4. Myopia- New Latin …… was derived from the original Greek word “mŭopia” …
contracting or closing the eye.
- 138–201 Galen was the first to use the term myopia
PM- 1988 Takashi Tokoro …Definition of pathologic myopia
Staphyloma - is a pathognomic feature of PM
- 1801 Antonio Scarpa First anatomical description of posterior staphyloma,
but did not make the link to myopia
- 1856 Carl Ferdinand von Arlt First connected staphyloma and myopic refraction
- 1977 Brian J. Curtin Classification scheme for staphyloma
8. Clinically- refractive error > -6 D.
Duke-Elder - Myopia with degenerative changes
especially in the post. segment.
Tokoro - Myopia caused by pathological axial
elongation.
A more specific - Myopic retinopathy, refers to the
degeneration of chorioretinal tissue ass. with axial
elongation of the eye.
10. Country % Country %
Myopia
Some Asian countries 70–90% Industrialized -West 10%–25%
Taiwan 84% Africa 10–20%
Industrialized - East 60%–80% India 6.9%
Europe and the US 30–40%
PM
Asian 9–21% Most countries 1–4%
Spain 9.6% USA 2%
Singapore 9.1% Bangladeshi 1.8%
Japan 8% Czechoslovakia 1%
Northern China 4.1% Egypt 0.2%
High myopia affects 27%-33% of all myopic eyes in Asia.
11. Interesting facts
Lengthening of the post. segment of the eye commences only during
the period of active growth. The eye and the brain show precocious
growth at the age of 4 years; the brain is 84% and the eye 78% and
the rest of the body 21%.
After this, both the eye and the brain increase slowly while the body
grows more rapidly. However, when axial myopia continues to
progress, it is interpreted as a precocious growth which has failed
to get arrested…………….!!!!!!!!!!
We do not as yet know what this influence is.
13. Etiology of Myopia is as diverse and controversial as one
can imagine. Everything in medicine has been blamed as a
cause of Myopia.
Two types of theories are put forward:
1) Mechanical and Environmental
2) Biological
14. Mechanical theories - distension of normal sclera - Increased IOP
caused by the action of EOMs or IOMs or by insidious chronic
glaucoma.
Others theories : weakening of the sclera - venous congestion,
inflammation or dietary deficiency.
16. Type of Class. Classes of Myopia
Cause Axil Myopia
Refractive Myopia ( Curvature & Index )
Clinical Entity Simple myopia
Nocturnal myopia
Pseudomyopia
Degenerative myopia
Induced myopia
Degree Low myopia (<-3.00 D)
Medium myopia (-3.00 D - -6.00 D)
High myopia (>-6.00 D)
Age of Onset Congenital myopia
(present at birth and persisting through infancy)
Youth-onset myopia
(<20 years of age)
Early adult-onset myopia
(20-40 years of age)
Late adult-onset myopia
(>40 years of age)
17. High Myopia is classified in a simple manner as:
i) Simple ii) pathological
Simple Myopia - not progressive, good vision- optical correction.
Pathological Myopia - changes in the posterior segment,
lengthening of AP axis of the globe.
19. Risk factors Description
Race & ethnicity Asians
Age Middle aged (working life) or younger
Gender Female
Social group Children(Asian)
professional working adults
Geography Industrialised/developed nations
Lifestyle Time spent outdoors
Education High level of education/academic achievement
Occupation Near work indoors (e.g. lawyers, physicians,
microscopists and editors)
Familial inheritance
(parental refraction)
Genetic
21. Family studies and twin studies have revealed the heritability of myopia since the
1960s.
In familial studies and twin studies, linkage analysis using microsatellite markers
has identified 19 loci for myopia: MYP1 to MYP19.
AD High Myopia AR High Myopia X-Linked High Myopia Common Myopia
MYP1
MYP13
MYP2 MYP18
MYP3
MYP4
MYP5
MYP11
MYP12
MYP15
MYP16
MYP17
MYP19
MYP7
MYP8
MYP9
MYP10
MYP14
MYP17
23. Anatomical Manifestations
Corneal astigmatism
Deep AC
Angle iris processes
Zonular dehiscences
Vitreous syneresis
Lattice retinal degeneration
Scleral expansion and thinning
↓ Ocular rigidity
↑ AL
Tilted disc
Peripapillary detachment in PM
Temporal crescent or halo atrophy
Macular lacquer cracks
Pigment epithelial thinning
Choroidal attenuation
Foveal retinoschisis
Post. staphyloma
24. Functional Manifestations
Suboptimal binocularity
Image minification
Anisometropic amblyopia
Subnormal visual acuity
Visual field defects
Impaired dark adaptation
Abnormal color discrimination
25. Ocular Manifestations
-Strabismus:exophoria/exotropia
-Cataract.
