Myopia

hmirzaeee 23,252 views 112 slides Feb 20, 2014
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MYOPIA

سانشراک روپدمحم یبتجم تسیرتموتپا

یرتموتپا دشرا

یرتموتپا دشرا سانشراک روپدمحم یبتجم تسیرتموتپا
mojtaba mohammadpour .optometrist,Msc.
univercity of medical scences Birjand ,Iran

• EMMETROPIA
Parallel incident rays come to a focus on the retina when the
accomodation is fully relaxed so far point is at infinity.

MYOPIA
eye having excessive refractive power for its axial length.
(borish)
This may be due either to the eye having
1-a relatively long axial length
2-increased dioptric power of one or more of the refractive elements.

myopia
Far point of the eye closer to retina than infinity

•Axial myopia
•if the total refractive power of an eye remains constant but the
axial length (i.e., the distance from the anterior corneal surface to
the retina measured along the visual axis) increases, a myopic
shift in refractive error will result
•Refractive myopia
• if the axial length of an eye remains constant but the
refractive power of one or more of its optical elements
increases, a myopic shift in refractive status will occur.

MYOPIA: REFRACTIVE vs AXIAL
Refractive Myopia
(Optics of the eye too strong)
Axial Myopia
(Eye too long)

•The proposed classifications may be grouped
under the following broad headings:
•1-Rate of myopic progression
•2-Anatomical features of myopia
•3-Degree of myopia
•4-Physiological and pathological myopia
•5-Hereditary and environmentally induced myopia
•6-Theory of myopic development
•7-Age of myopia onset

•Classification by Rate of Myopic Progression
•1-Stationary myopia
•2-temporarily progressive
•3-permanently progressive.

•1-Stationary myopia Stationary myopia
•(Donders )
• is generally of low degree (-1.50 to -2.00 D) and arises "in
the years of development."
•The degree of myopia remains stationary during adulthood
and may occasionally diminish with the approach of old age.

•2-temporarily progressive
•Temporarily progressive myopia generally arises in the early
teens and progresses until the late 20s.
• After this age, the rate of myopia progression approaches
zero. Interestingly, Donders reported that it was rare for
myopia to develop after 15 years of age in previously normal
eyes and, falsely, that it never developed after the 20th year
of life

•3-permanently progressive
•Permanently progressive myopia ascends rapidly until around 25
to 35 years of age, and there afteradvances more slowly.
•Subsequent increases in myopia are said to occur in jumps,
rather than in a smooth progression.
•Donders observed that because of pathological condi-tions such
as retinal detachment and macular degener-ation, in these cases
it was rare at 60 years of age "to find a tolerably useful eye."

•Classification by the Anatomical Features of Myopia
•1-Axial
•whereby the eye is too long for its refractive power
•2-Refractive
•whereby the refractive system is too powerful for the axial length of the eye.An increase in axial
length may occur in the anterior or posterior portions of the globe individually, or may occur
throughout the eye.
•The site of elongation may have implications for determining the etiology. For example, it has
been suggested that expansion of the posterior portion of the globe may be related to the
actions of the superior and inferior oblique muscles during vergence

•Borish further divided refractive myopia into
1-Index myopia
•in which one or more of the refractive indices of the media are anomalous.
•2-Curvature myopia,
• in which the reduced radius of curvature of one or more refractive surfaces produces increased dioptric power.
•3-Anterior chamber myopia
in which a decrease in anterior chamber depth increases the refractive power of the eye.

•Hirsch examined the refractive error of 562 eyes having myopia in
patients between 18 and 60 years of age. He divided the population into
three groups on the basis of the degree of myopia,
•1-alpha
•Using inferential statistics, he determined that the alpha group followed a
normal distribution curve, with a theoretically assumed peak of -0.50 D.

