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SELF-INSTRUCTIONAL MATERIALS IN
OPHTHALMOLOGY
SECOND EDITION
Marissa N. Valbuena MD, MHPEd, Editor
Professor
Department of Opnthaimoiogy and Visual Science
College of Medicine
University of the Philippines Manila
Philippine General Hospital
Teresita R. Castillo MD, MHPEd, Assistant Editor
Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Philippine General Hospital
Publication authorized by the University of the Philippines
SELF-INSTRUCTIONAL MATERIALS IN
OPHTHALMOLOGY
2ND EDITION
ISBN: 978-971-95319-0-6
Published by UP-PGH Ophthalmology Residence Association, Inc.
Address: 5/F Sentro Oftalmologico Jose Rizal, Philippine General Hospital, Taft Avenue, Ermita, Manila, 1000.
Marissa N. Valbuena MD, MHPEd, Editor
Teresita R. Castillo MD, MHPEd, Assistant Editor
©2012
All Rights Reserved
Book Design: mervin concepcion vergara
Printed by: Econofast Press, Philippines
CONTENTS
CONTRIBUTORS
INTRODUCTION
1
ANATOMY OF THE EYE
Marissa N. Valbuena MD, MHPEd & Andrea Kristina F Monzon-Pajarillo MD
2
PHYSIOLOGY OF THE EYE
Richard C. ,(ho, MD
3
EYE SYMPTOMS
Marissa N. Valbuena MD, MHPEd & Andrea Kristina F Monzon-Pajarillo MD
4 EYE EXAMINATION
Teresita R. Castillo, MD, MHPEd
5
DISTURBANCE IN VISION
5.1 Disorders of the Cornea
Ruben LimBonSiong, MD
60
5.2 Cataract
Richard C Kho, MD
66
5.3 Disorders of the Retina, Choroid and Vitreous
Pearl T Villalon, MD
5.4 Glaucoma
Norman M. Aquino, MD
91
5.5 Disorders of the Optic Nerve
Raul I-,
98
5.6 Errors of Refraction
Juan Ma. Paoio rs. I\OnGgas, MD, MPH, MSNA
6
105
RED EYE, TEARING AND DISCHARGE
6.1 A Clinical Algorithm for the Diagnosis of the Red Eye
Leo D. P Cubillan, MD, MPH
6.2 Uveitis and Scleritis
leresita R. Castillo, MD, MHPEd
6.3 Tearing
Alexander D. Tan, MD
Self-Instructional Materials in Ophthalmology I 2nd Edition
n
DEVIATION AND DISPLACEMENT OF THE EYE
7
139
7.1 Strabismus
Marissa N. Valbuena MD, MHPEd
150
7.2 Proptosis
Prospero Ma. C. Tuano, MD
8 SPECIAL TOPICS
161
8.1 Retinoblastoma
Rolando Enrique D. Domingo, MD
167
8.2 Ocular Manifestations of Systemic Diseases
Romulo N. Aguilar, MD, PhD & Teresita R. Castillo, MD, MHPEd
186
8.3 Eyelid Malpositions
Franklin P Kleiner, MD
197
8.4 Ocular Trauma and Emergencies
Marissa N. Valbuena MD., MHPEd
207
8.5 Ocular Pharmacology
Mary Rose L. Pe-Yon, MD
220
9
ANSWERS TO SELF- TEST
10 APPENDIX
224
10.1 Patient Census of the Department of Ophthalmology
and Visual Science of the Philippine General Hospital
Marissa N. Valbuena MD., MHPEd
229
10.2 Different Types of Eye Redness
Teresita R. Castillo, MD, MHPEd
10.3 Step-By-Step Diagnosis Of Ocular Emergencies
Teresita R. Castillo, MD, MHPEd
241
10.4 Eye Care Rules To Remember
Teresita R. Castillo, MD, MHPEd
Self-InstTuetional Materials in Ophthalrn010,3y 1 Ztit1ECIII1011
CONTRIBUTORS
Romulo N. Aguilar, MD, PhD
Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Ocular Manifestations of Systemic Diseases
Richard C. Kho, MD
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Physiology of the Eye; Cataract
Norman M. Aquino, MD
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Glaucoma
Franklin P. Kleiner, MD
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Eyelid Malpositions
Teresita R. Castillo, MD, MHPEd
Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Eye Examination; Uveitis and Scleritis ;
Ocular Manifestations of Systemic Diseases; Types of Red Eye;
Step-By-Step Diagnosis Of Ocular Emergencies; Eye Care Rules to Remember
Ruben LimBonSiong, MD
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Disorders of the Cornea
Leo D. P. Cubillan, MD, MPH
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
A Clinical Algorithm for the Diagnosis of the Red Eye
Andrea Kristina Monzon-Pajarillo, MD
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Anatomy of the Eye; Eye Symptoms
Raul D. Cruz, MD
Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Disorders of the Optic Nerve
Juan Ma. Pablo R. Nanagas, MD, MPH, MSNA
Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Errors of Refraction
Rolando Enrique D. Domingo, MD
Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Retinoblastoma
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Ocular Pharmacology
Mary Rose L. Pe-Yan, MD
Prospero Ma. C. Tuano, MD
Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Proptosis
Marissa N. Valbuena, MD, MHPEd
Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Anatomy of the Eye; Eye Symptoms ; Strabismus;
Ocular Trauma and Emergencies; Patient Census
Alexander D. Tan, MD
Clinical Associate Professor
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Tearing
Pearl T. Villalon, MD
Associate Professor & Chair
Department of Ophthalmology and Visual Science
College of Medicine
University of the Philippines Manila
Disorders of the Retina, Choroid and Vitreous
Milagros H. Arroyo , MD
Teresita R. Castillo, MD, MHPEd
Francis Raymond M. Castor, MD
Michelle D. Lingao, MD
Illustrators
Rolando Enrique D. Domingo, MD
Business Manager
Self-Instructional Materials in Ophthalmology I 2nd Edition
INTRODUCTION
n the Organ System Integration Curriculum of the UP College of Medicine, the
medical student will have their first exposure to the field of Ophthalmology at
Learning Unit IV. The Sensory Organs — Eye Module is a 4-day rotation consisting
of didactic lectures, small group discussions and practicum of skills in history
taking and ocular examination. Aside from the introductory lectures in Anatomy
and Physiology of the Eye and Ocular History and Eye Examinations, the rest of
the modules will be problem based, covering the different eye problems that
patients may present with in the clinic. These eye problems are Disturbances in
Vision; Red Eye, Tearing and Discharge; and Deviation and Displacement of the
Eye. This series of self-instructional materials is organized in the same manner, with
additional topics of Retinoblastoma, Ocular Manifestations of Systemic Diseases,
Eyelid Malpositions, Ocular Trauma and Emergencies and Ocular Pharmacology at
the end of the series.
Each chapter specifies the specific learning objectives relevant to its content.
In order to facilitate monitoring of learning by the students, each chapter also
provides the student with self-test and/or cases. Students can receive feedback
to their performance in the self-test by comparing their answers to the correct
answers provided at the end of the book.
These study materials will supplement the lectures the medical students will
receive, help them in preparing for the small group discussions and serve as a quick
reference for subsequent rotations in ophthalmology. Although this book was
designed for the medical students of the UP College of Medicine, medical students
from other schools may also benefit from reading this book.
Marissa N. Valbuena MD, MHPEd
smmnstructional Materials in Ophinalmolonv I 2nd Edition
Marissa N.Valbuena MD, MHPEd and Andrea Kristina Monzon-Pajarillo MD
INTRODUCTION
An understanding of the anatomy of the eye, orbit, visual pathway and the central control of ocular movements is essential in
understanding the eye diseases and other diseases which have ocular manifestations.Together with the module on "Physiology
of the Eye", this module will help the student understand how the eye functions, how patients can be evaluated and examined
and how the different eye disorders manifest in patients. This module is an overview of the anatomy of the eye and the student
is advised to read the references listed at the end of the module for more details.
OBJECTIVES
After the completion of this instructional material, the student is expected to
1.
Describe the different parts of the eye and adnexae.
2.
Describe the functions of the parts of the eye and adnexae.
CONTENT
I.
Orbit
II.
Eyeball
1. Conjunctiva
2. Tenon's capsule
3.
Sclera and episclera
4.
5.
6.
7.
8.
9.
Cornea
Uveal tract - iris, ciliary body, choroid
Lens
Aqueous
Anterior chamber angle
Retina
10. Vitreous
Ill. Extraocular muscles
IV. Ocular adnexae
1. Eyebrows
2. Eyelids
3. Orbital septum
4. Lid retractors
5. Lacrimal Complex
V. Optic nerve
A. ORBIT
lies within the annulus of Zinn. The inferior ophthalmic vein
passes though any portion of the SOF and joins the superior
ophthalmic vein before exiting the orbit.
The orbit is a pear shaped structure with the optic nerve as
its stem. It is 30 cc in volume in adults and the eye occupies
20 % of the space while the muscles and fat account for the
rest. The orbit is limited anteriorly by the orbital septum, which
serves as a barrier between the eyelid and the orbit. It is also
related to the frontal sinus above, maxillary sinus below and
the ethmoid and sphenoid sinuses medially.
ROOF OF THE ORBIT
Frontal bone
Frontal bone
Sphenoid body
■ Sphenoid body
(lesser wing)
Ethmoid
Lacrimal bone
LATERAL WALL
Maxillary bone
■ Sphenoid (greater wing)
■ Zygomatic bone
Nasal bone
FLOOR OF THE ORBIT
Palatine (orbital process)
Maxillary bone
■ Zygomatic bone
Figure 1. Walls of the left orbit
ORBITAL WALLS (FIGURE 1)
1. Roof : frontal bone, lesser wing of the sphenoid bone
2. Lateral wall : greater wing of the sphenoid bone,
zygomatic bone
3.
4.
bone, zygomatic bone, palatine bone
Medial wall : ethmoid, lacrimal bone, frontal bone,
Frontal N, Lacrimal N, Superior oculomotor N
Superior Ophthalmic V
Superior rectus M
Abducens N
Oeulomotor foramen
Floor : maxillary
maxillary bone, sphenoid bone
Levator M
Trochlear N
Superior oblique M
Optic N
Medial rectus M
Lateral rectus M
Nasociliary nerve
Inferior oculomotor N
Inferior rectus M
ORBITAL APEX
Figure 2. Orbital apex
The orbital apex is the entry site of all the nerves and blood
vessels to the eye and all the extraocular muscles except the
inferior oblique. (Figure 2). There are openings through or in
between bones in the orbit through which several structures
Supraorbital
notch
Optic Canal
Supenor orbital
fissure
pass (Figure 3). The superior orbital fissure (SOF) is located
between the body and the lesser wing of the sphenoid bone.
The following pass through the lateral portion of the SOF
that lies outside the annulus of Zinn: superior ophthalmic
vein, lacrimal, frontal and trochlear nerves. The following
pass through the medial portion of the fissure and within
the annulus: superior and inferior divisions of the oculomotor
nerve and abduscens and nasociliary nerves. The optic nerve
and ophthalmic artery pass through the optic canal which also
Infraorbital
groove
Inferior orbital
fissure
Infraorbital
foramen
Figure 3. Anterior view of the bony orbit showing fissures, canal and foramen
2.
BLOOD SUPPLY
A. Arterial Supply : Ophthalmic Artery (branch of
internal carotid artery)
Central retinal artery- supplies the retina
Lacrimal artery — supplies lacrimal gland and upper
eyelid
3. Muscular branches to the muscles — continue to form
the anterior ciliary arteries and supply the sclera,
episclera, limbus and conjunctiva and contribute to
the major arterial circle of the iris
4. Long posterior ciliary arteries — supply the ciliary
body. The 2 long posterior ciliary arteries anastomose
with each other and with the anterior ciliary arteries
to form the major arterial circle of the iris.
5. Short posterior ciliary arteries — supply choroid and
part of the optic nerve
1.
2.
6.
Medial palpebral arteries to both eyelids
B. Venous Drainage :
Blood drains to the superior and inferior ophthalmic veins,
into which drain the vortex veins, anterior ciliary veins and the
central retinal vein. The ophthalmic veins communicate with
the cavernous sinus.
The blood from the skin of the periorbital region drain to the
angular vein, and to the supraorbital and supratrochlear vein
branches of the superior ophthalmic vein. This provides a
direct communication between the skin of the face and the
cavernous sinus.
Bulbar conjunctiva — is loosely attached to the orbital
septum in the fornices and is folded many times. This
allows the eye to move and enlarge the secretory
conjunctival surface.The semilunar fold is a thickened
fold of bulbar conjunctiva at the inner canthus and
corresponds to the nictitating membrane of lower
animals.
The conjunctiva has the following layers:
1.
2.
Conjunctival epithelium — consists of 2-5 layers of
stratified columnar epithelial cells. The superficial
epithelial layer consists of mucous secreting goblet
cells. The basal epithelial cells are deeper and may
contain pigments near the limbus.
Conjunctival stroma has an adenoid (superficial)
layer and a fibrous (deep) layer. The adenoid layer
contains lymphoid tissue and 'follicle-like" structures
without germinal centers. and develops after the 2nd
or 3rd month of life. The fibrous layer is composed
of connective tissue that attaches to the tarsus and
is loosely arranged over the globe. The accessory
lacrimal glands (glands of Krause and Wolfring)
located in the stroma resemble the lacrimal gland in
structure and function.
The conjunctival arteries are derived from the anterior ciliary
and palpebral arteries and anastomose freely. Conjunctival
veins follow the arterial pattern. The conjunctival lymphatics
together with the lymphatics of the eyelids form a rich
lymphatic plexus. The conjunctiva is innervated by the
ophthalmic (first) division of the trigeminal nerve.
2. TENON'S CAPSULE
Clinical Pearl:
Cavernous Sinus Thrombosis
The direct communication between the ophthalmic
veins and the cavernous sinus may potentially cause
a posterior and intracranial spread of infection from
an orbital abscess or cellulitis. It is thus very important
to monitor patients with these disorders for rapid
progression of proptosis and any neurologic signs or
dysfunction.
B. EYEBALL
The Tenon's capsule is a fibrous membrane covering the
globe from the limbus to the optic nerve. At the limbus,
the conjunctiva, Tenon's capsule and the episclera are fused
together. Posteriorly,the inner surface of theTenon's capsule lies
against the sclera and the outer aspect lies in contact with the
orbital fat and structures within the extraocular muscle cone.
At the point where Tenon's capsule is pierced by the tendons
of the extraocular muscles, it sends out tubular reflections
around each of the muscles. These fascial reflections become
continuous with the fascia of the muscles and the fused fascia
sends out expansions to the surrounding structures and to the
orbital bones called check ligaments. Inferiorly, the Tenon's
capsule fuses with the fascia of the inferior rectus and inferior
oblique to form the suspensory ligament of Lockwood, upon
1. CONJUNCTIVA
which the globe rests.
The conjunctiva is a thin transparent mucous membrane
3. SCLERA AND EPISCLERA
covering the globe anteriorly. It consists of 2 parts:
1.
Palpebral conjunctiva — lines the posterior surface of
the eyelid and is adherent to the tarsus.
The sclera is the fibrous outer layer of the eye consisting
mainly of collagen. It is dense and white and continuous
1
ANATOMY OF THE EYE
El
with the cornea anteriorly and the optic nerve dural sheath
posteriorly. It is thinnest at the insertion of the recti muscles
(0.3 mm); elsewhere it is 0.6 mm thick. The outer layer of the
anterior sclera is covered with a thin layer of fine elastic tissue,
the episclera, which contains blood vessels that nourish the
sclera.
4. CORNEA
I he cornea is a transparent tissue inserted to the sclera at the
limbus. It is thicker at the periphery (0.65 mm) than at the
center (0.52 mm). Its horizontal diameter (11.75 mm) is slightly
bigger than its vertical diameter (10.6 mm).
Clinical Pearl:
Herpes Simplex Corneal Ulcer
Ihe Herpes simplex virus (HSV) commonly affects
the trigeminal ganglion which is the main source of
sensory nerve supply to the cornea.
Corneal sensation may be tested by light touch - tul
example, using a strand of cotton. When a patient has
a corneal ulcer caused by HSV, the cornea exhibits
hypoesthesia at the ulcer site. This is one characteristic
of an HSV corneal ulcer that helps differentiate it from
other types of corneal ulcers.
There are 5 layers of the cornea : (Figure 4)
Epithelium : 5-6 layers of cells, continuous with the 5. UVEAL TRACT
epithelium of the bulbar conjunctiva.
2) Bowman's membrane : clear acellular layer, a modified The uveal tract is composed of the iris, the ciliary body and
the choroid. It is the middle vascular layer of the eye and
portion of the stroma.
3) Stroma : 90 % of corneal thickness; composed of contributes to the blood supply of the retina.
intertwining lamellae of collagen fibrils that run
parallel to the surface of the cornea and because A. IRIS
of their size and proximity are optically clear. The
lamellae run within the ground substance of hydrated The iris is a flat surface with a central opening, the pupil. The
iris lies in contiguity with the anterior surface of the lens,
polyglycans in association with the keratocytes that
dividing
the anterior chamber from the posterior chamber,
produce the collagen and ground substance.
both
of
which
contain aqueous humor. Within the stroma of
4) Descemet's membrane : basal lamina of corneal
the iris are the sphincter and dilator muscles.The 2 pigmented
endothelium
posterior layers of the iris represent anterior extensions of the
5) Endothelium : single layer of cells ; responsible for
neuroretina and the retinal pigment epithelium (RPE).
maintaining the deturgescence of the cornea and
failure of function leads to corneal edema. Cell loss
occurs with age and injury. Endothelial repair occurs The blood supply of the iris is from the major circle of the iris.
with cell enlargement and sliding of existing cells The iris capillaries are non-fenestrated. The sensory supply is
from fibers of the ciliary nerve.
with minimal capacity for cell division.
1)
The cornea gets its nutrition from the vessels of the limbus, the
aqueous and the tears. The superficial cornea gets most of its
oxygen from the tears. The sensory nerves of the cornea are
from the ophthalmic division of the trigeminal nerve.
The pupil controls the amount of light entering the eye.
The pupillary size is determined by the balance between
constriction due to parasympathetic activity via the
oculomotor nerve and dilation due to sympathetic activity.
The transparency of the cornea is due to its uniform structure,
avascularity, and deturgescence.
B. CILIARY BODY
The ciliary body consists of 2 zones
1.
Epithelium
Bowmans
membrane
— Strome
Descemet's
membrane
Endothelium
Figure 4. Cross section of cornea
2.
Pars plicata: 2 mm wide; The ciliary processes arise
from this zone. The ciliary processes are composed
mainly of large fenestrated capillaries and veins
that drain to the vortex veins. The 2 layers of the
ciliary epithelium are the internal non- pigmented
layer (representing the anterior extension of the
neuroretina) and the external pigmented layer
(representing the RPE). The ciliary processes produce
the aqueous.
Pars plana - 4 mm ; flattened posterior zone
The ciliary muscle is composed of longitudinal, circular
and radial fibers.
1. Circular fibers: contraction and relaxation of the
zonular fibers alters the capsule of the lens thus giving
variable focus for far and near objects of fixation.
2. Longitudinal fibers : insert to the trabecular
meshwork, influencing its pore size
3. Radial fibers
The lens capsule (Figure 7) is a semi-permeable membrane
(to water and electrolytes). A subcapsular epithelium is present
anteriorly.The lens nucleus is harder than the cortex. With age,
the subepithelial lamellar fibers are continuously produced,
gradually making the lens larger and less elastic.
The lens consists of 65 0/0 water and 35% protein and minerals.
There are neither blood vessels nor pain nerve fibers in the
lens.
The blood supply of the ciliary body is from the major circle
of the iris (Figure 5) and the nerve supply is from the ciliary
nerves.
Anterior ciliary vessels
4- Vortex veins
Retinal vessels
Choroidal vessels
Long posterior ciliary a
Short posterior ciliary a
Conjunctival vessels
Major arterial circle of iris
Central vessels of the retina
Vessels of ciliary body
Figure 5. Blood supply of the eye
Lamellar lens
C. CHOROID
Lens capsule
The choroid is the posterior portion of the uveal tract, located
between the retina and the sclera. The internal portion of the
choroidal vessels is called the choriocapillaris (Figure 6). Blood
from the choroidal vessels drain via the four vortex veins, each
one located in each posterior quadrant of the globe. The
choroid nourishes the outer portion of the retina.
Pigment epithelium
ChorlocepiNerls
Bruch's membrane
Larger choroidal
vessels
.tir•
SCAM
Figure 6. Cross section of the choroid
6. LENS
The lens is a biconvex, avascular clear structure, which
is 4 mm thick and 9 mm in diameter. The lens, together with
the cornea, are the main refractive components of the eye. It
is suspended behind the iris by the zonules which connects it
with the ciliary body. Anterior to the lens is the aqueous and
posterior to it is the vitreous.
fibers
Lens epithelium
Figure 7. Magnified view of a section of the lens showing lens capsule
and epithelium
7. AQUEOUS
The aqueous is a clear fluid that fills the anterior and posterior
chambers of the eye. Its volume is about 230 pL and its rate
of production which is subject to diurnal variation is 2.5 LIL/
min. Its composition is similar to plasma except for higher
concentrations of ascorbate, pyruvate and lactate and lower
concentrations of protein, urea and glucose.
Aqueous is produced by the ciliary epithelium. From the
posterior chamber, the aqueous passes through the pupil to
go to the anterior chamber and then drains into the trabecular
meshwork, to the Schlemm's canal and into the venous system.
Some aqueous passes between the bundles of the ciliary body
and through the sclera (uveoscleral pathway).
1 ANATOMY OF THE EYE
Ei
8. ANTERIOR CHAMBER ANGLE
9. RETINA
The anterior chamber angle lies at the junction of the
peripheral cornea and the root of the iris. Its main anatomic
structures are Schwalbe's line, trabecular meshwork (which
overlies the Schlemm's canal) and the scleral spur. (Figure 8)
The retina is a thin, semi-transparent, multilayered sheet of
neural tissue that lines the inner wall of the posterior 2/3 of the
eye. It extends anteriorly as the ora serrata. The outer surface of
the retina is apposed to the retinal pigment epithelium (RPE).
Except at the disc and the ora serrata, the retina and RPE are
easily separated to form a subretinal space, such as occurs in
retinal detachment. The inner layer of the retina is apposed to
the vitreous.
The Schwalbe's line corresponds to the termination of the
corneal endothelium. The trabecular meshwork is triangular
in cross section with the base directed to the ciliary body.
It is composed of perforated sheets of collagen and elastic
tissue with decreasing pore size as the canal of Schlemm is
approached. The longitudinal muscles of the ciliary body
insert into the trabecular meshwork. The scleral spur is an
inward extension of the sclera between the ciliary body and
the Schlemm's canal, to which the ciliary body and the iris are
attached.
Clinical Pearl: Retinal Detachment
In some forms of inflammation, such as in uveitis, fluid
may leak out of the retinal vessels and accumulate in the
subretinal space separating the retina and RPE, causing
exudative retinal detachment
Antenor chamber angle
Schlemm's canal
Anterior chamber
The 10 layers of the retina (Figure 9), from the inner aspect are
the following:
1.
2.
Trabecular meshwork
Posterior chamber
Figure 8. Anterior chamber angle
Clinical Pearl :
Acute angle closure glaucoma
The eye's natural response of dilation to environmental or
chemical stimuli which can result to apposition and contact
between the lens and the iris is called pupillary block. In
addition, the forward-most surface of the lens is anterior
to the plane of the iris insertion into the ciliary body. As
a result, aqueous flow from the posterior chamber to the
anterior chamber is obstructed or altogether blocked.
The increasing pressure in the posterior chamber causes
the iris, particularly its peripheral region, to bow forward
(iris bombe). Iris bombe further closes the already narrow
angle and compromises aqueous drainage, thus increasing
intraocular pressure (10P).
internal limiting membrane
nerve fiber layer — ganglion cell axons passing to the
optic nerve
3. ganglion cell layer
4. inner plexiform layer — connections of the ganglion
cells with the amacrine and bipolar cells
5. inner nuclear layer — cell bodies of the bipolar,
amacrine and horizontal cells
6. outer plexiform layer — connections of the bipolar
and horizontal cells with the photoreceptors
7. outer nuclear layer — cell nuclei of photoreceptors
8. external limiting membrane
9. photoreceptor layer — rod and cones inner and outer
segments
10. retinal pigment epithelium (RPE) — The inner layer
of the Bruch's membranes is actually the basement
membrane of the RPE
The retina is 0.1 mm thick at the ora serrata and 0.56 mm thick
at the posterior pole. In the center of the posterior retina is
the macula (Figure 10). It is clinically seen as a 3 mm area of
yellowish pigmentation (due to xanthophylls pigments) and
bounded by the temporal vascular arcades. In the center of
the macula is the fovea, clinically seen as a depression and
corresponds to the "foveal reflex". It corresponds to the retinal
avascular zone on fluorescein angiography. Histologically, the
fovea is characterized by thinning of the outer nuclear layer and
the absence of the other parenchymal layers. The foveola is the
most central portion of the fovea, in which the photoreceptors
are all cones, and the thinnest part of the retina. All these
histologic features provide for fine visual discrimination
(Figures 11, 12). The normally empty extracellular space of
I
1 - INTERNAL LIMITING MEMBRANE
2 - NERVE FIBER LAYER
3 - GANGLION CELL LAYER
GANGLION CELL
4 - INNER PLEXIFORM LAYER
AMACRINE CELL
BIPOLAR CELL
- INNER NUCLEAR LAYER
HORIZONTAL CELL
6 - OUTER PLEXIFORM LAYER
7 - OUTER NUCLEAR LAYER
8 - EXTERNAL LIMITING MEMBRANE
9 - PHOTORECEPTOR LAYER
10 - RETINAL PIGMENT EPITHELIUM
Figure 9. Layers of the retina
1500pm
ILM
500µm
Muller cells in
inner nuclear
layer
#ifi —lie is al
Iczry %II.
AllligiNglainal
es,
- r,
Capillary
arcades
'
W
UM
,
•,"
XLM
,
RPE
Cones
Figure 12. Diagram of layers of the retina in the area of macula
Figure 10. Macula (white arrow)
the retina is potentially greatest at the macula, and diseases
that can lead to accumulation of fluid causes thickening of this
area.
The retina receives its blood supply from
1.
2.
Figure 11. Histophotograph of the retina at the area of the macula
choriocapillaris — supply outer third of retina, from
outer plexiform layer to RPE
central retinal artery — supplies the inner 2/3 of the
retina
The fovea is supplied entirely by the choriocapillaris and
is susceptible to irreparable damage when the macula is
detached. The retinal blood vessels have a non-fenestrated
endothelium, which forms the inner blood-retinal barrier. The
endothelium of the choroidal vessels is fenestrated. The outer
blood-retinal barrier lies at the level of the RPE.
1
ANATOMY OF THE EYE
10. VITREOUS
D. OCULAR ADNEXA
The vitreous is a clear, avascular body, comprising 2/3 of the
volume and weight of the eye. It fills the space bounded by the
lens, retina and optic disc. The hyaloid membrane, the outer
surface of the vitreous is in contact with the posterior lens
capsule, zonules, pars plana epithelium, retina and optic nerve
head. The base of the vitreous maintains a firm attachment
throughout life with the pars plana epithelium and the retina
immediately behind the ora serrata. The attachment to the
lens capsule and the optic nerve head is formed early in life
but soon disappears.
The vitreous is 99% water. Collagen and hyaluronic acid make
the vitreous gel-like because of their ability to bind large
amounts of water.
1. EYEBROWS
I he eyebrows are tolds of thickened skin covered with hair.The
glabella is the hairless prominence in between the eyebrows.
2. EYELIDS
I he upper and lower lids (palpebrae) are folds of skin that can
close to protect the anterior portion of the eye. Blinking helps
spread the tear film, keeping the cornea and conjunctiva wet.
Layers of the eyelids (Figure 14)
1.
EXTRAOCULAR MUSCLES
2.
Eye movement is facilitated by its six extraocular muscles
consisting of four recti and two oblique muscles. The four
recti muscles originate from the annulus of Zinn at the apex
of the orbit and are named after their insertion at the sclera on
the medial, lateral, superior and inferior aspect of the eye. The
superior oblique, which also originates from the orbital apex,
is the longest and thinnest of the extraocular muscles. The
inferior oblique originates from the nasal side of the orbital
wall and is the only extraocular muscle that does not originate
from the apex of the orbit. Table 1 summarizes the origin,
insertion, action and innervation of the extraocular muscles.
Figure 13 shows the spiral of Tillaux, which connects the
points of insertion of the four recti muscles to the sclera.
The blood supply to the extraocular muscles comes from the
muscular branch of the ophthalmic artery. The lateral rectus
and inferior oblique are also supplied by the branches from
3.
4.
5.
Skin — thin, loose, elastic, few hair follicles and no
subcutaneous fat.
Orbicularis oculi muscle — Circular muscle fibers
surround the palpebral fissure which functions to
close the eyelids. It is innervated by the facial nerve.
Areolar tissue — under the orbicularis oculi,
communicates with the subaponeurotic layer of the
scalp.
Tarsal plates — dense fibrous tissue layer ; main
support of the eyelids
Palpebral conjunctiva — adheres firmly to tarsal plate
Frontal Sinus
Levator palpebrae muscle
Gland of Krause
Gland of Wolfring
Orbital fat
Orbicularis oculi muscle
-Orbital septum
Levator palpebrae aponeurosis
Superior tarsal muscle
the lacrimal artery and infraorbital artery respectively.
Conjuctiva
Eyelash
SR
Spiral of
Tillaux
•
10.6
Melbomian gland in tarsal plate
f.
—
Lower eyelid retractors
Interior oblique muscle
4
Figure 14. Cross section of the eyelid
103 mrs.
Clinical Pearl : Eyelid swelling
g.g
IR
Figure 13. Spiral of Tillaux, showing the insertion of the recti muscles to the sclera
The thin, loose skin and the absence of subcutaneous
fat makes the eyelid vulnerable to swelling, such as
in accumulation of fluid in allergy or infection and
blood in trauma.
Table 1.
Muscle
Origin
Insertion
90'
iAt)rilk;tio!I
\11
7.7 mm from superior
limbus
23°
Elevation
Intorsion
Adduction
III
Annulus of Zinn
6.5 mm from inferior limbus
23°
III
Orbit apex above
Annulus of Zinn
(functional origin
at trochlea)
Behind lacrimal
fossa
Posterior equator at
superotemporal quadrant
51°
Depression
Extorsion
Adduction
Intorsion
Depression
Abduction
Posterior to the equator in
infero-temporal quadrant
51°
Extorsion
Elevation
Abduction
III
5.5 mm from medial limbus
Lateral rectus
(LR)
Annulus of Zinn
6.9 mm from lateral limbus
Superior rectus
(SR)
Annulus of Zinn
Inferior rectus (IR)
Superior oblique
Lacrimal caruncle
Innervation
Cranial Nerve
111
Annulus of Zinn
Inferior oblique
(10)
Action from
Primary Position
Adduction
Medial rectus
(MR)
(SO)
Direction of
pull
Lacrimal lake
Plica semilunaris
(,(1
IV
1. Anterior margin
a. Eyelashes
b. Glands of Zeis — modified sebaceous glands ; open
onto hair follicles at the base of eyelashes
c. Glands of Moll — modified sweat glands ; open in a
row near the base of the eyelashes
2. Posterior margin — in close contact with the globe ; along
its margins are the small orifices of the meibomian glands
(modified sebaceous glands)
3. Lacrimal punctum — at the medial end of posterior margin of
the lid; small elevation with a central opening; two puncta in
each eye, superior and inferior puncta which serves as passage
of tears for drainage. (Figure 16).
