Trans No. 2.

BLOCK XIII-A: DISORDERS of the EYES, EARS, NOSE and THROAT

HAZY VISION
Dr. Rosario Lahoz-Garcia

NOTES
 AUDIO
 NOTES FROM THE TUTOR’S POWERPOINT
 ADDITIONAL INFORMATION FROM THE TRANSCRIBERS

HAZY VISION

CASE

 55-year-old, male, complaining of hazy vision for six

months.

QUESTIONS

1. What possible structures are involved? Explain?

2. What further questions will you ask in your history? And
why?
3. Differential diagnoses and why?
4. What findings will you expect?
5. Anatomy and Embryology The most common causes of blurred vision include:
6. Pathophysiology of Cataract
1. Refractive errors (the most common cause overall)
7. Types of Cataract
2. Age-related macular degeneration
8. Management
3. Cataracts
4. Diabetic retinopathy
WHAT POSSIBLE STRUCTURES ARE INVOLVED?
EXPLAIN? Blurred vision has 4 general mechanisms:

1. Opacification of normally transparent ocular structures

(cornea, lens, vitreous) through which light rays must pass
to reach the retina
2. Refractive errors
3. Disorders affecting the retina
4. Disorders affecting the optic nerve or its connections

 Haze- made dim or cloudy by or as if by fine dust, smoke, A. CORNEA

or light vapor in the air; (Blurry, foggy).
 Blurred vision is the most common visual symptom.  Corneal opacification (eg, posttraumatic or postinfectious
 It usually refers to decreased visual clarity of gradual onset, scarring.
and corresponds to decreased visual acuity.
Cornea function:

 Transmit and refract light.

Transmission of Light:

 Cornea is transparent because it is avascular, has

uniform arrangement of fibrils and has Na pumps in
the endothelium, creating a relative
dryness/deturgescence —> light not diffracted,
therefore transmitted.
 Any disruption of the normal configuration of the collagen
fibrils will therefore cause failure in the efficient
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transmission of light and the cornea will appear hazy or  The (crystalline) lens- transparent (avascular) -focus
opaque. images on the retina.
 It is positioned just posterior to the iris and is supported by
Disruption in the transmission of light zonular fibers arising from the ciliary body and inserting
1. Corneal scars onto the equatorial region of the lens capsule
2. Corneal edema  Accommodation - eye’s ability to adjust its focus from
3. Corneal deposits distance to near due to changes of the shape of the lens.
4. Corneal melt Its inherent elasticity allows the lens to become more or
5. Corneal tumors less spherical depending on the amount of tension exerted
by the zonular fibers on the lens capsule. Zonular tension
Refraction of Light: is controlled by the action of the ciliary muscle that, when
contracted, relaxes zonular tension. The lens then assumes
 Normal: incoming parallel light rays enters eye—> bent/ a more spherical shape, resulting in increased dioptric
refracted—> focuses on retina power to bring near objects into focus.
 This is made possible by the smooth anterior  Ciliary muscle relaxation reverses this sequence of
shape/curvature of the cornea which is convex (thus light events, causing the lens to flatten and bringing distant
is bent inward or converged) and by the difference in the objects into view. As the lens ages, accommodation
indices of refraction between air, tear film, cornea and gradually reduces as lens elasticity decreases.
aqueous humor. So, any disturbance in the
shape/curvature of the cornea and the indices of refraction Problems with lens:
of the different structures can cause the failure of the  Loss of lens transparency (cataract) results in blurred
converged light rays to be focused on the retina leading to vision for near and distance.
blurry vision.  Aging is the most common cause, but many other factors
Disturbance in the refraction of light: can be involved, including trauma, toxins, systemic disease
(such as diabetes), smoking, and heredity. Age-related
1. Abnormalities of the corneal epithelium and tear film cataract is a common cause of visual impairment.
2. Abnormalities of corneal size/ shape / curvature  Protein aggregates that scatter light and reduce
transparency and other protein alterations that result in
B. LENS yellow or brown discoloration.

