 1.** *An OCT scan overlying an area of chorioretinal atrophy: a myopic CNV is also present.*

*Pathologic Myopia: Complications and Visual Rehabilitation DOI: http://dx.doi.org/10.5772/intechopen.85871*

#### **Figure 2.**

*Intraocular Lens*

In autofluorescence exam, they appear ipoautofluorescent. Spectral domain optical coherence tomography (SD-OCT) allows studying RPE and Bruch's membrane breaks; "en face" OCT angiography shows avascular bands in choriocapillaris segmentation [12]. Break of Bruch's-choriocapillaris complex leads to near RPE atrophy and fibrotic degeneration. Thus, fluoro angiography shows window-effect hyperfluorescence with no leakage; staining can appear during late phases, especially in fibrotic-evoluted breaks. In those cases, indocyanine angiography shows linear ipocyanescent lesions, which extension results longer than the one appreciable in fluoro angiography exam. Therefore, indocyanine angiography results in a most accurate examination in lacquer crack detection. Breaks on Bruch's-choriocapillaris complex lead to RPE damage and subsequent retina-epithelial "patchy atrophies" and, in 30% of

Choroid thinning and subsequent retinal involvement are typical findings in pathologic myopia. Retinal remodellation seems to be associated with choroidal hypoperfusion due to vascular axial stretching. There are three main atrophy morphologies.

Tessellated fundus is the most common. It consists in multiple linear choroid-RPE thinning, making fundus appear as tiger streaked. Tessellated fundus is a very early manifestation of myopic retinal changes, and it can evolve in other more severe lesions. In fact, it is associated to lacquer crack formation and myopic chorioretinal atrophies. Patchy atrophy appears as a gray-white lesion with well-defined edges; they can be found on staphyloma edges, near lacquer cracks, or as CNV evolution [15]. Coalescent patchy atrophies can lead to diffuse atrophy; furthermore, they have

Diffuse atrophy, instead, is a large yellowish-white lesion with no well-defined

SD-OCT allows the operator to study the retinal structures involved, measuring

The process that can lead to complications due to myopic chorioretinal atrophies

edges. Usually, it is located in peripapillary zone and its correlation with CNV formation is rare (3.7%). RPE atrophy, patchy ore diffuse, leads to photoreceptor atrophy and their loss of function. Thus, macular or foveal atrophy is responsible of important and irreversible central vision loss. Fluorescein and indocyanine angiographies show hyperfluorescence and hypercyanescence due to window effect. In autofluorescence, atrophy is hypoautofluorescent with mild hyperautofluorescent

been described as very important risk factor in CNV formation (20%).

cases, choroidal neovascularization (CNV) [19].

edges, especially in patchy atrophy.

is resumed in **Figure 2**.

progression of lesions over time (**Figure 1**).

**3.2 Chorioretinal atrophy (tessellation, patchy, diffuse)**

**70**

**Figure 1.**

*An OCT scan overlying an area of chorioretinal atrophy: a myopic CNV is also present.*

#### **3.3 Fuchs' spots**

Fuchs' spots are patch-like whitish retinal lesions characterized by a dark pigmented central formation. They are the result of previous myopic CNV and their atrophic evolution with subretinal and intraretinal pigment dispersion. As for patchy atrophies, multiple Fuchs' spots can coalesce forming macular atrophy. Presence of Fuchs' spots in a myopic eye is very important to understand the history of the pathology and its future prognosis [16].

#### **3.4 Myopic CNV**

Myopic CNV (mCNV) is found in 5–10% of high myopic eyes. Over time, many environmental and genetic risk factors have been detected. Among the main ones, lacquer cracks (29%), patchy atrophy (20%), female gender, and genetic proinflammatory protein expression are important to remember. However, the most important one is history of myopic CNV in the other eye (34%). Very often, mCNVs grow between RPE and neuroepithelium (CNV type 2 or "classic CNV") [17] in the macular region and precisely: 58% foveal and 23% juxtafoveal. Only 19% of mCNVs have extramacular location on the edges of a peripapillary diffuse atrophy (periconus-CNV).