Lacrimal
Anterior
punctum lid margin
Posterior
lid margin
Gray
line
Orifices of
Me ibomian
glands
Figure 15. Lid Margin (medial portion of the eyelids). Adopted from Riordan
E, Whitcher, J.2
3. ORBITAL SEPTUM
The orbital septum is the fascia behind the portion of the
orbicularis muscle that lies between the orbital rim and the
tarsus. It serves as a barrier between the lid and the orbit
Lid Margin (Figure 15) — free lid margin is 25-30 mm long
and 2 mm wide. It is divided by the gray line (mucocutaneous
junction) into anterior and posterior margin.
1
ANATOMY OF THE EYE
Superior canaliculus
Common canaliculus
Superior punctum
‘,."— Lacrimal sac
Interior canaliculus
Nasolacrimal
duct
Inferior punctum
Figure 16. Lacrimal drainage system
B.
Clinical Pearl:
Preseptal and Orbital Cellulitis
An infection which causes inflammation of the eyelids
and periorbital structures is termed preseptal cellulitis if
the orbital contents are not involved, since the orbital
septum serves as the barrier between the eyelids and
the orbit.
lo determine if the cellulitis is preseptal or orbital, we
need to check extraocular muscle function, pupillary
reaction and visual acuity. Restriction of ocular motility,
abnormal pupillary reaction and decreased visual acuity
suggest involvement of the cranial nerves in the orbital
apex and would mean that the cellulitis is already orbital
and would necessitate aggressive and immediate
management.
4. LID RETRACTORS
The lid retractors are responsible for opening the eyelids; have
striated and smooth muscle components
A. Upper lid
1. Levator palpebrae superioris
2. Muller's muscle (superior tarsal muscle)
B. Lower lid
1. Inferior rectus muscle
2. Inferior tarsal muscle
Accessory lacrimal glands of Krause and Wolfring
- located in the substantia propria of palpebral
conjunctiva
C. Canaliculi
D. Lacrimal sac
E. Nasolacrimal duct- drains out to the nasal cavity
The lacrimal drainage system is illustrated in Figure 16. Tears
drain thru the superior and inferior puncta to the superior
and infertior canaliculi, then to the common canaliculus, to
the lacrimal sac, nasolacrimal duct and out through the nasal
meatus.
Fhe lacrimal gland receives its blood supply from the lacrimal
artery and venous blood drain to ophthalmic vein. Lymphatics
drain into preauricular lymph nodes.
Nerve supply to the lacrimal gland is by
a. lacrimal nerve (sensory), a branch of the trigeminal
first division
b. great superficial petrosal nerve (secretory)
c. sympathetic nerves
E. OPTIC NERVE
The trunk of the optic nerve consists of about 1.2 million axons
arising from the ganglion cells of the retina and has four parts
(Figure 17)
1.
2.
5. LACRIMAL COMPLEX
3.
A.
Lacrimal gland - has orbital portion and palpebral
portion
self-Instructional Material, in Ophthalmcdmiy 12nd EdITIOn
4.
intra-ocular portion - optic nerve head ; 1.5 mm in
diameter, 1 mm long
orbital portion - 3 mm in diameter, 25-30 mm long,
located within the muscle cone
intra-canalicular portion — 4-9 mm long
intra-cranial portion - 10 mm long, and with the
opposite optic nerve joins to from optic chiasm
The optic nerve sheath is continuous with the meninges.
Figure 18 shows the cross section of the optic nerve.
intraocular
intraorbital
intracanalicular
intracranial
I he surface layer of the optic disc receives blood from the
branches of the retinal arterioles. The rest of the nerve in
front of the lamina cribrosa receives its blood supplyfrom the
peripapillary choroidal vessels. At the region of the lamina
cribrosa, the blood supply comes from the short posterior
ciliary arteries. The retrolaminar portion receives blood from
branches of the central retinal artery.The rest of the intraorbital,
intracanalicular and intracranial portions are supplied by pial
vessels from branches of the ophthalmic artery and other
branches of the internal carotid artery. (Figure 19)
SUMMARY
Figure 17. Parts of the optic nerve
Fibers of the
optic nerve consist of
1. visual fibers — 80%, synapse in the lateral geniculate
body on neurons whose axons terminate in the visual
cortex of the occipital lobe
2. pupillary fibers — 20% , bypass the geniculate body
en route to the pretectal area.
The ganglion cells of the retina and their axons are part
of the central nervous system and as such, do not
regenerate if severed.
An understanding of the anatomy of the eye, ocular adnexae,
orbit, visual pathways and the cranial nerves is important in
the proper diagnosis of ocular diseases and other disorders
with ocular manifestations.
REFERENCES
1.
2.
3.
Dura
Duane, Thomas and Jaeger, Edward. Clinical
Ophthalmology, Philadelphia : Harper and Row, 2006
Riordan-Eva, Whitcher, John. Vaughn and Ashbury's General
Ophthalmology, 17th Edition, New York: Lange Medical
Books/ McGraw Hill, 2007
Scheie, Harold, Albert, Daniel. Textbook of Ophthalmology,
Philadelphia : W.B. Saunders Co,
Subdural space
Central
retinal vein
Arachnoid
SELF-TEST
Subarachnoid space
Central
retinal artery
Pia
Nerve bundles
divided by septa
Figure 18. Cross section of the optic nerve
Choroid
---- Posterior Ciliary A
Retina-6\
r
Dura
Arachnoid
Subarachnoid
space
Optic Disc
1. An anti-glaucoma drug which decreases aqueous
production acts on the epithelial cells of the
A. Pars plicata
B. Choroid
C. Iris
D. Pars plana
2. The rectus muscle tendon that inserts on the sclera
nearest to the corneal limbus belongs to the
A. superior rectus
B. inferior rectus
C. medial rectus
D. lateral rectus
Pia
(
Central
Retinal Vein
Central Retinal
Artery
Figure 19. Blood supply of the optic nerve
3.
Paralysis of this cranial nerve will result in inability to
close the eyelid
A. Ill
B. IV
C. V
D. VII
1
ANATOMY OF THE EYE
4.
5.
The following structures are part of the medial orbital
wall, EXCEPT
A.
ethmoid bone
B.
C.
D.
lacrimal bone
maxillary bone
sphenoid bone
Layer of the retina that receives its oxygen supply from
the choriocapillaris is the
A. ganglion cell layer
B. nerve fiber layer
C. photoreceptors
D. inner nuclear layer
8.
In order to ensure good vision, the following structures
must maintain their clarity, EXCEPT
A.
B.
C.
D.
E.
9.
Cornea
aqueous
lens
vitreous
choroid
Axons comprising the optic nerve come from which cells
in the retina?
A. amacrine cells
B. bipolar cells
C. ganglion cells
D. photoreceptor cells
6.
Which of the following statements regarding the cornea
10. Which muscle is an abductor?
is FALSE?
A. medial rectus
A. The corneal endothelium is important in maintaining
corneal dehydration.
B. lateral rectus
C. superior rectus
B. The water content of the cornea is less than that of
the sclera.
D. inferior rectus
C. Normal central corneal thickness is 1.00 mm
D. Corneal diameter is greater horizontally than Answers to self-test on page 220.
vertically.
7.
Which is not a layer of the eyelid?
A. Skin
B. Conjunctiva
C. Tenon's capsule
D. Orbicularis muscle
E. Tarsus
Richard C. Kho, MD
INTRODUCTION
This self-instructional material is designed to help the medical student acquire an overview of the biophysical elements at work
within (and outside) the human eye. With the eye functioning as a sense organ, all these processes work together in order to
bring about the phenomenon we call visual perception. Understanding basic concepts of light energy, its transformation in the
human eye, its conversion to nerve impulses and eventual visual perception are vital in the diagnosis and management of eye
diseases.
OBJECTIVES
Upon completion of this instructional material, the student should be able to discuss the following:
1.
The physical properties of light
2.
The processes that occur as soon as light strikes the human eye
3.
The internal bending of light as it is focused on the retina, i.e., optics and refraction in the human eye
4.
Retinal processes which transform light energy resulting in visual perception
5.
Basic neuro-anatomic architecture of the visual pathway, as well as topographical localization of lesions in this pathway
CONTENT
I. THE EYE AS AN OPTICAL INSTRUMENT
A. Physical Optics
-The physical properties of light
B. Geometric Optics
-The process in which external light energy is focused on the retina
II. THE EYE AS A SENSE ORGAN
A. Physiologic Optics
-The biochemical and functional processes that occur in the retina to produce
visual energy
B. Psychologic Optics
or Neuro-Ophthalmologic Optics
-The conduction of visual energy to the occipital lobe
(primary visual center) resulting in vision
REFRACTION OF LIGHT
I. THE EYE AS AN
OPTICAL INSTRUMENT
As light passes through a transparent solid or liquid media,
it slows down depending on the density of the media. The
relative unit of measurement of this capacity is called the
index of refraction.
A. PHYSICAL OPTICS
Light is the basic stimulus for vision. The wavelength that is
visible to the human eye comprises only a small portion of the
electromagnetic spectrum of energy:
air = 1.0
water = 1.33
glass > 1.40
kilometer
Ymillion mp
Cosmic
rays
The Index of Refraction or Refractive Index (n) is a constant,
depending on the material; it determines the angle of
deviation. It is simply a relative unit compared to air.
X-rays
Infra
red
UV
waves
Radio - TV
Radar
Radium
rays
invisible
Hersian
V 130Y
visible
Invisible
As light passes from one medium to another with a different
refractive index and at a certain angle, there is bending of light,
i.e., light is refracted (Figure 2).
Figure 1. The electromagnetic spectrum. Adopted from Espiritu RB.'
AIR
GLASS
AIR
This small portion, called the visible spectrum, is the ONLY
portion of the spectrum that can stimulate the photoreceptors
of the human retina. It extends from 380p (3800 angstrom
units--violet) to 760p (7600 angstrom units--red). The
wavelength of each color increases as it moves toward the
direction of infrared rays (Figure 1).
Figure 2. Refraction of light as it passes from one medium to another (with a
There are three important physical characteristics of light:
PRISM
1) Velocity or Speed
Any media whose two sides are not parallel will refract light
rays. Light is deviated towards the base of the prism. (Figure 3)
-remains constant in vacuum , 3 X 1010 cm/sec
-slower in clear air and in denser media.
2) Wavelength
-size determines color; with violet (380p) the shortest, and
red (760p) the longest.
different refractive index)
APEX
light source
3) Frequency
-number of complete cycles moving past a specific point
over a given period of time.
BASE
Note: Velocity = Wavelength x Frequency
Figure 3. Prismatic effect on travelling ray
B. GEOMETRIC OPTICS
BASIS OF LENSES
Geometric optics, in-between physical optics and physiologic
optics, encompasses events that occur from the moment light
strikes the eye and eventually gets focused on the retina. Its
principal basis is the transmission and bending of the direction
of traveling light rays, i.e., refraction.
Lenses can be viewed as a certain arrangement of prisms
(remember that light is deflected towards the base of the
prism). A converging lens (positive lens) can be thought of as
two prisms joined at the base, while a diverging lens (negative
lens) can be thought of as two prisms joined at the apex
(Figure 4).
1!1
Ammetropia is a condition wherein parallel light rays DO NOT
fall into a pinpoint focus on the retina, i.e., there is an error of
refraction. They are generally classified as:
• Myopia
• Hyperopia
• Astigmatism
CONVERGING
DIVERGING
Figure 4. Converging and diverging lenses
Myopia, commonly known as "nearsightedness", is a condition
wherein parallel light rays focus at a point in front of the retina
(Figure 6). It can be axial (eyeball longer than average) or
refractive (corneal curvature steeper than average).
POWER OF THE LENS
A diopter (D) is a unit of measurement of lens power. It is a
measure of convergence or divergence, and is a reciprocal of
focal distance (f) in meters.
D = 1/f
For example:
A +1.00 diopter lens will converge light rays at 1 meter.
A +4.00 diopter lens will converge light rays at 25 centimeters
(0.25m), i.e., 4D = 1/(0.25m).
The power of the lens depends on its curvature and the
difference in its refractive index relative to air.
Figure 6. Myopia: Light is focused IN FRONT of the retina
To correct myopia, one would need a divergent lens ("negative"
or biconcave lens to neutralize the convergent effect of the
myopic eye) in order to focus light rays on the retina (Figure 7).
THE EYE
The human eye can be thought of as a series of lenses whose
main goal is to focus light rays from the external world unto
the retina. These "lenses" include: cornea, aqueous, lens and
vitreous
The average human eye has a total converging power of
about 60 diopters. The main refractive components with their
corresponding converging powers are as follows:
Cornea — + 40 Diopters
Lens
— + 20 Diopters
Emmetropia is a condition wherein parallel light rays fall into a
pinpoint focus on the retina (Figure 5).
Figure 7. A Negative Lens "pushes back" the image onto the retina
Figure 5. Emmetropia: Light is focused ON the retina
2 PHYSIOLOGY OF THE EYE la
Hyperopia, commonly known as"farsightedness'; is a condition
wherein parallel light rays focus at a point behind the retina.
It can be axial (eyeball shorter than average) or refractive
(corneal curvature flatter than average). (Figure 8)
is
SPHERICAL
ASTIGMATIC
Figure 10. The front curvature of two different balls illustrate the difference in the
curvature of spherical comeas (basketball) vs. astigmatic comeas (football).
Types of Astigmatism :
1.
Figure 8. Hyperopia: Light is focused BEHIND the retina
7.
To correct hyperopia, one would need a convergent lens
("positive" or biconvex lens) in order to focus light rays on the
retina (Figure 9).
3.
4.
5.
Simple Myopic - one image on the retina, one image
in front of the retina (Figure 11)
Simple Hyperopic - one image on the retina, one
image behind the retina (Figure 12)
Compound Myopic - both images in front of the
retina (Figure 13)
Compound Hyperopic - both images at the back of
the retina (Figure 14)
Mixed Astigmatism - one image in front of the retina,
one image at the back of the retina (Figure 15)
Figure 11. Simple myopic astigmatism. One image on the retina. other image in
front of the retina.
Figure 9. A Positive lens "pulls frontward" the image unto the retina
Astigmatism is a condition wherein the curvature of the
cornea or of the lens is not the same in different meridians.
Here, parallel light rays focus on two separate lines or planes.
One can imagine that the curvature of the eye in astigmatism
resembles one side of a football, instead of a basketball (in eyes
without astigmatism) (Figure 10). To correct astigmatism, one
would need cylindrical lenses (lenses each with power in two
different meridians/axes)
Figure 12. Simple hyperopic astigmatism One image on the retina, other image
behind the retina
PRINCIPLE OF ACCOMMODATION
Accommodation is the mechanism through which the eye
is able to increase its dioptric power allowing it to focus on
a nearby object. The brain sends out signals to contract the
smooth muscles of the ciliary body; this enables the zonules
to loosen up, which in turn increases the lens curvature
(lens thickens), and thereby increasing its converging power.
Accommodation is part of the synkinetic near reflex triad,
which includes convergence (to focus the near object on both
foveas) and miosis (to increase depth of focus).
Figure 13. Compound myopic astigmatism. Both images in front of the retina.
PRESBYOPIA
Figure 14. Compound hyperopic astigmatism. Both images at the back of the retina
With aging (around 40 years old), there is loss of focusing
or accommodative power of the human lens. Though the
refractive state of the eye remains relatively stable with age
(assuming one does not develop any media opacity like
cataract), near vision for an emmetrope (and hyperopes,
but not myopes) is practically lost because the lens cannot
accommodate to focus light rays nearer the eye. One would
then need "plus lenses" (presbyopic glasses/reading adds) to
make up for the lost automatic focusing power of the lens for
images closer to the eye. If one is emmetropic, only reading
glasses for near work are needed. For ammetropics, bifocals
are the norm --- eyeglasses with different refractive powers
in the upper (for distance ammetropia correction) and lower
segments (for near vision).
II. THE EYE AS SENSE ORGAN
A. PHYSIOLOGIC OPTICS
Figure 15. Mixed astigmatism. One image in front of the retina, one image at the
back of the retina
CORRECTION OF AMMETROPIA
1. Spectacles
2. Contact lenses
• soft, rigid gas permeable, hard, etc.
• multifocal
3. Refractive Surgery
• photorefractive keratectomy (PRK)
• radial keratotomy (RK)
• laser-assisted in situ keratomilieusis (LASIK)
• implantation of phakic lenses
• refractive lens exchange surgery
The human retina is a thin, semi-transparent, multilayered
sheet of neural tissue that lines the inner aspect of the posterior
2/3 of the wall of the globe. The young, adult retina contains
approximately 120 million rods, and about 6 million cones.
The human retina is capable of perceiving the following visual
senses:
• Light sense
• Form sense
• Color sense
LIGHT SENSE:THE ROLE OF VISUAL PIGMENTS
For the eye to perceive light, the latter has to be converted
into the biochemical energy of the visual nerve impulse. First,
it must be absorbed by the visual pigments located at the
outer segments of the rods and cones. These visual pigments
(rhodopsin, lodopsin, etc.) are lipid-protein complexes of a fatsoluble aldehyde of Vitamin A, plus a protein called opsin.'
2 PHYSIOLOGY OF THE EYE El
Vitamin A is present only in animal tissue. A molecule of its
precursor (beta-carotene) derived from plants, is split into
two to form molecules of Vitamin A in the form of an alcohol.
Vitamin A occurs in two forms (isomers), a cis-retinal and a
trans-retinal structure. Only the cis-retinal isomer combines
with opsin to form rhodopsin.'
These two lights subserve an angle at the nodal point of the
eye called the minimum visual angle.'
MINIMUM VISUAL ANGLE
PHOTOCHEMISTRY OF VISION
Experimentally, the smallest detectable line subtends one
minute of arc (Figure 17). The big "E" on the Snellen Chart
subtends an angle of 5 minutes
When light strikes rhodopsin, it is split into cis-retinal (cis-retinene)
and opsin (Figure 16) after passing through a series of orange
intermediate compounds (lumirhodopsin, metarhodopsin, etc)'
1)
A sudden reduction of sodium influx through the
photoreceptor plasma membrane together with
increased permeability of the membrane to calcium
ions result in a relative hyperpolarization of the
plasma membrane and initiates an electrical/nerve
impulse.
2)
The transformation of cis-retinene to trans-retinene
releases energy.
Trans-retinal is reconverted to cis-retinal by the action of the
retinene isomerase enzyme with energy provided by the
diphosphopyridine nucleotide (DPN) dehydrogenase system.
Cis-retinal, as soon as it is formed combines with opsin to
form the stable product rhodopsin. This combination also
releases energy which is utilized in the oxidation of retinol (Vit
A-alcohol) to retinal (Vit A-aldehyde or retinene).'
NODAL POINT
1 minute of arc
Figure 17. Minimum visual angle
FORM SENSE: VISUAL ACUITY
Form sense discriminates between stimuli, i.e., to see two
stimuli separately as two instead of fusing them into one. It
determines the acuity of vision. Simply put, it is the minimum
amount of separation between two light sources at a given
distance from the eye so that they can still be seen as two.
1
Figure 18. The Snellen "Big E" and its corresponding visual angles
Light energy
nerve impulse
orange
intermediates
cis-retinene + opsin
Opsin
cis-retinene
*
isomerase
1
DPN - H2.4\
\••
DPN
trans-retinene
(Dehydrogenase)
Figure 16. The photochemistry of vision. Adopted from Espiritu RB '
energy
TESTING VISUAL ACUITY USING THE SNELLEN CHART
In Trichromats, all 3 colors are present but has a
relative deficiency in one.
Letters are constructed so that they subtend the 5dnie visual
angle when viewed at distances of up to 200 ft (Figure 19).
—
Deuterdnornalous (green anornuly)
-
Trianomalous (blue anomaly)
Protanomalous (red anomaly)
•
In Dichromats, there is total loss of one color pigment
•
Deuteranopes (no green)
Protanopes (no red)
Trianopes (no blue)
Monochromats or Cone Monochromats (atypical)
have only one color pigment
Achromats or Rod Monochromat (typical) are totally
color blind
1 minute
5 minutes
60 meters
1111 I
I
0 20 40 80 80 100
distance from eye
B. NEURO-OPHTHALMIC OPTICS
200 feet
BASIC CONCEPTS
Figure 19. Construction of the Snellen Chart for consistency
Monocular vision, seen in lower vertebrates, is a less-advanced
One usually measures visual acuity at 20 ft (6 m) and is
recorded as two numbers: The numerator represents the
distance between chart and patient, while the denominator
represents the distance at which normal eyes can read the
given line. For example, a visual acuity of 20/40 simply means
that the patient's eye can only read from 20 ft, what a normal
(emmetropic) eye can read at 40 ft.
form of visual function wherein visual impressions from one
side cross-over to the contralateral cerebral cortex completely
(there is complete decussation)'. (Figure 21)
Lett half
Right half
COLOR SENSE: A FUNCTION
OF THE CONE PHOTORECEPTORS
White light or sunlight is a composite of different colors
corresponding to each wavelength in the visible spectrum
(Figure 20).
complete decussation
Left cortex
—4g
RED
Figure 21. Visual pathway in monocular vision.
ORANGE
YELLOW
GREEN
BLUE
INDIGO
VIOLET
Right cortex
Adopted from Espiritu RB.'
In binocular vision, there is nasal (partial) decussation of fibers
from the two sides (Figure 22). As a result, both retinas send
the same visual impressions to the visual cortex.
Left half
Right half
Figure 20. The Color Spectrum
COLOR BLINDNESS
"Color blindness" occurs in about 10% of all males and about
1% of all females. It has a sex-linked, recessive pattern of
inheritance. True color blindness (total absence of one type
of photo pigment or color-sensitive cone) is rare. Most of
the time, all photo pigments are present except for a relative
nasal decussation
Left cortex
Right cortex
Figure 22. Visual pathway in binocular vision. Adopted from Espiritu RB.'
deficiency of one color----an "anomaly".'
2
PHYSIOLOGY OF THE EYE
19
•
•
•
•
•
This partial decussation of fibers at the optic chiasm is the
basis for single binocular vision in humans. Stereopsis or depth
perception is possible only with binocular vision.
NEURO-ANATOMIC PATHWAYS
These are structures which perceive, relay, and process visual
information. From the external world, all the way to its end
terminal (occipital lobe), the following are its components':
4111 Nasal Fiekis
Temporal Fields
Left t ye
4—
Nasal FlaNes
of Retinas
Temporal Half,
Lett Retina
411--
Eyes (retina)
Optic Nerves (CN II)
Optic Chiasm
Optic Tracts
Lateral Geniculate Nuclei (LGN)
Optic Radiations
o
Parietal Lobes
Corresponds to inferior visual fields
(superior retina)
o
Temporal Lobes
Corresponds to superior visual fields
(inferior retina)
Striate Cortex (Occipital Lobes)
Temporal Fields
Right Eye
Temporal Half,
Note that the Visual Fields and the
Retina are optically Inverted
Right Retina
Optic Nerve
Optic Chiasm
IOptic Tract I
Lateral Geniculate
Nucleus
Geniculocalcarine Tract:
•Optic Radiations
-Parietal Lobes
•Temporal Lobes
•Occipital Lobes
Occipital Lobes
Primary Visual Cortex
Figure 23. The Afferent Visual Pathway
Note that the cortex of one side receives
images from the contralateral visual fields
of BOTH eyes
Note that the visual field and the retina are optically inverted,
i.e., the right visual fields (both the right field of right eye and
the right field of left eye) are projected to the left hemi-retina
of both eyes and, retro-chiasmally, the left visual pathway until
its termination in the left occipital lobe (Figure 23). Vertically,
visual field and retinal projections follow a similar pattern
of optical inversion. In addition, there is direct one-to-one
correspondence between visual direction in space and retinal
•
location.This retino-topic organization is preserved throughout
the entire visual pathway, and this logical architecture is the
basis for localization of lesions in the visual pathway via visual
field testing (perimetry).
Understanding the neuro-anatomy of the visual pathway
is the key to effective evaluation, localization, and eventual
diagnosis of many intracranial lesions (Figure 24).
LESION
A. Right optic nerve - central scotoma/
generalized depression of the right eye
B. Optic chiasm - Bitemporal hemianopia
C. Left optic tract - Right homonymous
hemianopia
D. Left optic radiation (temporal lobe)
- Right Superior Homonymous
Quadrantanopia ("pie in the sky")
E. Left optic radiation (parietal lobe)
- Right Inferior Homonymous
Quadrantanopia ("pie on the floor")
F. Left occipital lobe (visual/striate cortex)
- Right Homonymous Hemianopia
••
B
Cm*
D
(Temporal Lobe)
E
(Parietal Lobe
Figure 24. Location of Lesion with Corresponding Visual Field Defects
2 PHYSIOLOGY OF THE EYE
SUMMARY
I.THE EYE AS AN OPTICAL INSTRUMENT
A. PHYSICAL OPTICS
3 properties of light:
1) velocity
2) wavelength
3) frequency
B. GEOMETRIC OPTICS
•
refractive index (n)
•
prisms
lenses (converging and diverging)
•
emmetropia
•
ammetropia
•
•
myopia
•
hyperopia
•
astigmatism
simple myopic
simple hyperopic
compound myopic
compound hyperopic
mixed astigmatism
correction of ammetropia
•
spectacles
•
contact lenses
•
refractive surgery
II. THE EYE AS A SENSE ORGAN
A. PHYSIOLOGIC OPTICS
•
light sense: role of visual pigments
•
photochemistry of vision
•
form sense: visual acuity
•
minimum visual angle
•
testing visual acuity with the Snellen Chart
color sense: a function of photoreceptors
•
color blindness
•
Trichromat
•
Dichromat
•
Monochromat
•
Achromat
B. PSYCHOLOGIC OPTICS OR NEURO-OPHTHALMOLOGIC OPTICS
•
monocular vision
•
binocular vision
•
neuroanatomy of the afferent visual pathway
•
lesions and corresponding visual field defects
Recommended Reading
1. Espiritu RB. Ophthalmologic Optics. Manila: Department
of Ophthalmology and Visual Sciences-UP-PGH Medical
Center; 2001.
Riordan-Eva P, Whitcher JP. eds. Vaughan's and Asbury's
General Ophthalmology. 16th ed. New York, NY: McGraw
Hill Companies; 2004.
3. Spalton DJ, Hitchings RA, Hunter PA. eds. Atlas of Clinical
Ophthalmology. 2nd ed. London: Wolfe Publishing; 1994.
4. Goldberg S. Clinical Neuroanatomy Made Ridiculously
Simple. Miami: Medmaster Inc; 1979.
5. DeMyer W. Technique Of The Neurologic Examination: A
Programmed Text. 3rd ed. New York: McGraw-Hill Book
Company; 1980.
2.
REFERENCES
1.
2.
3.
Espiritu RB. Ophthalmologic Optics. Manila: Department
of Ophthalmology and Visual Sciences-UP-PGH Medical
Center; 2001.
Riordan-Eva P, Whitcher JP. eds. Vaughan's and Asbury's
General Ophthalmology. 16th ed. New York: McGraw Hill
Companies; 2004.
DeMyer W. Technique Of The Neurologic Examination: A
Programmed Text. 3rd ed. New York: McGraw-Hill Book
Company; 1980.
SELF TEST
1.
In the visible spectrum, which of the following colors
has the longest wavelength?
A. blue
B. green
C. orange
D. red
2.
What happens to the velocity of light as it passes from
a medium of low refractive index, to one of higher
refractive index?
A. slows down
B. speeds up
C. stays the same
D. is dissipated
3. True or False? A converging (positive) lens can be
thought of as 2 prisms stacked with the bases adjacent.
4. Which of the following structures accounts for about
one third (on average) of the total refracting power of
the human eye (about 20D)?
A. lens
B. cornea
C. vitreous
D. aqueous
5.
Match the following refractive states in reference to the
location of the image relative to the retina.
1. on the retina
A. myopia
2. in front of the retina
B.hyperopia
3. behind the retina
C. emmetropia
6.
Which statement best describes astigmatism?
A. The curvature of the lens is spherical.
B. The curvature of the cornea is not the same in
different meridians.
C. The curvature of the cornea is neutralized by the
curvature of the lens.
D. The convergence of rays in two different axes cancel
each other out.
E. The best type of lens for the correction of
astigmatism are prism lenses.
10. What stable product results from combination of cis-
retinal and opsin ?
A. metarhodopsin
B. beta-carotene
C. rhodopsin
D. lumirhodopsin
11. What angle does the entire big "E" in the Snellen Chart
subtend?
A.
B.
C.
D.
1 min
5 min
10 min
20 min
12. True or False? In recording visual acuity, the
denominator represents the distance between the chart
and the patient.
7.
To correct myopia, one would need which lens?
A.
B.
C.
D.
8.
diverging (negative) lens
cylindrical lens
converging (positive) lens
prisms
Which type of astigmatism has both images focused in
front of the retina?
A. simple myopic
B. simple hyperopic
C. compound myopic
D. compound hyperopic
E. mixed astigmatism
13. Which condition is described as having total loss of blue
color?
A.
B.
C.
D.
14. A symmetrically-growing pituitary macroadenoma
impinging on the optic chiasm would most likely
present with this kind of visual field defect:
A. binasal hemianopia
B. left homonymous hemianopia
C.
9.
Your neighbor who is an emmetrope develops difficulty
in reading for near on his 40th birthday and asks for
your casual advice. Which type of eyeglasses would you
recommend?
A.
B.
C.
D.
Bifocals to correct both distance and near vision
Toric lens with reading adds
Reading glasses for near work only
Prisms reading glasses
deuteranope
protanope
trianomaly
trianope
bitemporal hemianopia
D. left superior homonymous quadrantanopia
15. Which of the following lesions would most likely give
rise to a right inferior homonymous quadrantanopia?
A. left temporal lobe
B. right temporal lobe
C. left parietal lobe
D. right parietal lobe
Answers to Self-Test on page 220.
2
PHYSIOLOGY OF THE EYE
Marissa N.Valbuena MD, MHPEd and Andrea Kristina Monzon-Pajarillo MD
INTRODUCTION
One should have a good understanding of eye symptoms to be able to perform a complete ophthalmic history and examination,
which in turn are necessary to come up with accurate diagnoses.The student should have basic knowledge of the anatomy and
physiology of the eye and adnexae. In addition, the student should have the skills in interviewing a patient
OBJECTIVES
Upon completion of this unit of instruction, the student should be able to discuss the different eye symptoms.
CONTENT
PART I: The Eye as an Optical Instrument
(.Abnormalities of vision
1.Visual loss
2. Visual distortion
3. Flashing or flickering lights
4. Floaters
5. Oscillopsia
6. Diplopia or double vision
II. Abnormalities in appearance
1. Red eye
2. Color abnormalities other than redness
3. Ptosis
4. Focal growth or mass
5. Proptosis
6. Ocular deviation or strabismus
7. Abnormality in size
Ill. Abnormalities in ocular sensation
1. Eye pain
2. Eye irritation
3. Headache
Eye symptoms can be classified into three general types:
1.
2.
3.
abnormalities of vision
abnormalities of ocular appearance
abnormalities of ocular sensation — pain and
discomfort
These symptoms should always be described according to
a.
b.
c.
d.
e.
f.
onset — gradual, rapid or asymptomatic
Example of asymptomatic onset is that the blurring
of vision was discovered only when patient
inadvertently covered one eye.
duration — acute, chronic
frequency — continuous or constant, intermittent or
episodic
degree — mild, moderate or severe
location — focal or diffuse, unilateral or bilateral
progression — worsening of symptoms
Determine if forms of treatment have already been initiated
or tried. If so, to what extent have they helped to relieve the
symptoms? Are there circumstances that provoke or worsen
the condition? Is this the first time these symptoms are
experienced? Are there associated signs or symptoms?
I. ABNORMALITIES
OF VISION
Is the visual loss transient or permanent? Transient loss of
vision may be due to vascular disorders anywhere from the
retina to the occipital cortex.
Is the patient's vision worse or better in some circumstances?
Patients with error of refraction may have better vision when
they squint their eyes. Patients with presbyopia will read better
if they position their reading material further away from their
eyes. Patients with central focal cataracts, such as posterior
subcapsular cataracts, may have worse vision in bright sunlight.