The Eye Lens and Cataract Disease:

 The ocular lens is responsible for the fine focusing of light

onto the retina, and its transparency is vital for visual
acuity. The lens anterior is lined with a single layer of
epithelial cells, overlaying the lens cortex and nucleus, both
of which are composed of elongated fiber cells. The
epithelial cells maintain metabolic activity and undergo
mitosis to produce daughter cells that migrate to the lens
equator where they begin differentiating into fiber cells [1].
The differentiating cells elongate to yield long, thin, ribbon-
like structures that form the onion-like layers of the lens.
During this time major intracellular changes occur,
including very high expression of soluble crystallin proteins
followed by organelle degradation.
 The center of the lens, known as the nucleus, contains
terminally differentiated fiber cells of which the innermost
are formed in utero. The outer layers of fiber cells, known
as the lens cortex, surround the nucleus and maintain some
level of protein turnover and metabolic activity. The
development and structure of the lens is such that it
contains some of the oldest cells and proteins in the entire
body that must maintain their molecular structure and
organization over an entire lifetime.
 To enable sight, the lens must remain transparent to visible
light and numerous strategies have evolved to reduce or
remove light-scattering structures from the tissue. The lens
is avascular with no arterial or venous circulation. Fiber cells
are organized to compact membranes and reduce

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intercellular space. Coordinated organelle degradation is problems of perfusion, and, knowing the extent of supply
initiated during fiber cell maturation to remove nuclei, of each system, one can then predict the depth of retinal
mitochondria, ER, ribosomes, and other organelles, which involvement.
reduces light scattering. Crystallin protein expression is
highly upregulated during differentiation, resulting in the D. OPTIC NERVE AND NEURAL PATHWAYS
crystallins comprising 90% of protein in the mature lens.
Short-range ordered packing of the crystallins at
concentrations of 250–400 mg/mL contributes to the
transparency of the concentrated solution and a
polydisperse mixture of crystallins avoids crystallization [4,
5]. Because the lens is formed in utero and mature fiber
cells lack protein synthesis and degradation machinery
necessary for removing and replacing damaged proteins, a
major requirement of the crystallins is superior solubility
and long-term stability of their native conformations.

Opacification of eye structures

1. Cataracts
2. Gradual onset, often risk factors (eg, aging, corticosteroid
use), loss of contrast, glare
3. Lens opacification on ophthalmoscopy or slit-lamp
examination.

C. RETINA

OPTIC NERVE

 The optic nerve consists of about 1 million axons

srcinating from the ganglion cells of the retina. The optic
nerve can be divided into the intraocular (anterior) and the
retrobulbar (posterior) portions. The intraocular portion is
commonly referred to as the optic disc (papilla) is visible
with an ophthalmoscope.
 The retrobulbar portion starts behind the eyeball and
can be further divided into the intraorbital, intracanalicular
 Retina- light sensitive structure where images are
and intracranial segments. The longest division is the
focused.
intraorbital portion. As it enters the optic canal it is known
 Receives the visual image, produced by the optical system
as the intracanalicular portion. The intracranial portion
of the eye, and converts the light energy into an electrical
begins from the optic canal just before the optic nerves
signal, which undergoes initial processing and is then
converge toward each other to become the optic chiasm.
transmitted through the optic nerve to the visual cortex,
 Visual pathway lesions from the optic nerve, optic
where the structural (form, color, and contrast) and spatial
chiasm, optic tract, lateral geniculate body, optic radiation
(position, depth, and motion) attributes are perceived.
and the occipital lobe produce characteristic visual field,
 The 3 Neuron Relay System: has tall structure that has
and visual acuity defects.
ten layers.
 Optic neuritis- inflammation of optic nerve, demyelinative
 In the ten layers are three main cell types that relay
disease, including the typical acute demyelinative optic
visual/chemical information through the retina,
neuropathy that is associated with multiple sclerosis.
from outside to in, and to the optic nerve and finally into
 Optic atrophy is a nonspecific response to optic nerve
the brain.
damage from any cause and also occurs in primary retinal
 Any breakdown in the neurons, the supporting cells and the
disease, such as central retinal artery occlusion or retinitis
relay system itself can manifest as visual disorders.
pigmentosa. In general, in optic nerve disease, there is a
 The ten-layer system is supplied by two different vascular
correlation between degree of optic disk pallor and loss of
systems. The outer retinal layers derive nutrition from the
acuity, visual field, color vision, and pupillary responses, but
choriocapillaris of the choroid. The inner layers, from the
the relationship varies according to the underlying etiology.
inner nuclear layer inwards, are supplied by the retinal
vasculature itself. Certain retinal diseases can be traced to
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Error of refraction

