Hypermetropia

Group (5) Prepared by :-

1-Osama Tariq

2-Ihab Mahmood

3-Mustafa Ahmed

4-Yusra Mustafa
 Introduction
A normal developed eye act as a convex lens with a power of (+58D).
The two major components are cornea (+43D) and lens (+15D).

Refractive errors are most common eye disorders and not a disease.

It mean that the shape of the eye does not refract the light rays correctly on the retina resulting blurred
vision .

Emmetropia is a normal refractive condition of the eye in which the parallel light rays from infinity
(6meter&more) are focus exactly on the retina .so the vision is clear at all distances.

Ametropia are refractive errors in which the light rays are focused in front or behind the retina ,can be
classified as short sightedness or myopia and long sightedness or hypermetropia &astigmatism.

Ametropiamay be due to following causes :-

1- Axial ametropiaIn which too long and too short lengths of the globe result in myopia and
hypermetropia respectively .perhaps , the change in the axial length of the globe is the most important
cause of ametropia .

2-Abnormal curvature of the cornea or the lens _curvature ametropia

In which too much and too less curvatures cause myopia and hypermertopa, respectively.

3-Abnormal refractive indix of the media _index ametropia

Increase in the index of the refractive media (cornea,aqueous and lens) and decrease in the index of
vitreous cause myopia , while the opposite condition cause hypermetropia .

4-Abnormal position of the lens

A forward displacement of the lens leads to myopia and backward displacement to hypermetropia .
Hypermetropia
(Also known as hyperopia ,or far_sightedness)

Is error of refraction in which the parallel rays of light from infinity come to focus behind the retina
when the accommodation is at rest .

Etiology of hypermetropia

1-Axial hypermetropia

When the antero-posterior diameter of the eye is less than the normal (normal axial length is
24mm).1mm shortening will cause +3D hypermetropia .

*It is either :

Physiological;-Almost all eyes at birth are hypermetropic (+2.5 _3 D of HM) and with the growth of the
body their antero_pasterior diameter increase and reach normal length by the age of 4 to 5 years.If eye
remains under_developed ,hypermetropia is often found .

Pathological :-seen in orbital tumor ,oedema, coloboma& micropthalmos.

2_Refractive hypermetropia :

 Curvature HM :when the curvature of the cornea or lensis flatter than normal .increase of 1mm in
its radius of curvature produce a hypetmetropia of 6.OD.

Astigmatism is usually accompanied with curvature hypermetropia .

It is either:
Congenital (cornea plana ) or acquired (truma to the cornea with scar formation).

 Index HM :when the refractive index of the media is less than normal ,as found in cortical
cataract ,D.M patient .

(refractive index of cornea -1.37 ,,lens (cortex )-1.38 ,and nucleus of lens -1.40 )

 Positional HM :backward dislocation of the lens produce hypermetropia which is either congenital
or acquired (in truma ).

 Absence of lens (aphakia):either congenital or acquired .

 Classifications:

1. Based on the structure of the eye :

Physiologic Hyperopia (simple and functional)

The vast majority of cases of hyperopia are of a physiologic nature. From the perspective of
physiologic optics, hyperopia occurs when the axial length of the eye is shorter than the
refracting components the eye requires for light to focus precisely on the photoreceptor layer of
the retina. Hyperopia can result from a relatively flat corneal curvature alone or in combination
with insufficient crystalline lens power, increased lens thickness, short axial length, or variance
of the normal separation of the optical components of the eye relative to each other.

Astigmatism, the most common refractive error, is often present in conjunction with hyperopia.
High hyperopia is associated with high levels of astigmatism, suggesting a breakdown in the
process of emmetropization that results in a component-type refractive error. Hereditary factors
are probably responsible for most cases of refractive error, including physiologic hyperopia, with
environment playing some role in influencing the development and degree of the error.
However, environment probably plays a lesser role in influencing the course and magnitude of
hyperopia than of myopia.