-Glaucoma.. pigmentary / normal-tension glaucoma
-Tigroid, or blond fundus, with choroidal visible underneath
-Tilted optic nerve with peripapillary atrophy
-Peripapillary detachment
-Chororetinal atrophy
-PVD
-RD
-Lacquer cracks
-Lattice degeneration (spontaneous breaks in Bruch's membrane)
-Cobblestone degeneration
-Fuch's spot (RPE hyperplasia in response to CNV)
-Scleral thinning
-Peripheral retinal holes
-Macular holes causing RD
-CNV
26. Complications of Pathological Myopia
This review aims to provide an overview on some of the important
complications associated with PM.
Vitreous degeneration
Peripheral retinal
degenerations & RRD
Myopic foveoschisis &
Macular hole
CNV in PM Lacquer cracks
Post. Staphyloma
28. Liquefaction of the
vitreous gel
Hole in the posterior
hyaloid membrane
Fluid tru defect into
retrohyaloid space
Vitreous gel collapses
synchytic fluid in space
Detachment of posterior
vitreous from ILM Acute PVD
29. •PVD with gel collapse
Without vitreous hage, 4% develop retinal breaks
With vitreous hage, 20% develop breaks
PVD without gel collapse
Associated with future retinal hole or vitreous hage
Scaffold for proliferative new vessels
30. Symptomatic PVD
Approx 10-15 %
Retinal breaks at first
assessment
Approx 90 %
uncomlicated at first
assessment
High risk
break
Low risk
break
Low risk of
detachment
Approx 98 %
uncomplicated
At 4-6 weeks
1.5-3.4%
Retinal breaks
At 4-6 weeks
Detachment
In 33-46%
Within 6
weeks
Flow chart illustrating the natural history of an acute PVD
31. Ultrasound picture showing PVD.
Note that the vitreous is still attached
at the optic disc and the ora serrata.
32. Vitreous changes in PM
Vitreous liquefaction
Early PVD
Presence of CPVD
Years PM control
20- 39 27.8%
40-59 43% 8%
60 - 79 91% 60%
Larger posterior precortical vitreous pocket
Residual posterior cortex in CPVD
33. Myopic Foveoschisis
Prevalence – 9% to 34%
Pathogenesis :
1. Attachment of Contracted vitreous cortex to retinal surface
2. ERM
3. Retinal vascular traction
4. Rigidity of ILM
5. Progression of posterior staphyloma
34. Natural history:
Varied course with diverse visual outcomes- stable to development of
macular holes
Eyes with anterior traction had worst prognosis
Progressive disease with poor outcomes
Treatment:
PPV+ILM peeling(traditional/foveal sparing) +/- tamponade – useful
to relieve internal surface anterior traction
Scleral buckling – Addresses disparity between retina and elongated
sclera
Suprachoroidal buckling – hyaluronic acid injected through a catheter
into suprachoroidal space in the area of staphyloma to indent choroid
Complications:
Choroidal hemorrhage and hyperpigmentation around area of
indentation.
35. Macular hole
Myopic macular hole may occur, but the exact mechanism is
unknown.
Whether attenuation of the neural retina and its supportive pigment
epithelium and choroid are responsible is speculative.
36. Various surgical procedures have been performed for macular hole
with or without RD and they include :
PPV with gas or silicone oil tamponade
Macular buckling
Scleral shortening surgeries.
37. Myopic macular chorioretinopathy
DEF: is a rare, genetic eye disorder that causes vision loss.
Grading(shih et al)
MO - Normal post pole
M1 - Tesselation & choroidal pallor
M2 - M1+post staphyloma
M3 - M2+lacker cracks
M4 - M3+ focal deep choroidal atrophy
M5 - M4+geographic atrophy, CNV
M3>- myopic maculopathy
38. Peripheral retinal degenerations & RRD
“Lattice degeneration is a common retinal degeneration.”