Decline in visual acuity may be due to abnormalities anywhere
along the optical and neurologic pathway. Consider the
following as possible causes:
a.
b.
c.
d.
e.
f.
refractive error
ptosis
ocular media disturbance (corneal edema, hyphema,
cataract, vitreous hemorrhage)
retinal diseases
optic nerve diseases
intracranial visual pathway abnormalities
Clinical Pearl
Determining the characteristics of a patient's symptom is a
valuable tool in helping us direct our investigation towards
a suspected pathology.
,
.777:777:71
1. VISUAL LOSS
Patients can describe visual loss as "nanlalabo',' "maulap
ang paningin" "nawawala ang paningin", "hindi makakita" or
"nabulag"
When a patient reports impairment of vision, the examiner
should determine when it occurred, whether onset was
sudden or gradual, whether one or both eyes were affected.
If both eyes are involved, which is worse, which failed first and
how much time has elapsed between the two.
Actual onset of visual impairment may not coincide with the
time given by the patient. Vision in one eye may have been
deteriorating over the years, becoming noticeable when the
patient accidentally covered one eye.
One should distinguish between decreased central acuity
and peripheral vision. Disturbances in peripheral vision may
be focal such as scotoma, or may involve a bigger area as in
hemianopsia. A scotoma is a blind or partially blind area in
the visual field while hemianopsia is blindness in one-half of
the visual field. Abnormalities in the central nervous visual
pathway disturb the visual field more than the central visual
acuity.
Sudden
Gradual
Mild
Severe
check cornea
for dry eye
Check retina
for CRAO
Severe
Check refraction
for error of
refraction
Check lens for cataract
and optic disc for
glaucoma
CRAO - central retinal artery occlusion
2. VISUAL ABERRATIONS
A. Glare, photophobia
Patients may describe this as "silaw" or "nasisilaw"
Irritative disease of the conjunctiva or cornea especially
foreign bodies of the cornea may induce photophobia. Acute
inflammation of the iris may likewise make the eye sensitive to
ordinary light.
3 EYE SYMPTOMS 1111
Glare may also result from uncorrected error of refraction,
scratches on spectacle lenses, excessive pupillary dilatation
and hazy ocular media
B. Visual distortion
Visual distortion manifests as irregular patterns of dimness,
wavy or jagged lines, image magnification/ minification. This
may be caused by migraine, optical distortion from strong
corrective lenses and lesions involving the macula and optic
nerve.
3. FLASHING/FLICKERING LIGHTS
Patients may describe this as "may parang kidlat", "biglang may
maliwanag", "may kumikislap"
This may indicate retinal traction, posterior vitreous
detachments or migrainous scintillations or auras.
Clinical Pearl
Characterizing the particular quality ofvisual aberrations
can guide us in formulating a differential diagnosis
Glare/ Photophobia - corneal edema, cataracts
Visual Distortion - central serous chorioretinopathy,
age related macular degeneration
Flashing/ flickering lights - posterior vitreous
detachment, retinal detachment
Floating Spots - vitreous condensations
Oscillopsia - nystagmus
II. ABNORMALITIES OF
APPEARANCE
4. FLOATERS
1. RED EYE
"May lumulutang so harap ng mata","may insekto no sumusunod
so paningin"
One must differentiate between redness of the lids (Figure 1)
and periocular area (ocular adnexa) from that of the globe
(Figure 2).
Floaters represent normal vitreous strands due to "normal"
vitreous changes or may be secondary to pathologic presence
of pigments, blood, or inflammatory cells.
5. OSCILLOPSIA
"Gumagalaw o lumilikot ang paningin"
Shaking field of vision may be due to harmless lid twitching
(myokymia), or to certain forms of nystagmus
6. DIPLOPIA OR DOUBLE VISION
"Nagdadalawo ang paningin" "doble ang paningin', naduduling"
Monocular diplopia manifests as a split shadow or ghost
image. Causes include uncorrected error of refraction, media
abnormalities such as cataract, corneal irregularities and
intraocular lens dislocation.
Figure 1. Redness and swelling of the eyelid
Binocular diplopia disappears when one eye is covered. This
may be vertical, horizontal, diagonal or torsional. The diplopia
may be more severe (2 images more widely separated) in
certain direction of gaze or head position.
Figure 2. Eye redness due to a conjunctivitis
"Namamaga ang mata"
Preseptal cellutitis
Orbital cellulitis
External hordeolum (Figure 3)
VS
"namumula ang mate; "sore eyes"
Conjunctivitis (Figure 2)
Iritis (Figure 4)
Acute glaucoma (Figure 5)
Scleritis (Figure 6)
Pterygium (Figure 7)
"dumugo ang mata"
Subconjunctival hemorrhage (Figure 8)
Figure 3. External hordeolum
Figure 6. Scleritis
Figure 4. Iritis
Figure 7. Pterygium
Figure 5. Acute glaucoma
3 EYE SYMPTOMS
Eti
Figure 8. Subconjunctival hemorrhage
2. COLOR ABNORMALITIES OTHER THAN
REDNESS
jaundice
hyperpigmented spots (on the ocular surface)
— examples are nevus (Figure 9) subepithelial
melanosis
c. thinned out, bluish sclera — congenital glaucoma,
ciliary staphyloma
d. white opacity - opacity in the cornea (Figure 10),
a.
b.
opacity in the lens (Figure 11)
Figure 9.
Figure 10. Opacities in the cornea
golf !non srtional Mnteriala6, °pi-101011i iulUgY I
3. PTOSIS - drooping of the eyelids, "Napipikif; "kirat ang
mata" (Figure 12)
4. FOCAL GROWTH OR MASS in the eyelids or eye surface,
"bukol","maga'; "butlig" (Figures 13, 14)
S. PROPTOSIS - protrusion of the eyeball, "dilat ang mata"
(Figures 15), "Iumuluwa ang mata" (Figure 16)
6. OCULAR DEVIATION OR MISALIGNMENT - "duling':
"banlag"; esodeviation (inward turning of the eye) (Figure 17),
exodeviation (outward turning of the eye) (Figure 18), hypertropia
(upward turning oftheeye) (Figure 19) or hypotropia (downward
turning of the eye) (Figure 20)
Figure 11. Opacities in the lens
7. ABNORMALITY IN SIZE - cornea or globe may be smaller
(Figure 21) or bigger than normal (Figure 22)
Figure 12. Ptosis of the left eye
Figure 16. Proptosis, right eye
Figure 13. Lid masses
Figure 17. Esotropia. left eye
Figure 18.
Figure 14. Pinguecula
Figure 19.
Hypertropia, right eye
Figure 15. Lid retraction, left eye
3 EYE SYMPTOMS
29
Severe, localized one-sided eye pain radiating to the temporal
up to the occipital area of the head may be due to an attack
of glaucoma.
2. EYE IRRITATION
Figure 20. Hypotropia, left eye
Superficial discomfort is usually caused by ocular surface
abnormalities.
a.
b.
c.
Figure 21. Small right eye
Itching - Often a sign of allergic sensitivity, "makati"
Dryness - Burning, gritty, mild foreign body
sensation. Can occur with dry eyes or other types of
mild corneal irritation, "may buhangin: "may puwing",
"maaligasgas"
Tearing - may be due to irritation of the ocular
surface, corneal edema or may be a sign of abnormal
lacrimal drainage , "nagluluha, 'palaging basa ang
mata"(Figure 23)
Figure 22. Enlarged left eye
III. ABNORMALITIES OF OCULAR
SENSATION
1. EYE PAIN
Figure 23. Teaming
"Masakir "makiror "mahapdi"
Eye pain must be characterized in terms of location:
Periocular - may be tenderness of the lid, tear sac,
sinuses or temporal artery
b. Retrobulbar - may be due to orbital inflammation,
orbital myositis, optic neuritis
c. Ocular
- may be due to corneal abrasion,
corneal foreign body, glaucoma, corneal ulcer,
endophthalmitis
d. Non-specific - fatigue from ocular accommodation,
binocular fusion, or referred discomfort from nonocular tension or fatigue
d. Ocular Secretions - "nagmumuta: Characterize
discharge as to color, consistency, amount
a.
Deep seated aching, boring or throbbing pain may be due
to inflammation of the iris and ciliary body. Orbital infection
can give rise to severe pain. Herpes zoster may induce pain in
the eye before any visible involvement of the eyelid and may
persist after the disease has resolved.
Tenderness, soreness or pain on pressure may be due to
inflammation of the lids, corneal foreign body or any anterior
segment inflammation.
i. Watery - allergic (Figure 24)
ii. Mucoid discharge - allergic , viral conjunctivitis
(Figure 25)
iii. Ropy or stringy discharge - allergic (Figure 26)
iv. Mucopurulent - bacterial/viral conjunctivitis
v. Purulent and copious- gonococcal conjunctivitis
(Figure 27)
vi. Bloody - viral conjunctivitis (Figure 28), StevenJohnson's syndrome
vii. Dried matter-crusts on lashes - blepharitis
(Figure 29)
Figure 27. Purulent and copious discharge
Figure 24. Watery discharge
Figure 28. Bloody/serosanguinous discharge
Figure 25. Mucoid discharge (white arrow)
Figure 29. Crusting of discharge on lid
Figure 26. Stringy or ropy discharge (white arrow)
3 EYE SYMPTOMS
Es
3. HEADACHE
LEARNING ACTIVITY
Uncorrected errors of refraction and presbyopia frequently
cause headache referred to the eyes or brow and comes
with reading and computer work. Migraine headaches and
sinusitis are frequent causes of headache. Headaches may not
always come from the eye. High and low blood pressure may
also give rise to headaches around the eyes. Headache from
rise in intracranial pressure is usually severe and associated
with nausea and vomiting. Clearly demarcated one-sided
headache, originating from the ipsilateral eye, associated with
nausea and vomiting, with or without ciliary injection of the
eye may be due to angle closure glaucoma.
Students should pair and role play. One will be the doctor and
the other the patient. The doctor should take the history of the
patient with any of the following chief complaint:
1.
2.
3.
4.
"Malabo ang mata"
"may sore eyes"
"mahapdi ang mats"
"banlag"
The doctor will write the patient's history and the partner will
comment on the completeness and accuracy of the history
and the manner in which the history was taken.
SUMMARY
SELF-TEST
Eye symptoms consist of abnormalities in vision, appearance
and sensation. The student should ask clarifying questions in
order to get sufficient detail to pinpoint the etiology of the
ocular disorder.
REFERENCE
1.
Riordan-Eva, Whitcher, John. Vaughn and Ashbury's
General Ophthalmology , 16th Edition, New York: Lange
Medical Books/ McGraw Hill
2. Scheie, Harold, Albert, Daniel. Textbook of Ophthalmology.
Philadelpia : W.B Saunders
Case 1. You have a 20 year old female patient with chief
complaint of blurring of vision. What questions you will
ask the patient?
Case 2. You have a 15-year old patient with redness of the
right eye. What questions will you ask the patient?
Answers to Self-test on page 220.
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111111111',1111
Teresita R. Castillo MD, MHPEd
INTRODUCTION
This self-instructional material is designed to assist the student learn important concepts on how to perform the basic five-part
eye examination. It will explain how to examine the eye and basic visual function.
1 he proper method of basic eye examination in an individual is an important skill that every physician should possess. Performing
a systematic eye examination will enable the physician to evaluate ocular complaints and subsequently provide immediate
emergency care whenever the need arises. Furthermore, this will enable the physician to recognize ocular conditions that may
require further referral to an ophthalmologist for definitive management. An eye examination may also provide the physician
with information on the status or condition of certain systemic illnesses such as thyroid disease, tuberculosis, diabetes and
hypertension.
OBJECTIVES
Upon completion of this unit of instruction, the student should be able to discuss the principles of performing the live-part basic
eye examination. Specifically, the student should be able to:
1. discuss the value and rationale for performing the various parts of the basic eye examination
2.
determine a patient's visual acuity
3.
4.
perform gross examination of the eye and its adnexae
5.
6.
7.
8.
perform pupil examination and interpret its findings
evaluate ocular motility
determine intraocular pressure
perform direct ophthalmoscopy for a systematic fundus examination
report eye examination results accurately in an internationally acceptable format
CONTENT
I.Visual acuity testing
II.Gross examination of the eye and adnexae
I . Systematic examination of the eye and adnexae
2. Pupil examination
III.Ocular motility testing
IV.Intraocular pressure
V. Fundus examination
All patients should have an eye examination as part of a
general physical examination. Visual acuity, gross examination
of the eye and its adnexae, extraocular muscle movements,
intraocular pressure determination and fundus examination
using the direct ophthalmoscope constitute the basic eye
examination.
I. VISUAL ACUITY TESTING
Measurement of visual acuity (VA) is a fundamental element of
the basic eye examination. It should be performed prior to any
manipulation of the eye to avoid any medico-legal issues that
may arise. Distance visual acuity testing should be performed
in all patients, including children. Near visual acuity testing on
the other hand, is routinely performed only for patients over 35
years of age. Otherwise, this is done only if the patients have
complaints with their near vision. Occasionally, near vision
testing is done in lieu of distance vision testing if the latter is
difficult or not possible as in instances when vision testing has
to be performed at bedside.
Distance Visual Acuity is generally performed using the Snellen
Chart (Figure 1), which may come in the form of letters,
numbers, tumbling E or pictures.
eye during occlusion as this may affect subsequent
visual acuity testing of the occluded eye.
3.
Ask the patient to read the chart starting at the
first line (20/200 or 6/60 line) proceeding until the
smallest line that he/she can distinguish more than
half of the figures.
4.
Record the acuity using a ratio or fraction which
compares the performance of the patient with an
agreed upon standard.
Visual Acuity (VA) = distance of patient from the chart
distance at which normal eye can
read the given line
For example, a patient whose VA = 20/50 indicates that
the patient can see at 20 feet what a person with normal
acuity can see at 50 feet.
Table 1 shows the various notations commonly used for
recording distance visual acuity.
5.
Instruct the patient to occlude his/her other eye and
repeat steps 3 and 4.
Table 1. Alternative Notations for Recording Distance VA
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Figure 1. Snellen Charts used for distance visual acuity testing. (A) Letter chart,
(B) Tumbling E chart, (C) Lea Kindergarten chart
The standard distance of the patient from the chart is 6 meters
or 20 feet. 1 he general steps are as follows:
1.
0I
Position the patient 20 feet or 6 meters from a wellilluminated Snellen Chart. In patients consulting
•
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If the patient's visual acuity is less than 20/20 in either eye,
pinhole visual acuity testing is performed to determine if the
vision problem is due to an uncorrected refractive error. This is
performed as follows:
1.
With one eye occluded, instruct the patient to place
the pinhole (Figure 2) over the eye being tested
and ask him/her to try to read the chart through the
pinhole.
2.
Record the acuity using a ratio or fraction.
3.
Repeat steps 1 and 2 with the opposite eye looking
thru the pinhole if warranted.
for the first time, naked visual acuity (without any
correction) is initially taken. Follow-up patients who
wear corrective lenses should be asked to wear their
correction during the test.
2.
Instruct the patient to occlude one eye using his/her
palm or an opaque occluder when available. Care
should be taken to avoid exerting pressure on the
5.
Figure 2. Patient looking thru pinhole (white arrow) as she reads the
Snellen Chart.
Light Perception (LP). If the patient is unable to correctly
identify the direction of the light source but is able to
detect its presence, record the patient's response as light
perception. If the presence of light can not be detected
by the patient, this is recorded as No Light Perception
(NLP). This procedure is ideally performed in a dimly lit
room to accentuate the presence or absence of light
stimulus.
When the patient is illiterate or in toddlers who are still unable
to read, tumbling E, Lea charts or picture Snellen charts are
used instead. The patient is provided with hand-held cards
bearing the same figures on the chart. He/she is asked to
match the figures on the chart with those in the hand-held
cards. As with previous methods described, visual acuity
testing should be performed one eye at a time.
Standard charts can not be used to measure visual acuity
If a patient is unable to see the largest letter on the Snellen in infants or very young children (less than three years old).
chart, distance VA is measured using the following methods While visual function can be assessed in infants, it is not
possible to measure visual acuity. When evaluating vision in
(listed in order of decreasing vision):
this age group, the examiner should take note of certain signs
1. Reduce the distance between the patient and the chart that may indicate poor vision. The presence of misalignment
until he/she is able to read the 20/200 or 6/60 line. of the eyes, pendular, jerky or rotatory eye movements may
Record the new distance as the numerator and retain the be indicative of poor vision. Withdrawal or a change in facial
denominator. For example, if a patient is able to see the expression in response to light or sudden movement would
20/200 (6/60) line at a distance of 10 feet, the patient's indicate the presence of vision. If vision in one eye is poorer
VA is recorded as 10/200 (3/60). If the patient is unable compared to the other eye, the child usually becomes irritable
to read the 20/200 line at a distance of 3 feet, proceed to once the good eye is occluded or covered. Vision may be
assessed by passing light or brightly colored objects before
Step 2.
the baby and observing if the infant is able to fixate and follow
2. Counting Fingers (CF). Hold up one hand and ask the the moving object. Vision is recorded as presence or absence
patient to count the number of extended fingers. Record of fixation.
the distance at which counting fingers is done accurately.
For example, if a patient can count fingers accurately up Near Visual Acuity testing is performed using near vision
charts (Figure 3). Near vision charts usually contain numbers
to a distance of 2 feet, VA is recorded as CF at 2 feet.
or figures in varying sizes corresponding to particular point size
3. Hand Movements (HM). If a patient is unable to count or Jaeger notation. The standard near vision chart is held at a
fingers accurately even at a distance of one foot, determine distance of 14 inches or 35 cm under well lighted conditions.
if the patient can distinguish presence or absence of hand If a patient normally wears glasses for reading, these should be
motions at a distance of one foot. A positive response is worn during testing. Since number or figure size designations
recorded as (+) HM. A negative response is recorded as and test distances may vary, reporting of near VA usually
reflects both the size and distance of the smallest figures that
(-) HM.
a patient is able to read correctly (ex. is at 14 inches, 6 pt at
35 cm). In the absence of a standard near vision card, any
4. Light Projection (LPj). If the patient can detect hand
movements, use a penlight to determine if the patient can printed material such as a telephone book or newspaper may
instead be used. Both the approximate type size read and the
correctly detect the direction of the light source. Shine
distance at which the material was held should be recorded.
the light on four quadrants. Record findings as follows:
good LPj: able to identify light source in all four quadrants
fair LPj: able to identify light source in 2-3 out of the four
quadrants
poor LPj: able to identify light source in only one quadrant
Table 2 shows commonly used abbreviations used in
recording visual acuity.
4 EYE EXAMINATION El
the eyeball. Take note of the position of the eyelids relative
to the iris. The white of the sclera is normally covered by the
upper and lower lids superiorly and inferiorly. If the white of
the sclera can be seen all around the iris, this can be due to
exophthalmos or lid retraction. On the other hand, if the lids
are encroaching on the patient's pupil, this could be due to
ptosis or enophthalmos.
Figure 3. Near VA testing in a patient using the Rosenbaum (Jaeger)
Pocket Vision Chart.
Table 2. Abbreviations Used in Recording Visual Acuity
VA
visual acuity
OD
(oculus dexter) Right eye
Os
(oculus sinister) Left eye
OU
(oculus uterique) Both eyes
so
without correction
cc
with correction
ph
pinhole
NV
near vision
Inspection of the conjunctiva and sclera is subsequently done.
Instruct the patient to look down while holding the upper
lid to inspect the upper conjunctiva. Instruct the patient to
look up while retracting the lower lid to inspect the lower
conjunctiva. The patient is asked to look sideways to facilitate
inspection of the medial and lateral conjunctival regions. Take
note of the presence of redness, discharge, lumps and masses,
or any other abnormality.
Proceed with inspection of the cornea and iris. The cornea
is inspected for clarity as well as presence of localized areas
of opacities or other abnormalities, while the iris is inspected
for pigment changes as well the presence of any masses or
nodules (Figure 4).
II. GROSS EXAMINATION OF THE
EYE AND ADNEXAE
A systematic gross examination of the eye should be
performed to ensure that all structures are evaluated. It is
recommended that one proceed from the more external
towards the more internal eye structures.
The position of the eyes in relation to other facial structures is
first assessed. Check for the presence of any gross asymmetry
between the two eyes. Eye position should be examined from
the front, above (looking down over the patients brow while
seated) and from the side. These views would highlight any
possible protrusion of the eye ball.
With the aid of a flashlight, one inspects the lids, the
surrounding tissues and palpebral fissure. The exposed
portion of the eye between the upper and lower eyelids,
called the palpebrai fissure should be symmetrical. Take note
of the presence of redness, masses or abnormal pigmentation/
discoloration on the eyelids or periocular tissue. The eyelashes
should not touch the eye and should be directed outward.
The lid margins should be smooth and well opposed against
Figure 4. Gross picture of normal eye. Note the outwardly directed
lashes and the lids partially covering the superior and inferior limbos
Patient has deer cornea, brown iris and round pupil.
Pupil examination is composed of three components.
are
These
1.
Assessment of pupil size and shape. Darken the room
and instruct the patient to fixate on a distant target. Shine
just enough light onto both eyes and observe the size of
the patient's pupils.The normal pupil size ranges from 2 to
4 mm. Although size of individual pupils of a patient may
fall within this normal range, any asymmetry in pupil size
of more than two millimeters is considered abnormal.
2.
Assessment of pupil reaction to light (Light Reflex
Test). This test is used to evaluate the integrity of the
pupillary light reflex pathway. Cranial nerve II (optic nerve) and
cranial nerve III (oculomotor nerve) comprise the afferent
and efferent arms of the pathway respectively.
a.
Direct pupillary reaction. This is performed by shining
a penlight at the patient's eye. Normal response is a
brisk constriction of the pupil.
b.
Consensual pupillary reaction. To perform this test,
light is directed at one eye while the opposite eye is
observed for a response. Normal response is a brisk
constriction of the pupil of the opposite eye.
Absence of a direct response to light would indicate a
problem in the afferent arm of the same eye, while absence of
a consensual response would generally indicate a problem in
the afferent arm of the opposite eye. If vision is intact and both
direct and consensual response is absent, it is likely that the
problem lies in the efferent arm of the involved eye. In such
cases, however, this finding should be associated with ptosis
or drooping of the lids of the involved eye as the muscles
responsible for lid opening is also innervated by CN Ill or the
oculomotor nerve.
3. Assessment of the reactions of the pupils to a
swinging light (Swinging Flashlight Test). This test is
performed by shining a light on one eye, then swinging it
across to the opposite eye. The process can be repeated
several times, allowing for about one second interval for
each swing. Change in pupil size of both eyes is noted
as light is moved from one eye to the other. The normal
reaction is for the pupil to constrict slightly and to remain
constricted as light shines on it. If dilation is observed
when light is shone on an eye, it means that its direct
light reflex is weaker than its consensual light reflex and
is suggestive of an optic nerve problem in the dilating
eye. This test compares direct and consensual responses
of each eye and provides an objective way to rule out a
unilateral optic nerve lesion or bilateral but asymmetric
optic nerve pathology. The abnormal response is called a
relative afferent pupillary defect (RAPD). A positive RAPD
signifies that an optic nerve lesion is present on the side
of the dilating pupil. Note that as this is a comparative
test, hence it is not possible to have bilateral RAPD.
III. OCULAR MOTILITY TESTING
Examination of eye movements begins by examining ocular
alignment in the primary position (straight gaze). The simplest
method to observe this is by observing the position of the
corneal light reflections. This is performed by instructing the
patient to look straight and fixate at a distant object while
a light is shone towards both eyes. A reflection of light will
appear in the cornea of each eye. If the eyes are properly
aligned, the reflection should appear in the center of the pupil
in both eyes (Figure 5). The presence of misalignment will be
observed as appearance of the corneal reflection outside of
the center of the pupil in the deviating eye. Table 3 lists the
common abnormalities in the alignment of the eyes.
Table 3. Common Abnormalities in Alignment of the Eyes
Esotropia
inward
misalignment
light reflection appears It!!
displaced laterally in the
non-fixating eye
Ipotio
-pie
outward
misalignment
light reflection appears
displaced medially in
the non-fixating eye
downward
misalignment
light reflection appears
displaced superiorly in
the non fixating eye
upward
displacement
light reflection appears
displaced inferiorly in
the non-fixating eye
'
Left Esottopia
Left Esotropia
Hypotropia
Right Hypotropia
tHypertropia
Right Hypeiti opia
4 EYE EXAMINATION
Figure 5. Normal ocular alignment showing comeal reflexes at center
of pupils.
Proceed to examine eye movement by instructing the patient
to follow your finger, a penlight or a small target through the
six cardinal positions of gaze. Move the target slowly through
the different positions (Figure 6) keeping it roughly 14
inches or 35 centimeters from the patient. This will allow for
systematic testing of each of the extraocular muscles in their
primary fields of action (Figure 7). When extraocular muscle
(EOM) movement is tested with both eyes open, this is referred
to as version test. When performed one eye at a time, it is
referred to as duction test.
Observe the excursion of each eye as it moves from one
position of gaze to another and take note of any limitation in
movement. Also observe for parallelism of eye movements
between the two eyes and presence of jerky, oscillatory or
rotational movements like nystagmus in any direction of gaze.
While conducting the examination, the patient is also asked if
double vision occurs at any point.
Figure 6. Motility examination being conducted on a patient.
(A) cardinal positions of gaze to be tested following the arrows or the
letter "H", (B) Examiner asks patient to follow his finger thru the different
cardinal gaze positions.
Normally, the white of the sclera should disappear completely
with sideways movement. On upward movement, only a
small part of the cornea should disappear behind the upper
eyelid, while with downward movement, at least half of the
cornea should disappear. In order to allow better visualization
of downward movement of the eye, the patient's upper eyelids
may be lifted.
Results of EOM testing are recorded diagrammatically as
shown in Figure 8A. The limits of gaze in the various positions
are delineated by small lines while the EOM movements are
represented by lines ending in arrows or circles. For duction
tests a separate diagram is used to represent each eye.
Version test results are presented in a similar manner except
that the diagrams for each eye overlap each other. When
movement in any direction is limited, the lines representing
RSR
LIO
Sup Recii & Inf Obliques RIO
LSR
RLR
LM R PRIMARY POSITION RMR
LLR
RIR
LSO
LIR
Id Recli & Sup Obliques RSO
Figure 7. Cardinal positions of gaze. Note the primary positions acting in each of the positions.
muscle movement is shorter and does not reach the limits of
gaze. Length of said lines should approximate the extent of
imitation in EOM. Figure 8B shows the results for limitation in
movement of the right lateral rectus muscle for both duction
and version tests.
if globe perforation is suspected, as in cases wherein a
history of ocular trauma is elicited from the patient.
Additional motility examinations are performed in cases when
abnormalities in ocular alignment and EOM movements are
noted when performing the basic eye exam.
MOTION
SR
10
LR 1e
sf MR le
provides a quantitative
method for determination of 10P by measuring the
amount of pressure required to indent the cornea with
the use of the Schiotz tonometer (Figure 10). While
this is the preferred method for 10P measurement in
patients with corneal scars, its main disadvantage is
that it is affected by scleral rigidity. Furthermore, this
method requires that patients be placed in supine
position.
2. Indentation Tonometry
VERSION
SO
IR
Right
Bilateral on
Ll
VERSION
\IP
Bilateral a
Figure 8. Motility examination results (A) Full EOMs shows normal
duction and version test results, (B) Abnormal duction and version tests
showing limitation in movement of the right lateral rectus
IV. INTRAOCULAR PRESSURE
DETERMINATION
Figure 9. Palpation tonometry is performed by alternately pressing on
the patient's upper lid using the index fingers of both hands while patient
looks down without closing her eyes.
Intraocular pressure (10P) refers to the pressure that is created
within the closed environment of the eye. This is governed by
a balance between the production of aqueous humor and its
drainage.
Intraocular pressures (IOP) vary from individual to individual
and exhibit normal fluctuations during the day. 10P is
considered normal if it falls within the range of 10 to 21 mm
Hg and if the difference in 10P between the two eyes does not
exceed 2 mm Hg.
Intraocular pressure is measured by tonometry. Various
methods commonly used for determining 10P levels follow:
provides a
rough estimate of 10P. This is performed by first asking
the patient to look down without closing his/her eyes.
The examiner then places his two index fingers on the
patient's upper lid over the globe and alternately exerts
pressure on the globe (Figure 9). Findings are reported
as soft (normal), hypotonic or firm. Care is taken that only
pressure sufficient to slightly indent the globe is applied.
Note that this method of 10P determination is avoided
1. Finger Palpation/Tension Tonometry
Figure 10. Indentation Schiotz tonometry gives a quantitative
measurement of the 10P by measuring the amount of pressure required to
indent the cornea
using the Goldman
Applanation Tonometer is considered as the gold
standard for lop determination (Figure 11). Its primary
disadvantage Is that it requires special equipment and
can only be used by an ophthalmologist. Intraocular
pressure measurements are based on the amount of
pressure required to flatten a standard diameter (3.06
mm) or area (7.35 mm2) of the cornea. Unlike the Schiotz
tonometer, the instrument requires a smooth cornea and
3. Applanation tonometry
4 EYE EXAMINATION
El
flattening by the fixed air puff pressure delivered against
the cornea. Unlike the Schiotz and Goldman applanation
tonometers, this method does not require the use of
topical anesthetic agent. This instrument provides
reasonably accurate readings and is generally used for
mass screening purposes.
V. FUNDUS EXAMINATION
Figure 11. Applanation tonometry which uses the Goldman Applanation
Tonometer, considered the gold standard for 10P determination takes 10P
by measuring the amount of pressure required to flatten a specified area
of the cornea
can not be used in individuals with corneal abnormalities
such as scars. This instrument is more accurate than the
Schiotz tonometer in determining the 10P of patients with
altered scleral rigidity. 10P measurements taken with the
applanation tonometer are however affected by corneal
thickness and irregular or altered corneal curvatures (e.g.
in post refractive surgery patients and patients with high
corneal astigmatism).
4.
The air puff noncontact tonometer is a machine that
takes 10P readings by calculating the amount of corneal
The fundus can be examined using various methods: direct or
indirect ophthalmoscopy, and use of special lenses with the
aid of the slit lamp biomicroscope. It is essential that every
physician learn and gain confidence in performing fundus
examination using the direct ophthalmoscope as this is
generally used for screening purposes.
Prior to performing direct ophthalmoscopy, it is essential to
gain familiarity with the instrument's basic parts (Figure 12).
Ophthalmoscopy is best performed in a darkened room.
Sufficient examination of the fundus can be done even in a
non-dilated pupil, provided that there are no media opacities.
However, a more thorough examination of the peripheral
retina can be performed through a dilated pupil.
Before beginning the procedure, one should ensure that the
ophthalmoscope is working properly and that both you and
the patient are positioned comfortably.
HEAD
PATIENT SIDE
EXAMINER SIDE
OPHTHALMOSCOPE PARTS
1 - Brow rest for examiner
2 - Viewing Aperture where examiner
looks thru to see structures
3 - Polarizing Filter eliminates
unwanted reflection
4 • Lens Selection Dial is used to
choose lens for focusing of
fundus structures
5 - Aperture Selection Dial is used to
select preferred aperture for
fundus examination
6 - Lens Power Indicator shows the
dioptric power of the lens being
used for the examination
7 - Power Switch/Rheostat is used to
control strength of illumination
HANDLE (contains battery)
Fig 11 ro 12. Direct ophthalmoscope and its basic parts
40
Calf
clonal Matc!
1.
Check the light source and select the large beam
aperture. The intensity of light from the ophthalmoscope
should not be too much as this could lead to excessive
constriction of the patient's pupil.
2.
Place your index finger on the lens selection dial and
adjust the lens setting to 0 diopter. The index finger is
placed on the lens selection dial to allow for adjustment
of the lens power during the conduct of the examination.
3.
When examining the patient's right eye, hold the
ophthalmoscope with your right hand and use your right
eye to view the patient's eye. Use the left hand and left
eye to examine the patient's left eye.