Physiologic hyperopia is not solely an anomaly of physiologic optics. Significant effects on visual
system function are closely related to the underlying structural anomaly. Active accommodation
mitigates some or all of hyperopia's adverse effects on vision. The impact of accommodation is
highly dependent upon age, the amount of hyperopia and astigmatism, the status of the
accommodative and vergence systems, and the demands placed upon the visual system.

Active accommodation typically enables young patients to overcome facultative and latent
hyperopia, but it may not be sustainable for long periods under conditions of visual stress. Signs
and symptoms such as optical blur, asthenopia, accommodative and binocular dysfunction, and
strabismus may develop. These signs and symptoms occur more readily and to a greater degree
in manifest and absolute hyperopia. In general, younger individuals with lower degrees of
hyperopia and moderate visual demands are less adversely affected than older individuals, who
have higher degrees of hyperopia and more demanding visual needs.
Pathological hyperopia :

Use of the term "pathologic" implies that the hyperopia has an etiology other than normal
biologic variation of the refractive components of the eye. Pathologic hyperopia may be due to
maldevelopment of the eyeduring the prenatal or early postnatal period, a variety of corneal or
lenticular changes, chorioretinal or orbital inflammation or neoplasms, or to neurologic- or
pharmacologic-based etiologies. It is rare in comparison with physiologic hyperopia and may
have a genetic inheritance pattern. Because of the relationship of pathologic hyperopia to
potentially serious ocular and systemic disorders, proper diagnosis and treatment of the
underlying cause may prove critical to the patient's overall health.

Microphthalmia (with or without congenital or early acquired cataracts and persistent

hyperplastic primary vitreous) and this condition's often hereditary form, nanophthalmia, may
produce hyperopia in excess of +20 D. Anterior segment malformations such as corneal plana,
sclerocornea, anterior chamber cleavage syndrome, and limbal dermoids are associated with
high hyperopia. Acquired disorders that can cause a hyperopic shift result from corneal
distortion or trauma, chalazion, chemical or thermal burn, retinal vascular problems, diabetes
mellitus, developing or transient cataract or contact lens wear. When extreme enough to lead to
relative aphakia, ectopia lentis produces high hyperopia. Conditions that cause the
photoreceptor layer of the retina to project anteriorly (idiopathic central serous choroidopathy
and choroidal hemangioma from Sturge-Weber disease) also induce hyperopia. Similarly, orbital
tumors, idiopathic choroidal folds, and edema can mechanically distort the globe and press the
retina anteriorly, thereby causing hyperopia. Adie's pupil occasionally causes a mild hyperopic
shift. Cycloplegic agents may induce hyperopia by affecting accommodation, and a variety of
other drugs can produce transient hyperopia.

A number of developmental disabilities and syndromes are associated with high hyperopia.
Conditions having foveal hypoplasia (albinism, achromatopsia, and aniridia) or early retinal
degeneration (Leber's congenital amaurosis) appear to disrupt emmetropization grossly and
result in high hyperopia and astigmatism. Other disorders with a high prevalence of hyperopia
are Aarskog-Scott, Kenny, Rubinstein-Taybi, fragile X, and Down's syndromes.
2. Based on degree of the refractive error.
. Low hyperopia consist of an error of +2.00 diopters (D) or less
. Moderate hyperopia includes a range of error from +2.25 to +5.00 D
. High hyperopia consists of an error over +5.00 D

3. Based on patient’s accommodative system .

.Latent hypermetropia is the amount of error corrected by involuntary tone of ciliary muscle.

. Manifest hypermetropia is the amount of error that is not corrected by the involuntary tone of
ciliary muscle. It equals the highest plus lens by which the patient sees clearly without the use of
cycloplegic drugs.

. Absolute hypermetropia is the amount of error not corrected by contraction of ciliary muscle.
It equals the lowest plus lens by which the patient can see clearly without the use of cycloplegia.

.Facultative hypermetropia is the amount of error corrected by voluntary contraction of ciliary

muscle.