1. Epidemiology
8-10% of general population (but 20-40% of RD)
More commonly in moderate myopes and is the most important
degeneration directly related to RD
Location: Commonly -temporal superiorly fundus Between equator and
ora serrata
2. Pathology
Discontinuity of internal limiting membrane
Atrophy of inner layers of retina
Overlying pocket of liquefied vitreous
Adherence of vitreous to edge of lattice (posterior edge)
Sclerosis of retinal vessels
39.
40. Lattice degeneration - predispose to RRD
Retinal tears - posterior and lateral margins of the lattice
degeneration
Role of prophylactic Laser photocoagulation:
History of RD in the fellow eye
Family history of RD
Prior to ocular surgeries
Symptomatic pt
41. In eyes with RD, laser photocoagulation alone is insufficient to treat
the condition and V-R surgery is required.
Surgical modalities for RRD - pneumatic retinopexy, SB surgery
with cryopexy, and PPV+BB+EL+ C3F8/ SIO.
CLINICAL PEARLS
Lattice degeneration both with and without atrophic holes is generally
benign and does not require prophylactic treatment, as the complications of
treatment are more severe than the natural history of the untreated
condition.
42. Myopic RD
• Incidence of RD in general population range between
0.005 and 0.01 % .
• RD occurs far more frequently in patients with myopia.
• Disease Case-control study Group found that subjects with
sepherical equivalent refractive error of -1 to -3 diopters
had a fourfold greater risk of RD then a nonmyopic
individual.
• For refractive errors greater than -3 diopters the risk was
tenfold greater
More than half of nontraumatic RRD occurs in myopic
eyes.
43. Syneresis of the
central vitreous
Traction caused
by spontaneous
or PVD
RETINAL TEAR
44. CNV in Pathological Myopia
Among various lesions associated with high myopia, macular CNV
is one of the most vision threatening complications.
It develops in around 5 to 10% of eyes with high myopia and is the
commonest cause of CNV in young individuals and accounts for
around 60% of CNV in young patients aged 50 years or younger.
Macular hage ass. with CNV in high myopia
45. - Develops from laquer cracks.
- Smaller, less exudation.
- Type 1 (severe myopic degeneration)- Leakage does not
extend beyond initial CNVM border- Quiescent scar.
- Type2( Minimal degeneration)- Leakage beyond CNVM
borders- Fibrovascular scarring.
46. The mechanism of CNV formation in myopic CNV is still
unclear.
A possible explanation includes, certainly, the induced
hypoxia in the outer retina, which is a large source of
VEGF secretion. Chorioretinal stretching, lacquer crack
formation, choroidal thinning, choroidal flow disturbance
with reduced flow, choroidal filling delay, RPE and
overlying retina atrophy, loss of photoreceptors, all of
them can be involved in growth factor release and myopic
CNV formation. The role of each of these features and the
interconnections between them remain unclear
47. Treatment of myopic CNV
More recently, the use of anti-VEGF agents
The most commonly used currently is PDT with
verteporfin.
A combination therapy of PDT with anti-VEGF
agents appears efficacious in the treatment of eyes
with CNV secondary to pathological myopia, and
may afford better visual outcomes as compared to
PDT monotherapy
•Laser photocoagulation of …. no longer performed.
• Other treatment modalities
- Submacular surgery
- Macular translocation surgery
48. Features of choroid in PM
Stretched choroid without additional vasculature
Thinner choroid
Choriocapillaries and larger ch.vessel have decreased lumen
Choriocapillaries have loss of fenestrations
Increased number of vortex veins(>4)
Posterior vortex veins(ciliovaginal veins)
Reduction of choroidal thickness is proportional to age and refractive status
Per dioptermyopia caused 8μm reduction in choroidal thickness
Per decade causing 12-15μm reduction in choroidal thickness
Intrachoroidal cavitation – the expansion of distance between inner wall of
sclera and posterior surface of bruch’s membrane
Attenuated choroid to absent choroid – myopic chorioretinal atrophy
49. Lacquer cracks
Spontaneous ruptures in the Bruch's membrane .
Small hages may develop within the lacquer cracks.
Lacquer cracks predispose - macular CNV
Small ingrowth of fibrovascular tissue may also give rise to small
elevated pigmented circular lesions and are known as Fuchs‘ spots.
51. post. staphyloma (ectasia)
Equatorial staphyloma with scleral dehiscence - STQ.