•2-beta groups
•The beta group was represented by a second normal
distribution curve, with its peak around -4 D.
• Hirsch suggested that the myopia in this group may be hereditary in
origin

•3-gamma groups
•The gamma group ranged from -9 to -15 D, and this degree
was described by Hirsch as malignant, pathological,
degenerative, or congenital.
•Sorsby et al in an investigation of 341 eyes between 20 and 60
years of age, concluded that 95% of refractive errors fell
within ±4 D. They also suggested that the etiology of myopia
of less than 4 D differed from that myopia exceeding 4 D,

•Classification Based on Age of Onset
•1-Congenital myopia:
•Myopia is present at birth and persists through infancy .although many children are born with myopia (low birth
weight) lose their myopia during first year of life this classification includes only children whose myopia persist
in infancy and present when entering school. prevalence is about 2%.
•2-Youth-onset myopia:
•The onset of myopia occurs between 6 years of age and the early teens .from 2% at 6 years to 20% at 20 years.
•3-Early adult-onset myopia:
•The onset of myopia occurs between 20 and 40 years of age.
•4-Late adult-onset myopia:
•Myopia onset occurs after 40 years of age.

•Physiological (correlation ) myopia
•All of the component of refraction are within normal limits .but lack of correlation.(-
0.50D) per years.
• intermediate myopia
•Similar to Physiological myopia but
•1-age is slightly younger.
•2-amount of myopia tends to be higher.
•3-axial length is longer.
•Pathologic myopia
•Highly myopic refractive error is present from early childhood
and is progressive. prognosis is poor with legal blindness

•Other Myopias
•Night Myopia
•The phenomenon of increased myopia under low luminance
conditions was first reported in 1789 by the Revere and Nevil
Maskelyne
• More recent evidence has demonstrated that night myopia is
produced by an increased accommodative response (typically
on the order of 0.50 to 1.00 D) under degraded stimulus
conditions changes in chromatic aberration may also be
involved in this myopic shift.

•Pseudomyopia
•Pseudomyopia has been defined as a reversible form of
myopia that results from a spasm of the ciliary muscle.
• The excessive accommodative response produces an apparent
myopic shift that will disappear when a cycloplegic agent is
administered to produce relaxation of accommodation

Ocular disorder Associated with Myopia
•1-Retinopathy of prematurity
•2-retinitis pigmentosa
•3-Albinism
•4-Congenital or juvenile glaucoma
•5-keratoconus
•6-isolated ectopic lentis
•7-CSNB
•8-subset of Lebers s Congenital amaurosis
•(majority are hypropic)
•9-Cone dystrophy
•10-Interruption of light passing through ocular media
•11-Genetics! autosomal dominant pathologic myopia to gene18p11.31

•6-Cataract -Nuclear cataract causes a myopic shift

Retinopathy of prematurity
•1-VEGF
•Treatment
•1-laser photocoagulation
•2-anti VEGF (bevacizumab )

Albinism
Albinism, a group of inherited disorders, results in little or no production of the pigment
melanin
Foveal hypoplasia
Tyrosine negative –positive

Systemic disorder Associated with Myopia
•1-Marfan’s syndrome
•2-Down syndrome
•3-Fetal alcohol syndrome
•4-Ehler’s-Danlos syndrome
•5-homocysinuria
•6-Stickler’s syndrome
•7-weill – marchesani syndrome

•4-Congenital or juvenile glaucoma
•5-keratoconus
•6-isolated ectopic lentis
•7-CSNB
•8-subset of Lebers s Congenital amaurosis
•(majority are hypropic)
•9-Cone dystrophy
•10-Interruption of light passing through ocular media
•11-Genetics! autosomal dominant pathologic myopia to gene18p11.31

Marfan syndrome
most often affects the connective tissue of the heart and blood
vessels, eyes, bones, lungs, tall, thin build.
•Long arms, legs, fingers, and toes and flexible joints.
•A spine that curves to one side. This condition is called scoliosis .
•A chest that sinks in or sticks out. These conditions are called pectus
excavatum and pectus carinatum respectively.
•Teeth that are too crowded.
•Flat feet.

Pathological Conditions Associated with Myopia
•Marfan’s syndrome
–Suspensory ligaments break
–dislocation of lens occurs superiorly and temporally and
results in a very high increase in myopia
Lens dislocation is common in Marfan's, affecting 50% to 80% of patients. The
dislocation is usually superior

•Marfan's syndrome is an autosomal dominant disorder
caused by mutations in the fibrillin gene on chromosome 15.
• Fibrillin is a glycoprotein that is a major component in elastic
tissue and is important in lens zonules. 50-80 percent of
patients with Marfan’s syndrome have ectopia lentis.