4.
The patient's glasses should be removed. The examiner
may also opt to remove his glasses while performing
direct ophthalmoscopy. Contact lenses worn by the
patient or examiner may be left in place.
5.
Instruct the patient to focus on a distant target. The
patient should also be instructed to maintain that gaze
throughout the examination.
6.
Begin to look at the patient's eye thru the instrument's
viewing aperture from about a distance of one to two
feet. When you look straight down the patient's line of
sight at the pupil, the red-orange reflex should be visible.
7.
Slowly come closer to the patient at an angle of about 150
temporal to the patient's line of sight keeping the pupil
in view at all times. Turn the lens selection dial with your
index finger to bring the patient's retina into focus.
8.
You may place your free hand on the patient's upper lid
to keep the eye open, or on the patient's shoulder to keep
yourself steady. Hold the ophthalmoscope comfortably
against the arch of your brow.
9.
Move the beam until a retinal vessel comes into view. If
the image is not clear, turn the lens selection dial up and
down until it becomes clear. Follow the retinal vessel
until it converges to the optic disc, which lies nasal to the
center of the retina. Take note of the disc color, its margins
10. Examine the retinal vessels by moving the beam slowly
along the nasal retinal vessels and the temporal retinal
vessels.
11. Inspect the retinal background for the presence of
hemorrhages, exudates or any other abnormality.
12. Examine the macular area. Take note of the presence of
the foveal reflex.
13. Repeat the procedure with the opposite eye.
There are five structures that should be observed in a systematic
fundus examination: (1) ocular media, (2) optic disc, (3) retinal
vasculature, (4) retinal background and (5) the macular area.
Figure 13 shows these areas in an actual fundus photograph.
1)
Ocular Media is observed for presence of the red-orange
reflex (ROR) which is a result of the reflection of light
coming from the ophthalmoscope that bounces off the
patient's fundus. The status of the ROR is an indication of
the clarity of the ocular media (cornea, lens, aqueous and
vitreous humor) and condition of the retina. A normal
ROR (Figure 14) is evenly colored and is not interrupted
by shadows. The presence of any opacity in the lens or
cornea, cells or bleeding in the aqueous/vitreous humor
will generally appear black or create a silhouette against
the red-orange reflex. Retinal detachment will also affect
the bouncing of light as it is reflected from the retina and
alter the appearance of the ROR.
-RETINAL VEIN
- RETINAL ARTERY
f---- DISC
FOVEA
r- - - —)
F,ACKGROUND
MACULA
TEMPORAL
PHYSIOLOGIC CLIP
NASAL
Figure 13. Normal Fundus. Photo shows the different parts of the right
fundus.
and size of the optic disc cup.
Figure 14. Red Orange Reflex (A) Normal ROR, (B) dull ROR due to retinal detachment, (C) no ROR due to
presence of mature cataract
4
EYE EXAMINATION
2)
The optic disc is examined taking note of its color, shape
arid margins. In most cases, when viewed through the
ophthalmoscope, the normal optic disc will appear slightly
oval vertically and yellowish-orange to pink in color. Its
margins should be sharp or distinct. Also note for the
presence of abnormal structures such as new vessels or
hemorrhages within the disc (Figure 15). A central pit
or depression seen on the surface of the disc is called the
"physiologic cup" which is comprised by the aggregation
of ganglion cells from the retina as it forms the optic
nerve. It is also the area where the retinal arteries and
veins enter and exit and provides the observer with a
marker for the edge of the cup since the blood vessels
would he noted to bend in this area. The relative size of
the optic cup to the disc (cup:disc ratio) should be noted.
Approximation of the vertical cup-to-disc ratio (CDR) is
described in Figure 16. Normal cup-to-disc ratios should
be less than 0.5. The cup becomes enlarged when the
ganglion cells die as observed in glaucoma (Figure 17).
The optic disc is often used as a "yardstick"of the ocular fundus.
Lesions seen with the ophthalmoscope are measured and
described in terms of disc diameters.
Figure 17. Optic cup enlargement (A) shows CDR between 0.4 to
0.5 which is generally considered as upper knit of normal; (B) cupping
resulting from glaucoma with CDR of approximately 0.6
Figure 15. Examples of presentations of the optic disc.
(A) normal disc showing healthy neuroretinal rim with distinct margins and
approximate CD ratio of 0.3. (B) tilted optic disc with a scleral crescent often
seen in myopic patients, (C) disc with neovascularization as seen in diabetic
retinopathy, (D) disc with blurred disc margins as seen in optic disc edema
3) The retinal vasculature is composed of arteries and
veins. Note that the retinal vessels emerge from the nasal
portion of the optic disc. The vessels on the temporal
aspect of the disc follow an arching course while those
on the nasal side have a radial course. The arteries
usually appear brighter red in color than the veins with a
prominent shiny reflex stripe. Examination should focus
\\p
Figure 16. Estimation of vertical cup-to-disc ratio (A) Delineation of limits of optic nerve disc and cup, (B) estimation of cup-to-disc ratio
(CDR); this is estimated by imagining a grid that divides the disc into 10 vertical portions and counting the number of grids occupied by the cup.
Above example's CDR is approximately 0.5
kip it, .11 I R.Avyy I 211C1 LUIIIVI I
on evaluating the course of the vessels; caliber of the
arteries in comparison to the veins (normally 2:3 to 4:5);
presence of pressure effects of the arteries on the more
pliant veins at areas of their intersection (indentation
or displacement of the veins); transparency of the
vessels; presence of focal narrowing particularly of the
arterioles; and presence of abnormal structures within or
surrounding the vessels such as atheromatous plaques,
perivascular infiltration (sheathing) or hemorrhages.
4) The retinal background is generally reddish orange in
color. The retinal pigment epithelium, blood and pigment
of the choroid contribute to the appearance of the retinal
background. Take note of changes in its color as observed
in retinal detachment or ischemic conditions. Note for
the presence of pigmented lesions or other abnormal
structures within or on the retina such as hemorrhages
and exudates (Tables 4 and 5).
5)
The macular area is located approximately 2.5 disc
diameters temporal to the optic disc. There are no
blood vessels in the area and it appears darker than the
surrounding retina. This is due to the specialized retinal
pigment epithelial cells of the macula that are taller and
more heavily pigmented. At the center of the macula is
a central depression called the fovea which may act as
a convex mirror and produce a light reflection known
as the foveal reflex. As with other areas of the retina, it
is important to take note of the presence of abnormal
pigmentation as well as other structures such as exudates
and hemorrhages which may prevent the appearance of
the foveal reflex.
Table 4. Yellow-White Lesions on the Retina
Yellow-White
Lesions
Distinctive
Ophthalmoscopic
Features
Common Associated
Conditions
Hard Exudate
Deep yellow with
sharp margins, often
circinate
Diabetes, hypertension
von Hippel Lindau
disease, radiation
Soft Exudate
Fluffy gray-white;
usually near optic disc
Hypertension, diabetes,
connective tissue
disease, HIV
Drusen
Clusters of yelloworange spots, usually
centered around
fovea
Age-related macular
degeneration
Laser Marks
Clusters of yellowwhite spots, usually
uniform in size and
regularly distributed in
entire retina or around
macular area
Post retinal
photocoagulation
Photo
4 EYE EXAMINATION
Table 5. Hemorrhages (red lesions) commonly observed in the fundus
Hemorrhages
Source
Common Associated
Conditions
Dot Hemorrhages
Bleeding from capillaries
Diabetes
Flame Hemorrhages
Bleeding from superficial precapillary arterioles, small
veins
Hypertension. retinal
vein occlusion. blood
dyscrasia. trauma
Boat Hemorrhage
Bleeding from large
superficial retinal veins into
the space between the retina
and vitreous: sometimes
these bleeds break into the
vitreous cavity
Trauma, blood
dyscrasia. sudden
increase in intracranial
pressure
Vitreous Hemorrhage
Bleeding from superficial
retinal vessels or vessels on
a fibrovascular stalk
extending into the vitreous
Diabetes. hypertension.
trauma
Su bmacular/
subfoveal
Hemorrhage
Bleeding from choroidal
vessels under the fovea
Age-related macular
degeneration
Phot0911111.
Reporting of Fundus Findings
Findings on fundus examination should be reported in a systematic manner. Table 6 shows a listing of the normal and common
abnormal findings encountered when performing a fundus examination.
Table 6. Listing of Normal and Common Abnormal Fundus Findings
Red Orange Reflex (ROR)
present
dull or absent (cornea and lens opacities, retinal
detachment)
Media
clear
hazy
Optic Disc
disc margins
color
shape
cup to disc ratio (CDR)
sharp/distinct
yellowish orange to creamy pink
round or oval
< 0.5
blurred/indistinct (papilledema, papillitis)
pale (optic atrophy)
AV ratio
2:3 to 4:5
narrowed arteries, AV nicking and AV crossing
defects
Median light reflex
normal median light reflex
widened arteriolar median reflex (chronic
hypertension)
red orange
—
gray, pale (retinal detachment)
pale (central retinal artery occlusion)
absent
—
-
pigmentation
> 0.5 (glaucoma)
Retinal Circulation
Retinal Background
color
pigment changes.
hemorrhages and
exudates
-
hemorrhages (diabetes. hypertension)
exudates (diabetes, chronic hypertension)
Macula
vessels
exudates
hemorrhages
drusen
absent
absent
absent
absent
present (neovascularization)
macular star (hypertension)
present (macular degeneration)
present (macular degeneration)
fovea! reflex
present
absent
SUMMARY
Acquiring the skills to be able to properly perform the basic
eye examination will allow physicians to recognize potentially
vision threatening conditions early so that such cases are
referred to the ophthalmologist for appropriate management.
Summary of the steps in performing the basic eye exam is
listed in Table 7.
The following is an example of an eye exam report of a 54/M
patient with Left Lateral Rectus Palsy.
VA
OD
OS
Sc
6112
PH
617.5
NV
J5
6115
617.5
J5
T OD soft
OS
soft
000111111mIeftioi
1/4,
Table 7. Summary of conduct of basic eye exam
Pupils equal and briskly reactive to light
Intact direct and consensual light reflex
(-) RAPD
(+) L esotropia
1
Measure the distance and near visual acuity
2.
Inspect the lids. ocular adnexae. Palpate the orbit if
necessary.
3.
Inspect the conjunctiva, sclera. cornea and iris.
4.
Inspect the pupil and check the pupillary reflexes.
5.
Check the ocular alignment and test the extraocular
movements.
OD
6.
Perform tonometry.
OD
7.
Examine the fundus (red orange reflex, disc. vessels, retinal
background and macula.
EOMs
It><)1 MX I
F
OS
(+) diplopia on
left gazes with
version: (-)
diplopia with
duction test
(+)ROR, pink disk with distinct borders, CD 0.4, AV 2:3,
hemorrhages, exudates. good fovea! reflex
(+)ROR pink disk with distinct borders, CD 0.4, AV 2:3,
OS (-) hemorrhages, exudates. good foveal reflex
4 EYE EXAMINATION
A. replace the Snellen Chart since it is possible that he is
just not familiar with its figures
B. instruct the patient to count your extended fingers at
a distance less than one meter
C. Shine your penlight on his left eye to check for
presence of pupillary light reflexes
D. Repeat visual acuity testing, this time asking patient
to look thru a pinhole
RECOMMENDED FOLLOW-UP
ACTIVITY
This self-instructional material should be utilized as a guide
to identify specific areas that should be focused on by the
student concerning the Basic Eye Examination. It should
be supplemented by the following small group activities to
maximize the learning experience: (1) a demo-return demo
session with a faculty member and (2) examination of patients
at the General Clinic under the supervision of a faculty member.
Students are further encouraged to practice the examination
skills during their self-study session.
Shown below is a gross picture of the patient's left eye.
Based on the picture below, which of listed findings are
present in this patient (may have more than one answer
A. round, normal sized pupil
B. Mild redness of the conjunctiva
C. Clear cornea
D. Presence of opacity in pupillary area
3.
REFERENCES
1. Chandrasekhar, Ai. Eye Exam Lectures. September 17,
2002: http://www.meddean.luc.edu/lumen/MedEd/
medicine/pulmonar/pd/eye (accessed April 15, 2011).
2. Hamrah, P and Pavan-Langston, D. Ocular Examination
Techniques and Diagnostic Tests.
In:
Manual of
Ocular Diagnosis and Therapy. Pavan-Langston, D. (ed).
Philadelphia: Lippincott Williams and Wilkins. 6th ed. 2008.
chap 1: 1-35.
3. Root, T. Physical Exam. In: The Eyes Have It. httpi/www.
ophthlbook.com (accessed September 30, 2008).
4. Riley, HD. Using the Direct Ophthalmoscope. January,
2007:
http://www.opt.indiana.edu/Riley/HomePage/
Direct_OscopeiText_Direct_Oscopt (accessed April 20,
2011).
5. The Eye Examination. In: Basic Ophthalmology for Medical
Students and Primary Care Residents. Berson, FG. (exec ed).
San Francisco: American Academy of Ophthalmology.
1993. chap 1: 1-26.
L.
4.
Shown below is a diagram of patient looking at straight
gaze.
SELF-TEST
Case. A 23 year old patient consults for decrease in vision of
his left eye after hitting his left temple against a lamp post. He
has been wearing soft contact lenses for both eyes for the past
five years.
1. After taking his history, the first thing that should be
done is
A. ask patient to remove his contact lenses
B. take the patient's visual acuity without removing his
contact lenses
C. palpate the patient's orbital rim for any fractures
D. palpate the left globe to rule out globe rupture
2.
On visual acuity testing, the patient was unable to read
even the first line of the Snellen chart with his left eye
despite moving him closer to a distance of 1 meter. You
should
Based on this diagram, you conclude that the patient has
A. Left esotropia
B. Left hypertropia
C. Right exotropia
D. Right hypotropia
5.
On EOM testing, you note that the patient is unable to
abduct his left eye. Movement was full on all positions
of gaze for the right eye. This would imply weakness of
his left
A. lateral rectus
B. medial rectus
C. inferior rectus
D. superior rectus
5.
The left eye was hypotonic on palpation. To get a more
accurate 10P, the best instrument that should be used
would be
A. Schiotz tonometer
B. Non-contact tonometer
C. Applanation tonometer
D. None of these, since patient has history of trauma to
the eye
7.
You attempt to do funduscopy and note the absence of
ROR on the involved eye. Fundus exam was however
possible on the opposite eye as shown below. True
regarding this patient's fundus would be presence of
(may have more than one answer)
A. normal retinal background
B. enlarged CDR
C. tilted disc with scleral crescent
D. retinal pigment abnormalities
E. normal vasculature
F. abnormal macular area
Answers to Self-Test on page 220.
4 EYE EXAMINATION
• Disor ers o t e ornea
Ruben Urn Bon Siong, MD
INTRODUCTION
phis instructional material intends to serve as supplementary reading for the medical students and focuses primarily on pray( in
the knowledge of how corneal pathologies affect vision and of the common corneal diseases or problems that can affect
vision. The discussion is divided into major headings based on how certain corneal disorders affect the two main functions of
the cornea as mentioned below. The aim is to make the student appreciate the close relationship between the structure and
function of the cornea, and know the common etiologies that can affect each function. It is not the main aim of this material to
make the student adept in diagnosing these conditions since specialized instruments and tests, which are not available to the
student, are usually required to make an accurate diagnosis. Pictures of typical cases are also presented. Students are however
encouraged to apply the knowledge that they will acquire from this instructional material to actual and simulated clinical cases
during their rotation. The student is advised to review the anatomy and physiology of the cornea, as well as the principles and
definitions of basic physical optics before going through this SIM.
OBJECTIVES
After going through this material, the student is expected to:
1.
Explain how corneal pathologies and diseases affect vision.
2.
Discuss the common corneal diseases that affect vision.
3.
Formulate differential diagnosis of corneal diseases that affect vision.
CONTENT
I. Functions of the cornea
II. Common causes of blurring of vision due to corneal diseases
A. Disruption in the transmission of light
1. Corneal scars
2. Corneal edema
3. Corneal deposits
4. Corneal melt
5. Corneal tumors
B. Disturbance in the refraction of light
1. Abnormalities of the corneal epithelium and tear film
2. Abnormalities of corneal size/ shape / curvature
III. Guide to diagnosis of corneal diseases
IV. Principles of management of corneal diseases
The two main refracting components of the eye are the cornea
and the lens. Of the two, the cornea, together with the pre
corneal tear film is responsible for two-thirds of the total refractive
power of the eye, thus making it more powerful than the lens.
I. MAIN FUNCTIONS OF THE
CORNEA
1.
Transmission of Light: The cornea is a highly transparent
tissue and this is largely due to its unique anatomy. It
is devoid of blood vessels and has a paucity of cellular
elements. It is composed of collagen fibrils with uniform
diameter and uniform spacing and arrangement. In
between the collagen fibrils is the extracellular matrix
ground substance composed of proteoglycans (PG) with
a constant water content of 78%, a lot less than the water
content of other tissues of the body. This relative dryness
or deturgescence is responsible for maintaining the
homogeneity of the collagen fibrils. Since the diameter of
the collagen fibrils and the distance between them is less
thane the wavelength of visible light, light is notdiffracted
and is therefore transmitted (Figure 1). Any disruption
of the normal configuration of the collagen fibrils will
therefore cause failure in the efficient transmission of Ugh'.
and the cornea will appear hazy or opaque.
A-
2.
Refraction of Light: In order for light entering the eye to oe
focused on the retina, incoming parallel light rays have to be
bent or refracted. This is made possible by the smooth anterior
shape and curvature (measured in radius of curvature;
(Figure 2) of the cornea which is convex (thus light is bent
inward or converged) and by the difference in the indices of
refraction between air, tear film, cornea and aqueous humor.
Therefore any disturbance in the shape or curvature of the
cornea and the indices of refraction of the different structures
can cause the failure of the converged light rays to be focused
on the retina leading to blurry vision.
radius of curvature
Figure 2. Radius of curvature the cornea
II. COMMON CAUSES OF BLURRING
OF VISION DUE TO CORNEAL
PATHOLOGY OR DISEASES
A. Conditions causing Disruption in the
•
• • • • • • 0 • • •
• • • • • • • • • • • •
• • • • • • • • • • •
•
•
Transmission of Light
0411 • • • • • • • •
1. Corneal Scars
• • )10 • • •
Corneal scars are usually tan to white in color. They may involve
different areas of the cornea and may come in different shapes
and sizes depending on the etiology and pathology (Figure 3).
Scars are usually formed after an inflammatory process when
fibrosis sets in. In fibrosis, new and abnormal collagen fibrils and
other cellular elements are laid down in a "haphazard" manner,
.4• • • •ii • •
i• •
• • • • • • •
• •
•
Figure 1. Theory of comeal transparency. Since the oiameter of tne
collagen fibrils (black dots) and the distance between them is homogenous
(arrows) and measures less than one-half the wavelength of visible light (top),
light is not diffracted and is therefore transmitted through the cornea.
Figure. 3 (A) Typical appearance of corneal scar, (B) Hypertrophic corneal scar
5
DISTURBANCE IN VISION 15.1 Disorders of the cornea
49
causing the disruption of the normal homogenous arrangement
of the collagen fibrils. This prevents proper transmission of light
and is reflected back instead; thus, making the cornea appear
opaque.
Causes of corneal scar:
a.
Microbial keratitis: These are infections of the cornea
which can be caused by viruses, bacteria, fungi and
protozoans (Figure 4). Invasion of microorganisms
into the cornea induces an intense inflammatory
response and with the actions of microbial toxins and
enzymes, causes corneal tissue necrosis, melting and
sometimes rupture of the cornea. During the active
infection, corneal opacity is associated with marked
eye redness, tearing and photophobia. Once healing
ensues, either due to treatment or due to the natural
course of the disease, redness and other symptoms
will disappear except for blurring of vision (more so
if lesion is overlying or affecting the pupillary area)
which perists, as it is caused by the corneal opacity.
b. Corneal trauma: This includes mechanical and
chemical injuries to the cornea and is among the major
causes of corneal problems in the Philippines. Corneal
lacerations and perforations are usually caused by sharp
objects (knife, scissors, nails, glass etc), and high velocity
projectiles (iron nails due to hammering, shattered
glass, darts, bullets etc). Most of these injuries require
surgical management in the form of corneal repair
or suturing with the goal of closing the wound and
restoring the integrity of the globe (Figure 5 A). Similar
to skin lacerations, healing will bring about fibrosis and
subsequent corneal scarring along the wound and
suture track (Figure 5 B). Depending on the extent
of involvement, vision will be variably affected either
by the opacity itself or the distortion of the shape of
the cornea. Acid chemical burns of the cornea cause
denaturation and precipitation of the collagen and lead
to scar formation. In alkali burn, corneal destruction is
generally more severe since it causes corneal necrosis
and melting due to its ability to penetrate deeply into
the cornea. Contact burns from molten metal and
other heated materials can also cause severe corneal
injuries and scarring.
Figure 5. (A) Sutured comeal laceration, (B) Comeal scar from healed
corneal laceration
Figure 4. (A) Active fungal keratitis, (B) Acute bacterial keratitis
c. Exposure keratopathy: The cornea is prone to
desiccation if left exposed to the environment.
Failure of the lids to close properly (lagophthalmos)
will lead to a condition called exposure keratopathy
wherein the exposed cornea (usually the inferior
half) opacifies due to the drying effect (Figure 6).
This condition can also lead to severe scarring if
secondary microbial keratitis occurs. This problem
is usually seen in comatose patients, those with
CN VII palsies, lid and orbital deformities, acute
proptosis, nocturnal exposure etc. Bilateral inferior
corneal scars are commonly seen in patients with a
history of severe measles occuring in childhood. The
condition usually starts as exposure keratitis in a very
sick child compounded by dehydration, pneumonia,
malnutrition, immunodeficiency, vitamin A
deficiency and lack of tears. The exposed cornea
develops secondary bacterial infection and usually
ends in corneal rupture and subsequent scarring. It
should be noted that exposure keratopathy can be
prevented.
Figure 6. Exposure keratopathy secondary to lagophthalmos due
to CN VII palsy
d.
Lid margin and lash disorders: Abnormalities of the
lid margins may cause misdirection of the eye lashes
towards the cornea.The constant and chronic rubbing
can lead to surface vascularization and eventual
scarring. This condition is seen in trichiasis, trachoma,
chronic blepharitis, epiblepharon, entropion. It is also
as sequelae of Stevens Johnson Syndrome.
e.
Congenital corneal scars: Corneal scars (leukoma)
can develop while in utero due to anomalies during
embryogenesis. Peter's anomaly is part of a spectrum
of disorders known as anterior segment dysgenesis
and presents as central corneal leukoma with defects
in the posterior stroma, Descemet's membrane and
the corneal endothelium. Strands of iris may attach to
the posterior border of the leukoma. This condition
is bilateral in 80% of cases and more than half have
glaucoma.
2. Corneal Edema
The corneal endothelium is the single most important
structure of the cornea and is responsible for the active
pumping of water away from the cornea to the aqueous
humor, thereby maintaining corneal clarity. the human
corneal endothelial layer does not regenerate when lost or
injured and the endothelial cells decrease in number as a
person ages. An adequate number of endothelial cells must
be present throughout life for the endothelium to function
properly. When the cell density dips below a critical level, the
direction of the flow of water is reversed and the cornea will
retain water and swell like a sponge (corneal decompensation)
resulting in the disruption of the normal arrangement of the
collagen fibrils.The edematous and markedly thickened cornea
becomes hazy or ground glass in appearance. Affectation may
be diffuse or focal. Patients will usually complain of marked
blurring of vision, recurrent eye pain, redness, foreign body
sensation and tearing.
Causes of corneal edema:
a. Endothelial dystrophy: Infants with bilateral diffuse
corneal haziness and ground glass appearance,
thickened cornea with normal corneal diameter and
eye pressure and absence of birth trauma should be
suspected to have Congenital Hereditary Endothelial
Dystrophy (Figure 7). Fuchs' Endothelial Dystrophy,
on the other hand, is usually seen after age 50,
more so in females than males. These patients have
an abnormally high rate of endothelial cell loss as
compared to the normal population. All cases will
initially present with central corneal guttata located at
the posterior side of the cornea. The corneal guttata
will increase in number and spread toward the
periphery. With the decrease in the total endothelial
cell density, corneal decompensation may ensue.
Figure 7. Congenital hereditary endothelial dystrophy (CHED)
5 DISTURBANCE IN VISION 1 5.1 Disorders of the Cornea 1111
b.
c.
Surgical trauma : Anterior segment intraocular
surgery such as cataract extraction can cause trauma
to the corneal endothelium (Figure 8). Direct trauma
may come in the form of mechanical contact of
instruments or lens implants or intraocular structures
like vitreous to the corneal endothelium. Trauma
may also be indirect like inadvertent introduction of
noxious chemicals into the eye.
Chronic elevation of intraocular pressure (glaucoma):
Abnormally high eye pressure can affect corneal
metabolism and damage the corneal endothelium
by causing relative hypoxia and hypoglycemia in
the anterior chamber of the eye. Since the cornea is
avascular, the corneal endothelium depends on the
aqueous humor for its nutrients and oxygen supply.
Corneal decompensation is seen in both congenital
glaucoma in children and chronic glaucoma in adults.
Figure 9. (A) Granular Type 3 Stromal dystrophy, (B) Avelino Stromal
dYslroPhY
b.
Figure 8. Post cataract extraction corneal edema
3. Corneal Deposits
Aside from acting like a sponge, the cornea is also like a sieve.
Substances can get trapped within the corneal collagen
lamellae or within intracytoplasmic vacuoles or organelles and
cause opacities that will lead to blurring of vision.
Causes of corneal deposits:
a. Corneal dystrophy (Figure 9): This is a large group of
hereditary corneal disorders sharing several common
features like bilateral and symmetrical involvement,
absence of any form of inflammation, absence of
vascularization, and presence of proven or suspected
chromosomal abnormalities. Chromosomal defects
cause problems in normal metabolism leading to
deposition of substances in different layers of the
cornea. Diagnosis is based on clinical presentation
and
histopathology. Each form affects vision
differently primarily due to difference in appearance
and location.
Lipid keratopathy: This is usually seen in vascularized
corneal scars of various etiologies (trauma, infection,
immune-mediated). The invasion of blood vessels
into the cornea will lead to leakage and eventual
deposition of glycoproteins, cholesterol and neutral
fat into the cornea. The opacities are usually yellow
or cream-colored located at the corneal stromal layer
typically associated with a branch or several branches
of blood vessels at the core (Figure 10)
Figure 10. Lipid keratopathy secondary to herpes simples keratitis
c.
Calcific band keratopathy: This is usually seen in eyes
with chronic inflammation like anterior uyf3itis and
or lysosome-like intracytnnintmi
or these
conditions are rare and are autosomal recessive.
Examples are systemic mucopolysaccharidoses,
hyper- and hypolipoproteinemias, sphingolipidoses,
in phosphate metabolism. Calcium hydroxyapatite
particles deposit at the Bowman's layer starting
at the 3 and 9 o'clock areas. These eventually meet
at the center over time to form a white horizontal
band across the cornea with a Swiss cheese pattern
d.
sLruc-ture
a result of a single enzyme defect. Most
in patients with high serum calcium and disorders
mucolipidoses, and an array of protein and amino
acid metabolic disorders.
(Figure 11).
4. Corneal Melt
Corneal staining: Hyphema (blood in the anterior
chamber) coupled with high eye pressure will lead
to deposition of heme in the corneal stroma. This
appears as a central golden brown to yellow discoid
opacity on the cornea (Figure 12).
Apart from microbial keratitis, corneal melt or necrosis can be
brought about by Vitamin A deficiency, chemical burn and
autoimmmune diseases (Figure 13). Prompt and appropriate
therapy may arrest the process and lead to healing and fibrosis,
leaving the cornea scarred and opacified. Corneal melting
is brought about by a complex interaction and cascade
of enzymatic and molecular events involving a myriad of
substances and is beyond the scope of this material.
Figure 11. Calcific band keratopathy
Figure 13.
Autcommune peripheral corneal melting
Causes of corneal melt:
a.
Figure 12.
e.
Corneal staining secondary to heme deposition
Metabolic disorders: Systemic metabolic disorders
can cause alterations in corneal clarity due to
abnormal storage of metabolic substances within
the epithelium, stroma or endothelium. Abnormal
substances typically accumulate in lysosomes
Vitamin A deficiency: this leads to xerophthalmia,
which is responsible for at least 10,000 — 20,000
new cases of blindness worldwide each year. At
greatest risk are the malnourished infants and babies
born to Vitamin A-deficient mothers, especially if
the infant has another biological stressor such as
measles or diarrhea. Prolonged vitamin A deficiency
leads to external eye involvement, including xerosis
(dryness of the conjunctiva and cornea), metaplastic
keratinization of areas of the conjunctiva (Bitot spots),
corneal ulcers and scars and eventually, diffuse
corneal necrosis (keratomalacia).
b.
Alkali chemical burn: Strong alkali raise the pH of
tissues and cause saponification of fatty acids in
cell membranes and ultimately cellular disruption.
5
DISTURBANCE IN VISION 1 5.1 Disorders of the Cornea
Egi
Alkaline solutions rapidly penetrate the corneal
stroma, destroying the proteoglycan ground
substance and collagen fibers. It also destroys the
limbal stem cells, preventing normal epithelial
healing. Severe scarring and corneal vascularization
are seen in severe cases (Figure 14).
lesion that behaves malignantly. It is a wing-shaped
or triangular fold of conjunctiva and fibrovascular
tissue with its apex invading the superficial cornea
(Figure 15 C). Strong correlation with UV exposure
has been documented. It affects vision in two ways:
(1) it grows progressively towards the center of the
cornea and covers the pupil area; (2) it pulls on the
peripheral cornea which causes distortion of Its
shape resulting to astigmatism.
Figure 14. Comeal scarring and vascularization due to alkali bum
5. Corneal Tumors
New growths, either benign or malignant can occur on the
ocular surface involving the cornea and conjunctiva. Vision
may or may not be affected depending on the location
of the lesion and whether or not it will interfere with the
transmission of light. These lesions are easily diagnosed by
their clinical presentation and appearance and are confirmed
by histopathology.
Causes of corneal tumors:
a.
Dermoid choristoma: This
congenital lesion typically
occurs on the inferotemporal limbus as a smooth,
elevated, tan to fleshy color, round to oval solid
mass embedded in the superficial cornea and sclera.
Dermoids are composed of fibrous tissue and hair
with sebaceous glands that is covered by conjunctival
epithelium. Epibulbar dermoids are located over the
central cornea and can severely affect vision (Figure
15 A).
b.
Corneal intraepithelial neoplasia: The lesion appears
as a translucent, gray or frosted epithelial sheet
starting from the limbus and extending onto the
cornea with fimbriated or scalloped borders and
pseudopodia-like extensions. Blurring of vision will
occur once the growing epithelial sheet reaches the
central area (Figure 15 B).
c. Pterygium: Strictly speaking, this condition is
primarily a conjunctival disorder but due to its
intimate relationship with the cornea, it will be
included here. Pterygium is a benign conjunctival
Figure 15. Comeal Tumors; (A) Dermoid choristoma, (B) Corneal and
conjunctival neoplasia, (C) Pterygium covering the pupil axis
B. Disturbance in the Refraction of Light
1. Abnormalities in the Corneal Epithelium
Film
components are abnormal, patients will complain
of dry eye symptoms even if there is adequate tear
volume. They will also complain of fluctuating vision
due to rapid evaporation and break up of the tear
film in between blinking. In some patients, all three
and Tear
The main refractive surface of the eye is the anterior cornea.
An important prerequisite for any refractive surface is that
it should be smooth. Presence of cracks, smudges and
the like will cause degradation in the quality of the image.