Visual loss is most often due to macular involvement of a post. pole
staphyloma.
52. Curtin classified the staphylomas into ten categories. The first five were simpler
configurations, while the last five were either more intricate in their configuration
53. Tesselated Fundus
Hypoplasia of the RPE following axial elongation reduces
the pigment, allowing the choroidal vessels to be seen.
Commonly seen in elderly or brunette patients.
May not be associated with any clinical significance
55. Ohno-Matsui K, Yoshida T, Futagami S, Yasuzumi K, Shimada N, Kojima A, et al. Patchy
atrophy and lacquer cracks predispose to the development of CNV in PM. Br J Ophthalmol
2003; 87: 570-573.
Cheung BT, Lai YY, Yuen CY, et al. Results of high-density silicone oil as a tamponade agent in
macular hole RD in patients with high myopia. Br J Ophthalmol 2007;91:719-721.
Chinese Medical Journal 2013;126(8):1578-1583
Bhatt N S, Diamond J G, Jalali S, Das T. Choroidal neovascular membrane. Indian J
Ophthalmol 1998;46:67-80
Hamelin N, Glacet-Bernard A, Brindeau C, et al. Surgical treatment of subfoveal
neovascularization in myopia: macular translocation vs surgical removal. Am J Ophthalmol
2002;133:530-6.
Flower RW. Expanded hypothesis on the mechanism of photodynamic therapy action on CNV.
Retina 1999;19:365-69.
Albert & Jakobiec,Principles and Practice of Ophthalmology, Volume 2, Chapter 154 PM P
2023-2027, 3rd ed 2008.
Pathological Myopia, Richard F. Spaide, Kyoko Ohno-Matsui, Lawrence A. Yannuzzi Editors
Kyoko Ohno – Matstui MD, Phd, Muka Moriyama MD, PhD Staphyloma II: Analyses of
Morphological Features of Posterior Staphyloma in Pathologic Myopia Analyzed by a
Combination of Wide-View Fundus Observation and 3D MRI Analyses Pathological Myopia
2014, pp 177-185
56. Pukhrai Rishi, … et al …..Photodynamic monotherapy or combination treatment with
intravitreal triamcinolone acetonide, bevacizumab or ranibizumab for choroidal
neovascularization associated with pathological myopia.. 2011
Editor's Notes
The word “myopia” is thought to be derived from New Latin, which in turn was derived from the original Greek word “mŭopia” (μυωπία, from myein “to shut” + ops [gen. opos] “eye”), which means contracting or closing the eye.
There are several other terms also used to describe pathological myopia such as ‘‘degenerative myopia’’ and ‘‘malignant myopia
MAGNA OR DEGENERATIVE MYOPIA
The definition of pathological myopia as a refractive error of –6 dpt is clinically useful, though it may exclude a number of eyes. Some authors have considered pathological myopia as refractive errors greater than –4 dpt in children less than 5 years of age
Duke-Elder defined PM as myopia with degenerative changes especially in the post. segment.5
Tokoro defined PM as myopia caused by pathological axial elongation.6
A more specific definition, myopic retinopathy, refers to the degeneration of chorioretinal tissue associated with axial elongation of the eye.7
In the Blue Mountains Eye Study, myopic retinopathy included the presence of staphyloma, lacquer cracks, Fuchs’ spot, myopic chorioretinal thinning or atrophy, peripapillary atrophy, cytotorsion or tilting of the optic disc, and the T sign found in central retinal vessels.
The prevalence of myopia has been reported as high as 70–90% in some Asian countries, 30–40% in Europe and the United States, and 10–20% in Africa
some research suggests the prevalence of myopia in India in the general population is only 6.9%.
High myopia is more common in Asian populations, with rates of 9–21%
There is a wide variation in the prevalence in different ethnic groups: 0.2% in Egypt, 1% in Czechoslovakia, 2% in the USA, 8% in Japan or 9.6% in Spain were documented, with most countries having a prevalence of approximately 1–4%
Prevalence of high myopia in Bangladeshi adults was 1.8%.
Prevalence of myopia of in urban and rural adults of northern China population of high myopia (<-6.0 D) was 4.1%.
In Singapore, reported 9.1% prevalence of high myopia among adult Chinese in Singapore.
In Taiwan, between the ages of 16 and 18 years have a rate of myopia of 84%.