SUMMARY:

What structures involves, what structures you will

think about if your patient came with hazy vision?
 Anteriorly, anterior to the cornea, you have your tear
film.
 If you have a dry eye, your vision will also be affected,
even if everything is normal. So you should also consider
dry eye.
 Next to the tear film is the cornea, then your aqueous,
lens, vitreous and your retina.
 Your retina, the vascular supply coming from the retinal
arterial and the choroid should be intact. From the
retina, your optic nerve, optic chiasm up to your cortex.
 So, if a patient comes in with a hazy vision, you think of
many structures, from the anterior (tear film) until the
brain. Not just cataract.

WHAT FURTHER QUESTIONS WILL YOU ASK IN

YOUR HISTORY? AND WHY?

 The age is there for that reason.

 In your exams or in seeing patients, there are diseases
found in the elderly, for most of this is cataract. Only DIFFERENTIAL DIAGNOSES AND WHY?
some are found in the young.
 So, age is so important. Sometimes there are sexual 1. Any corneal disease
predilection. For example, for vision deficiency, 8% in 2. Cataract
males while 1% only in females. 3. Capsular opacification
 Occupation is also important. For example, an 4. Vitreous opacity
accountant whose vision is 20/25 will already complain
of hazy vision because it will already affect her work. OPACIFICATION OF EYE STRUCTURES
 Unlike a farmer whose vision is 20/200 already but will 1. Cataracts
not complain of hazy vision. The farmer will come in with 2. Corneal opacification
other complain. Another thing, in determining if a patient
needs cataract surgery, it’s the visual needs of the DISORDERS AFFECTING THE RETINA
patient, not the visual acuity. 1. Age-related macular degeneration
 Another important thing is if the patient is smoking,
2. Infectious retinitis (eg, cytomegalovirus, Toxoplasma)
medications, and presence of comorbidities.
3. Retinitis pigmentosa
4. Retinopathy associated with systemic disorders

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- By history taking, you can already know if the
DISORDERS AFFECTING THE OPTIC NERVE OR NEURAL patient is hypertensive and diabetic
PATHWAYS 5. Glaucoma
1. Optic neuritis 6. Optic nerve and central connections pathology

DISORDERS AFFECTING FOCUS

1. Refractive errors
1. CORNEAL DISEASE
 The cornea is not only a clear window through which light
passes on its way into the eye, it provides most of the
focusing power in the eye as well.
 Corneal disease is a serious condition that can cause
clouding, distortion, scarring and eventually blindness.
There are several common conditions that affect the
cornea.
 Injuries
 Allergies
 Keratitis
 Dry eye
 Corneal dystrophies.
2. CATARACT
 The term cataract refers to any opacity in the lens.
 Aging is the most common cause, but many other factors
can be involved, including trauma, toxins, systemic
disease (such as diabetes), smoking, and heredity.
 Age-related cataract is a common cause of visual
impairment.
 The prevalence of cataracts is around 50% in individuals
age 65–74, increasing to about 70% for those over 75.
3. CAPSULAR OPACIFICATION
 Posterior capsular opacification (PCO) occurs when a
cloudy layer of scar tissue forms behind your lens implant.
This may cause you to have blurry or hazy vision, or to see
a lot of glare from lights. PCO is fairly common after
cataract surgery, occurring in about 20% of patients.
4. VITREOUS OPACITY
 Vitreous opacity occurs when the vitreous, a gel-like
substance that fills most of the eye, shrinks and forms
strands that cast shadows on the retina, the light sensitive
tissue at the back of the eye. These shadows manifest in
the visual field as ‘floaters’.
DIFFERENTIAL DIAGNOSIS FOR HAZY VISION:
(from doctora’s discussion)
Conjunctivitis or any conjunctiva diseases are not
included. why? – because your visual axis will not
include your conjunctiva. It will not cause hazy vision since
it is not part of the visual axis. The conjunctiva, the lids and
the sclera will not cause hazy vision.
WHAT FINDINGS WILL YOU EXPECT?
 Visual acuity
– Reduction of vision even with correction
 Intraocular pressure
– Most patients: normal
– With glaucoma: elevated
– With uveitis: very soft or hypotonic
 Extraocular pressure
– Full movement on all directions
 Slit lamp examination
o Provides more details about the character,
location and extent of the opacity
 Ancillary examinations
o Ultrasound of the eye
 Important to determine the status of
the posterior segment of the eye which
includes the vitreous and retina
 Most useful if cataract is associated with
trauma
 Systemic examinations
o Congenital rubella is associated with
development of cataract at birth
o Diabetes is associated with cataract formation in
the younger age group
Clinical features
Symptoms:
 An opacity of the lens may be present without causing any
symptoms; and may be discovered on routine ocular
examination.
Common symptoms of cataract are as follows:
1. Glare. One of the earliest visual disturbance with the
cataract is glare or intolerance of bright light; such as direct
sunlight or the headlights of an oncoming motor vehicle.
2. Uniocular diplopia or polyopia. It is also one of the
early symptoms. It occurs due to irregular refraction by the
lens owing to variable refractive index as a result of
cataractous process, seen commonly with incipient stage of
cortical category (spoke or cuneiform).
3. Colored halos around light. These may be perceived by
some patients owing to breaking of white light into colored
spectrum due to irregular refractive index being more
common in nuclear cataract.