Aortic root dilation
m.v.p

Unlike Marfan syndrome, in which the joints tend to be "loose," in homocystinuria
the joints tend to be "tight."
rare inherited metabolic disorder involving the amino acid methionine and resulting in a
harmful accumulation of homocysteine in the body.
Mental retardation
Skeletal abnormalities
Scoliosis Kyphosis
Chest abnormalities
homocysinuria

Stickler syndrome
•Stickler syndrome is a
•connective tissue disorder
• a genetic malfunction in the connective tissue
• bones
•Eyes
•and ears
•flattened facial appearance.
•abnormal curvature of the spine (scoliosis or kyphosis)

•Ocular disorder
•glaucoma
•Cataracts
•retinal detachment

Ehlers-Danlos syndrome
Ehlers-Danlos syndrome is a group of inherited disorders that affect your connective tissues —
primarily your skin, joints and blood vessel walls.

Ehlers-Danlos syndrome
Skin thin and hyperelastic

Weill–Marchesani syndrome
short stature;
an unusually short, broad head (brachycephaly)
facial abnormalities;
hand defects,
including unusually short fingers (brachydactyly);
distinctive eye abnormalities.
A six year old female with Weill-Marchesani syndrome, which has caused a dislocated
lens.

Weill–Marchesani syndrome
•microspherophakia
• myopia
• lens subluxation
•and glaucoma secondary to progressive
shallowing of the anterior chamber.

A lens dislocation caused by Weill-Marchesani syndrome

A lens dislocation caused by Weill-Marchesani syndrome

Pathological Conditions Associated with Myopia
•Diabetes
–High blood glucose levels cause increased sorbital levels in
the lens
–Water rushes in and dilutes the sorbital in the lens
–Lens bulges and results in a myopic shift

•Classification into
• Physiological
•Pathological Myopias

•1-Physiological myopia
•was denned by Curtin as myopia in which each component of refraction
lies within the normal distribution for that population. Thus, the myopia
arises from a failure of correlation between the refractive components.
• However, physiological myopia may be defined as normal as opposed to
pathologic myopia Therefore, physiological myopia might simply and
more accurately be defined as nonpathological myopia

•2-Pathological Myopia(malignant or degenerative myopia)
•Duke-Elder and Abrams defined pathological refractive errors as "those refractive
• anomalies determined by the presence in the optical system of the eye of an
element which lies outside the limits of the normal biological variations.
•These authors adopted the term degenerative myopia to describe myopia that is
accompanied by degenerative changes, particularly in the posterior segment of the
globe. This is most frequently found in high (>6 D) degrees of myopia

Pathologic Myopia
Eyes with pathologic myopia have progressive elongation of the
eye, thus creating a propensity for thinning of the RPE and choroid
The spherical equivalents of an eye with high myopia are more
than -6.00 D, or an axial length greater than 26.5 mm, whereas
patients with pathologic myopia are more than —8.00 D, or an
axial length greater than 32.5 mm.

•Degenerative myopia is also known as other terminology
including:
•High Myopia
•Degenerative Myopia
•Pernicious Myopia
•Malignant Myopia

• Pathological change in myopic eyes

•TOOLS TO MONITOR
•Fundus photography
•A- and B-scan ultrasonography
•Visual fields
•OCT
•Monitor corneal health if CL wearer
•Fundus photos

•FUNDUS SIGNS

It is important as primary eye care providers to be cognizant of the signs of degenerative myopia
which commonly include:
•Tilting of the optic disc
•Peripapillary chorioretinal atrophy
•Lacquer cracks
•Round, subretinal hemorrhages that clear spontaneously
•Fuchs spots + CNV
•Posterior staphyloma
•Paving-stone degeneration
•lattice degeneration
•Hole formation in the peripheral retina
•Elongation and atrophy of the cilliary body
•POAG

TIGROID FUNDUS
•As the eye enlarges, the retinal pigment epithelium thins,
resulting in a tessellated (checkered) appearance of the
fundus and increased visibility of the choroidal vasculature.