The outermost layer of the corneal epithelium per se is not
smooth. When seen under scanning electron microscopy,
the surface is thrown into dense microvilli. To make the
corneal surface a perfect refractive surface, it is intimately
related to the tear film, which coats the anterior surface
of the cornea. Additionally, the tear film has a high index
of refraction when compared to air. This physical attribute
allows further convergence of light rays as it passes from
air then through the tear film and the cornea. Thus, any
abnormalities of the tear film and/or the corneal surface
epithelium, especially over the central area overlying the
pupil, can cause blurring of vision.
components are affected. As in dry eye syndrome, the
corneal surface epithelium can also be injured. Mucin
deficiency can be caused by vitamin A deficiency,
severe dry eye, alkali chemical burn, Stevens-Johnson
syndrome (Figure 17), and cicatricial pemphigoid.
Lipid deficiency can be caused by blepharitis and
meibomian gland dysfunction.
Causes of abnormalities in corneal epithelium and tear
film:
a. Deficiency in tear volume: Dry eye syndrome is a
common disorder with different etiologies wherein
there is decreased tear production. Most cases are
mild and just cause occasional symptoms. In severe
and chronic cases however, it can cause irregularities
on the corneal surface due to microtrauma to
the epithelium (Figure 16). Patients complains of
dryness, foreign body sensation, burning sensation
and blurring of vision. This condition is also known
as keratoconjunctivitis sicca.
Figure 17. Severe dry eye disease with ocular surface damage due to
Stevens-Johnson syndrome
keratitis: This pertains to microtrauma to the
corneal surface epithelium secondary to contact
with chemicals (such as alcohol-based products like
hair spray) or topical medications (active ingredient,
preservatives or both). Presence of these superficial
punctate lesions makes the surface irregular and will
thus affect vision.
C. Toxic
2.
Abnormalities of Corneal Size/Shape/Curvature
The total refractive power of the eye is around 60 diopters (D).
The cornea and tear film together contribute 40 D and
the rest is contributed by the crystalline lens. This 40 D
is a result of a constant range of radii of curvature and
indices of refraction of the cornea as provided by normal
anatomy. If the radius of curvature of the cornea decreases
(steep cornea), light rays will converge more, moving the
Figure 16. Dry eye disease with ocular surface damage (stained with
Rose Bengal dye)
b.
Tear quality abnormalities: The tear film is a complex
structure composed of three main components: lipid,
aqueous and mucin. The lipid component prevents
rapid tear evaporation and mucin allows molecular
interaction between the tear film and the corneal
surface (surface tension). If one or both of these
focal plane in front of the retina, resulting in myopia. If the
radius of curvature increases (flat cornea), the opposite
effect will occur, which is termed as hyperopia. If light
rays pass through a cornea with variable radii of curvature,
light rays will converge on different focal planes. This
is known as astigmatism. Myopia, hyperopia and
astigmatism are collectively known as errors of refraction
and are discussed in another chapter of this SIM. Only
corneal diseases and disorders that result in severe errors
of refraction and therefore severe blurring of vision will be
discussed in this section.
5
DISTURBANCE IN VISION
I Disorders of the Cornea 1111
Causes of abnormalities of corneal size, shape or curvature:
a. Keratoconus: This is a common disorder where the
central or paracentral cornea undergoes progressive
thinning and bulging, so that the cornea takes on the
shape of a cone (Figure 18). Hereditary pattern is
not prominent. Its etiology is unknown and is most
likely, multifactorial. Due to the progressive bulging
of the cornea, the cornea becomes abnormally and
irregularly steep resulting in very severe myopia and
astigmatism. It is almost always bilateral but usually
asymmetrical. The patient complains of rapidly
progressive blurring of vision during adolescent
years which then stabilizes when the patient attain
full growth. The cornea usually appears grossly clear,
except in severe cases where an apical scar is visible.
On profile view, one may see a focal area of bulging
which is best appreciated when examined using the
slit lamp biomicroscope.
III. GUIDE TO DIAGNOSIS
It was mentioned at the start of this chapter that one needs
specialized equipments to arrive at an accurate diagnosis. The
lack of such equipment should not be a hindrance for a rational
differential diagnosis to be formulated as to what corneal
condition is causing the blurring of vision. All one needs are a
good history, an appropriate light source, an observant
eye and a firm foundation of the basic pathophysiology of
corneal diseases as discussed above.
When blurring of vision due to a corneal pathology
is suspected, the first step is to examine the cornea
with an appropriate light source such as a penlight, an
ophthalmoscope or a transilluminator. Determine if the
cornea is clear/transparent or not. If an opacity is observed,
one has to decide if it is due to a corneal scar, edema,
deposition of substances, corneal melt or tumor growth. If
the cornea looks clear, the blurring of vision can be due to
an abnormal corneal shape and curvature or to problems
with the tear film and surface epithelium.
With Corneal Opacity
Figure 18. (A) Keratoconus with acute hydrops, (B) Slit lamp view of
comeal profile in keratoconus
b. Corneal distortion due to peripheral scars or lesions:
This is to emphasize the fact that you do not need
to have direct involvement, like a scar, on the center
of the cornea to cause disturbance in vision. This
concept becomes easy to understand if one imagines
the cornea as a silver mylar balloon. By looking at
your reflection at the flat surface of the balloon,
you will notice that the image can be distorted by
either pulling or pushing the sides of the balloon,
because by doing so, you change the curvature of
the center. Always remember that the cornea is one
whole integral structure. Flattening of one meridian
causes a corresponding steepening in the meridian
90 degrees away and vice versa. This effect is seen in
pterygium, scars from peripheral corneal perforations,
effect of sutures after cataract surgery and peripheral
thinning disorders.
If the corneal opacity has been present since birth, consider
a congenital etiology like Peter's anomaly or sclero-cornea.
If the opacity started in infancy or early childhood, with a
history of malnutrition or systemic illness at the onset of the
eye problem, measles-related microbial keratitis leading to
scar is an important differential diagnosis. Equally probable is
the differential diagnosis of xerophthalmia with all its ensuing
corneal complications. These two conditions usually involve
both eyes.
If there is a history of mechanical trauma or of the eye being
injured by foreign bodies, then consider scars from previous
corneal infections like central microbial keratitis or from
corneal lacerations or perforations. Central microbial keratitis
is also associated with improper use of soft contact lenses.
Chemical (acid and alkali) burn usually manifests as diffuse
corneal haze or cloudiness, which may or may not lead to frank
melting of the cornea.
If there is inability of total lid closure, exposure keratopathy
should be entertained. If you see corneal opacities
accompanied by lid margin irregularity and inward turning
of lashes, you should think of trichiasis, trachoma, entropion,
chronic blepharitis and sequelae of Stevens Johnson
Syndrome.
Corneal edema gives the cornea a diffuse ground glass
appearance. Bilateral involvement since birth is due to congenital
hereditary endothelial dystrophy. Bilateral involvement noted in
the middle-aged or the elderly is most probably due to Fuchs'
endothelial dystrophy. If the patient had undergone cataract
extraction surgery, then it is most probably induced by the
surgery leading to what is known as pseudophakic bullous
keratopathy. If the corneal edema is accompanied by acute rise in
intraocular pressure or chronically high intraocular pressure, then
the cause is glaucoma. Corneal edema is typically accompanied
by recurrent eye pain, foreign body sensation and tearing due to
bullae formation and sloughing of the corneal epithelium.
Opacities on the cornea that are golden brown to yellow in
color with a previous history of blunt eye trauma is probably
due to blood staining as a complication of hyphema. Cream
or ivory colored corneal opacities accompanied by blood
vessels growing into the cornea are due to lipid keratopathy.
This is usually a sequelae of interstitial keratitis due to Herpes
simplex virus, Herpes zoster virus, tuberculosis or syphilis.
Horizontal dirty-white band-shaped Swiss cheese-like opacity
involving the exposed portion of the cornea is due to calcium
deposition (band keratopathy). This condition is usually seen
in eyes with a chronic history of inflammation such as uveitis.
Symmetrical corneal opacities found in a patient with a family
history of the same condition should make one consider the
large group of corneal dystrophies. Discrete bread crumblike white deposits is typical of granular stromal dystrophy.
Macular stromal dystrophy presents as diffuse central corneal
haze not accompanied by thickening of the cornea. Lattice
stromal dystrophy is difficult to diagnose with just a pen light
but should be suspected if recurrent eye pain is elicited in
the history. Bilateral corneal opacities seen in patients with
multiple systemic anomalies are usually related to metabolic
storage diseases like systemic mucopolysaccharidoses, hyper
and hypolipoproteinemias, sphingolipidoses, mucolipidoses,
and an array of protein and amino acid metabolic disorders.
Tumors or growths on the cornea can easily be seen by the
naked eye. If the mass is a triangular fleshy vascular conjunctival
mass with the apex growing towards the central area of the
conjunctiva from the nasal side of the eye, then this is most
probably a pterygium. If the mass is elevated, tan-colored,
located at the outer lower quadrant of the cornea and is
present at birth, the mass is usually a dermoid choristoma. If an
elderly patient complains of blurring of vision and you see an
elevated gelatinous vascular mass from the limbus extending
to the visual axis, then you have to think of a conjunctival
neoplasia.
epithelium may have occurred due to lack of normal tears in
patients with severe dry eye disease.
Recent onset of blurring of vision in patients with long-term
use of multiple preserved eye drops may have toxic epithelial
keratitis. This is especially common in glaucoma patients
who are usually on multiple anti-glaucoma medications. This
condition is also seen in patients with a history of inadvertent
exposure of the cornea to noxious chemicals or alcohol based
agents.
If a teenager or young adult patient complains of very poor
vision and has a history of frequent change of glasses due to
rapid and progressive increase in myopia and astigmatism, one
should consider corneal thinning disorders like keratoconus.
The cornea is clear in early keratoconus and is quite difficult
to diagnose without sophisticated instruments. However, in
advanced cases, the paracentral or central conical protrusion
of the cornea can be seen by examining the profile of the
cornea or by eliciting the tenting of the lower lid margin as the
patient looks downwards (Munzon's Sign).
IV. PRINCIPLES OF
MANAGEMENT
As a rule, corneal scars are permanent. There is no medical
therapy available to turn scar tissue into normal corneal
tissue. Depending on the location, size and degree of visual
involvement, management is geared towards two goals,
either improvement of vision or cosmetic or both. To improve
vision, management is usually surgical, which may range from
manual excision to laser removal to corneal transplantation.
To improve appearance, corneal scars may be covered with
cosmetic contact lenses, dyed by tattooing or removed by
corneal transplantation (Figure 19).
No Corneal Opacity
If a middle-aged female patient complains of fluctuating
blurring of vision occurring by the later part of the day,
with symptoms of eye discomfort and irritation, a tear film
abnormality must be considered. This consideration is most
likely if the symptoms are associated with feelings of eye
fatigue, dryness and burning sensation. If the blurring is not
fluctuating and fairly constant, desiccation of the surface
Figure 19. Clear corneal graft. Post penetrating keratoplasty
(full thickness corneal transplant). Note radial 10-0 nylon sutures.
5
DISTURBANCE IN VISION I 5.1 Disorders of the Cornea El
Corneal edema due to endothelial damage or dysfunction
and is also permanent because the cells do not regenerate.
Definitive treatment is corneal transplantation. The role of
medical therapy is to minimize pain and discomfort and to
prevent secondary infections. If it is due to high eye pressure,
then the therapy should be directed towards lowering the
pressure to appropriate levels.
Disorders that can disrupt the normal transmission of light are
corneal scars, corneal edema, corneal deposits, corneal melt
and corneal tumors. Scars are caused by infection, trauma,
exposure, vascularization or can be congenital. Corneal edema
can be congenital, due to surgical and non surgical trauma
or due to chronic glaucoma. Deposits in the cornea can be
caused by metabolic products, calcium, hemoglobin, iron,
lipids, proteins, amyloid and other amorphous substances.
Corneal deposits due to systemic metabolic disorders or from Corneal melting caused by vitamin A deficiency, chemical
corneal dystrophy may recur after a corneal transplant since the burn or autoimmune diseases can lead to permanent corneal
underlying condition is not corrected. Corneal transplantation scarring. Masses on the cornea like dermoid, pterygium and
is reserved only for those conditions with significant visual neoplasia can block the transmission of light or alter the shape
loss. Calcium deposits can be removed by chelation since the of the cornea.
location is superficial while deeper ones like lipid and heme
cannot be removed. Corneal transplantation may be the only Disorders of the cornea that can disturb the refraction of
light includes dry eye disease, corneal epithelial dysfunction,
option.
and corneal disorders that affect its normal size, shape and
In treating corneal melting, the underlying etiology should curvature.
immediately be addressed. Surgical management is usually
done later to treat sequelae, unless it is for an emergency
procedure aimed to restore the integrity of the globe. Corneal
transplantation is usually done.
Corneal masses are usually treated by surgical removal if the
indications for surgery are present. Sometimes corneal grafts
are also used to restore corneal clarity.
Dry eye syndrome is treated by using topical lubricating agents
and/or by preserving existing natural tears by preventing tear
drainage. With adequate lubrication, the health of the corneal
epithelium will be restored. Moreover, all other possible risk
factors that may aggravate tear quality should be removed
or minimized. This principle also holds true in treating toxic
keratitis.
There are several treatment options for corneal disorders with
abnormal shape or curvature in order to improve vision. The
goal is to correct the refractive errors so that the image will
be sharply focused on the retina. This is done by employing
optical appliances or by surgically altering the cornea so that
the shape will be restored to normal. Depending on the
indications, choices may include glasses and contact lenses,
incisional or laser refractive procedures, or corneal grafting and
transplantation. A recent treatment option for keratoconus
is corneal collagen cross-linking wherein topical riboflavin
drops are applied on the cornea and exposed to ultraviolet
light which promotes formation of new collagen bonds.
This procedure increases corneal rigidity to stop or delay the
progression of keratoconus.
SUMMARY
The main function of the cornea is to transmit and refract light.
If the normal anatomy of the cornea is altered, it will lead to
blurring of vision.
Management of these disorders involves the restoration of
the cornea's normal anatomy primarily through corneal tissue
transplantation; excision of abnormal growths or tissues;
control or removal of etiologic and contributing factors;
surgical interventions to improve corneal shape and curvature
and use of optical appliances to enhance the transmission and
refraction of light into the eye.
REFERENCES
2.
Krachmer JH, Mannis MJ, Holland EJ. (Eds) Cornea . St
Louis MO, Mosby ,1997, Vol 1 to 3.
Smolin G,Thoft RA. (Eds) The Cornea: Scientific Foundations
and Clinical Practice, 3rd Ed, Little, Brown & Company, 1994
SELF-TEST
1.
Two thirds of the refractive power of the eye is supplied
by the:
A. cornea
B. lens
C. tear film
D. vitreous
2.
To maintain the transparency of the cornea, the water
content should be:
A. 50%
B. 67%
C. 78%
D. 95%
3.
The following affects the normal refraction of light into
the eye, EXCEPT:
A. color of the iris
B. index of refraction
C. quality of the corneal surface
D. radius of curvature of the cornea
1.
The major causes of corneal scarring in the Philippines
is/are:
A.
B.
C.
D.
5.
anterior segment dysgenesis
corneal dystrophy
corneal infection and trauma
surgical complications
Which statement about the corneal endothelium is
FALSE?
A. The corneal endothelium can be damaged by
intraocular surgery
B. The corneal endothelium is a monolayer of cells
lining the posterior surface of the cornea
C. The corneal endothelium is responsible for actively
pumping water out of the corneal stroma
D. The human corneal endothelium retains its mitotic
activity throughout life
6.
What is the main mechanism of corneal scarring in a
patient suffering from measles?
A. deposition of blood in the cornea
B. direct invasion of the cornea by measles virus
C. exposure of the cornea due to poor lid closure with
secondary bacterial infection
D. misdirection of eye lashes towards the cornea
7. White horizontal band-like opacity across the cornea
with Swiss-cheese pattern is due to deposition of what
substance ?
A.
B.
C.
D.
8.
amyloid
calcium
iron
lipid
9.
Steepening of the cornea caused by keratoconus leads
to what form of refractive error?
A.
B.
C.
D.
hyperopia and astigmatism
monocular diplopia
myopia and astigmatism
presbyopia
10. The following are treatments options on the cornea to
improve vision, EXCEPT:
A.
B.
C.
D.
corneal tattoo
corneal transplantation
excimer laser photoablation
hard contact lenses
17. You are suspecting that the patient's complaint of
problem. But
blurring of vision is due to a cornea
you cannot see any obvious corneal abnormality after
examining with a penlight. What will you do next to
confirm your suspicion?
A.
B.
C.
D.
dilate the pupils
have refraction done
measure the diameter of the cornea
request for test to measure corneal curvature
12. The patient and other family members have bilateral,
symmetrical corneal opacities. Your main differential
diagnosis is
A. bullous keratopathy
B. corneal dystrophy
C. dermoid choristoma
D. lipid keratopathy
Answer to Self Test on page 220.
Peripheral corneal lesions can cause blurring of vision
by:
A.
B.
C.
D.
blocking the transmission of light
decreasing tear production
increasing central corneal thickness
inducing astigmatism by changing the central
corneal curvature
5
DISTURBANCE IN VISION 1 5.1 Disorders of the Cornea
59
5.2 Cataract
Richard C. Kho, MD
INTRODUCTION
This self-instructional material (SIM) is designed to give an overview on cataracts. Philippine statistics on cataract suggest that
medical students will likely encounter this common ocular condition in the elderly population during their clinical rotation in
ophthalmology (and possibly in other departments as well), as it is still one of the most common causes of visual impairment
in the country'. Being inevitable with aging and hence, in all patients eventually, physicians in every specialty should acquire
some basic knowledge and skill in recognizing cataracts, giving sound advice to the patient, and making the appropriate referral.
OBJECTIVES
Upon completion of this SIM, the student should be able to discuss the following:
1. Definition of cataract
2. Etiology and associated predisposing factors for cataract formation
3. Types of cataracts
4. Symptoms of cataract
5. Gross examination and ancillary evaluation for surgical planning
6.
Principles of management
CONTENT
I.
Definition of cataract
II. Types of cataract
III. Symptoms of cataract
IV. Evaluation of cataract
V.
Ancillary tests for cataract
VI. Management of cataract
:ASE:
'our friendly neighbor tells you that his 78 year-old
grandfather who lives with him has been complaining of
)ad vision lately. Knowing that you are a senior medical
student, he wants you to drop by his house, take a look at his
grandfather and give them sound medical advice on what
`o do next. Are you up to the task?
WHAT IS A CATARACT?
(DEFINITION AND ETIOLOGY)
A cataract is defined as any opacity in the lens that precludes
optimal vision (Figure 1). Aging is the most common
cause of cataracts. The human lens is normally clear at birth
but undergoes changes that result in gradual loss of its
transparency over time. On average, a younger person's
lens should be clearer than an older person's. In reality, this
"degeneration" varies from individual to individual, with some
having relatively clear lenses well into their 60's, while others
already requiring cataract surgery in their early 40's.
Many other factors are involved in cataract formation. These
include trauma, toxins, systemic disease (e.g. diabetes, etc.),
smoking and heredity.2 There are also congenital and juvenile
cataracts that are seen in the pediatric population. The
pathophysiology of cataract formation is not fully understood
but is likely to be multi-factorial in nature. Biochemical
changes in the lens are characterized by protein aggregates
that alter its optical properties. These changes take the
form of discoloration (from yellow to brown in increasing
maturity), the appearance of vacuoles (lens hydration clefts),
and aberrant migration and enlargement of epithelial cells.
Other contributing factors include malnutrition, damage from
ultraviolet light rays, and other causes of oxidative damage
resulting in free radical formation?
Figure 1. Cataract - an opacity of the lens.
Upon history taking, you found out that the patient has
been having gradual and progressive cloudiness of distance
vision in both eyes (right eye worse than the left) over the
past several years. He notes that recently, he seems to be
able to read small prints better. He does not report any
eye pain, discharge, itchiness, redness, or tearing. He has
given up driving especially at night time, because he says
he has "difficulty with oncoming headlights': Systemically,
he reports having been diagnosed with hypertension and
diabetes for the past 6 months, both of which are fairly
controlled. Are his symptoms consistent with cataract
formation?
TYPES AND SYMPTOMATOLOGY
Cataracts usually cause a gradual decrease in visual acuity that
worsens with aging. This process of senile cataract progression
and worsening of vision may take years (or decades) and
can vary from individual to individual. Knowledge of basic
lens anatomy enhances our understanding of cataract types,
symptomatology, and surgery (Figure 2).
ANTERIOR CAPSULE
z
0
n
n
U
0
S
NM.
S
POSTERIOR CAPSULE
Figure 2. Review of basic lens architecture.
Variations in cataract description and grading system have
prompted efforts to come up with a unified scheme. The
Lens Opacities Classification System (LOCS) 111, based on
standardized photographs, is popularly used in teaching
institutions for grading and comparison of cataract severity
and type - (Figure 3)
For practical purposes, we describe three common types of
cataracts seen in the elderly population. Nuclear cataracts
are by far the most common type seen in the clinics. Around
middle age, the normal condensation process in the lens
results in a denser central portion. With further progression,
this may cause visual disturbances such as decreased acuity,
color discrimination and contrast sensitivity. In the early
stages, this type of cataract may occasionally improve near
vision--so called "phenomenon of second sight"---as there
is a myopic shift and increased focusing power of the lens
(precluding a patient from seeking early consult).This apparent
improvement in vision, however, is only temporary and will
eventually be overtaken by the progression of cataract density.
Nuclear cataracts are usually bilateral but can be asymmetric in
5
DISTURBANCE IN VISION I S2 Cataract
61
LENS OPACITIES CLASSIFICATION SYSTEM III
(LOCS III)
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Figure 3. LOCS Ill
their progression Cortical cataracts affect the outermost and The visual symptoms mentioned in the different types of
youngest layers of the lens. Lens hydration changes produce cataracts are usually not accompanied by any ocular pain.
clefts in a radial pattern around the equatorial region. This can Other ocular signs and symptoms such as discharge, itchiness,
result in glare, seeing haloes around lights, and monocular redness, tearing, or foreign-body sensation are also absent
diplopia (seeing double or"shadow images").This type can also in an isolated cataract. It should be noted that patients with
be bilateral and quite asymmetric, with the visual deterioration cataracts may also have an ocular co-morbidity (glaucoma,
depending on the involvement of the visual axis. Posterior diabetic retinopathy, age-related macular degeneration,
subcapsular cataracts (Figure 4) affect the region near the etc). Pre-operative evaluation and exclusion of these other
central posterior capsule. Being in the center, they usually pathologies are important in prognosticating visual outcomes
cause early visual symptoms (and hence, cataract surgery) in after surgery.
the form of night time glare/haloes around lights and poor
vision under bright illumination (as the pupil constricts while You examine his eyes with a penlight and notice that both
the central visual axis is obscured by the cataract). This type pupils react briskly to light and do not demonstrate a relative
is also more commonly associated with diabetes, trauma, afferent papillary defect (RAPD). You attempt funduscopy
corticosteroid-use, inflammation, and exposure to ionizing but is prevented by hazy media, and you notice that the redradiation.'
orange-reflex appears distorted. Using the pocket Snellen that
you brought along, you noted that his best vision (with reading
glasses) on the right eye is 20/100, and on the left eye, 20/70. He
asks you for advise on what his options are.
EVALUATION
he uncorrected and corrected (pinhole and refraction) visual
acuity should be recorded. In mature cataracts with poor vision,
one may test for color discrimination (using the different hues
of the direct ophthalmoscope) and light projection. These are
fairly reliable gross tests of visual (especially macular) function
and may be useful for visual prognostication in dense cataracts.
Figure 4. Posterior subcapsular cataract seen thru slit lamp biomicroscope
The Swinging Flashlight Test is a simple and very useful
bedside examination when evaluating cataracts. If the
pathology is a cataract ONLY with NO other ocular co-
morbidity, then there should be NO gross RAPD, however
tense the cataract may be.* This is especially helpful when
assessing the potential visual outcome in dense cataracts.
if RAPD is present, the patient must be forewarned about
the possible existence of an ocular co-morbidity that may
preclude good visual outcome after surgery. Effort must be
undertaken to look for other etiology causing poor vision.
Further evaluation may be warranted to rule out the existence
of posterior pole pathology (e.g. diabetic retinopathy, optic
atrophy, age-related macular degeneration, etc.).
* In a hypermature unilateral cataract, one may actually be able to
demonstrate a trace RAPD in the opposite eye—likely due to more
scattering of light (and hence diminished afferent input) in the
cataractous eye.
Funduscopy with the direct ophthalmoscope may be difficult
in the presence of significant cataract as the media is hazy.
With mature cataracts, the patient's pupil might appear
whitish/opaque, called leukocoria (Figure 5). With less
mature cataracts, this might not be obvious. Grossly, using
the hyperopic correction of your direct ophthalmoscope
(green numbers), one can look through" the patient's lens
at a distance of about 12 inches. Especially for cortical and
posterior subcapsular cataracts, a distortion of the normally
round and homogenous red-orange-reflex may be seen with
this maneuver.
Cataracts are best viewed via a slit lamp biomicroscope.
This instrument allows for visualization of the layers of the
lens and the extent of cataract involvement. In addition, the
ophthalmologist uses the slit lamp to look for associated
findings that may make the surgery difficult. For example, the
presence of phacodonesis (lens movement), Irldodonesis (iris
movement) on slit lamp exam, as well as pseudoexfoliation
(from pseudoexfoliative glaucoma) on the lens capsule may
indicate weak zonules and can lead to complications during
surgery. Other factors that may affect the course of surgery
include the presence of uveitis, posterior synechiae, nondilating pupils, shallow anterior chamber, corneal opacity and
low endothelial cell count.
Dilated fundus examination should be performed in an
attempt to view the fundus pre-operatively. Checking for
posterior pole pathology (glaucomatous optic neuropathy,
optic atrophy, retinopathy, age-related macular degeneration,
etc.) is very important for prognosticating visual outcome in
cataract surgery. When there is virtually no view of the fundus
because of the density of the cataract, an ocular ultrasound is
sometimes performed as part of the pre-operative evaluation.
A detailed medical history is important in assessing other
factors that may affect surgical outcome. These include the
patient's cardio-pulmonary status (surgical risk), the presence
of diabetes (non-dilating pupil makes the surgery more
difficult), and even drug history as certain medications may
predispose patients to intra-operative complications.
Figure 5. Leukocoria
Additional ancillary tests that may be performed by the
ophthalmologist for surgical planning include refraction
and biometry (a procedure that extrapolates the refractive
outcome with various IOL powers), corneal topography (to
address astigmatism), and specular microscopy (to assess the
health of the corneal endothelium) among others.
SURGERY
Despite all the technological advances and innovations in
ophthalmic science, there is still no proven medical treatment
to reverse the progression of cataracts. It would be safe to say
that anyone who lives long enough will eventually develop
significant cataracts and require surgery. Surgical removal of the
opacified lens to clear the visual axis is the only treatment option
for cataracts. Visual rehabilitation after cataract removal is varied
and depends on the type of procedure performed. The evolution
of cataract removal and visual rehabilitation highlight one of the
great success stories in medical innovation.
CAPSULOTOMY
z
z
0
n
0
n
IOL Optic
1
e
e
S
IOL Haptic
CAPSULAR BAG
IOL Haptic
Figure 6. Post-op appearance in Extracapsular Cataract Extraction (Manual)
Phacoemulsification/Small Incision) with IOL secure in the capsular bag.
Cataract surgery had evolved from intracapsular cataract
extraction (ICCE), which leaves a patient aphakic, to extracapsular
cataract extraction (ECCE) with intraocular lens (IOL) implantation
(Figure 6). Procedures for ECCE have evolved from manual
nucleus expression and irrigation/aspiration of the cortical
material with rigid IOL implantation to phacoemulsification with
implantation of foldable 10Ls. Table 1 lists the characteristic
features of the various types of procedures performed for surgical
removal of cataracts.
5
DISTURBANCE IN VISION 15.2 Cataract
63
The trend in cataract surgery has gone towards smaller incisions,
usually 2-4mm (to minimize the surgically-induced astigmatism of
larger incisions) and foldable 10Ls (to maintain the small incision
during lens implantation). Phacoemulsification, a form of ECCE,
utilizes an ultrasonic probe to break up the cataract into smaller
pieces, which can then be removed by aspiration. Manual Small
Incision Cataract Surgery (MSICS) is another surgical option
that boasts of the advantages of small incision cataract surgery
without the need for a phacoemulsification machine. A shelved,
self-sealing incision, usually 5-7mm, is dissected from the sclera
and into the anterior chamber. The nucleus is prolapsed out of
the bag and out of the eye with the advantages of a suture-less,
closed system like phacoemulsification.
Cataract extraction surgery has evolved into a 10 to 30-minute,
surgical procedure that is often performed on an out-patient
basis and under topical anesthesia. As a result of these, recovery
period has shortened and the faster visual rehabilitation allows
patients to return to their regular activities even a day after their
surgery. Furthermore, advances in intraocular lens technology
have widened a patient's choice. When formerly only regular
monofocal lenses (which correct for only one focus - either distance
or near vision depending on the patient's choice) were available,
there are now toric 10Ls that can correct a patient's pre-existing
corneal astigmatism (which cannot be corrected by a monofocal
lens), as well as multi-focall0Ls that allow vision for both distance
and near without the aid of spectacles.
You were able to convince the patient that his cataracts
probably need surgery. Before he sees an ophthalmologist,
he asks for your advice on the risks of cataract surgery. What
will you tell him?
COMPLICATIONS OF CATARACT SURGERY
In a well-equipped ophthalmic surgical operating room and
under an experienced surgeon's hand, present day cataract
surgery should be 99.99% successful. As with any other
surgical procedure, however, complications can and do occur.
Complications may range from minor to severe, potentially sightthreatening ones. Intra-operative complications include posterior
capsule rupture, vitreous loss, retention of lens fragments in the
vitreous and thermal or mechanical trauma from the phaco
probe. Post-operative complications include inflammation
and/or increased intraocular pressure. unplanned refractive
outcomes, i.e., biometry was off-target or the wrong IOL power
was inserted , cystoid macular edema and pseudophakic bullous
keratopathy. A severe and the vision-threatening complication
of this procedure is intraocular infection or endophthal mitis. The
key to prevention of permanent loss of vision that can result
from this complication is its early recognition and treatment.
Hence, close and regular follow-up of patients following cataract
extraction surgery should always be performed in order to
immediately address any post-operative complication that may
arise.
Table 1. Types of cataract surgeries
Extracapsular Cataract Extraction (ECCE)
n racapsular
Cataract Extraction
(ICCE)
Manual
retrobulbar
peribulbar
retrobulbar
peribulbar
Incision
180.. limbal
Part of lens that
is removed
IOL used
Anesthesia*
Phacoemulsification
Manual Small
Incision
retrobulbar
peribulbar
retrobulbar
peribulbar
160°, limbal
2-4 mm. corneal
5-7 mm. scleral
Entire lens
Anterior capsule. nucleus
and cortex (nucleus
delivered without
fragmentation)
Anterior capsule nucleus
and cortex (nucleus
fragmented using
phacoemulsification
machine)
Anterior capsule.
nucleus and cortex
(nucleus fragmented
manually)
No IOL
(Visual rehabilitation thru
aphakic spectacles or
contact lenses)
Rigid Intraocular lens (IOL)
Foldable IOL
Foldable
Rigid IOL
*Local anesthesia (LA) generally used although general anesthesia or IV sedation also performed in certain instances. Note that the specific route of LA used is
subject to surgeon and patient preference.
SUMMARY
Definition and Etiology
Types of Cataracts
Nuclear
Cortical
Posterior Subcapular
Symptomatology
Evaluation
Funduscopy
Slit lamp Examination
Medical and Drug history
Ancillary Procedures
• Refraction
• Biometry
• Corneal Topography
•Specular Microscopy
Cataract Surgery
Types off Cataract Surgeries
• Intracapsular Cataract Extraction (ICCE)
• Extracapsular Cataract Extraction (ECCE)
• Phacoemulsification with IOL implementation
2.