In this case, the considerations are: 4. Poor color discrimination, especially at blue end of
1. Cataract
visible light spectrum, occurs due to progressive yellowing
- Because of his age.
or browning of the lens.
2. Refractive error
3. ARMD (age-related Macular degeneration)
4. Retinopathies- HPN, DM, CRVO, BRVO 5. Buick spots in front of eyes. Stationary black spots may
be perceived by some patients.
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6. lmage blur, and misty vision may occur in early stages
of cataract. Especially loss of ability to see objects in bright
sunlight, blinded by light of oncoming headlamps when
driving at night. This occurs due to loss of contrast
sensitivity and also due to the fact that constriction of pupil
in bright light cuts of the peripheral vision from non-
cataractous lens (typically in axial cataract: posterior polar,
posterior subcapsular and nuclear cataract).
7. Deterioration of vision. Visual deterioration due to senile
cataract has some typical features. It is painless and
gradually progressive in nature.
SUMMARY:
 Before doing physical exam, we should go back to our
differentials.
 The first thing you should do in examining the patient is
measure the visual acuity. Even before touching the
patient and just with the visual acuity, you will be able
to eliminate one from your differentials. For example,
your visual acuity is 20/200 improves to 20/20 with
pinhole test, that’s refractive error. If it does not
improve or it became worst, then you should think of the
other conditions.
 After visual acuity, you do pupillary examination. So if
you have positive RAPD (relative afferent pupillary
defect) that means you have defect on your optic nerve.
The normal reaction is , when you shine a light in one
eye, pupil will constricts and also the other eye. That
Transcribers: SIBAYAN, K., SANTOS SAGMAYAO, SERDENIA
means no pathology and even with a very dense
cataract, it will not be positive in RAPD. But if you shine
a light in one eye for example the right eye and it does
not constrict, and you shine a light in the eye and it
constrict, you can tell now there is a problem. First, you
can have a problem in your optic nerve because it is the
receptor, it receives the light. If the optic nerve is
disease, nothing will receive the light, nothing can
perceive the light, and nothing will transmit the light so
the pupils will stay dilated. Just by doing this
examination, you will be eliminating your optic nerve
and your central connection as differentials.
 Next, do Fundoscopy. Just with your red orange reflex,
you will already be ruling in or ruling out one of the
differentials. If your orange-red reflex is bright all
throughout, that means the pathology can be refractive
error, ARMD or retinopathies.
 If your orange-red reflex are not bright, there are
opacities, that means you have cataract. If you see
opacities in your ocular media you think of cataract.
Ocular media means cornea, aqueous, lens and your
vitreous.
 So, in summary of the PE, In visual acuity, you can
eliminate a refractive error. In pupillary exams, you can
eliminate now optic nerve and its connections. In
orange-red reflex, you can already eliminate cataract. In
your fundoscopy, you go nearer the eye, focus on the
fundus and you can able to see retinopathies or age-
related macular degeneration or glaucoma (you see
optic capping).
ANATOMY AND EMBRYOLOGY
LENS ANATOMY
 Biconvex, avascular, colorless- transparent
 4mm thick, 9mm diameter
 Suspended behind the iris by the zonules of Zinn- ciliary
body
 Aqueous – LENS – vitreous
Composed of:
 Capsule
 Elastic, transparent basement membrane (Collagen
type IV)
 Molds the lens during accommodation
 Zonular lamellae: outer layer of the capsule,
attachment for the zonular fibers.
 Lens epithelium
 Single layer of cuboidal epithelial cells just behind the
anterior capsule
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 Metabolically active  the ciliary muscle,
 Mitotic cells occurring greatest in a ring around the  the fibroblasts of the sclera,
anterior lens (germinative zone)  the vitreous, and the optic nerve meninges.
 Cortex
 peripheral part  It is also involved in the formation of the orbital cartilage
 comprises the youngest lens fibers and bone, the orbital connective tissues and nerves, the
 Nucleus extraocular muscles, and the subepidermal layers of the lids.
 central part containing the oldest fibers
 consists of different zones which are laid down  The neural ectoderm gives rise to the:
successively as the development proceeds  optic vesicle
 optic cup and is thus responsible for the
Lens Sutures formation of the retina and retinal pigment
 Formed by the end to end joining of lamellar fibers epithelium
 Upright anteriorly  the pigmented and nonpigmented layers of
 Inverted posteriorly ciliary epithelium
 the posterior epithelium, the dilator and sphincter
muscles of the iris, and the optic nerve fibers and
glia.