. Total hypermetropia is the total error. It equals the power of the plus lens by which the patient
can see clearly under complete cycloplegia.
 Symptoms
Principle symptoms is blurring of vision for close work.
Symptoms vary depending upon age of patient & degree of refractive error.
Corrected by accommodation of patient

1- Asymptomatic
Small e Small error produce no symptoms
Corrected by accommodation of patient

2- Asthenopia
Refractive error are fully corrected by accommodative effort
Thus vision is normal
Sustained accommodation produce symptoms
Asthenopia increase as day progresses
Increase after prolonged near work.

Symptoms
Tiredness
Frontal or frontotemporal headache
Watering
Mild photophobia

To keep the image focused on retina an excessive amount of accommodation is required in

uncorrected hyperopia, the visual system has three choices:
1- The visual system can let the letters go out of focus, making reading impossible.
2- One eye may turn inward, toward the nose, releaving the eyestrain but causing double vision.
3- Single vision may be maintained, but at the cost of large amount of stress due to the continual
unconsciousness effort to keep the eye from overcovering, and thus avoid double vision.

3- defective vision with asthenopia

Not fully corrected by accommodation.
Defective vision for near more than distance.
Asthenopia due to sustained accommodation.
Refractive error more(>4D).

4- Defective vision only

Refractive vision more than 4D
Adults who usually do not accommodate.
Marked defective vision for near and distance.

5- The effect of aging on vision:

Progressive loss of accommodative power with aging-> progressive loss of vision.

6- Intermittent sudden blurring of vision:

May occur due to spasm of accommodation inducing pseudomyopia.
 Cycloplagic refraction reveals the underlying hyperopia.

Diagnosis

Diagnosis of hypermetropia is based on the symptoms and clinical signs observed.

Clinical signs:
Visual acuity: Visual acuity varies with degree of hypermetropia and power of
accommodation. Patients with low degree of refractive error may have normal visual
acuity. However, there is decrease in visual acuity for seeing near objects.

Cover test: Cover test reveals an accommodative convergent squint. Due to altered
accommodative convergence (AC) and accommodation (A) balance (AC/A ratio),
maintaining binocular vision becomes difficult. The advantages of binocular vision are
sacrificed in favour of more obvious advantages of clear vision. The better eye
dominates for vision and the other eye develops accommodative convergent squint.

Eyelids: One may develop blepharitis, stye or chalazion. The correlation between lid
conditions and hypermetropia is not clear.

Eyeball: Size of the eyeball may be normal or small.

Cornea: Cornea may also be slightly smaller in size. There may be associated condition
of cornea plana (flat cornea).

Anterior chamber: Anterior chamber is relatively shallow in high hypermetropia.

Glaucoma: The eye is small in high hypermetropia along with small size of cornea and
shallow anterior chamber. Due to increase in size of the lens with ageing, the eye
becomes prone to an attack of narrow angle closure glaucoma.

Lens: Lens may be dislocated backwards.

Fundus: Fundus examination shows small optic disc which may look hyperaemic
(vascular) with ill- defined margins. This appearance may simulate papillitis. Since there
is no swelling of the disc, it is called pseudo-papillitis. The retina is shiny due to reflection
of light, called as shot silk appearance. Reflex of retinal vessels may be accentuated
simulating arteriosclerotic changes. Vessels may be tortuous and may show abnormal
branching.

Management
Medical optical therapy:

Assessment of Vision:

The most common component of assessment of visual function is to test central vision through
visual acuity. Visual acuity determines ability to read symbols of varying sizes at a standard
testing distance. This reference distance approximates optical infinity and is typically 6 meters.
A 6/6 letter on the standard eye chart devised by Snellen is considered normal visual acuity.
Refractive errors may result in uncorrected visual acuities that fall below 6/6. In the absence of
other diseases, the condition of hypermetropia may be corrected with restoration of normal visual
function. This may be achieved with spectacles or contact lenses.

Basic principle of therapy is to converge and focus the light rays on the retina with the help of
convex (plus) glasses.

Rules for prescribing glasses in hypermetropia:

 Cycloplegia: Total hypermetropia is determined by performing refraction (checking

power of glasses) under complete cycloplegia.

 Small total manifest hypermetropia: For small total manifest hypermetropia e.g. 1 D or
less, correction may be required only if the patient is symptomatic.

 Spherical power: Spherical power is prescribed to the extent that it is suitably acceptable
to the patient.