The prevalence of myopia in young adolescent eyes 10%–25% and 60%–80%, respectively, in industrialized societies of the West and East.
After this, both the eye and the brain increase slowly while the body grows more rapidly. However, when axial myopia continues to progress, it is interpreted as a precocious growth which has failed to get arrested. We do not as yet know what this influence is.
Mechanical theories explained the development of high myopia by distension of normal sclera. This is caused by several factors. Increased intra-ocular pressure caused by the action of extra-ocular muscles or intra-ocular muscles or by insidious chronic glaucoma.
Others put forward the theory of weakening of the sclera by various causes like venous congestion, inflammation or dietary deficiency.
Among these theories two factors were prominently discussed - excessive close work and general debility. Incidence of High Myopia: among school going children was attributed to excessive close work. However, this was disapproved when high myopia was reported among illiterate population.
Classification
By cause
Borish and Duke-Elder classified myopia by cause:[3][4]
Axial myopia is attributed to an increase in the eye's axial length.[5]
Refractive myopia is attributed to the condition of the refractive elements of the eye.[5] Borish further subclassified refractive myopia:[3]
Curvature myopia is attributed to excessive, or increased, curvature of one or more of the refractive surfaces of the eye, especially the cornea.[5] In those with Cohen syndrome, myopia appears to result from high corneal and lenticular power.[6]
Index myopia is attributed to variation in the index of refraction of one or more of the ocular media.[5]
Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens as a result of sorbitol (sugar alcohol) accumulating in the lens. This edema often causes temporary myopia (nearsightedness).
Clinical entity
Various forms of myopia have been described by their clinical appearance:[4][7]
Simple myopia, more common than other types of myopia, is characterized by an eye that is too long for its optical power (which is determined by the cornea and crystalline lens) or optically too powerful for its axial length.[8] Both genetic and environmental factors, particularly significant amounts of near work, are thought to contribute to the development of simple myopia.[8]
Degenerative myopia, also known as malignant, pathological, or progressive myopia, is characterized by marked fundus changes, such as posterior staphyloma, and associated with a high refractive error and subnormal visual acuity after correction.[5] This form of myopia gets progressively worse over time. Degenerative myopia has been reported as one of the main causes of visual impairment.[9]
Nocturnal myopia, also known as night or twilight myopia, is a condition in which the eye has a greater difficulty seeing in low-illumination areas, even though its daytime vision is normal. Essentially, the eye's far point of an individual's focus varies with the level of light. Night myopia is believed to be caused by pupils dilating to let more light in, which adds aberrations, resulting in becoming more nearsighted. A stronger prescription for myopic night drivers is often needed. Younger people are more likely to be affected by night myopia than the elderly.[10][11]
Pseudomyopia is the blurring of distance vision brought about by spasm of the ciliary muscle.[12]
Induced myopia, also known as acquired myopia, results from exposure to various pharmaceuticals, increases in glucose levels, nuclear sclerosis, oxygen toxicity (e.g., from diving or from oxygen and hyperbaric therapy) or other anomalous conditions.[8] The encircling bands used in the repair of retinal detachments may induce myopia by increasing the axial length of the eye.[13]
Index myopia is attributed to variation in the index of refraction of one or more of the ocular media.[5] Cataracts may lead to index myopia.[14]
Form deprivation myopia occurs when the eyesight is deprived by limited illumination and vision range,[15] or the eye is modified with artificial lenses[16] or deprived of clear form vision.[17][18] In lower vertebrates, this kind of myopia seems to be reversible within short periods of time.[18] Myopia is often induced this way in various animal models to study the pathogenesis and mechanism of myopia development.[18]
Nearwork-induced transient myopia (NITM) is defined as short-term myopic far point shift immediately following a sustained near visual task.[19] Some authors argue for a link between NITM and the development of permanent myopia.[20]
Degree
Myopia, which is measured in diopters by the strength or optical power of a corrective lens that focuses distant images on the retina, has also been classified by degree or severity:[21]
Low myopia usually describes myopia of −3.00 diopters or less (i.e. closer to 0.00).[5]
Medium myopia usually describes myopia between −3.00 and −6.00 diopters.[5] Those with moderate amounts of myopia are more likely to have pigment dispersion syndrome or pigmentary glaucoma.[22]
High myopia usually describes myopia of −6.00 or more.[5] People with high myopia are more likely to have retinal detachments[23] and primary open angle glaucoma.[24] They are also more likely to experience floaters, shadow-like shapes which appear singly or in clusters in the field of vision.[25] Roughly 30% of myopes have high myopia.[26]
Age at onset
Myopia is sometimes classified by the age at onset:[21]
Congenital myopia, also known as infantile myopia, is present at birth and persists through infancy.[8]
Youth onset myopia occurs in the early childhood or teenage, and the ocular power can keep varying until the age of 21, before which any form of corrective surgery is usually not recommended by ophthalmic specialists around the world.[8]
School myopia appears during childhood, particularly the school-age years.[27] This form of myopia is attributed to the use of the eyes for close work during the school years.[5]
Adult onset myopia
Early adult onset myopia occurs between ages 20 and 40.[8]
Late adult onset myopia occurs after age 40.[8]
Simple Myopia is not progressive beyond the amount included within normal development; is associated with good vision and requires no treatment except optical correction.