 The mesoderm contributes to the vitreous, extraocular

and lid muscles, and the orbital and ocular vascular
endothelium.

Formation of Eye

 Embryonic plate → neural plate → optic pits → optic

vesicles → optic cups
 65% water 35% protein, trace minerals
Optic Pit
 Potassium
– forms at day 23 of gestation
 Ascorbic acid, glutathione- oxidized, reduced form
Optic Vesicle
- anterolateral outpouching of primitive brain stem
EMBRYOLOGY - evaginates on day 25
- becomes the globe
 The eye is derived from three of the primitive embryonic - induces the lens placode at day 27
layers:
 surface ectoderm, including its derivative—the neural Optic Cup
crest; neural ectoderm; and mesoderm. - anterolateral evagination of the forebrain
 Endoderm does not enter into the formation of the eye.
 Mesenchyme, derived from mesoderm or the neural a. Inner Layer
crest, is the term for embryonic connective tissue. Most • Becomes the retina
of the mesenchyme of the head and neck is derived b. Outer Layer
from the neural crest. • Becomes the retinal pigment epithelium
c. Potential Space Between the Inner and Outer Layers
 The surface ectoderm gives rise to the: • Becomes the subretinal space (which
 Lens was the cavity of the neural tube and
 lacrimal gland optic vesicle).
 epithelium of the cornea
 Conjunctiva
 adnexal glands
 epidermis of the lids.

 The neural crest, which arises from the surface ectoderm

in the region immediately adjacent to the neural folds of
neural ectoderm, is responsible for the formation of the:
 corneal keratocytes
 endothelium of the cornea
 the trabecular meshwork
 stroma of the iris and choroid
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Pathophysiology of Cataract (Age Related):

PATHOPHYSIOLOGY OF CATARACT
During aging, we have increased light scattering in the eye.
Etiology: When we age, instead of the light transferring doon sa center
ng retina for it to be interpreted by the brain, ang nangyayari it
 Aging (the most common cause). Most cataracts develop becomes scattered. That’s why the image which is presented in
slowly as a result of aging, leading to gradual impairment our brain becomes blurred.
of vision (Harrison’s 20th Ed.)
Decreasing elasticity
 Other factors:
 As the lens becomes thicker, the nucleus of the lens
- Trauma (Ocular Trauma)
becomes less elastic.
- Uveitis
- Toxins Post-translational changes to the lens crystalline
- Vitrectomy
- Systemic disease (such as diabetes)  Deamination - modification of the structure of the
- Smoking proteins into an insoluble structure of α- and β-crystalline.
- Heredity such as myotonic dystrophy, neurofibromatosis  Glycation - most important glycators are fructose,
type 2, and galactosemia. glucose, some pentoses, glyoxal, threose, ascorbate, along
with some products of degradation.
Factors that contribute to cataract formation:

1. Oxidative damage (from free radical reactions)

- Free radicals, they are very toxic to oxygen. So, it
causes oxidative stress because they are unstable. So,
for them to become stable, they will get oxygen from
any other proteins, or DNA. Yung kukunan niya ng
oxygen eh magiging unstable, kung ano man yung
DNA na yun na kukunan niya ng oxygen eh magiging
unstabe, and that would cause mutations or diseases
that involves our eye.
2. Ultraviolet light damage
- UV light damage, it is actually a light that we cannot
perceive. It is under the violet rays. Ang visible lang sa
atin ay and RYGBV. Ultraviolet rays ay mas mataas din
ang kanyang energy content/level that/s why it can
affect our eyes and can cause damage

3. Malnutrition

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CORTICAL

SUMMARY:

Loss of chaperone function

 The activity of α-crystallin chaperone significantly
decreases with age, and this is the reason of the
increased aggregation, and insolubility of proteins along
with the increased scattering of light and loss of
transparency of lens.

TYPES OF CATARACT

A. AGE-RELATED (SENILE)

 Any cataract without any known cause that develops in

elderly people.

Three main types:

1. Nuclear (“Hard Cataract”)- diffuse opacity principally

affecting nucleus

2. Cortical
(1) cuneiform (in the peripheral cortex)
(2) punctate perinuclear (in the cortex next to the nucleus)
(3) cupuliform (in the posterior cortex) POSTERIOR SUBSCAPULAR (PSC)

3. Posterior Subcapsular
– plaque of granular opacity on posterior capsule
– may be rapidly progressive

NUCLEAR CATARACT

B. CHILDHOOD CATARACT

Childhood cataracts are divided into two groups:

1. Congenital (infantile) cataracts- present at birth or

A, The red reflex shows the “oil droplet” effect of the nuclear appear shortly thereafter
cataract. 2. Acquired cataracts- occur later and are usually related to
B, Slit-lamp examination of another case shows the cataractous a specific cause.
yellow pigmented nucleus.
***Either type may be unilateral or bilateral

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Childhood cataracts can be:  Visual prognosis is not as good as in ordinary age-related
A. Hereditary cataract.
B. Secondary to metabolic or infectious diseases or associated
with a variety of syndromes V. CATARACT ASSOICATED WITH A SYSTEMIC DISEASE
C. Undetermined causes
 Diabetes mellitus
 Hypocalcemia (of any cause)
Congenital Cataract  Myotonic dystrophy
 Unilateral cataracts
 Atopic dermatitis
 usually isolated sporadic incidents
 Galactosemia
 can be associated with
 Down, Lowe (oculo-cerebro-renal), and Werner syndromes
 Ocular abnormalities (eg, posterior lenticonus,
persistent hyperplastic primary vitreous, anterior VI. DRUG-INDUCED CATARACT
segment dysgenesis, posterior pole tumors).
 Trauma  Corticosteroids (systematically – oral/inhaled; drop form)
 Intrauterine infection (rubella) - It will decrease the permeability of our lens,
therefor it will affect the potassium and sodium
 Bilateral cataracts
pumps. Normally, ang ating ions ay PISO
 Often inherited and associated with other diseases
(Potassium In and Potassium Out). If you take
 Common causes:
these steroids, it will alter the normal function of
 Hypoglycemia our ion, papasok si sodium.
 Trisomy (eg, Down, Edward, and Patau  Amiodarone
syndromes) - It is an anti-arrhythmic drug. According to one
 Myotonic dystrophy journal, taking Amiodarone for 6 months and
 Infectious diseases (eg, toxoplasmosis, above, it may cause opacities or pigment
rubella, cytomegalovirus, and herpes deposition on the anterior part of the lens.
simplex [TORCH])  Phenothiazines
 Prematurity - Same mechanism with corticosteroids.