TIGROID FUNDUS: As the eye enlarges, the retinal pigment epithelium thins, resulting in
a tessellated (checkered) appearance of the fundus and increased visibility of the
choroidal vasculature.

Myopic crescent
•a white or grayish white crescentic area in the fundus of the
eye located on the temporal side of the optic disc; caused by
atrophy of the choroid, permitting the sclera to become
visible.

Optic disc crescents are common in myopes. They can vary in size and location
but are typically situated at the temporal disc margin as in this three dioptre myope.

A much larger crescent in a nine dioptre myope

Myopic crescent

•Posterior Staphyloma
•The posterior staphyloma is a pathognomonic feature of eyes with pathologic myopia. It is a
localized
• ectasia of the sclera, choroids, and retinal pigment epithelium that can be of variable size and
involve different aspects of the posterior fundus.
•These staphylomas are best observed with indirect binocular ophthalmoscopy and B-scan
ultrasonography.
•The posterior staphylomas are usually present from a young age and
•may progress with age, particularly with high myopias and long axial
•lengths.
•Vision progressively deteriorates in eyes with staphylomas that amacula-centered because of
the progressive thinning of the choroids and
•retinal pigment epithelium in the macula.

POSTERIOR STAPHYLOMA: Staphylomas are localized ectasia (“enlargement”) of the
sclera, choroid, and RPE. It can be easily seen on B-scan or a CT Scan. Staphylomas can
eventually lead to atrophy and loss of vision.

The most common type 1 posterior staphyloma. The edge of thestaphylomatous region is
arrowed

Lacquer Cracks
•With the thinning of the retinal pigment epithelium and
choroid,ruptures of Bruch’s membrane occurs in up to 4.2%.
• These typically occur with a streak of retinal hemorrhage that is not
associated with any underlying choroidal neovascularization.

Lacquer Cracks

•The lacquer cracks are best defined as linear hyperfluorescence in the early
phase of fluorescein angiography and late hypofluorescence on indocyanine
angiography.
•Over time, the cracks may widen and join with areas of atrophy. Central vision
may be affected depending on the course of the lacquer crack, especially if
there is foveal involvement. It should be noted that the presence of lacquer
cracks does put the eye at risk of choroidal neovascularization.
•In our series of 28 Asian eyes with myopia of greater than –6.0 DS, sixeyes
(21.4%) were found to have lacquer cracks as the underlying cause.

LACQUER CRACKS: are spontaneous ruptures of the elastic lamina of Bruch’s membrane
that appear yellowish-white and are usually located in the posterior pole. They generally
have linear or stellate patters. IVFA will show hyperfluorescence, as the fluorescein leaks
through Bruch’s membrane, highlighting these cracks. These can lead to CNV in the 4th-
6th decade of life.

Myopic macula chorioretinal degeneration with lacquer crack across the fovea.

Lacquer cracks near the macula

Myopic Foveoschisis
•As a consequence of the ectasia secondary to the posterior
staphyloma,highly myopic individuals can develop foveoschisis.
• This is the splitting of the retinal layers in the macula which can cause
blurring of vision and metamorphopsia.
• It can then progress on to a myopic macular hole formation that may be
associated with a retinal detachment
•.Surgical intervention may be necessary to restore the anatomy and
visual function. The surgical procedures that have been performed
include vitrectomy with gas tamponade and macular buckling.

•Postsurgical developments in a myopic macular hole with associated retinal detachment. (a) Posterior pole of the left eye shows a tilted optic disc with myopic
crescent, and a horizontally oval macular hole with extensive subretinal fluid, which masks the retinal pigment epithelial (RPE) atrophy around the hole. Subretinal
precipitates suggest chronicity of the retinal detachment. (b) Optical coherence tomogram (vertical 10 mm scan) shows the macular hole, the surrounding sensory
retinal detachment, and the posterior staphyloma. (c) One month after vitrectomy, the retina is reattached with closure of the macular hole. The central geographic
patch of RPE atrophy is now prominent. (d) Repeat OCT (10 mm horizontal scan) confirms the anatomical outcomes; and reveals the residual central defect between
the flattened edges of the macular hole ('flat open' configuration), as well as the presence of posterior staphyloma. Central sub-RPE hyperreflectivity is suggestive of
geographic atrophy. (e) A small blister is evident within the nasal edge of the closed hole as early as 4 months on repeat mode OCT, which, however, disappeared on
subsequent visits. (f) In a 4-year review, a full-blown foveoschisis has developed, with irregular but attached central edges. Status quo continued for 6 months.

tilted optic disc with myopic crescent
macular hole

Color fundus photo of a highly myopic patient who presented with progressive
reduction in vision. Notice the significant myopic degeneration in the posterior pole.
The patient was found to have myopic foveoschisis (MF) with foveal detachment.