Pathological Myopia on the other hand is a degenerative myopia accompanied by changes in the posterior segment of the eyeball with lengthening of AP axis of the globe. Besides, the axial pathological myopia, there are other types of myopia due to defects in the curvature of cornea and lens and due to trauma. Today, I will confine my remarks only to pathological axial Myopia.
Race and ethnicity
Highest prevalence among Asians, i.e. Taiwanese , Japanese , Singaporeans
and Chinese Compared to Asians lower prevalence in African and Pacific Island groups When compared to African Americans and/or Mexican Americans, higher prevalence found in Whites
Age
Clinically significant pathologic changes have also been found in patients who are middleaged (working life) or younger . The incidence and severity of pathologic signs increases with age. For instance, the visual acuity of high myopes decreases significantly as individuals age, which may be the result of complications including lacquer cracker, submacular hage, Fuchs spots and chorioretinal atrophy
Gender
Higher prevalence in women than men
Social group
Higher prevalence in young (particularly Asian) children and young and professional working adults
Geography
Higher prevalence in industrialised/developed nations Within nations there are rural–urban differences, i.e. inner-city urban areas have higher odds of the condition than outer suburban areas
Lifestyle
Associated with amount of time spent outdoors, i.e. total time spent outdoors was associated with less myopia, independent of indoor activity, reading and engagement in sports
Education
High prevalence in individuals with high level of education/academic achievement
Occupation
Associated with near work indoors . For example, people whose profession entails substantial reading during either training or performance of the occupation (e.g. lawyers, physicians, microscopists and editors) have higher degrees of myopia
Familial inheritance
(parental refraction)
Heritable myopia susceptibility – there is a positive correlation between parental myopia and myopia in their children , particularly if both parents are myopic
Ethnicity
Higher prevalence in Asians, Arabs, and Jews
Lower prevalence in Caucasians, Blacks, and South Sea Islanders
Myopia is more common in urban communities than in rural ones
MYP19
In 2010, a genetic locus was mapped to 5p13.3–5p15.1 in a
Chinese family with autosomal dominant high myopia
Patients who have excessive myopia often have strabismus, especially exophoria and exotropia, and are more likely to develop premature nuclear sclerosis or, in some cases, posterior subcapsular lens opacities. Glaucoma is more common among highly myopic eyes and is particularly insidious. Its prevalence is related to the degree of myopia. Also, pigmentary and normal-tension glaucoma occurs more frequently in myopes.
Retinal degenerations can be broadly divided into benign degenerations and those associated with higher risks of RD
Retinal degenerations can be broadly divided into benign degenerations and those associated with higher risks of RD
Conclusions. SS-OCT clarified the boat-shaped PPVP structure in vivo. Although the central height increased with the myopic refractive error, the width was unchanged. A channel connecting Cloquet's canal and PPVP suggested the route of aqueous humor into the PPVP.
In more advanced stage, myopic macular hole can develop which may be associated with RD and patients will suffer from severe visual loss with reduced visual acuity. Various surgical procedures have been performed for macular hole with or without RD and they include pars plana vitrectomy with gas or silicone oil tamponade, macular buckling, and scleral shortening surgeries.*
However, despite these interventions, reopening of the macular hole and retinal redetachment may still develop and some patients will require multiple surgeries to achieve attachment due to the loss of chorioretinal tissue and retinal pigment epithelial atrophy.