Acquired cataracts

Causes:
 Trauma (most common) - blunt or penetrating
 Uveitis
 Acquired ocular infections
 Diabetes
 Drugs
 Often do not require the same urgent care (aimed at
preventing amblyopia) as infantile cataracts because SUMMARY:
the children are usually older and the visual system  When taking the history of the patient, you have to ask
more mature. “Are you taking steroids? are you diabetic,
hypertensive?”
III. TRAUMATIC CATARACT  How to ask if the patient is taking corticosteroids,
sometimes they don’t know that what he/she is taking is
 It is most commonly due to a foreign body injury to the corticosteroid, so you have to ask the name of that
lens or blunt trauma to the eyeball; medication.
 Air rifle pellets and fireworks are a frequent cause;  You can ask “meron po ba kayong asthma, gout,
 Less-frequent causes include arrows, rocks, contusions, arthritis, allergy,uminom po ba kayo ng metacort,
histacort etc.? ganun kasi hindi nila alam. Kung minsan,
and ionizing radiation.
‘tong binigay ng kapitbahay nakakataba daw because
you increase weight and appetite.
IV. “COMPLICATED CATARACT” / CATARACT  So, it is important to ask for the medications that the
SECONDARY TO INTRAOCULAR DISEASE patient is taking, systemic diseases, history of trauma,
any blood injury.
 Intraocular diseases commonly associated with the  Kunwari naman the patient is just 7 years old or 10 years
development of cataracts are: old and the patient already has cataract. So, consider
o chronic or recurrent uveitis congenital cataract. You ask the mother if she had any
o glaucoma sickness during pregnancy.
o retinitis pigmentosa  Another cause is ionizing radiation, electrocution etc.
o retinal detachment  Cataract is not only from aging.

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 BLOCK XIII-A Disorders of the Eye, Ears, Nose, and Throat | Hazy Vision
MANAGEMENT  The different methods are:

o Conventional ECCE
 No medical treatment has been shown to have any o ECCE by small-incision cataract surgery (SICS) or
significant effect in inducing the disappearance of cataract o small-incision manual nucleus fragmentation
once opacities have developed. o Lensectomy
 Cataract is at the early stages of hydration and is due to a o Phacoemulsification
systemic disease such as diabetes, control of the causal o Femtosecond laser assisted cataract surgery
condition may result in a disappearance of early lens
changes.
 If opacification has occurred, control of the general
condition may stay its progress, but once the proteins of
the lens have become coagulated, the change is
irreversible.

CATARACT SURGERY
Phacoemulsification
Removal of the crystalline lens is performed if the lens is causing
visual loss by:  The most popular method worldwide and has now virtually
 opacification (cataract) replaced all other techniques in most countries
 displacement from its normal position  The nucleus is emulsified by a phacoemulsifier and the lens
(subluxation or dislocation) matter removed by suction while a physiological aqueous
 defect in shape (coloboma, lenticonus, substitute such as balanced salt solution (bss) replaces the
spherophakia) evacuated fluid under electronic control
 lens-induced complications  This technique requires a small incision and the surgery is
sutureless.
Intracapsular Cataract Extraction

 The entire lens including the capsule is removed by

rupturing the zonules
 Can be done mechanically by pulling on the lens with
special forceps to hold the lens capsule
 Cryoextraction using a cryoprobe to freeze and hold the
lens or by inducing the lens to slide out or tumble out using
a lens hook and spatula.
 The technique is no longer used because of:
o Large incision needed,
o Inability to implant a posterior chamber
intraocular lens
o A high rate of complications particularly
astigmatism, vitreous loss, retinal detachment and
cystoid macular edema
 indicated only if the lens is dislocated or there is zonular
dialysis affecting more than 180°.

Extracapsular Cataract Extraction

 Done by making an opening in the capsule (capsulotomy),

removing the nucleus and washing out the cortical
substance
A. Incision with a keratome
 There are different techniques of performing extracapsular
B. anterior capsulotomy by capsulorhexis assisted by the use
cataract extraction. They vary in terms of:
of Trypan blue dye
o Incision size C. phacoemulsification of the nucleus
o shape of capsulotomy, D. aspiration of the residual cortex by automatedirrigation–
o Instruments used for capsulotomy aspiration
o technique of removing the hard lens nucleus E. implantation of a foldable intraocular lens.
 Instruments used for removal of the residual lens cortex