•OCT AND MF
•The standard test to detect MF remains OCT

Clinical photographs of the fundus of the right (A) and (B) left eyes in a patient with MFS.
(c) Fluorescein angiogram of the right eye in the early (C) and late (D) phases,
demonstrating staining of the optic nerve crescents and small window defects along the
macular region.

On OCT scans
•eyes with MF exhibit a thickened retina in the posterior pole
and hyporeflective splitting between the less reflective outer
retina and the more reflective inner retina.

There is splitting of the retinal layers of the macula in the presence of myopic
foveoschisis as seen on this OCT scan.

SD-OCT image of a 60-year-old woman with high myopia and posterior staphyloma
demonstrating typical MF (large arrow), premacular structure (small arrow), and foveal
detachment (star).

• Lattice degeneration
•Lattice degeneration is a peripheral vitreoretinal thinning that is clinically
•important because of the potential risk of developing retinal tears and
•detachments.
•Lattice lesions can vary in their appearance. They can be linear or oval
•lesions of retinal thinning that can be of various sizes and extents of pigmentation.
•They are usually anterior to the equator
•Some may have round atrophic holes within them.

•These are not considered to be major risk factors for retinal detachment, however,lattice
degeneration has been reported in up to 20% of all detachments,and Byer showed that the
risk of developing retinal detachment in the presence of lattice degeneration is about 0.3 to
0.5%.

LATTICE DEGENERATION: is a vitreo-retinal degeneration that causes retinal atrophy
(“thinning”). It can be classified as pigmented or non pigmented. It takes on a lattice
formation (“crisscrossing”) because the retinal vessels become sclerotic, and the
collagen is laid down in this crisscross pattern. Due to the retinal thinning, it is prone to
causing retinal breaks, tears, or holes, which of course might lead to retinal detachment.
However it is important to remember that retinal breaks due to lattice degeneration
rarely turn into retinal detachments.

Lattice Degeneration

Peripheral lattice degeneration with pigmentation and an atrophic round hole within.

Figure 9. Retinal detachment involving the macula secondary to multiple retinal breaks
superiorly.

Prevalence of fundus changes in 1584 consecutive eyes with high myopia

Fuchs’ spot
•The most serious outcome of myopic chorioretinal degeneration is the
presence of a Fuchs’ spot, which is a round or elliptical, circumscribed lesion
in the macular or perimacular area.
• It occurs as a result of breaks in Bruch’s membrane and the development of
a neovascular membrane, giving rise to a hemorrhage that becomes
pigmented.
•A Fuchs’ spot initially causes symptoms of metamorphopsia - as found on
the Amsler grid - and can eventually cause a partial or complete loss of
central vision.

FUCHS SPOTS: Fuch’s spots are dark spots due to RPE hyperplasia. They can involve
subretinal neovascular membrane with an overlying retinal pigment epithelial hyperplasia.
The CNV can eventually cause disciform scars on the macula in the 4th-6th decade of life.

A developing Fuchs’ spot together with haemorrhage and a serous detachment of
the macula. Vision was markedly reduced

Paving Stone Degeneration
•well-delineated, flat yellow foci in the size
range of 0.5–2.0 disc diameters .
• Irregular black pigmentation frequently is
present on the margins of the lesions and red
lines, which correspond to choroidal blood
vessels

Pavingstone degeneration (also known ascobblestone) (Image courtesy
of Dr HD Riley andthe Indiana University School of Optometry, USA)

Myopic Chorioretinal Atrophy
•The areas of atrophy may be focal or diffused, defined or irregularly
•shaped, isolated or composed of multiple pale white areas in the posterior pole
•. There may be clumps of pigment within these areas.
•The choroidal vessels are usually easily seen beneath the thinned out retina.
Fundus fluorescein angiography would show staining of these atrophic areas
while they are hypofluorescent with indocyanine green angiography.
•The natural history of these areas of atrophy is gradual enlargement
•and coalescence. As the fovea becomes more extensively involved, centralvision
becomes progressively affected.