Shih and co‐authors used a grading system for myopic macular chorioretinopathy.8 MO indicated a normal posterior pole with no tessellation pattern in the macular area; M1 indicated tessellation and choroidal pallor pattern in the macular area; M2 indicated choroidal pallor and tessellation, and the border of an ectasia posteriorly was visualised: M3 indicated pallor and tessellation with several yellowish lacquer cracks in Bruch's membrane and posterior staphyloma; M4 showed choroidal pallor and tessellation, with lacquer cracks with posterior staphyloma and focal areas of deep choroidal atrophy, M5 indicated choroidal pallor and tessellation with lacquer cracks, posterior staphyloma, geographic areas of atrophy of retinal pigment epithelium and choroids, and choroidal neovasculariation were visualised. M3 or greater was defined by Shih et al in this issue of BJO as “with maculopathy.”
A greater appreciation of pathological myopia by eye care practitioners would facilitate a better understanding of approaches for screening and management
Hayashi et al. [4] found some problems with this scale, following a large number of highly myopic eyes during a mean time of 12.7 years. For these authors, lacquer cracks, placed into a relatively advanced group (M3), often develop at the early stage of myopic maculopathy, and they are often observed in young individuals without an obvious staphyloma or early atrophic changes of the retina
lattice degeneration is the most important peripheral retinal degeneration which can predispose to RRD.** This is because retinal tears can develop at the posterior and lateral margins of the lattice degeneration caused by strong vitreoretinal adhesions following PVD.
In eyes with RD, laser photocoagulation alone is insufficient to treat the condition and V-R surgery is required. Surgical modalities for RRD include pneumatic retinopexy, scleral buckling surgery with cryopexy, and pars plana vitrectomy with intravitreal tamponade such as gas or silicon oil.
The goal of the surgery is to identify and seal off all retinal breaks.
For patients in whom the macula is still attached, they will generally have favourable visual outcome postoperatively. However, for patients in which the central of the macula i.e. the fovea is detached, the visual prognosis of the patient is more variable and some patients might develop irreversible visual loss despite successful RD surgery. Therefore, prompt ophthalmic consultation is advised for early detection of RD in order to prevent irreversible visual loss.
More recently, the use of anti-VEGF agents
The most commonly used method in the treatment of myopic CNV currently is PDT with verteporfin.
Direct thermal laser photocoagulation of myopic CNV has been attempted for treatment but this will lead to considerable visual loss due to expansion of the laser scar in the long term and therefore thermal laser treatment is no longer performed for myopic CNV.
Other treatment modalities
Submacular surgery
Macular translocation surgery
The most commonly used method in the treatment of myopic CNV currently is PDT with verteporfin.
More recently, the use of angiogenesis therapy with anti-VEGF agents
Now there is a new, safer alternative that can preserve vision. Visudyne(R) (verteporfin for injection), also known as photodynamic therapy (PDT), is the first clinically proven therapy to treat pathological myopia.
Visudyne is currently approved for treating pathological myopia in over 40 countries, including the U.S. and Europe.
Visudyne is generally well tolerated and has a well-established safety profile. Infusion-related transient back pain occurred with Visudyne only at an incidence of 2.5%. Infusion induces temporary photosensitivity; patients should avoid exposure of skin and eyes to direct sunlight or bright indoor light for 5 days.
Severe vision decrease was reported within seven days in 1-5% of patients. Partial recovery occurs in some patients. Do not re-treat these patients until vision completely recovers to pretreatment levels and potential benefits and risks of subsequent treatment are carefully weighed.
The most frequently reported adverse events (10-30% incidence) were injection site reactions (including extravasation and rashes), blurred vision, decreased visual acuity, and visual field defects.
The abnormality seen in the myope that justifies use of the term degenerative is posterior staphyloma (ectasia), with its devastating secondary effects in the post. pole. The progressively myopic eye expands in all its post. dimensions, and the formation of an equatorial staphyloma with scleral dehiscence is not uncommon, especially in the superotemporal quadrant. Visual loss is most often due to macular involvement of a posterior pole staphyloma. [11]
In 1977, Curtin [ 1] classified a posterior staphyloma in eyes with pathologic myopia into ten different types. Types I to V are considered a primary staphyloma, and types VI to X are considered a combined staphyloma.
To date, this has been the most frequently used classification for staphyloma.