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OPTICAL REHABILITATION OR CORRECTION OF
APHAKIA
 Removal of the cataractous lens renders the patient
aphakic, which is a refractive state of extreme
hypermetropia.
 For the patient to be able to see clearly some form of
optical rehabilitation must be provided
 This may be in the form of spectacles, contact lenses
or an intraocular lens.
 Aphakic spectacles and contact lenses have inherent
disadvantages
 implantation of an intraocular lens after removal of the
lens is the norm today and is in fact
consid_x0002_ered to be very much a part of cataract
surgery
Intraocular Lenses
 Implantation of an intraocular lens is the best optical
rehabilitation following removal of a cataractous lens
 the central part overlying the optic axis is called the
optic and the peripheral arms used for placement and
stabilization are the haptics
 The optimal intraocular lens position is within the
capsular bag following an extracapsular procedure.
This is associated with the lowest incidence of
postoperative complications such as:
o pseudophakic bullous keratopathy
o glaucoma
o Iris damage
o Hyphema
o lens decentration
Transcribers: SIBAYAN, K., SANTOS SAGMAYAO, SERDENIA
 The newest posterior chamber lenses are made of
flexible materials such as silicone and acrylic polymers
allowing the lens implant to be folded, thus decreasing
incision size.
 Lens with multifocal optics can provide good vision
for both near and distance without glasses.
 In event of some complication during surgery such as
posterior capsule tear or zonular dialysis, intraocular
lens can be placed in the anterior chamber or sutured
to lie in the ciliary sulcus
 The power of the intraocular lens to be implanted is
calculated by various formulas.
 The most widely used formula is the modified
Sanders–Retzlaff–Kraff (SRK) formula, which is
based on a statistical correlation between calculated
and observed refractive error after intraocular
implantation
 If an intraocular lens cannot be safely placed or is
contraindicated, post-operative refractive correction,
postoperative refractive corrections generally requires
a contact lens or aphakic spectacles
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 BLOCK XIII-A Disorders of the Eye, Ears, Nose, and Throat | Hazy Vision
 Next, because you remove the total/whole lens (what is
behind the lens?) the vitreous, so the chance of
complication of vitreous coming out is larger. So, there
are more complications with intracapsular procedure.
 In ophthalmology, it very important to talk about
refractive errors, the shape of the cornea that there
should be no distortion or else you will have
astigmatism. It should be perfect in any meridian.
 If you have a big incision. There are more chances of
distortion of the shape of cornea, so there’s more
distortion in intracap compared to extracap. and least
with phacoemulsification.

INTRACAPSULAR CATARACT EXTRACTION

 We remove the whole lens by using special forceps or
we use a cryoprobe. We have a cryopencil and we put a
dry ice, we touch the lens. The capsule sticks to the
pencil and you pull out the whole lens. Or we use
“tumbling” wherein we put a pressure, you break the
nucleus and the lens will come out.
 Tumbling or using pressure to remove the nucleus.
 Since we remove the lens, the refractive power has been
diminished by 20 diopters or 1/3 of the refractive
power of the lens.
 So, we need to replace that power by eyeglasses
(aphakic lens- plus 1000 or 10.00 power), contact
lenses, and intraocular lenses.
 Intraocular lens can be placed on the posterior
capsule (anatomically pareho parin).
 In extracapsular, you can still place intraocular lens but
anterior to the iris. Or there are special lenses which we
can suture behind the iris.

PHACOEMULSIFICATION
 We don’t need any pushing from the outside because
SUMMARY: you just suction out the content.
 “Phaco”-latin for lens
 “Emulsification”-lens is broken down
 You breakdown the lens.
 So, the difference between intracapsular, extracapsular
and phacoemulsification:
 In intracap, the whole lens including the capsule is
removed.
 In other procedures, you leave behind the posterior
capsule. You just make an opening in the anterior
capsule and you remove the lens. That is extracapsular.
 So now, in extracapsular, you make an opening

INCISION (at the limbus):

 Intracapsular- the lens diameter is 9mm, so you have
to make an opening large enough for that lens to go out.
Yu make a 180-degree incision.
 In intracapsular, you remove the lens nucleus, so it
has a smaller diameter than the whole lens, the incision
is smaller.
 In phacoemulsification, you breakdown the nucleus
(you breakdown nucleus by using the phacoprobe. Using
ultrasound power on the lens nucleus, you will
breakdown the nucleus and at the same time, you
suction out the broken-down nucleus, so you just need
incision large enough for the probe tip to enter). It is just
2.7 or 2.2 mm depending on the probe.

Transcribers: SIBAYAN, K., SANTOS SAGMAYAO, SERDENIA Page 13 of 13