The pathogenesis of mCNVs is still controversial. Their subretinal growth associated to underlying RPE atrophy (75–94% of mCNVs occur on lacquer cracks), together with strong association of choroidal thinning, suggests that an angiogenic stimulus due to choroidal hypoxia could be a plausible pathogenic mechanism, when RPE barrier breaks are present (patchy atrophies and lacquer cracks). Axial length and refractive error, if considered by themselves, do not represent risk factors for mCNVs development [18]. mCNVs growth is asymptomatic until the activation, which leads to rapid reduction of visual acuity with metamorphopsia and scotoma.

On the funduscopic examination, they appear as small grayish spots with pigmented edges; subretinal hemorrhages' and intraretinal exudation are modest.

Fluoro angiography remains the benchmark test for early diagnosis of myopic CNVs, presenting a higher sensitivity than SD-OCT in the detection of early active forms [19].

These lesions appear as hyperfluorescence in the early phases. When active, they show late fluorescein leakage, which is modest when compared to CNV in

age-related macular degeneration (AMD). Furthermore, fluoro angiography, when a subretinal hemorrhage occurred, is a fundamental tool in the differential diagnosis between mCNV and Lacquer crack, which typically does not show fluorescein leakage. However, factors such as staining of dye in fibrotic tissue and hemorrhagic blocking defect may reduce the reliability of fluoro angiography exam.

Indocyanine angiography has a better penetration through bleeding, pigment, and exudates; it also allows a more accurate visualization of lacquer cracks. However, sensitivity in identifying CNVs is lower than fluoro angiography. Neovascularizations are shown as inconstant hypercyanescent lesions, sometimes surrounded by a hypocyanescent halo. For these reasons, indocyanine angiography is used only in case of extensive macular hemorrhages and in case of doubtful fluoro angiographic results.

SD-OCT exam is a primary, rapid, and noninvasive test in the diagnosis and follow-up of myopic CNV (**Figure 3**). However, modest exudation and bleeding of active mCNVs can sometimes lead to misdiagnosis on OCT examination. They appear as hyperreflective subretinal formations; signs of exudation (such as intraretinal fluid, retinal thickening, and outer limiting membrane interruption) can be detected only in 48% of cases, while fluorescein leakage is found in 82%. A multimodal approach, combining OCT and fluoro angiography, allows reaching high sensitivity in the diagnosis of myopic CNVs [20].

Overmore, implementation with OCT angiography function allowed us to study the retinal flow in the single tomographic segmentation of the retina, managing to identify 94.1% of mCNVs with a specificity of 93.75%. In "en face" visualization, active CNVs appear as vascular organizations in a typical lacy wheel shape or glomerular pattern, with many anastomoses and thin capillaries, in addition to the typical perilesional dark halo. In the quiescent phase, instead, they assumed the typical aspects of mature neovessels: large caliber and linear course, without anastomosis, with a filiform aspect, or dead tree appearance.

The most effective treatments to date are intravitreal injections of anti-VEGF drugs. While bevacizumab and ranibizumab demonstrated a comparable efficacy, aflibercept allowed the resolution of the CNV with a single administration in 55% of cases, resulting in the best medication for the "result/number of injection" ratio [21].

Photodynamic treatment has been shown to be less effective than ranibizumab; therefore, it is considered as a second choice treatment [22]. Natural evolution of mCNVs consists in a remodellation of the neuroepithelial and pigmented epithelial tissues, leading to the formation of typical Fuchs' spots and patchy atrophies with loss of function of involved retina.

**73**

**Figure 4.**

*Pathologic Myopia: Complications and Visual Rehabilitation*

capability compared to choroidal and scleral structures.

**3.5 Myopic tractional maculopathy (VMT, foveoschisis, macular hole, macular** 

The definition of "myopic tractional maculopathy" includes a wide range of

High myopic eyes, with a posterior pole staphyloma, undergo tractional phenomena between stretchable structures and nonelastic structures. To understand the biomechanics underlying these modifications, it is important to consider the physiological adherence of posterior vitreous cortex on the fovea. Furthermore, inner limiting membrane (ILM) and retinal vessels showed a reduced stretching

The extreme bulbar elongation caused by staphylomas creates axial vitreomacular traction with increased macular thickness; it is usually an asymptomatic condition, or it may lead to metamorphopsia, with preserved or mild altered visual acuity. Axial traction may result in alterations of vitreous body, such as cortical vitreoschisis or posterior vitreous detachment (PVD) (43.2%) with subsequent cellular proliferation and increased risk of epiretinal membrane (ERM)