 Astigmatism: Astigmatism should be fully corrected.

 Children younger than 4 years: Children younger than 4 years requiring hypermetropic
correction may usually accept full cycloplegic correction. It may be reduced in older
children.

 Older children: Older children may not accept full cycloplegic correction because of the
blur for distance. It may be increased gradually till the child accepts for the manifest
hypermetropia.

 Exophoria: Hypermetropia should be under-corrected by about 1- 2 D if there is

associated exophoria.

 Accommodative convergent squint: Full cycloplegic correction should be given if there

is accommodative convergent squint.
  Amblyopia (lazy eye): In the presence of associated amblyopia (Functionally reduced
vision not correctable with glasses and is not due to any eye disease) in one eye, full
correction with occlusion therapy should be given.

 Growth of child: Hypermetropia decreases with growth of the child. Periodic refraction
should be conducted and the correction should be reduced accordingly.

Prescription of convex power:

 Spectacles: Convex lenses may be prescribed as spectacles.

 Contact lenses: Contact lenses may be prescribed for cosmetic reasons once the
refractive power of the eye stabilises. Contact lenses may be prescribed for unilateral
hypermetropia as well.

Surgical therapy:
It may be:

 Non- contact Holmium:YAG laser thermokeratoplasty: Non- contact Holmium:YAG

laser thermokeratoplasty is suitable for hypermetropia of about + 1 D to + 2.5 D. With
this, multiple radially distributed spots are produced in the para-central cornea, which
leads to shrinkage of the collagen in the mid- peripheral stroma and consequent
steepening of the central cornea.

 Hypermetropic photorefractive keratectomy (H- PRK): The principle of this

procedure is to steepen the anterior corneal curvature. The cornea is sculpted in to a
steeper convex lens by creating a furrow- like ring zone in the corneal periphery.

 Conductive keratoplasty: Conductive keratoplasty is a non-invasive procedure in which

radiofrequency is used to correct low hypermetropia with or without astigmatism. It may
also be used to correct residual refractive error after cataract surgery or laser assisted in-
situ keratomileusis.

 Hypermetropic laser assisted in- situ keratomileusis (LASIK): It is used to correct

mild- to- moderate hypermetropia varying from + 1 D to + 4 D.
  Phakic intraocular lens (IOL) implants: Phakic intraocular lens (IOL) implants are
used to correct higher degrees of hypermetropia, varying from about + 4 D to + 10 D.
Phakic IOLs are especially designed, foldable, convex, thin lenses implanted in the
posterior chamber behind the iris and in front of the normal crystalline lens.

 Refractive lens exchange: Extraction of clear lens with implantation of an IOL,

preferably foldable IOL or a piggyback IOL. In piggyback IOL, two IOLs are placed in
the eye one on top of the other. This is done if the biometry is + 40 D or so, and one does
not have a lens of high power to implant. Moreover, there is high level of spherical
aberration with thick lenses.

Prognosis:
Asymptomatic children up to about 10 years with low to moderate hypermetropia usually do not
require any glasses. Visual acuity decreases as the child grows due to loss of accommodation.

Hypermetropia decreases quality of life. Poor vision may also decrease in the ability to learn and
develop. Hypermetropia that is not fully compensated with accommodation may produce
complications.

Complications:
Uncorrected hypermetropia may produce complications such as:

 Accommodative convergent squint: Excessive use of accommodation may produce

accommodative convergent squint, usually by the age of about 2- 3 years.

 Amblyopia: Amblyopia may develop as

– Anisometropic amblyopia as in cases with unequal or unilateral hypermetropia.
– Strabismic amblyopia as in children who develop accommodative squint.
– Ametropic amblyopia as seen in children with uncorrected bilateral high hypermetropia.

 Lid diseases: Repeated rubbing of eyes in hypermetropic blurred vision may produce
blepharitis, stye or chalazion.

 Primary narrow angle glaucoma: The eye in hypermetropia is proportionately small.

The size of the lens keeps on increasing with age. This predisposes the already small eye
to the primary narrow angle glaucoma.
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