A myopic CNV which is seen as a greyish subfoveal membrane with surrounding
subretinal blood.

Fluorescein angiogram showing the classic CNV.

A 53-year-old female with myopia of –8.50 DS, presented with a subfoveal
hemorrhagein the right eye with visual acuity 6/15 (a).
The fluorescein anigoram showed the presenceof a myopic CNV involving the macula
(b).
(a)
(b)

(c)
(d)
(e)
The OCT scan showed the subretinal fluid space and the subretinal neovascular membrane (c).
(d) and (e) She received a singledose of intravitreal bevacizumab 1.25 mg/0.05 ml and the vision
improved to 6/9 after one month and this was maintained after 12 months. However there was
formation of chorioretinalatrophy around the involuted mCNV (black arrow).

Myopic macular hole detachments
•Macular holes can develop in highly myopic eyes. This usually
occurs as aconsequence of tractional forces from the
vitreoretinal interfaceOften, a localized detachment arises
within the macula, which over time,can extend peripherally

Myopic macular hole

Chorioretinal atrophy: larger geographic areas involving the posterior pole

. A myopic retina with a macular hole with surrounding retinal detachment within the macula

•Some unfortunate consequences of myopia
•1-chorioretinal degeneration
•2-retinal detachment
• 3-glaucoma
•4-cataract

Management
•Divergent or minus lenses in
• spectacles
• contact lenses
•Refractive surgery

•Low myopia <1.00 has little significant in infant and preschool children and is not
usually corrected.
•Moderately low degrees of myopia (1- 3D) should be corrected in children who are 3
years of age or older.
•Moderately high degrees of myopia (3.00- 5.00D) should be corrected in children
who are 1 years of age .
•high degrees of myopia (- 5.00D) should be corrected in any age .
•Bruce D.MOOR,OD. eye care for infants and young children.

Correction of myopia
1-minus glass
2-contact lens

Uncorrected, light focuses in front of fovea
Corrected by divergent lens, light focuses on fovea

•Contact lenses
–Soft contact lenses
–Rigid gas permeable contact lenses
–Ortho-keratology contact lenses

Management
•Surgery
–Radial keratotomy (RK)
–Post-surgical complications
•Hyperopic shift
•Diurnal fluctuations of refractive error and visual acuity
•Glare
•Corneal scarring

Management
•Refractive surgery
–Photorefractive keratectomy (PRK)
–Technique
•High energy photons from an excimer laser are used to
photoablate a small amount of tissue from the anterior corneal
surface and sculpt the cornea

Management
•Refractive surgery
–Photorefractive keratectomy (PRK)
–Post-surgical complications
•Eye pain
•Corneal disruption
•Blurry vision
•Prolonged duration of drug use
•Greater time needed for eyesight recovery

Management
•Refractive surgery
–Laser in-situ keratomileusis (LASIK)
–Technique
•A microkeratome is used to cut a flap of superficial corneal tissue
•The flap is lifted back, exposing the underlying corneal stroma
•The excimer laser is used to perform tissue removal in the corneal
stroma
•The flap is repositioned in its original position and adheres to the
underlying corneal stroma without the need for sutures
Flap creation
Laser intervention Flap repositioning

Management
•Refractive surgery
–Laser in-situ keratomileusis (LASIK)
–Post-surgical complications
•Severe dry eye syndrome
•Poor night vision
•Reduced contrast sensitivity
•Astigmatism

Management
•Refractive surgery
–Points to consider after the surgical procedure
–Use eyedrops, as prescribed by the ophthalmologist
–Wear sunglasses when outside to protect the eyes from sunlight
–Remember to go back to the hospital for regular follow up visits with
the ophthalmologist and to get eyedrops

mojtaba mohammadpour .optometrist,Msc.
univercity of medical scences Birjand ,Iran