Progression of staphylomatous bulbar elongation comes up against lower elasticity of retinal internal structures (ILM, retinal vessels, incomplete PVD with vitreoretinal adhesion, ERM), causing an intraretinal cleavage and configuring a foveoschisis (9%) [23]. Cleavage can occur in the inner, outer, or both retinal layers, but more often, it affects the inner limiting membrane. This condition has a variable progression, and some studies demonstrate its stability in 88.4% of cases. However, further progression of axial traction may lead to a detachment of the

The alteration of posterior pole profile due to the staphyloma, the presence of an ERM, and the incomplete PVD are factors that can lead to the development of tangential traction forces, which, combined with axial traction, can make the foveoschisis evolve into lamellar or full thickness macular holes with important visual acuity impairment. Furthermore, a full-thickness macular hole may cause a rhegmatogenous retinal detachment that can be confined to the macula or also

Diagnostic strategy of all the clinical presentation analyzed is based on fundus

examination and, above all, on the SD-OCT exam. The latter allows a precise characterization of the single vitreoretinal structures involved, through a tomographic study of the bulbar structures. OCT exams also make an accurate, rapid,

and noninvasive follow-up possible (**Figure 4**) [24].

*An OCT of a myopic patient showing a macular pucker and a foveoschisis.*

pathologies: vitreomacular traction, foveoschisis, and macular hole.

*DOI: http://dx.doi.org/10.5772/intechopen.85871*

**detachment)**

formation.

macular neuroepithelium.

involve the peripheral retina.

**Figure 3.** *An OCT scan of a myopic patient showing active myopic CNV.*

*Intraocular Lens*

angiographic results.

age-related macular degeneration (AMD). Furthermore, fluoro angiography, when a subretinal hemorrhage occurred, is a fundamental tool in the differential diagnosis between mCNV and Lacquer crack, which typically does not show fluorescein leakage. However, factors such as staining of dye in fibrotic tissue and hemorrhagic

Indocyanine angiography has a better penetration through bleeding, pigment, and exudates; it also allows a more accurate visualization of lacquer cracks. However, sensitivity in identifying CNVs is lower than fluoro angiography. Neovascularizations are shown as inconstant hypercyanescent lesions, sometimes surrounded by a hypocyanescent halo. For these reasons, indocyanine angiography is used only in case of extensive macular hemorrhages and in case of doubtful fluoro

SD-OCT exam is a primary, rapid, and noninvasive test in the diagnosis and follow-up of myopic CNV (**Figure 3**). However, modest exudation and bleeding of active mCNVs can sometimes lead to misdiagnosis on OCT examination. They appear as hyperreflective subretinal formations; signs of exudation (such as intraretinal fluid, retinal thickening, and outer limiting membrane interruption) can be detected only in 48% of cases, while fluorescein leakage is found in 82%. A multimodal approach, combining OCT and fluoro angiography, allows reaching

Overmore, implementation with OCT angiography function allowed us to study the retinal flow in the single tomographic segmentation of the retina, managing to identify 94.1% of mCNVs with a specificity of 93.75%. In "en face" visualization, active CNVs appear as vascular organizations in a typical lacy wheel shape or glomerular pattern, with many anastomoses and thin capillaries, in addition to the typical perilesional dark halo. In the quiescent phase, instead, they assumed the typical aspects of mature neovessels: large caliber and linear course, without

The most effective treatments to date are intravitreal injections of anti-VEGF drugs. While bevacizumab and ranibizumab demonstrated a comparable efficacy, aflibercept allowed the resolution of the CNV with a single administration in 55% of cases, resulting in the best medication for the "result/number of injection" ratio [21]. Photodynamic treatment has been shown to be less effective than ranibizumab; therefore, it is considered as a second choice treatment [22]. Natural evolution of mCNVs consists in a remodellation of the neuroepithelial and pigmented epithelial tissues, leading to the formation of typical Fuchs' spots and patchy atrophies with

blocking defect may reduce the reliability of fluoro angiography exam.

high sensitivity in the diagnosis of myopic CNVs [20].

anastomosis, with a filiform aspect, or dead tree appearance.

loss of function of involved retina.

*An OCT scan of a myopic patient showing active myopic CNV.*

**72**

**Figure 3.**