Type of cataract that gives the worst visual symptoms
outdoors (in bright sunlight)
A. Nuclear
B. Cortical
C. Posterior subcapsular
D. All of the above
3.
The following symptoms are typical for isolated
cataract EXCEPT:
A.
B.
C.
D.
E.
decreased visual acuity and color perception
glare
haloes
ocular pain
monocular diplopia
4. Bedside examination most useful for evaluating and
prognosticating cataracts
A. Direct ophthalmoscopy
B. Slit lamp examination
C. Ocular ultrasound
D. Swinging flashlight test
5.
Complications
• Intra-operative complications:
• Post-operative Complications
The following slit lamp findings may warn the surgeon
of potential difficulties during surgery EXCEPT:
A. Posterior synechiae
B. Corneal Opacity
C. Phacodonesis
D. Pseudoexfoliative material on the lens
E. Well-dilated pupil
REFERENCES
1. Cubillan LDP, Olivar-Santos EO. Third national survey on
blindness. Philipp J Opthalmol. 2005:30(3);100-114.
2. Riordan-Eva P, Whitcher JP. eds.Vaughan's and Asbury's
General Ophthalmology. 16th ed. New York: McGraw Hill
Com pan ies;2004.
3. Kahn HA, Leibowitz HM, Ganley JP, et al., The Framingham
eye study. II. Association of ophthalmic pathology with
single variables previously measured in the Framingham
heart studyAm J of Epidemio. 1977:106 (1);33-41.
4. Stanga PE, Boyd SR, Hamilton AMP.Ocular manifestations
of diabetes mellitus.CurrOpin Ophthalmology.1999:10(6);
483-489.
5. Chylack LT Jr., Wolfe JK, Singer DM, et al.The Lens opacities
classification system III. The longitudinal study of cataract
study groupArch Ophthalmol. 1993;111(6):831-836.
6. Awwad S. Cataract surgery. http://www.eyeweb.org/
cataract_surgery.htm. Accessed April 28, 2011.
SELF-TEST
1. The following factors are associated with cataract
formation:
A. diabetes
B. trauma
C. damage from UV rays
D. toxins
E. All of the above
6. In the setting of a very dense/mature cataract with
media opacity and poor vision, the following exams
may be useful for prognosticating visual outcome
EXCEPT:
A. Color discrimination
B. Fluorescein angiography
C. Ocular ultrasonography
D. Swinging flashlight test
7. Which type of cataract surgery will routinely require
aphakic lenses for visual correction post-operatively?
A. ECCE
B. ICCE
C. phacoemulsification
D. A and B
8.
Which type of IOL is best suited for patients who do not
wish to wear spectacles for both distance and near after
cataract surgery?
A. Monofocal IOL
B. Multifocal IOL
C. Phakic IOL
D. Toric IOL
Answers to Self-Test on page 220.
5
DISTURBANCE IN VISION I
5.3 Disorders of the Retina,
Vitreous and Choroid
Pearl M. Tamesis- Villalon, MD
INTRODUCTION
This chapter provides an overview of disorders of the retina, vitreous and choroid that cause disturbances in vision.
vsented, with typ c cases discussed at
Photographs representative of various vitreo-retinal and choroidal pro:_ ems wil,
the end of each clinical section. The basic knowledge acquired from this material should serve as a springboard for further self
study, for possible research and should be applied to cases which the student will encounter in the actual clinical setting of the
Department of Ophthalmology and Visual Sciences.
OBJECTIVES
After reading this material, the medical student in ophthalmology is expected to:
1. Recognise the uniqueness of the human retina, vitreous, and choroid that lend it susceptible to certain problems.
2. Identify the elements in a patient's history and ophthalmologic examination that will lead to the formation of a
working diagnosis (primary and differential diagnoses) of vitreo-retinal and choroidal disease.
3. Differentiate selected vitreo retinal and choroidal disorders according to the appearance of typical lesions, their
location, etiology and pathophysiology.
4. Analyze available data and formulate a management plan.
RECOMMENDED PREPARATION
The student is advised to review the anatomy, histology and physiology of the retina, vitreous and chorord, as well as the optic nerve, before going
through this material.The student is also advised to review the mechanics of taking a good dinical history and the method of conducting a complete
eye examination.
CONTENT
I. Uniqueness of the Microstructure of the Vitreous, Retina, Choroid
II. Diagnosis of a retinal, vitreous and choroidal disorder
1. History
2.
3.
4.
Ophthalmologic examination
Ancillary examinations
Systemic examination
III. Diseases of the retina, choroid and vitreous
1. Diabetic retinopathy
2. Central retinal vein occlusion
3. Central retinal artery occlusion
4. Age related macular degeneration
5. Retinitis pigmentosa
6. Retinal detachment
7. Vitreous hemorrhage
8. Ocular toxoplasmosis
9. Vogt- Koyanagi- Harada Syndrome
10. Choroidal capillary hemangioma
11. Metastatic choroidal tumor
I. UNIQUENESS OF THE
Crystalline lens
MICROSTRUCTURE OF THE
Lacuna developing in
vitreous during syneresis
VITREOUS, RETINA, CHOROID
A. THE VITREOUS
Subhyaloid space: between
posterior hyaloid and retina
The globe is filled with a gel called the vitreous. This gel is 99%
water and only 1% solid. The solid portion consists of collagen
fibrils that make up the meshwork, hyaluronic acid molecules,
and the very few cells called hyalocites. The vitreous has a
peripheral or outer layer called the cortex, and a central part,
the gel. The outermost limit of the cortex is the hyaloid face,
both anterior and posterior. The anterior hyaloid is just behind
the lens.The posterior hyaloid is adjacent to the retina's internal
limiting membrane all over the inner surface of the globe where
there is retina, and is loosely attached to it, creating a potential
space called the subhyaloid or preretinal space (Figure 1). The
vitreous is firmly attached to the optic nerve, the macula, along
blood vessels and also at the so called vitreous base (where
the retina ends peripherally and anteriorly). Many disorders in
vision originate from problems with the vitreoretinal interface.
For example, vitreous liquefaction and anterior displacement
(towards the lens) can cause undue traction on the vitreous
base and may cause the formation of a retinal tear or dialysis,
possibly leading to retinal detachment. Another example is
undue traction of the vitreous gel and posterior hyaloid of the
vitreous, on the macula, causing the formation of a macular
hole, or the formation of an epiretinal membrane.
Figure 1. Diagram of vitreous in relation to lens, retina and optic disc.
Adopted from Yanoff P.'
and posterior vitreous detachment (PVD) may also occur
after vitreous hemorrhage, inflammation, trauma, and after
intraocular surgery. When liquefaction and PVD have set in,
patients usually start seeing "floaters" and occasionally "flashes"
B. THE RETINA
The human retina is a tall
structure that has ten layers. In the ten layers are three main
cell types that relay photochemical information through the
retina , from outside inwards, and to the optic nerve, and finally
into the occipital cortex. These are, from scleral (outer side),
towards the vitreous (inner side) : photoreceptor cells, the
bipolar cells and the ganglion cells. The axons from these cells
form the nerve fiber layer, and course towards the optic disc,
and into the optic nerve (Figure 2, 3). There are supporting
cells that keep the tall ten layered retina "together These
are the Muller cells which are structural cells, and horizontal
and amacrine cells which allow multiple photoreceptors to
"plug into" a smaller number of bipolar and ganglion cells.
Any breakdown in the neurons, the supporting cells and the
relay system itself can manifest as visual disorders. The tenlayer system is supplied by two different vascular systems. The
1. The 3 Neuron Relay System:
Vitreous syneresis is degeneration
of the vitreous gel
(liquefaction of the gel) with eventual detachment of the
vitreous from the retina. This event is a normal physiologic
occurrence starting at age 45-50 years and is present in around
70% of 70-year old individuals . Liquefaction of the vitreous
RPE •""10"
Rods & Cones
Horizontal Cells
0•
1\1
Bipolar Cells
1
,
1
1
Arnacrine Cells
Ganglion Cells
Internal Limiting
Membrane
Figure 2. Diagram of the layers of the retina showing the different cell types in the human retina. In this diagram, only the
Muller cell, a structural cell that serves as a scaffold supporting the entire thickness of the multi-layered retina is not shown.
Light enters the eye and stimulates the Photoreceptors (Rods and Cones). Visual information is then carried by the 3 neuron
relay system: from photoreceptors to bipolar cells to ganglion cells (blue arrow) Adopted from Yanoff P.'
5
DISTURBANCE IN VISION I 7 3 Disorders of the Retina, Vitreous and <hnrniri
INTERNAL LIMITING MEMBRANE
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GANGLION CELL LAYER
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4-- OUTER NUCLEAR LAYER
•
EXTERNAL LIMITING MEMBRANE
•
PHOTORECEPTOR CELL LAYER
RETINAL PIGMENT EPITHELIUM
4— CHOROID
Figure 3. Histopathologic section of the human retina showing the 10 layers and the choro.a. Adopted from Yanoff P.'
outer retinal layers derive nutrition from the choriocapillaris
of the choroid. The inner layers, from the inner nuclear layer
inwards, are supplied by the retinal vasculature. Certain retinal
diseases can be traced to problems of perfusion. Knowledge
of the blood supply of the inner and outer retina will help the
clinician predict the severity and depth of retinal involvement.
2. The Retinal Pigment Epithelium: The retinal pigment
epithelium (RPE) is the first of the ten layers, and is the
outermost layer, adjacent to the choriocapillaris of the choroid,
separated only by Bruch's membrane. It takes care of most
metabolic processes of the outer retinal layers, keeps the retina
"dry" with its "outer blood-retina barrier", participates in the
recycling of retinol and disposes of metabolic wastes of the
other cells. A breakdown of the"outer blood-retina barrier"can
lead to accumulation of fluid in the subretinal space and the
sub RPE space. This can lead to retinal edema. A physiologic
"pump" also exists in the human RPE layer and this pumps
fluid away from the retina and back into the choriocapillaris,
keeping the retina" dry".
3. The Blood -Retina Barriers: There are two so called bloodretina barriers that keep the retina "dry":
a.
b.
1111MI
The Inner Blood-Retina Barrier: This is attributed
to the tight endothelial cell junctions of the retinal
capillaries. Any disturbance in the integrity of these
tight attachments leads to oozing of fluid and/or
blood, as well as lipids and proteins from the retinal
vascular tree. This manifests as retinal edema, hard
exudates, and/or hemorrhages.
The Outer Blood-Retina Barrier: This is found in the
RPE.The tight intercellular attachments between RPE
cells, called "zonula occludens" keep the RPE layer
leak proof from the highly vascular choriocapillaris
,nritr,r,nni tonrcrinil
I F, Ili. ,F1
of the choroid, to which it is adjacent. An additional
feature is the presence of a physiologic "pump" that
keeps fluid contained outside the retina.
C.THE CHOROID
The choroid is the middle coat of the wall of the globe. It is a
vascular layer that comes from the long and short posterior
ciliary arteries, mostly from the short, that in turn emanate
from the ophthalmic artery. The choroid is arranged in
lobules , giving rise to some peculiarities in choroidal disease
presentations. More importantly is its role in 'maintaining" the
health of the outer retina and providing the vascular supply
especially to the macular area. The dense barrier between the
RPE of the retina and the choriocapillaris (the layer of choroid
made of finer vessels and closest to the retina) is called Bruch's
membrane. It is impermeable to fluids, and diseases involving
Bruch's membrane can lead to subretinal accumulation of fluid
and blood.
II. DIAGNOSIS OF A RETINAL,
VITREOUS AND CHOROIDAL
DISORDER
There are four elements needed for making a working
diagnosis that involves the retina, vitreous and/or choroid.
1. History: Good history taking is a must, especially
in patients where loss of vision or changes in vision
are the chief complaints. Many vitreo-retinal and
choroidal diseases have peculiar affectations of vision
which immediately suggest the type of problem.
2. Ophthalmologic Examination: A basic eye
examination should be done for all patients:
1. Visual Acuity
2. Gross Eye Examination
3. Pupils
4. Intraocular Pressure Determination
5. Extraocular Muscle Movements
6. Funduscopy
Floaters (muscae volitantes) are black to gray spots and/or
fibers that move about in the field of vision of the patient.
They seem to float freely and may vary In number. They are
commonly observed after the age of 45 to 50 when vitreous
liquefaction and vitreous collapse and/or detachment have
begun as part of the ageing process. The onset of this process
occurs earlier in individuals who are myopic. Floaters may also
be caused by particles suspended in the pre-corneal tear film.
3. Ancillary Examinations: Special ophthalmologic
and laboratory examinations are done to help the
ophthalmologist confirm his working impression
and establish an etiologic diagnosis for patients
suspected to have disorders of the retina, vitreous
and choroid.
Flashes (photopsias) caused by retinal problems are described
as arcuate lightning like streaks of bright light in the periphery,
noted with or without eye and/or head movements. Patients
describe them as" gumuguhit sa gilid "parang kidlat sa gilid".
Photopsias, however, may be of optic nerve origin. Care must
be taken not to confuse these lightning like flashes with the
visual aura of migraine headaches.
4. Systemic Examination: A thorough physical
examination of all systems is done in cases where
the eye problem is suspected to be part of a systemic
condition or distant trauma (away from the eye).
When a systemic disease is suspected, a referral to an
internist is recommended.
Sometimes patients do not know that they have color vision
problems, and only discover it at work (seamen's pre- boarding
tests, fabric factory mishaps in color choices), or unusual
personal choices in colors of their clothes and similar activities
requiring precise color recognition.
2. Did the visual disturbance come gradually or
suddenly?
The patient should be interviewed regarding the onset and
development of the visual complaints. Inquire if the change in
vision occurred suddenly; or whether it was gradual or rapidly
progressive and where the blurring started, from the center or
from the periphery. One must take pains to extract this from
the patient who may not volunteer the information, thinking
that it is not important or relevant.
HISTORY TAKING IN CASES SUSPECTED
OF POSTERIOR SEGMENT DISORDERS
The importance of history taking cannot be over emphasized.
The information gathered, either volunteered by the patient or
extracted by the clinician helps in the formulation of a working
diagnosis, that guides the clinician to request for ancillary
examinations, to help confirm it. The information also gives
the clinician an idea as to possible etiology, present state of
severity, treatment response and prognosis.
3. What other eye problems accompanied the visual
disturbance?
Pain is rarely present in retinal, vitreous and choroidal disorders.
The pain in diabetic retinopathy with neovascular glaucoma,
for example, is due to the severely elevated intraocular
pressure. Ocular discomfort and/ or redness may accompany
intraocular inflammatory conditions with retinal involvement.
The following are important questions to ask patients
suspected of having a vitreo-retinal, or choroidal problem:
1. What is your patient's chief complaint?
These patients usually complain of some type of visual
disturbance.
This may come in the form of:
•
persistent blurry vision
•
transient blurry vision
•
change in shape or distortion (metamorphopsia)
•
change in image size (usually smaller : micropsia; if
bigger-macropsia)
color
vision problems : difficulty in identifying colors
•
(dyschromatopsia),
change in shade, contrast, brightness
visual field loss : (scotoma) central, peripheral, other
4. How long has this been going on?
The duration of the problem is a significant information. It
is also important to know how long the problem has been
present, if this is the first episode, or if it is recurrent. If the
problem is recurrent, be sure to ask about the timing and
sequence of events, duration, interval, and treatment as well
as treatment responses.
5. Which eye is involved?
Laterality is as important as knowing if the same or similar
problems have occurred in the fellow eye, Do not forget to
ask when the problem started. If bilateral, ask which eye was
affected first, followed by questions regarding the sequence of
signs and/or symptoms.
patterns
difficulty in the dark (nyctalopia or night blindness)
difficulty in bright light (hemeralopia)
floaters (muscae volitantes)
flashes (photopsias)
5
DISTURBANCE IN VISION I i Disorders of the Retina, Vitreous and Choroid
69
6. Were there previous consultations and treatments ? When?
What medications have been used? What medications
are being used? Did the patient have any eye operation
or interventions like laser treatment, injections into the
eye, for this or other problems?
These information has bearing on the present state of the eye,
if you are seeing a patient who was or is under treatment by
someone eke.
7. Other aspects of the patient's history that should be
considered include:
be deliberately withholding information. The clinician must
be observant of patient responses, reactions, attitude and
demeanor. For example, history taking of AIDS patients and
drug addicts is particularly challenging.
OPHTHALMOLOGIC EXAMINATION
OF THE PATIENT
The basic tools needed for an examination of a patient
suspected of posterior segment disease are:
Visual acuity charts : both for distance and near vision
2. Penlight : for nross examination of the eye , adnexae and
pupils
3. Tonometer: .,ed to determine intraocular pressure. For
medical students, the technique of finger palpation is
performed to estimate intraocular pressures.
4. Ophthalmoscope: used to examine the fundus ( retina
and optic disc)
5. Slit lamp: a biomicroscope that allows for a highly
magnified view of the eye and assessment of the ocular
media, optic nerve and retina with the help of special
lenses.
6. Amster grid: a black and white card with a fine grid and
a fixation point, used to detect and quantify central visual
changes.
1.
Family History : Is there a history of similar eye problems
in the family? Is there a history of any hereditary illness? It is
also very important to ask about hypertension and diabetes
mellitus.
Social History: Does the patient smoke? Does he drink and
how much alcohol does he consume? Does he have pets and
what kinds of pets (particularly interested in dogs and cats)?
Does he eat raw food? Does he engage in contact sports or
other unusual sports like deep sea diving, sky diving, bungee
jumping, competitive weight lifting, boxing, contact sports,
etc, and has he been injured in the head and/or eyes? Does
he take prohibited drugs or has he ever taken any? What is
his occupation? Is there exposure to chemicals or toxic fumes?
Does he travel often and has he been to places like Africa, the
Middle East, China?
Medical History: Does he have cardiac disease, hypertension,
diabetes mellitus, asthma, hematologic disease, cancer ,
pulmonary tuberculosis and other diseases? Has he ever had
accidents that required surgery and/or hospitalization? Has he
been operated on and for what? Does he have symptoms like
angina, pedal edema, joint pains, oral ulcers, intractable fever,
to name a few. Has he ever had a blood transfusion and when?
Has he ever had cobalt therapy? Is he on any medications for
other illnesses? What are these medications? How long has
he been taking these? A perfect example of knowing about
systemic medications is that of ethambutol toxicity and its
effect on the optic nerve. Sudden usually bilateral painless
significant visual loss ( for example, sudden deterioration
in visual acuity from 20/20 to 20/400) in a patient who has
been on ethambutol for pulmonary tuberculosis for several
months, should raise suspicion about a possible ethambutol
optic neuropathy. In ethambutol toxicity, all other ocular
findings including posterior segment findings, are normal.
Sexual History: The presence of a history of any sexually
transmitted disease should likewise be elicited from the
patient. What is his sexuality?
During history taking keep your mind open to the possibility
that the patient may not be volunteering information because
he does not think it is relevant or important, or the patient may
AAr
ole
ninktk.dry-InInew I -)nri r, itinn
Gross Eye Examination: In the absence of any systemic
illness or trauma, the ocular adnexae are usually not affected in
retinal disease. Except in some retinal disorders of inflammatory
origin, there will be no ciliary flush or redness.The pupils must
be examined for direct and consensual light reactions. Severe
retinal damage as well as some optic nerve diseases can cause
abnormal pupillary responses . A'white pupil" in a small child
is always an alarming and significant finding. The absence of,
or a faint 'red orange reflex' or 'ROW may indicate vitreous
opacities like hemorrhage or inflammatory material. One must
remember however, that an absent ROR can also be caused by
a dense cataract or a dense corneal opacity or dense material
in the anterior chamber.
Visual Acuity: Vision is usually affected in some way in most
vitreo-retina and choroidal posterior segment disorders.Typica l
affectations in vision are seen in specific diseases. For example
retinal edema at the macula can cause decreased vision and
metamorphopsia. In retinal detachments, many patients
report seeing floaters and light flashes before the onset of
"wavy vision", actual blurring, visual field "cuts". Macular disease
causes blurry central vision while extramacular retinal diseases
will cause peripheral visual loss. Vitreous opacities also cause
blurry vision and/ or floaters. Many retinal disorders come
with vitreous abnormalities. A few affect all three structures:
retina, vitreous and choroid.
itraocular Pressure: As with visual acuity, there is no set
attern for intraocular pressures in disorders of the retina,
itreous and choroid. Retinal detachments usually cause some
mount of hypotony due to the accompanying inflammatory
hanges and involvement of the ciliary body in the
etachment. The elevated intraocular pressures in end stage
Iroliferative diabetic retinopathy with neovascular glaucoma
re due to blocking of the drainage angles by new vessel
irowth (neovascularization) of proliferative disease. Macular
liseases usually do not cause pressure changes. Choroidal
letachments are accompanied by ocular hypotony.
Extraocular Muscle Movements (EOM): Patients usually
?xhibit normal EOMs in retinal, vitreous and choroidal
Diseases. Long standing retinal disease with retinal scarring
rnd poor vision may result in outward deviation of that poorly
ieeing eye. Inward or outward deviation of the eye can be a
presenting sign of retinoblastoma, a tumor most commonly
3een in infancy.
Figure 5. Indirect ophthalmoscopy. Examiner views fundus using an
indirect ophthalmoscope on his head while holding an aspheric lens.
Patient is examined lying down.
Funduscopic Findings: Fundus changes depend on the
problem. The vitreous always has to be considered in assessing
the status of the retina. The inter-relationship of the vitreous
and the retina will be discussed in a separate section. The
fundus can be examined using a direct ophthalmoscope,
which allows a very limited and magnified view of the fundus.
(Figure 4 A,B). The indirect ophthalmoscope is a better
instrument, as it gives one a wider view of the fundus. The
image magnification depends upon the lens held by the
examiner. Indirect ophthalmoscopy is more difficult to learn
and its use is a "must" for residents in ophthalmology (Figure 5).
Figure 6. Fundus examination using slit lamp biomicroscopy with
non-contact fundus lens.
Slit Lamp Biomicroscopy with Special Lenses: A third method
of fundus examination is with the slit lamp and a fundus lens
(Figure 6).This examination allows the examiner to see details
of the vitreous, retina and optic disc in high magnification.
Findings of slit lamp examination depend on the disorder and
will be discussed in a separate section. Problems in the vitreous
and the anatomic-pathologic vitreoretinal relationships can be
determined with this examination.
Amster Grid Examination: This is a simple examination
performed in a clinic on patients complaining of central
visual problems. The patient can also perform this at home
to monitor changes in central vision. He observes changes in
the grid presented to him on a black and white chart (black
card with white grid or vice versa) , relative to a central fixation
point. These changes can be blind spots of varying densities,
Figure 4. (A) Physician performs direct ophthalmoscopy on a patient, (B) direct ophthalmoscope
5
DISTURBANCE IN VISION I 5.3 Disorders of the Retina, vitreous and Choroid
AMSLER'S GRID
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the grid that a patient may see if he has a macular problem
and distortion. The grid allows the patient to measure the
approximate size of the perceived changes and note their
location on the chart (Figure 7).
ANCILLARY EXAMINATIONS
Additional examinations may be necessary to confirm a
diagnosis. Even if the diagnosis is clinically obvious these
examinations may still be requested to document changes.
This will help with monitoring progress of treatment.The more
commonly requested examinations are:
Fundus Fluorescein Angiography
(FA) : Fluorescein
angiography is a procedure that involves the injection of a
dye, sodium fluorescein, into the antecubital vein. The dye
is carried with the circulation and outlines the retinal and
choroidal vascular system. This is then picked up by a special
fundus camera. Retinal and choroidal diseases have typical
fluorescence qualities and patterns, thereby allowing the
observer to confirm certain clinical observations. The optic
nerve head also has typical angiographic fluorescence . Any
changes seen on FA may thus, be pathologic and can then be
correlated with clinical findings (Figure 8).
Figure 8. Fundus fluorescein angiography. (A) Sodium fluorescein
dye is injected into the antecubital vein and pictures of the retina are
taken and recorded with a fundus camera, (B) Color picture showing
hard exudates (clusters of punctuate yellowish dots, examples indicated
by black arrows), microaneurysms (small punctuate reddish dots, red
arrows), small retinal hemorrhage (white arrow) in diabetic retinopathy,
(C) Fundus angiography of B showing microaneurysms (small punctuate
white dots, red arrows), small retinal hemorrhage, in the angiogram seen
as a small dark area that corresponds with the hemorrhage in the color
picture (white arrow)
Idocyanine Green Angiography (ICGA):
This is similar
) FA but uses indocyanine green dye instead of sodium
Jorescein.The choroidal circulation is better highlighted with
:GA. It is helpful in studying problems of the choroid not seen
FA.
Ieular B scan Ultrasonography: In the presence of media
pacities the ultrasound is a useful tool to evaluate the
natomic relationships among the three structures (vitreous,
"tina, choroid) and may indicate changes in the vitreous cavity
Jch as the presence of densities and masses . For example, in
le presence of a very dense cataract, the presence or absence
f a retinal detachment can be determined. It is used to assess
le density, size and height of intraocular tumors, giving clues
s to the type of tumor, and possibly a diagnosis. It is also very
seful in assessing the amount of and density of intravitreal
laterial such as blood, and to locate intraocular foreign
ladies in trauma cases (Figure 9).
(blood sugar, cholesterol, triglycerides, BUN, creatinine, etc.)
and x-rays form an important part of "systemic examination"
and must be done when a patient is suspected of having a
certain disease. Patients can present with pedal edema, skin
discoloration of the lower extremities, non healing ulcers and
wounds in the lower extremities in diabetes mellitus.
Figure 10. OCT of normal macula , showing retinal layers (white arrow
indicates fovea, red arrow indicates choroid, yellow arrow indicates RPE )
III: DISEASES OF THE RETINA,
CHOROID AND VITREOUS
Examples of Retinal, Vitreous and Choroidal Disorders are
enumerated in this section.Those discussed in this chapter are
in bold italic print. The student is encouraged to read about
each disorder in more detail and to read about the other
disorders as well.
Retinal Vascular Diseases : diabetic retinopathy,
hypertensive retinopathy, central retinal vein occlusion
•
(CRVO), central retinal artery occlusion (CRAO),
Ocular B scan ultrasound showing retinal detachment
(yellow arrow), optic nerve shadow (white arrow).
Figure 9.
)ptical Coherence Tomography (OCT): Optical Coherence
tomography is a "scan" of the retina, made possible by light
Naves , creating images of the ten layers of the retina at the
nacular area, Bruch's membrane , the choriocapillaris and
arger choroidal channels, and defects in these layers. It can
ilso be used to image the optic disc and cup (Figure 10).
branch retinal vein occlusion (BRVO), branch retinal artery
occlusion (BRAO), retinopathy of prematurity (ROP), Von
Hippel Lindau disease
Maculopathies: age related macular degeneration
(ARMD), central serous chorioretinopathy (CSCR), macular
hole, cystoid macular edema ((ME.), macular pucker
Heredodegenerative diseases of the retina: retinitis
pigmentosa (RP), color blindness, Stargardts disease,
juvenile foveal retinoschisis, Best's vitelliform macular
degeneration
Tumors: metastatic tumors, melanomas,
retinoblastoma, intraocular lymphomas, choroldal
•
Electroretinography (ERG) and Electro-oculography
;EOG): These examinations assess retinal function, by
measuring electrical activity of the retinal layers. In essence,
:hese are similar to an electrocardiogram( ECG).
capillary hemangiomas
Retinal Detachments, retinoschisis
Vitreous opacities and degeneration : vitreous
scintillans,
hemorrhage, asteroides hyalosis, sync hisis
SYSTEMIC EXAMINATION
•
Viany retinal diseases are part of systemic problems like diabetes
mellitus, hypertension, systemic lupus erythematosus and
Dther collagen diseases, pulmonary tuberculosis, malignant
disease or hematologic disorders . Some of these like diabetic
-etinopathy, hypertensive retinopathy, collagen disease, may
present with typical funduscopic findings. Blood chemistry
vitritis, amyloidosis
Retinochoroiditis : toxoplasmosis, toxocariasis,
serpiginous choroiditis
Uveal Effusion : Vogt-Koyanogi-Harada syndrome
Infectious Retinopathies : HIV retinopathy
5
DISTURBANCE IN VISION I 5.3 Disorders of the Retina, Vitreous arid Choroid
DIABETIC RETINOPATHY
Diabetic retinopathy is a complication of Diabetes Mellitus
and manifests mainly as vascular changes in the retina. The
retinal problem usually starts after many years of diabetes.
After 20 years, 90% of Type 1 diabetics and 60% of Type
diabetics will have some form of retinopathy. Good blood
sugar control has been proven to be a key modifiable factor
by wide based landmark studies, such as the Diabetes Control
and Complications Trial (DCCT) and the United Kingdom
Prospective Diabetes Study (UKPDS) . The DCCT showed
that strict glucose control in Type I diabetics can reduce the
chance of development of diabetic retinopathy by 76% and
slow progression in those who already have retinopathy by
54%. It also reduced the occurence of nephropathy by 50%
and neuropathy by 60%. The UKPDS showed that with strict
glucose control there was a 31% risk reduction in progression
to advanced retinopathy in Type II diabetics. It further
demonstrated the importance of blood pressure control in
delaying the progression of diabetic retinopathy to higher
stages. In summary, these studies recommend that normal
blood glucose levels must be maintained to delay the onset
of , or slow down the progression of the complications of
diabetes mellitus. Diabetic retinopathy is only one such
complication, and is closely related to the onset of diabetic
nephropathy.
it
A
There are two stages of diabetic retinopathy : non proliferative
diabetic retinopathy (NPDR) and proliferative diabetic
retinopathy (PDR). NPDR has 4 stages: mild, moderate, severe
and very severe. PDR has 2 stages, early and high risk. The
typical fundus findings in non proliferative diabetic retinopathy
are: microaneurysms, dot and blot retinal hemorrhages, hard
exudates, soft exudates, venous beading and intraretinal
microvascular angiopathies (IRMAs). The hallmark of the
proliferative stage is the growth of abnormal new vessels
(neovascularization) either on the disc (NVD) or on the retina
(NVE) (Figure 11). The pregnant diabetic is of particular
concern and must be monitored more closely.
Vision deteriorates when the patient develops macular
edema which can occur at any stage of retinopathy
including the earlier stages of NPDR. The standard of
care is to monitor fundus changes if the retinopathy is
diagnosed in its earlier stages, followed by laser treatment
in the form of pa nretinal photocoagulation (PRP) when
PDR characteristics are present. Macular focal and grid laser
treatment can be done at any stage if maculopathy causes
significant visual loss. Intraocular injections with anti-vascular
endothelial growth factors (anti-VEGF) preparations are under
study for the treatment of macular edema related to diabetic
retinopathy. Vitreoretinal surgery is indicated if there are non
clearing vitreous hemorrhage, premacular hemorrhage,
vitreoretinal traction, traction and bullous retinal detachment.
Figure 11. Retinal findings in diabetic retinopathy. (A) NPDR with
hard exudates (black arrows), microaneurysms (red arrows), dot and blot
hemorrhages (yellow arrows), soft exudates (white arrow), (B) PDR High
Risk with Pre-retinal hemorrhages (white arrow), NVDs (black arrow),
NVEs (yellow arrow), (C) PDR with retinal hemorrhages and extensive
fibrovascular membranes (white arrows) with vitreoretinal traction.
Diabetic retinopathy causes varying degrees of visual loss
depending on the fundus and vitreous changes. It is, however,
possible to have a patient with fairly good vision despite the
resence of PDR if the macula is minimally affected. Diagnosis
made with a thorough history and good clinical assessment
f the fundus. To confirm the working impression and identify
Ither possible retinal changes, a fluorescein angiogram (FA)
nd optical coherence tomography (OCT) are performed. An
icular B scan ultrasound may be requested if there are media
goblems such as vitreous hemorrhage and/ or a cataract
)recluding adequate visualization of the fundus.
Treatment of ischpmir CRVO is retinal
(scalier laser treatment similar Lo FliF' of diabetic retinopathy)
when certain criteria are met, as recommended by the Central
Vein Occlusion Study. Usually the non-ischemic type needs
no definitive ocular treatment but the primary cause must be
identified and addressed.
:ENTRAL RETINAL VEIN OCCLUSION
Central retinal artery occlusion or CRAO , is one of only
two "true" emergencies in ophthalmology. It does not
occur as frequently as CRVO.
CENTRAL RETINAL ARTERY OCCLUSION
ventral retinal vein occlusion or CRVO manifests in two types:
schemic and non ischemic (also called stasis retinopathy) .
rhe ischemic type is more severe. The fundus is covered with
multiple splinter and blot hemorrhages . One typically finds
;oft exudates (cottonwool spots) indicating retinal ischemia.
Retinal veins are tortuous and dilated. The optic nerve may
lave blurry borders covered with splinter retinal hemorrhages
-adiating from the disc and which appear to be following the
disposition of the nerve fiber layer. Vision is very poor in this
situation due to macular edema, and/or macular ischemia.
Retinal hemorrhages covering the fovea also cause poor
vision (Figure 12). With examination of the pupils one may
find afferent pupillary defects (APD).
It manifests as sudden painless loss of vision.Visual loss is severe,
and residual vision just after the episode is usually in the area
of light perception to count fingers . The retina is very pale so
that the usually darker macula becomes more prominent and
is described as a "cherry red spot". "Box tarring" of blood flow in
the arterioles is oftentimes observed. Occasionally a glistening
thrombus called a Hollenhorst plaque is seen blocking an
arteriole (Figure 13).
Figure 13. Central retinal artery occlusion showing pale retina and a
cherry red spot at macula
Figure 12. Central retinal vein occlusion showing numerous flame
shaped retinal hemorrhages, blurry disc borders, cotton wool spots
Some patients report a prodrome of temporary vision
"wipeouts" several times in a span of days to weeks before
the actual CRAO. This "wipeout" is very brief and lasts for a
few seconds. At this time the patient's vision appears white
or gray with all details gone temporarily. When vision returns,
everything is normal. Even the retina appears normal except
perhaps for vascular changes indicative of hypertension and
arteriosclerosis.
In contrast,
the non-ischemic type of CRVO, shows fewer retinal
hemorrhages and usually no soft exudates. The disc borders
are not markedly obscured by splinter hemorrhages. However,
there is definite retinal venous tortuosity and dilation. Vision
and prognosis are much better than in the ischemic type.
CRVO can happen to both elderly and young individuals. In
the elderly, one should consider systemic vascular diseases CRAO is usually related to systemic vascular diseases like
such as hypertension, diabetes and arteriosclerosis
as hypertension, arteriosclerosis, collagen disease or hematologic
possible causes of these vaso- occlusive episodes. In the disorders. Embolic and thrombotic phenomena must be
younger individual, one thinks of inflammatory disease, considered, such as internal carotid stenosis, arrhythmias,
collagen disease, hematologic disorders, etc. An FA will help cardiac valvular disease, peripheral vascular disease, or
confirm the type of CRVO. An OCT may confirm or rule out the intravenous medications with particulate matter such as
presence of macular edema.
steroids, heroin, others. Extraocular causes may include
5
DISTURBANCE IN VISION I 3 Disorders of the Retina, Vitreous and Choroid
prolonged pressure on the globe or massive retrobulbar
hemorrhage usually after trauma. Prognosis for visual recovery
is very poor. Most patients are left with vision of counting
fingers to light perception after the retinal edema has settled.
Treatment must be instituted within 5 minutes of the attack
and comes in the form of immediate lowering of eye pressure
to improve intraocular perfusion, by reducing intraocular
resistance to blood flow. Some reports have pegged the
"golden period" for treatment with salvage of vision, to 90
minutes from onset of visual loss.
AGE RELATED MACULAR DEGENERATION
Age related macular degeneration (ARMD) is one of the major
causes of central visual loss in the western world, in people
over 50 years of age. It is more common in the elderly and the
incidence rises sharply after the age of 75 years. There are two
types, the non-neovascular (dry) type and the neovascular
(wet) type. The non-neovascular type is more common and
visual loss is not as severe as in the neovascular type. The
neovascular type accounts for only 10% of all ARMD, but
is responsible for 90% of those with vision of 20/200 and
less. The basic pathology of the non-neovascular type is the
accumulation of cellular debris and formation of "drusen"
under the retina.There is accompanying atrophy of the retinal
pigment epithelium. In the neovascular type, a choroidal
neovascular membrane grows under the retina from the
choroid. This membrane bleeds under the retina and causes
scarring and extensive damage of the retina above it (Figure 14).
Age is a definite risk factor in ARMD. Other risk factors
implicated, but with no established causal relationship are:
smoking, cardiovascular disease, ethnicity, undue exposure to
UV light, lack of vitamin C and other factors related to oxidative
stress. Recent studies show that there is association of smoking
to ARMD.
The non-neovascular type causes gradual painless
deterioration of central vision while the neovascular type
causes sudden onset of central visual problems such as blurry
vision, metamorphopsia and scotomas (blind spots).
A good clinical examination of the fundus, an FA and an
OCT are necessary for the confirmation of the type of ARMD,
and for monitoring response to treatment especially in the
neovascular type. Occasionally, an ICGA is needed.
Management of the neovascular type is thermal laser
treatment to the abnormal vascular complex, if extrafoveal
(outside the foveal center). The subfoveal (under the foveal
center) types are treated using intravitreal injections of antivascular endothelial growth factor (anti-VEGF) medications.
Photodynamic therapy (PDT), a "cold laser", is also a treatment
option for neovascular ARMD. There is no current treatment
for the non-neovascular type. Monitoring must be done, as
a few convert to the neovascular type. Patients with both
Splf-InctrurtionAl WtpriAlc in Onhthalmoloav I 2nd Edition
A
Figure 14. Age related macular degeneration (A) Non-neovascular
type, showing round patch of atrophy of the retinal pigment epithelium at
the macula (black arrowheads), (B) Neovascular type, showing subretinal
hemorrhage and choroidal neovascular membrane (black arrows) at the
macula and perirnacula
types must be advised regarding managing the modifiable
risk factors such as smoking, diet, excessive UV light exposure,
dyslipidemia and hypertension.
RETINITIS PIGMENTOSA
Retinitis pigmentosa (RP) is a retinal disorder belonging to
the family of heredo-degenerative diseases and" ta petoreti na I
diseases. It is characterized by progressive degeneration of the
rods and cones, and in most cases is associated with migration
of pigment epithelial cells into the retina. There are several
patterns of inheritance: autosomal recessive, X-linked recessive
and autosomal dominant .The first two have the earliest onset
and worst prognosis. Patients with the autosomal dominant
form may be symptom free until middle age. Genetic analysis
has shown that the defect in most affected individuals is in the
gene that encodes for rhodopsin.There are 2 types of RP: type
I in which the rods are affected earlier than the cones, and type
II in which the cones are affected earlier than the rods.
Symptoms include night blindness or nyctalopia for most cases
of type I , progressive contraction of peripheral visual fields,
)Iurring of vision in some cases (with macular involvement),
ind development of cataracts . Absence of night blindness is
)ossible especially in type II RP.
tumors, accelerated hypertension as in eclampsia or other
vascular diseases like diabetes mellitus. Causes of traction
detachments are diabetic retinopathy, trauma or ischemic
retinopathies. (Figures 16, 17, 18)
- undus findings include vitreous cells and opacities, narrowed
irteries, diffuse pigmentation of the retinal pigment
pithelium (RPE), bone spicule and comma shaped intraretinal
Noliferation of pigmented cells, and waxy pallor of the optic
iisc in the late stages (Figure 15). RP with very little or no
)igment is possible (sine pigment()) and is usually type II.
Figure 16. Rhegmatogenous retinal detachment, superior half retinal
break most likely at 12:00 o'clock area
Figure 15. Fundus picture of retinitis pigmentosa showing bone spicule
like pigments ( red arrows) and other retinal pigment epithelial changes
(gray mottling) outside the macula
Other causes of night blindness (e.g. vitamin A deficiency,
systemic syndromes, congenital stationary night blindness)
must be ruled out.
RP is usually a bilateral disease. If findings are unilateral
other causes (e.g. blunt trauma, uveitis, long standing retinal
detachment, retained intraocular foreign body, diffuse
unilateral subacute neuroretinitis ) must be ruled out.
Figure 17. Traction retinal detachment in diabetic retinopathy: white
There is no known treatment for retinitis pigmentosa. Cataract
extraction may help improve vision. Daily doses of 15,000
IU of Vitamin A in the form of retinol palmitate (with liver
function monitoring) may help slow down deterioration of
ERG changes, with no known demonstrable effect on vision.
arrows indicate areas of retinal traction from the fibrovascular membranes
RETINAL DETACHMENT
Retinal detachments are conditions where the retinal pigment
epithelium is separated from the inner retinal layers, with
accumulation of fluid in the"subretinal space" (space between
the RPE and photoreceptor "rods and cones" layer). Retinal
detachments can be "rhegmatogenous" (with a retinal
break: tear or hole) or "non-rhegmatogenous" (without
a break). Causes of non-rhegmatogenous detachments are
exudation and traction. Causes of exudative retinal detachment
are inflammatory diseases of the choroid and retina, subretinal
Figure 18. Exudative retinal detachment in eclampsia
5
DISTURBANCE IN VISION I 5.3 Disorders of the Retina, Vitreous and Choroid
Rhegmatogenous retinal detachments are associated with
the formation of a retinal break(s) usually located in the retinal
periphery. These breaks are associated with peripheral retinal
thinning of high myopia, peripheral retinal degeneration such
as lattice degeneration, vitreoretinal traction during vitreous
liquefaction , posterior vitreous detachment as well as trauma.
The loss of vision in rhegmatogenous retinal detachments is
described as a "curtain falling": with blurry vision starting in
the periphery and steadily moving towards the center. Vision
changes are also described as wavy vision and/or visual field
cuts. The symptoms of flashes and floaters in some patients
may be an early warning sign of a serious impending retinal
tear and detachment. Occasionally a patient may present with
normal central vision but with peripheral visual field defects
due to a beginning retinal detachment.
Management of rhegmatogenous retinal detachment is
surgical. The basic principles of retinal reattachment surgery
are: 1) to find the break, 2) to close the break 3) to seal the
retinal breaks with a chorioretinal scar 4) neutralize vitreoretinal
traction. Management of traction detachment is surgical as
well. The management of exudative detachment is primarily
medical, addressing the primary cause.
Figure. 19. Fundus partially obscured by dark red patches of vitreous
hemorrhage; optic disc is hardly seen (black arrow)
ocular B scan ultrasonography must be done to determine if
retinal detachment, tumors or other abnormalities are present
behind the blood.
The general rule is, if no retinal detachment or tumor is
detected, the hemorrhage may be observed for 4-6 months
and allowed to resorb by itself. In the presence of retinal
detachment, tumor or other diseases requiring immediate
VITREOUS HEMORRHAGE
attention, vitreoretinal surgery is advised. If a retinal brea K
Floaters followed by decreasing vision with no history of without a detachment is found, the break is sealed with laser.
trauma are common reasons for emergency consults with the If there is a vitreous hemorrhage accompanying the traction
neovascularization, surgical
eye doctor. When a vitreous hemorrhage is seen, one must detachment and/or retinal
consider the possibility of an avulsed retinal vessel secondary removal of the vitreous hemorrhage and traction membranes,
to posterior vitreous detachment. The presence of a retinal with /or without laser treatment is considered within the
break must be carefully eliminated as a possible cause of the context of management of the retinopathy.
vitreous hemorrhage. This is especially true if the patient has
no systemic vascular disease like diabetes or hypertension,
OCULAR TOXOPLASMOSIS
or hematologic disorders. Any condition causing peripheral
neovascularization may result in vitreous hemorrhage, Ocular toxoplasmosis, caused by an intraocular obligate
including the chronic stages of pars planitis and other parasite is one of the more common forms of posterior
uveitides, sickle cell disease. Trauma, including the battered uveitis. The organism Toxoplasma gondii, is a protozoan
child syndrome, should always be ruled out in children.
that has predilection for the retina. The classic finding is
Symptoms are sudden onset of blurry vision, frequently with
floaters in the form of "many dust like particles" which are
dispersed RBC, or "streaming dark lines". Massive vitreous
hemorrhage can cause significant loss of vision without the
floaters. Lighter hemorrhages may manifest as large clumps of
floaters. Occasionally there are reports of light flashes in the
peripheral field of vision (Figure 19).
Management is directed at finding the cause and clearing
the blood. In most cases where the bleeding is mild, retinal
examination will permit adequate assessment of the situation
and identification of cause.When vitreous hemorrhage is dense
retinochoroiditis. There are two types of ocular toxoplasmosis:
congenital and acquired. The congenital type is acquired by
the pregnant immune-incompetent mother, and passed on
to the unborn child. The later in pregnancy the infection is
acquired by the mother, the more serious the ocular problem.
The acquired type is by ingestion of the organism in uncooked
food or infected fomites. The infection is easily quelled by the
patient but the organism finds its way into the eye and causes
an inflammatory reaction in the vitreous, retina and choroid
hence, a retinochoroiditis.
Scarring of the retina and choroid are prominent in the
quiescent phase. Recurrences of activity are possible and can
>e found at the edges of scars from previous attacks. Visual
iffectation is dependent on the part of the retina affected.
lacular involvement will certainly lead to poor vision
Figures 20, 21).
The patient usually complains of sudden onset of blurry vision,
photophobia, perhaps floaters, sometimes with headache,
neck stiffness an/or tinnitus. The disease presents with
yellowish white patches of retinal edema, wide areas of serous
retinal detachments, retinal vasculitis and/or optic disc edema.
(Figure 22) There may be a heavy anterior uveitis. Later in
the course of the disease the patient develops vitiligo (white
patches on the skin) and poliosis (whitening of eyelashes). A
high index of suspicion based on clinical presentation and
findings, a spinal tap and immunologic tests will help make a
diagnosis of VKH. Fundus fluorescein angiography may help
define the structures involved. Patients are given systemic
steroids and/or immunosuppressives. They usually require
prolonged treatment with maintenance doses.
The final outcome of VKH depends on control of the
inflammation and scar formation. Vision is relatively good
except where the macula has been affected. The course is long
and indolent.
Figure 20. Fundus picture showing typical toxoplasmosis scar at
temporal paramacular area
Figure 22. Multiple foci of serous retinal detachments
(black arrows) in VKH
a•
Figure 21. Composite fundus picture of two scars (red arrows, toxoplasmosis, and an active lesion with indistinct borders (yellow arrow ;
with hemorrhage at its upper and nasal borders
CHOROIDAL CAPILLARY HEMANGIOMA
:_horoidal capillary hemangiomas are benign, isolated, round ,
well circumscribed reddish orange tumors under the retina, of
varying sizes, usually discovered as an incidental finding during
a routine eye examination. On occasion the patient complains
of gradual onset of blurry vision due to induced hyperopia
or to serous exudation from the tumor. These rarely grow in
Diagnosis is best made clinically although immunolog.:
examinations are helpful. Treatment is in the form of oral
antibiotics that interfere with the organism's pathway for
protein transcription, such as sulfadiazine, clindamycin,
pyrimethamine. Intraocular injection of antibiotics has also
been shown to be an effective route of treatment. The use of
steroids whether oral, topical, peri-bulbar or intra-ocular is not
without hazard.
size. Large ones can cause exudative retinal detachments and
eventually have pigmentary retinal changes overlying the
choroidal mass. These tumors have distinct angioigraphic and
ultrasound features (Figure 23).
VOGT-KOYANAGI-HARADA SYNDROME
Management options are laser treatment, cryopexy,
Vogt-Koyanagi-Harada syndrome (VKH) is a rare and unusual
form of diffuse granulomatous uveitis. This is found more in
pigmented individuals and is a bilateral disease.
photodynamic therapy, external beam irradiation and
transpupillary thermotherapy if vision is threatened by retinal
detachment.
S
DISTURBANCE IN VISION 1 5.3 Disorders of the Retina, Vitreous and Cilurold
HUMAN IMMUNODEFICIENCY SYNDROME
RETINOPATHY
The human immunodeficiency syndrome (HIV) may affect the
eye directly. More frequently, the eye becomes vulnerable to a
number of opportunistic infections and neoplastic conditions
because of the underlying systemic immunodepression.
These include CMV retinitis, toxoplasmosis, Candida retinitis,
Pneumocystis carinii -fection and Kaposi's sarcoma.
Figure.23. Choroidal capillary hemangioma with classic red orange
color (white arrow)
METASTATIC CHOROIDAL TUMOR
Metastatic tumors to the uveal tract are the most common
intraocular malignancies. Most are found in the choroid more
often than in the iris or ciliary body. Metastasis to the retina
and optic disc are rare. Spread from the primary cancer is
by the hematogenous route. The primaries are, in men, lung
carcinomas, and in women, breast carcinomas. They may
appear as bumpy elevations under the retina, with or without
surrounding exudation, or an almost flat mottled lesion under
the retina, also with or without exudation (Figure 24). They
may be solitary or multiple, big or small.
Visual symptoms occur if the tumors or exudative detachments
are at or close to the macula. Extramacular or peripheral
detachments may cause photopsias and visual field problems.
Small tumors that do not cause visual symptoms frequently
go undetected.
Figure 24. Choroidal metastasis from lung adenocarcinoma with
leopard skin-like mottling (black arrow) of the elevated mass, and
surrounding shallow exudative retinal detachment (red arrows)
The most consistent retinal manifestations are fleeting cotton
wool spots (retinal nerve fiber infarcts) which are present in
almost 100% of HIV positive patients at some time during the
course of the systemic HIV infection.These localized ischemic
areas are located at the posterior pole and may be related to
circulating immune complexes. In most cases cotton wool
spots are asymptomatic and blurry vision occurs only if the
lesion is at or close to the macula. Diagnosis must exclude
other causes of cotton wool spots (diabetic retinopathy,
collagen vascular disease, retinal vaso-occlusive disease).The
other ocular manifestations of disease depend on the type of
opportunistic infection.
The eye disease is managed together with the systemic
treatment of AIDS. Intravitreal implantation of gancyclovir
and foscarnet is an option . Vitreoretinal surgery is indicated
when there is vitreoretinal traction, non-clearing vitreous
hemorrhage and/or retinal detachments.
SUMMARY
It is the primary objective of this material to guide the medical
student through the steps needed in order to recognize
posterior segment "vitreo-retinal and/or choroidal" disorders
by taking a good history and performing a thorough eye
examination. One should remember that even if these
problems have typical presentations, the atypical may happen.
It is for the wise student in ophthalmology to unravel the
mystery in each case he sees by correlating the knowledge
he would have learned from this book and the clinical picture
he would have obtained from his interaction with his patient .
As medical practitioners we should be aware of the many
different manifestations of retinal, vitreous and choroidal
diseases. Just as importantly, the medical practitioner should
realize that many eye problems can be traced to systemic
diseases or etiologies originating from systems other than the
eye, as in distant trauma. It is thus possible that fundus findings
can alert the ophthalmologist regarding the presence of a
systemic illness that would have otherwise been missed e.g.
diabetic retinopathy. Subsequent referrals can then be made
and the patient holistically co-managed with other specialists.
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
American Academy of Ophthalmology . Basic and Clinical
Science Course, Retina and Vitreous. San Francisco USA.
LEO. 2008
Diabetes Control and Complications Trial Research (DCCT)
Group. The Effect of Intensive Treatment of Diabetes
on the Development and Progression of Long-term
Complications in Insulin-dependent Diabetes Mellitus.
N Engl J Med 1993; 329:997
Kanski. Clinical Ophthalmology : A Systematic Approacn.
London. Elservier. 6th ed. 2007.
Yanoff, Podos. Textbook of Ophthalmology, Retina and
Vitreous. London. Mosby. 1st ed. 1994. Vol 9
Riordan-Eva, Witcher, Vaughn & Asbury's General
Ophthalmology. Lange Medical Books/McGraw-Hill. 16th
ed. 1999
Ryan S. ed. Retina. The Mosby Company. 4th ed. 2006
Tasman, Jaeger. Duane's Ophthalmology. Lippincott,
William & Wilkins. 2009
United Kingdom Prospective Diabetes Study
(UKPDS) Group: Intensive Blood Glucose Control with
Sulphonylureas or Insulin Compared With Conventional
Treatment and Risk of Complications in Patients with
Type 2 Diabetes ( UKPDS 33), Lancet 352: 837-853, 1998
United Kingdom Prospective Diabetes Study (UKPDS)
Group: Tight Blood Pressure Control and Risk of
Macrovascular and Microvascular Complications in Type
2 Diabetes ( UKPDS 38), BMJ 317: 7160-7176, 1998
Based on the data given above:
1. What is your working diagnosis of the case ?
2. Why ?
3. Is there anything else that you would want to ask the
patient?
4. What ancillary procedures would you ask for?
Case 2.
A // yr old female consults you for blurring of central vision in
the left eye, since 3 weeks ago. Right eye is "somewhat blurred"
but is better than the left eye. She had cataract surgery in both
eyes 10 years ago and has intraocular implants. She is not
diabetic, is a hypertensive with good control with medications,
has no heart disease, but is on lipid lowering medications.
Your findings are:
Best corrected vision OD: 20/30 J2
10P OU: 16 mm Hg
OS: 20/100 J16
EOMs are normal in both eyes
Slit lamp findings of anterior segment OU: clear cornea, +arcus
senilis,. deep AC, + 10Ls in place, no AC cells and flare
Fundus findings: OD: Normal optic disc with CD 0.3, +
retinal arteriolar attenuation; Macula has no foveal reflex but
otherwise normal. A few drusen are noted in posterior pole
area. Peripheral retina is normal.
SELF-TEST
Fundus findings OS: Normal optic disc with CD 0.3, + arteriolar
attenuation; there is a small subretinal hemorrhage at macula,
covering fovea, around 2 disc diameter size. Peripheral retina
is normal.
Case 1.
A 50 year old female comes to you with a complaint of sudden
onset of blurry vision of the right eye since a week prior to
consult. She reports that she has had diabetes mellitus for
the past 15 years and is on insulin, with poor control of blood
sugar.
Based on the data given above
1. What is your working diagnosis of the case?
2. Why?
Vision OD: Counting Fingers 2 feet
OS: 20/20 .11 with correction
3. What else would you want to ask the patient?
Intraocular Pressure OU: 15 mm Hg
4. What ancillary procedures would you ask for?
Slit Lamp findings: OD: clear lens; no anterior chamber cells;
hazy vitreous with no view of the retina
OS: clear lens ; no anterior chamber cells; clear
vitreous
Funduscopy OD: negative ROR
OS: occasional microaneurysms noted all over
the fundus. Several cottonwool spots and blot
hemorrhages are also seen all over the fundus.
Macula appears normal.
EOMs OU: normal
Answers to Self- Test on page 221.
5
DISTURBANCE IN VISION 3 Disorders of the Retina, Vitreous and Choroid
81
5.4 Glaucoma
Norman M. Aquino, MD
INTRODUCTION
Glaucoma is a progressive neurodegenerative disease affecting the eye that may res;.. : v spa field disturbance or blindness. In
this condition, there is death of retinal ganglion cells resulting in a characteristic opt;c neuropathy with cupping, or excavation,
of the optic nerve head. (Figure 1).
OBJECTIVES
This chapter aims to provide a comprehensive overview of glaucoma. After reading this material, the —edlcal student In
ophthalmology is expected to be able to:
1.
Discuss the pathophysiology of glaucoma
2.
Discuss the eye examinations for glaucoma
3.
Discuss the principles of management of glaucoma
CONTENT
I.
Pathogenesis of glaucoma
II. Patient Evaluation
1. History
2. Eye examination
A. Visual acuity tests
B. Refraction
C. Slit lamp examination
D. Tonometry
E. Optic nerve head evaluation
F. Gonioscopy
G. Visual field examination
III. Management
NORMAL AQUEOUS
FLOW
fff
Trabecular
meshwork
Conjunctiva
Episciera
vein
Aqueous veal'
Schlemm's canal
Aqueous
flow
Lens
Figure 1. Glaucomatous optic nerve
Glaucoma is a leading cause of irreversible blindness and
is second only to cataracts as the most common cause of
blindness overall. Worldwide, glaucoma affects more than 70
million people, of whom about 10% are estimated to be blind.
In the Philippines, this condition ranks among the top 3 causes
of blindness. The economic and social impact of this disease is
enormous but is very difficult to quantify.
The understanding of the glaucomatous disease process
entails a thorough comprehension of the complex physiologic
relationship that exists between aqueous humor dynamics,
intraocular pressure and their effects on the optic nerve.
Aqueous humor is an intraocular fluid that is vital to the
health and function of the eye. It is produced in the anterior
portion of the pars plicata along the tips or crests of the ciliary
processes.The circulating aqueous humor enters the posterior
chamber and flows around the lens and through the pupil
into the anterior chamber. It leaves the eye at the anterior
chamber angle through the outflow system consisting of
trabecular meshwork, Schlemm's canal, intrascleral channels,
and episcleral and conjunctival veins. This is referred to as
the conventional or trabecular outflow (Figure 2). In the
unconventional or uveoscleral outflow, aqueous humor exits
by passing through the root of the iris, between the ciliary
muscle bundles, then through the suprachoroidal-scleral
tissues.
Intraocular pressure is a function of the rate at which aqueous
humor enters the eye (inflow) and the rate at which it leaves
the eye (outflow). An impediment in outflow would therefore
result in elevation of intraocular pressure leading to pathologic
alteration and loss of the nerve fibers of the optic nerve.
Although elevated intraocular pressure (10P) is the most
frequent causative risk factor for the development of glaucoma,
there are other factors that are also known to play a role. Thus,
attempts to define glaucoma solely on the basis of IOP alone
may not always be appropriate. Other pathophysiologic
mechanisms, either working separately or in combination with
10P, may contribute to retinal ganglion cell death. Impaired
Figure 2. Aqueous is produced by the chary body in the posterior
chamber, circulates around the lens, passes through the pupil, and flows
into the anterior chamber. Eighty percent of the outflow goes through the
trabecular meshwork and drains into the episcleral venous system; the
remaining 20% passes through the uveoscleral pathway via the interstitial
spaces between the iris root and ciliary muscle. Adopted from Adatia FA,
Damji KR.,
microcirculation, ischemia, deprivation of neuronal growth
factors, neurotoxic agents like glutamate and nitric oxide have
been shown to affect retinal ganglion cell viability (Figure 3).
The elucidation of cellular and molecular events that occur
during the glaucomatous disease process will most certainly
evolve over the next decade and will provide a more definitive
biologic basis for the disease.
Mechanical
Tissue Damage
Decreased
Elevated —4. Axoplasmic
10P
Flow
Retinal Ganglion
Cell Death
Vascular ..„,,,„,„,,,,,Ischemia
Dysregulation
1
Free Radicals
Neurotoxic
Agents
Figure 3. Concept of glaucoma pathogenesis . Adopted from the
European Glaucoma Society.
There are several approaches by which the glaucomas may be
classified.
Based on etiology, they can either be "primary" or "secondary'l
In the "primary" form, there are no identifiable ocular or
systemic conditions that contribute to the condition. These
typically affect both eyes and probably have a genetic basis.
In contrast, glaucomas are classified as"secondary"when there
is a partial understanding of underlying or predisposing ocular
or systemic events. These may be unilateral or bilateral, some
may have genetic basis, while others are acquired conditions.
However, as our knowledge about the mechanisms of the
glaucomatous disease process continues to expand, we realize
5 DISTURBANCE IN VISION 15.4 Glaucoma
83
that the "primary and secondary" classification approach has
become increasingly inadequate.
diagnosis and proper management of glaucoma.
A classification system based on the mechanism and site ofaqueous
outflow obstruction may be a more appropriate approach.
In open angle mechanisms, there is no obstruction to aqueous
outflow by iris tissue (Figure 4). Elevation of I013 results from
obstruction within the trabecular meshwork and beyond.
Many patients with open angle glaucoma are asymtopmatic.
They may have blurring of vision, which they usually attribute
to an error of refraction or the development of cataracts. Focal
loss of vision, unless severe, is rarely noticed by the patient.
When meeting a patient for the first time, it is helpful to observe the
patient as he or she walks into the examination room. Can the patient
walk unassisted? Does the patient walk confidently or does he or she
shuffle into the room wary of the surroundings? Is the patient able
to locate the examination chair accurately? All these clues give the
examiner an idea of the degree of visual deficiency that the patient
may have.
In angle closure mechanisms, the peripheral iris is in apposition
to the peripheral cornea blocking egress of aqueous humor
through the conventional anterior chamber angle outflow
tract resulting in the elevation of 10P.
It is important that the examiner ask the patient the reason for his
or her visit. In particular, detailed inquiries about visual problems,
accompanying ocular signs and symptoms, family history of eye
disease, previous eye surgery, trauma, other systemic or medical
conditions, and medications being taken systemically or topically are
essential. A comprehensive history may eliminate, or rule out, some
of the diagnostic possibilities or corroborate a suspected diagnosis.
B. Examination of the Eye
Examination should begin with an accurate assessment of
visual acuity. Proper refraction, or at least a pinhole vision test,
must be performed in order to determine the eye's refractive
status and visual potential. The refractive status can also be a
clue to diagnosis - as open angle glaucoma is found to be more
common in myopes while angle closure glaucoma is more
associated with hyperopes.
Figure 4. Open angle vs. angle closure mechanism. Adopted from Kwon
YH.s
Occlusion of the anterior chamber angle can occur
intermittently and is characterized by the development of
peripheral anterior synechiae. Elevation of I013 is gradual in
these cases. These patients may be asymptomatic or may
have recurrent short episodes of unilateral pain, redness and
blurring of vision associated with haloes around lights. These
attacks may resolve spontaneously.
An acute angle closure attack occurs when there is sudden
complete obstruction of the outflow tract by peripheral iris.
This is an ocular emergency. Because of the sudden rise in
10P, patients experience blurring of vision, eye redness with
severe eye pain, headache, nausea and vomiting. Treatment
must be instituted at the soonest possible time and is directed
at reducing 10P. A peripheral laser iridotomy, which creates a
connection between the posterior and anterior chamber, can
relieve the obstruction in the outflow tract. In many cases, the
fellow eye, which most likely is also anatomically predisposed
to angle closure, should receive a prophylactic laser iridotomy.
In patients found to have impaired vision, it is important to try and
determine why there is such. Is it because of a simple error of refraction?
Is there pathology affecting the transmission of light from the cornea
thru the crystalline lens to the retina? Are the retina and optic nerve
normal? Is there pathology invoMng the brain? It must be remembered
that although glaucoma alone can cause visual disturbance, it may
also co-exist with any of the conditions previously cited.
The slit lamp biomicroscope is an ophthalmological instrument
that allows stereoscopic examination of ocular tissue under good
magnification and illumination (Figure 5). It is used to visualize
and evaluate the various tissues and layers of the eye. Its use in
glaucoma evaluation is invaluable.
DIAGNOSING GLAUCOMA
A. Patient History
Careful history-taking, followed by a comprehensive physical
examination, will most likely provide enough information for
Figure 5. Slit lamp biomicroscope examination
Tonometry
The clinical measurement of the 10P is called tonometry
(Figure 6).
of 10P elevation in a particular case of glaucoma. In patients,
it allows for determination whether patient's glaucoma has an
open or closed angle mechanism.
(Image of Iridocomeal Angle)
Elevation of lop is considered the most significant causative
risk factor for the development and progression of glaucoma.
Therefore, it should be measured in all patients old enough to
cooperate with the procedure.
It is generally accepted that in the non-glaucomatous eye, 10P
ranges from about 10 - 21 mm Hg (mean 16 ± 2.5 mm Hg). Most
clinicians however agree that there is no sharp demarcation
line between what is "normal"and "abnormarlOP. A statistically
abnormal 10P is not synonymous with present or impending
disease. Many people with elevated eye pressures maintain
normal optic nerves and visual function. Glaucomatous optic
nerve damage can, on the other hand, occur in eyes with
pressures within the "normal" range.
Gonioscope Mirror
Ocular Lubricant
Cornea
Iridocorneal Angle
Iris
Figure 7.
Principle of gonioscopy
Figure 8. Structures in the anterior chamber angle (as viewed thru a
gonioscopic lens)
Figure 6. Applanation tonometry
Gonioscopy
The examination of the anterior chamber angle is called
gonioscopy. This is accomplished by using a variety of special
lenses that need to be coupled to the eye. Under normal
conditions, the anterior chamber angle cannot be visualized
through the intact cornea because light coming from the
angle undergoes total internal reflection at the cornea-air
interface. These special lenses eliminate this interface allowing
visualization of the angle and the structures that lie within it
(Figure 7).
The anterior chamber angle is where the main outflow system
for aqueous humour is located.This area is comprised of a series
of structures lying between the iris root and the peripheral
cornea. These include, from posterior to anterior, the ciliary
body band (CBB), scleral spur (SS), trabecular meshwork (TM)
and Schwalbe's line (SL) (Figure 8). Examination of each of
these structures and their relationship to one another provides
valuable information regarding the etiology and mechanism
The chamber angle is considered closed when none of the
angle structures are seen on gonioscopy. It is considered open
when the structures anterior to the scleral spur are visible.
An accurate gonioscopic assessment is essential in planning for
appropriate therapy since the therapeutic approach to angle
closure glaucoma differs from that of open angle glaucoma.
Optic Nerve Head Evaluation
The assessment of the morphologic features of the optic disc or
optic nerve head is important in glaucoma evaluation.
This structure can be examined clinically with a direct
ophthalmoscope, an indirect ophthalmoscope, or a posterior
fundus lens. The direct ophthalmoscope, although providing
high magnification, does not provide sufficient stereoscopic
detail. On the other hand, while the indirect ophthalmoscope
provides for stereoscopic view, its main disadvantage is the small
image size one can view with it.The best method to examine the
optic nerve head is with a posterior fundus lens at the slit lamp.
This system provides high magnification, excellent illumination
and a stereoscopic view of the optic disc.
5
DISTURBANCE IN VISION 1 5.4 Glaucoma
85
The optic disc is usually round or slightly oval in shape and
contains a central cup. The tissue between the cup and the
disc margin is referred to as the neuroretinal rim. In normal
patients, this rim has a relatively uniform width and a color that
ranges from orange to pink (Figure 9).
Generalized enlargement of the cup may be the earliest
change detected in glaucoma (Figure 10). It is also useful to
compare the optic cups of both eyes as asymmetry is unusual
in most individuals.
Thick neurorethel rim
9,40,.
:ka
, .. •
\ SW
1.4
Smarr cup
Figure 10. (A) Normal cup: (B) Enlarged cup in glaucoma
Focal enlargement of the cup appears as localized notching or
narrowing of the neuroretinal rim (Figure 11).
Figure 9. Normal optic nerve head
It is a common clinical practice to describe an optic disc by
comparing the diameter of the optic cup to the diameter of
the disc in both the horizontal and vertical meridians. This
is usually expressed as a ratio such as 5/10 or 0.5. Usually, a
horizontal cup-to-disc ratio of 3/10 or 0.3 is considered normal.
Cup-to-disc ratio increases slightly with age. There are also
racial differences in cup-to-disc ratios.
The appearance and configuration of the optic disc often
provides essential information about the existence and
severity of the disease (Table 1)
Table 1: clinical evaluation of the optic Nerve head
1.
Size and shape of the optic disc
2.
Size, shape, and color of the neuroretinal rim
3.
Size of the optic cup in relation to the area of the optic disc
4.
Configuration and depth of the optic cup
5.
Cup-to-disc diameter ratio and cup-to-disc area ratio
6.
Position of the central retinal vessel trunk on the disc
7.
Presence and location of splinter-shaped hemorrhages
8.
Presence and location of peripapillary chorioretinal atrophy
9.
Visibility of the retinal nerve fiber layer (RNFL)
Figure 11. Notching at the inferior rim (arrow)
If this occurs at either, or both, the superior or inferior pole of
the disc, the cup becomes vertically oval. In more advanced
glaucoma, the tissue destruction extends behind the cribriform
plate and the lamina bows backward. The optic nerve head
then takes on an excavated and undermined appearance that
has been likened to a "beanpot" (Figure 12).
In the normal eye, the nerve fiber layer can be best visualized
with red free illumination, and appears as a pattern of striations
that radiate toward the optic disc. With the development of
glaucoma, the nerve fiber layer thins and becomes less visible.
Diffuse loss of the nerve fiber layer may be a very important
sign of early glaucomatous damage.
Funduscopic evaluation of the optic disc and nerve fiber layer
can be difficult in the presence of media opacities like cataracts.
Detecting subtle anatomic changes in these structures
through time also presents a challenge. Optical coherence
tomography, scanning laser polarimetry and confocal
scanning ophthalmoscopy are new imaging techniques that
have significantly improved our capability for early disease
detection and monitoring of disease progression.
Visual Field Testing
Visual field testing, or perimetry, is an important diagnostic tool
in glaucoma. It also plays a critical role in monitoring disease
progression. There are various ways of testing and mapping
out a patient's visual field.
Figure 12. (A) Normal optic disc, (B) Histologic cross section of normal optic disc,
(C) Glaucomatous optic disc, (D) Histologic cross section of glaucomatous optic disc
(beanpot appearance)
Splinter hemorrhage usually appears as a linear red streak on or
near the disc surface (Figure 13). The hemorrhage clears over
several weeks but is often followed by localized notching and
pallor of the neuroretinal rim with subsequent visual field loss.
The confrontation method of visual field testing will quickly
demonstrate gross field defects. It may be the only practical
method to evaluate patients who are unable to perform well
using the more sophisticated instruments used in perimetry
testing. The detection of small field defects in early glaucoma
may be missed using this technique.
Kinetic visual field testing is performed, as the name implies,
with a moving test object.The object, usually a light of variable
size and intensity projected on an evenly illuminated surface,
is moved from a non-seeing area toward a seeing area. The
location is recorded when the patient sees the object. The
process is repeated until a boundary of seeing and non-seeing
is determined. This boundary line is called an isopter. Several
isopters are usually obtained using test objects of different size
and/or intensity. The Goldmann perimeter is an example of a
manual kinetic perimeter.
Static visual field testing involves the use of non-moving test
spots. During the examination, fixed test spots of varying
intensity of light are presented for a short period of time. The
patient responds when light is perceived in each test spot.
Static testing attempts to find the light sensitivity of the eye
at preselected locations in the visual field. Currently available
automated perimeters, like the Humphrey visual field analyzer
and the Octopus, employ the static type of visual field testing.
With the eye open and looking straight, the visual field of that
Figure 13. Splinter hemorrhage at inferior border of optic disc
eye is defined as all the space that it can see. The di rnerisiom
of the normal field of vision are defined relative to fixation. The
normal visual field extends approximately bu degrees superior
and nasal, 70 degrees inferior, and 90 -100 degrees temporal
to fixation. The blind spot occupies the area defined by the
5
DISTURBANCE IN VISION l 5,4 Glaucoma
87
optic nerve head and is typically located 15 degrees temporal
to fixation. Visual sensitivity is greatest in the center, the fovea,
and decreases toward the periphery. By convention, the visual
field of each eye is plotted as the patient sees it (Figure 14).
60°
Bllndspot
Fixation
Superior
60
100°
Glaucomatous damage at the optic nerve head produces
visual field defects in the region subserved by the affected
nerve fibers. The location, distribution, size and shape of the
resulting visual field defect, called a scotoma, are therefore
determined by the location and extent of the anatomic
defect. Typical glaucomatous visual field defects include
localized paracentral scotomas, arcuate defects, nasal steps,
and temporal wedges (Figure 16). It is important to correlate
changes in the visual field with changes in the optic disc. If an
appropriate correlation is not present, other causes of visual
field loss must be considered.
Inferior
70°
Figure 14. Normal limits of the visual field of the right eye
The dimensions of the visual field can be influenced by other
factors in addition to glaucoma. These include facial structure,
eyelid anatomy, pupil size, clarity of the ocular media, and
refraction. Many neurologic, neuro-ophthalmologic and
retinal conditions also alter the visual field.
Visual field changes seen in glaucoma reflect retinal and optic
nerve anatomy. Retinal nerve fibers radiate from the optic
nerve head and are distributed in an arcuate manner around
the foveal region (Figure 15).
30
30
30
30
30
Figure 16. (A) Bjerrum's region extends from the blind spot to the medial
raphe 10-20 degrees from fixation, (B) Siedel scotoma, (C) Paracentral
scotoma, (D) Arcuate or Bjerrum scotoma, (E) Double arcuate scotoma
(F) Temporal wedge defect. Adopted from Epstein DL.3
Figure 15. Arcuate distribution of retinal nerve fiber bundles.
Adopted from Epstein DL.3
MANAGEMENT OF GLAUCOMA
SUMMARY
The goal of treatment in glaucoma is to preserve vision by
slowing down the progression of the disease process. This
involves the lowering of KW and the adoption of therapeutic
strategies to protect the optic nerve from further damage
(Table 2)
Table 2: Treatment of Elevated 10P
Medical Treatment
A. Suppression of aqueous production
1. Beta adrenergic blocking agents - betaxolol, levobunolol
Timolol
2. Alpha adrenergic agonists - apraclonidine. brimonidine
Glaucoma is a progressive neurodegenerative disease affecting
the eye that may result in visual field disturbance or blindness.
In this condition, there is death of retinal ganglion cells
resulting in a characteristic optic neuropathy with cupping, or
excavation, of the optic nerve head. Although elevated 10P is
the most frequent causative risk factor for the development
of this condition, there are other factors that are also known
to play a role. The key to successful glaucoma management
is early detection, appropriate and adequate treatment, and
regular monitoring of the disease.
REFERENCES
3. Carbonic anhydrase inhibitors - brinzolamide,
Dorzolamide. oral acetazolamide
B. Facilitation of aqueous flow
1. Parasympathomimetic agents - pilocarpine
2.
2. Prostaglandin analogs - bimnatoprost. latanoprost,
travapost
C. Reduction of vitreous volume
3.
1. Hyperosmotic agents - oral glycerol. intravenous
mannitol
4.
Surgical and Laser Treatment
A. Peripheral iridotomy or iridectomy
5.
B. Laser 1- abeculoplasty
C. Glaucoma Drainage Surgery
1.
Trabeculectomy
2.
Glaucoma shunts and filtration devices
D. Cyclodestructive Procedures
I reatment should be appropriate to the type and severity of
the glaucoma that is present in a patient.
One or a combination of topical medications is given to lower
intraocular pressure. Laser therapy is used, when appropriate,
to improve fluid drainage within the eye.
In instances when there is progression or worsening of
the glaucomatous condition, despite maximum use of
medications and laser, glaucoma surgery is done. This would
involve the surgical creation of new drainage systems in the
eye to relieve pressure buildup. Intolerance to medications
and inability to sustain medical treatment are also indications
for surgery.
6.
7.
Allingham, R. Rand (ed.). Shield's Textbook Of Glaucoma.
Philadelphia, PA: Lippincott Williams and Wilkins. 5th
Edition, 2005
American Academy of Ophthalmology. Basic and Clinical
Science Course Section 10: Glaucoma. San Francisco, CA.
2008.
Epstein, David L. (ed.). Chandler and Grant's Glaucoma.
Baltimore, MA. Williams and Wilkins. 1997.
Higginbotham, Eve J. and Lee, David A. (ed.). Clinical Guide
To Glaucoma Management. Woburn, MA. Butterworth
Heinemann. 2004.
Kwon, Young H. (ed.). A Patient's Guide To Glaucoma.
Coralville, IA. F.E.P. International, Inc. 2008.
South East Asia Glaucoma Interest Group. Asia Pacific
Glaucoma Guidelines. Sydney, Australia. 2nd Edition. 2008.
Weinreb, Robert N., et al (eds.). Glaucoma In The 21st
8.
Century. London, UK. Mosby International. 2000.
Weinreb, Robert N., et al. (eds.). World Glaucoma Association:
Consensus Series. Amsterdam, The Netherlands. Kugler
9.
Publications. 2010.
Adatia FA, Damji KF. Chronic open angle glaucoma.
http://www2.cfpc.ca/cfp/2005/Sep/vo151-sep-cme-3.asp
accessed October 24, 2011
SELF-TEST
1.
Visual disturbance in glaucoma is the direct result of:
A. elevation of lop
B. death of retinal ganglion cells
C. obstruction of flow at the trabecular meshwork
D. presence of cataract
E. error of refraction
At this time, generally speaking, glaucoma cannot be cured,
but it can be controlled. With the availability of new topical
medications, lasers and new surgical technology and
techniques, we are now better able to control this disease.
S DISTURBANCE IN VISION
I
2.
The following structure is NOT found in the anterior 7. Aqueous humouroutflow thru the trabecular meshwork
chamber angle:
and Schlemm's canal is referred to as:
A.
B.
C.
D.
E.
3.
scleral spur
trahecular meshwork
ciliary body band
Schwalbe's line
lamina cribrosa
Morphologic finding in the optic nerve head is NOT be
suspicious for glaucoma:
A.
B.
C.
D.
E.
A. conventional outflow
B. extraocular outflow
C. infrachoroidal outflow
D. suprachoroidal outflow
8. Impediment in aqueous humour outflow would result
in:
A.
B.
C.
D.
E.
notching
splinter hemorrhages
drusen
enlarged cup-disc ratio
thinning of the nerve fiber layer
9.
4.
Which of the following does NOT affect the character
and dimension of the visual field of an eye:
A.
B.
C.
D.
E.
5.
lateral rectus muscle paralysis
miotic pupil
glaucomatous optic neuropathy
ptosis
high bridge of nose
Which of the following statements is true?
A. Automated perimeters employ kinetic visual field
testing strategies.
B. Blindness in glaucoma is reversible.
C. Genetics does not play a role in the causation of
glaucoma.
D. Peripheral anterior synechiae are found in open
angle glaucoma.
E. Preservation of vision is the goal of glaucoma therapy.
6.
Aqueous humour is produced in:
A. ciliary processes
B. pars plana
C. Schlemm's canal
D. trabecular meshwork
E. vitreous
IOP elevation
optic disc edema
pupillary block
retinal detachment
swelling of the crystalline lens
Which of the following eye medication lowers IOP thru
the facilitation of aqueous humour outflow:
A. orinzp,a
B. dorzolar
C mannitol
D. pilocarpine
E. timolol
10. In kinetic visual field testing, the boundary of "seeing"
and "non-seeing" is called:
rs. olinaspot
B. fixation
C. isopter
D. nasal step
E. scotoma
Answers to Self-Test on page 221.
5.5 Disorders of the Optic Nerve
z
Raul D Cru MD
INTRODUCTION
The optic nerve transmits visual impulses from the retina to the brain. A knowledge of the basic neuro-anatomy and a detailed
clinical examination of the optic nerve function are essential requisites in the evaluation of a patient with visual problems.
OBJECTIVES
After reading this chapter the student should be able to:
1,
2.
3.
Discuss the basic anatomy of the optic nerve
Discuss the signs and symptoms of optic nerve disorders
Discuss various tests used in evaluating optic nerve function
4.
Recognize disorders of the optic nerve
Identify field defects along the visual pathway
5.
CONTENT
I.
II.
Anatomy of the optic nerve
Evaluation of patients with optic nerve disorders
1.
2.
3.
History taking
Ocular examination
A. Visual acuity
B. Pupillary testing
C. Ophthalmoscopy
Ancillary tests
A. Visual field test
B. Other ancillary tests
III. Optic nerve disorders
1. Papilledema
2. Optic neuritis
3. Anterior ischemic optic neuropathy
4. Toxic optic neuropathy
5. Optic atrophy
6. Developmental anomalies
I. ANATOMY OF THE OPTIC
2. OCULAR EXAMINATION
NERVE
A. Visual Acuity
Measurement of the best corrected visual acuity is an absolute
requirement in assessing visual disturbances. Corrected visual
acuity should be 6/6 (20/20) or better in individuals with
normal vision.
The optic nerve is approximately 50 mm long and consists of
about 1.2 million axons originating from the retinal ganglion
cells. The optic nerve is composed of an anterior (intraocular)
and posterior (retrobulbar) portions.
The intraocular portion (-1mm long) can be visualized using
an ophthalmoscope. The retrobulbar portion starts behind
the eyeball and can further be divided into the intraorbital
(-30 mm long), intracanalicular (-6 mm long), and intracranial
(-10 mm long) segments. Normally, myelin covers the entire
retrobulbar portion and myelination ends just behind the
intraocular portion.
The short intraocular portion of the optic nerve is commonly
referred to as the optic disc (papilla). The longest section of
the optic nerve is the intraorbital segment. The intraorbital
segment is S-shaped to permit the eye to move without
stretching. Within the orbit, the intraorbital segment is
encircled by dura, arachnoid, and pia mater of the brain
meninges. As it exits the orbital space and enters the optic
foramen together with the ophthalmic artery, this division
is known as the intracanalicular segment. The intracranial
segment begins from the optic foramen to just before it joins
the contralateral optic nerve to form the optic chiasm.
IL Pupils
Patients with optic nerve problems may have abnormal
pupaary responses. Clinicians should be able to differentiate
normal from abnormal pupils. See Chapter 4 for pupillary
tests. One should suspect optic nerve problems in patients
with unequal or unreactive pupil or pupils with relative afferent
pupillary defects (RAPD) (Figures 1 and 2).
RIGHT EYE
LEFT EYE
Most of the intraocular portion is supplied by the branches of
the posterior ciliary artery. The intraorbital segment is mainly
supplied by the branches of the ophthalmic artery. Branches
of the internal carotid artery supply both the intracanalicular
and intracranial segments.
II. EVALUATION OF PATIENTS
WITH OPTIC NERVE DISORDERS
1. HISTORY AND SYMPTOMS
The most important initial step in the evaluation of a patient
is taking a good and complete history. Pertinent details such
as eye pain, headache, unilateral or bilateral involvement must
not be neglected. Review of the past medical, family, social,
personal history and other contributory factors are valuable
information.
The common complaint among patients with optic nerve
disease is blurring of vision.
1111
Solf-Inonirtinnal lubtarialc in nnhtrulmolonv I lnd Edition
Figure 1. Normal response to swinging flashlight test. Pupils
remain constricted as light is transferred from eye to eye.
RIGHT EYE
LEFT EYE
Short
ciliary nerve
Ciliary .--ganglion
Ill nerve "
EdingerWestphal
nucleus
Lateral
geniculete
body
Posterior commissure
Superior colliculue
Figure 3. Diagram of light reflex pathway
C. Ophthalmoscopy
Direct ophthalmoscopy allows visualization of the optic
disc (Figure 4). It is an indispensable diagnostic procedure
in establishing proper diagnosis. It also permits not only a
detailed visualization of the optic disc but also the entire
fundus.
Figure 2. Relative afferent pupillary defect (RAPID; ;n
:._tested
with the swinging flashlight test. Note dilation of pupils wne- i;-.1
Any acute injury, ischemia, trauma or irritation to the optic
disc can cause swelling or edema to the nerve axons. On
ophthalmoscopy the optic disc margins become blurred
and indistinct. Various diseases may cause optic disc edema
(Table 1).
Table 1. Conditions that can cause optic disc edema
transferred to the affected left eye.
ANISOCORIA
Papilledema
Raised ICP
Inflammatory
Optic neuritis, uveitis
Pupillary control is basically an interplay between the
parasympathetic (constriction) and the sympathetic system
(dilation). The parasympathetic constriction pathway which
originates in the midbrain pretectal area (Edinger-Westphal
nucleus) sends impulses to the eye via the ciliary ganglion
to connect to the cranial nerve Ill. The sympathetic dilation
pathway which originates in the hypothalamus sends impulses
down to the C-8 to T-2 spinal cord level (ciliospinal center of
Vascular
Toxic
Ischemic optic neuropathy, CRVO,
hypertension
Ethambutol, methanol, lead
Infiltrative
Leukemia. lymphoma. metastasis
Budge) then to the superior cervical ganglion via the ciliary
nerves to connect to the dilator muscles (Figure 3).
Unequal pupils or anisocoria may be a sign of a neurologic
disease. A dilated pupil may be caused by cranial nerve
III paralysis, head trauma, brain herniation or Adie's pupil
(ciliary ganglion damage). A constricted pupil can be seen in
Horner's syndrome, neurosyphilis (Argyll-Robertson pupil) or
parasympathomimetic drug intake.
Traumatic
Traumatic optic neuropathy
Compressive
Meningioma orbital tumors
N
Vitamin B deficiency
InfeCtiOUS
Herpes, cavernous sinus thrombosis.
AIDS
Hereditary
Leber's hereditary optic neuropathy,
drusen, myelination, crowded disc
(small CID ratio)
Medications
Sildefanil, amiodarone, omeprazole,
interferon
5
DISTURBANCE IN VISION I S S Disorders of the Optic Nerve
93
Table 2. Common terms used to describe visual field defects
A7rtt
Definition
,
Scotoma
015iammatic
Representation
general term used for area's of reduced or absent
vision
Central
area of depressed vision
corresponding with
fixation point that
interferes with or
abolishes central vision
Cecocentral
a horizontal oval defect
in the visual field situated
between and embracing
both the fixation point
and the blind spot
Paracentral
adjacent to the fixation
point
Arcuate
arc-shaped defect
ansing in an area near
the blind spot
Attitudinal
involves the inferior or
supenor area
Figure 4. Normal optic disc
3. ANCILLARY TESTS
A. Visual Field Test
The visual field is the area of vision of each eye with the
patient fixating centrally. A basic and reliable clinical method
of field testing is the confrontation test (Figure 5) This
method compares the examiner's field of vision and that of
the patient's. Any difference between the examiner's and
the patient's visual field is confirmed and documented. The
examiner is about 2-3 feet away from the patient. Each eye is
examined separately. It is important that the patient maintains
fixation on the examiner's nose. A test target or usually finger
counting is used. Automated perimetry is requested to confirm
and document visual field defects.
mianopia
Homonymous
loss of the right or left
half of the visual field in
both eyes
Bitemporal
loss of the nght half of
the visual field of the
right eye and left half of
the visual field in the left
eye
Quadrantanopia
loss of one fourtn of tne
visual field
Table 2 lists the various visual field defects, their definitions
and their diagrammatic representations.
VISUAL FIELD DEFECTS
Visual pathway lesions from the optic nerve, optic chiasm,
optic tract, lateral geniculate body, optic radiation and the
occipital cortex produce characteristic visual field defects
(Figure 6). Optic nerve disorders result in monocular loss of
vision causing various nerve fiber layer abnormalities that lead
to visual full defects such as central, cecocentral, paracentral,
arcuate and altitudinal scotomas. Complete destruction of
the optic chiasm causes bitemporal hemianopia. Because of
the crossing of the optic nerve fibers in the chiasm, disorders
affecting the visual pathway posterior to the chiasm result
in contralateral defects. A lesion involving the optic tract
produces homonymous hemianopia. Partial involvement
of the optic radiation results in quadrantanopia. A total
involvement of the optic radiation and occipital cortex may
produce a homonymous hemianopia. Macular sparing is
associated with occipital cortical lesions.
Figure 5. Confrontation Test
•
••
LESION
Ae•
BCE)
c44
Ef4 14
F
(Temporal Lobe)
Right optic nerve — central scotoma/generalized
depression of the right eye
Optic chiasm- bitemporal hemianopia
Left optic tract- Right Homonymous Hemianopia
Left optic radiation (temporal lobe)- Right Superior
Homonymous Quadrantanopia ("pie in the sky")
Left optic radiation (parietal lobe)- Right Inferior
Homonymous Quadrantanopia ("pie on the floor)
Left occipital lobe (visual/striate cortex)- Right
Homonymous Hemianopia
Figure 6. Visual Pathway with corresponding visual field defects
1. Other Ancillary tests
\ncilliary tests such as color vision, contrast sensitivity, visual
?yoked response, and imaging studies (ultrasound,CTscan and
\ARI ) are very helpful and can provide valuable information.
III. OPTIC NERVE DISORDERS
1. PAPILLEDEMA
Papilledema is an optic disc edema secondary to elevated
intracranial pressure. The optic nerve which is an extension of
the brain is encircled by the cranial meninges. Any increase in
the intracranial pressure will be transmitted to the meningeal
subarachnoidal space surrounding the optic nerve. Causes
of papilledema include brain tumors, intracranial trauma,
meningitis, hydrocephalus, subarachnoidal hemorrhage and
conditions that obstruct the flow of cerebrospinal fluid.
True papilledema is almost always bilateral. Symptoms include
headache, nausea and vomiting. The severity of papilledema
is proportional to the increase in intracranial pressure. Visual
acuity in the initial stages may be normal. Enlargement of the
physiologic blind spot is an early visual field defect.
Ophthalmoscopy findings include optic disc edema which
causes the disc margins to become blurred and indistinct. The
swollen disc obliterates the physiologic cup and displaces the
central vessels forward. There is dilation and tortuosity of the
retinal veins. Papilledema when fully developed will show a
severely hyperemic disc with hemorrhages, nerve fiber layer
infarcts (cotton-wool spots) and exudates (Figure 7). Absence
of spontaneous venous pulsation may be noted.
Once the diagnosis of papilledema is considered, neuroimaging studies should be done. Treatment is directed to the
underlying cause. Untreated papilledema will eventually lead
to optic atrophy and permanent visual loss.
Figure 7. Papilledema
2. OPTIC NEURITIS
Inflammatory edema of the optic nerve is known as optic
neuritis. Any portion of the optic nerve can be affected.
Therefore, the inflammation may be localized anteriorly
to the optic disc (papillitis), posteriorly behind the eyeball
(retrobulbar neuritis) or may even extend to the adjacent
retina (neuroretinits).
The foremost symptom is severe loss of vision. This is
accompanied by eye pain that is aggravated by movement of
the eye. A diffuse central visual field loss is a common finding.
Optic neuritis is usually unilateral and RAPD can easily be
detected.
Ophthalmoscopy will show a swollen hyperemic optic
disc with blurred margins (Figure 8). It may be difficult
to differentiate papillitis from papilledema based on the
ophthalmoscopic appearance alone. In retrobulbar neuritis,
there may be no visible ophthalmoscopic changes of the optic
disc. Neuroretinitis would frequently present with disc edema
and a swollen macula (macular star).
5
DISTURBANCE IN VISION 15.5 Disorders of the Optic Nerve
95
Other substances that can cause toxic optic neuropathy include
lead, methanol, chloramphenicol, isoniazid, amiodarone,
tobacco and alcohol.
5. OPTIC ATROPHY
Optic atrophy is the result of a severe long standing damage
or injury to the optic nerve. Degeneration of the nerve axons
causes pallor of the optic disc (Figure 9). Optic disc pallor is a
sign of advanced optic nerve disease. This condition leads to
loss of vision and carries a poor prognosis.
Figure 8. Papillitis
A demyelinating etiology, particularly multiple sclerosis, is always
considered during an attack of optic neuritis. Meticulous neurologic
history and examination are mandatory. A spontaneous resolution of
the visual loss may occur. However, corticosteroids preferably given
intravenously may shorten the clinical course.
3. ANTERIOR ISCHEMIC OPTIC
NEUROPATHY
Anterior ischemic optic neuropathy (AION) presents as a
sudden painless, non-progressive blurring of vision in patients
over 50 years of age.
Occlusion of the posterior ciliary arteries typically results in
optic disc edema and an altitudinal field defect.
AION has two types: non-arteritic (NAION) and arteritic
(AAION). The NAION occurs more frequently and is commonly
seen in patients with hypertension, diabetes mellitus,
dyslipidemia and coronary artery disease. Less common is the
Figure 9. Opoc Atroohv
6. DEVELOPMENTAL ANOMALIES
Developmental optic disc anomalies when they occur
bilaterally may mimic true papilledema. These congenital
disc disorders are called pseudopapilledema or structural
congestion of the optic disc. On the basis of ophthalmoscopy
alone, they may be mistaken for papilledema. The common
causes of pseudopapilledema are severe hyperopia, optic disc
drusen and myelination of the optic disc.
AAION which is associated in patients with temporal and giant
cell arteritis. Management of NAION is directed towards the
predisposing medical problem. Administration of steroids is
necessary in patients with AAION.
Disc margins can appear blurred in certain conditions despite
absence of disc edema. Severe hyperopic (far-sighted) eyes
4. TOXIC OPTIC NEUROPATHY
have significantly smaller eyeballs than normal. This results
in crowding of the optic disc structures resulting in blurring
of the disc margins. Optic disc drusen (deposition of hyaline
Ethambutol has been known to be harmful to the optic
crystals) frequently cause the disc borders to be indistinct.
Abnormal myelination that extends to the optic disc results in
nerve. It is commonly prescribed by physicians because
a white feathery opacified disc margin (Figure 10).
of the high incidence of tuberculosis in the Philippines. A
slowly progressive symmetrical bilateral painless blurring of
vision is characteristic of toxic optic neuropathies. Impaired
color vision may be detected early and the typical visual field
defects are central or cecocentral scotomas. If ethambutol
is not immediately discontinued, vision may not recover and
prognosis becomes poor when optic atrophy occurs.
Other optic disc anomalies include optic disc hypoplasia
(small disc), optic malformation (colobomas) and a tilted optic
disc (seen in myopia). These abnormalities can be associated
with developmental disorders of the central nervous system.
4.
A visual field defect involving the same side of both eyes
is
A. Congruent
B. Conjugate
C. Congruous
D. Homonymous
5. What type of visual field defect can an optic nerve
disorder cause?
A. Peripheral
B. Absolute
C. Heterogenous
D. Altitudinal
6.
How far away from a patient do you do a confrontation
test?
A. 1 foot
B. 3 ft
C. 10 ft
D. 20 ft
7.
Optic disc edema can be a result of
A. Cortical blindness
B. Complicated neck surgery
C. Orbital meningioma
D. Serous retinopathy
8.
The color of the optic disc in optic atrophy is
A. pale yellow
B. light brown
C. pastel pink
D. soft red
9.
On ophthalmoscopy, signs of papilledema include
A. hemorrhage, macular star
B. tortuous vessels, crowded disc
C. exudates, hyperemic disc
D. cotton wool spots, cupping
Figure 10. Myelinated nerve fibers
REFERENCES
1.
Martin Ti Corbett ii. Optic nerve disorders. In: Neuroophthalmology the requisites in ophthalmology. Stiouis.
Missouri: Mosby. 2000. 57-94.
2. Kline LB. Optic nerve disorders ophthalmology monographs.
San Francisco: American Academy of Ophthalmolgy.
1996
3. Maas EF, Tomsak RL. Diseases of the optic nerve. In: The
basics of neuro-ophthalmology. St. Louis. Missouri: Mosby.
4.
1991. 241-275.
Fajardo RV, Noche RR. Neuro-ophthalmology. Fajardo RR,
Espiritu, RB Naval CIN. In: Textbook of ophthalmology.
Quezon City: JMC Press. 1980. 115- 123.
SELF-TEST
1.
2.
3.
What is the shortest portion of the optic nerve?
A. Intraocular
B. intraorbital
C. I ntraca nalicular
D. Intracranial
What artery supplies the intraorbital portion of the
optic nerve?
A. Ciliary
B. Optic
C. Carotid
D. Ophthalmic
10. The pupillary parasympathetic pathway passes
through the
A. Edinger Westphal nucleus
B. Hypothalamus
C. Cervical ganglion
D. Center of Budge
Answers to Self-Test on page 221.
What is the efferent limb of the pupillary light reflex?
A. cranial nerve II
B. cranial nerve III
C. cranial nerve IV
D. cranial nerve VII
5
DISTURBANCE IN VISION 1 5.5 Disorders of the Optic Nerve
97
5.6 Errors of Refraction
Juan Ma. Pablo R. Nanagas MD, MPH, MNSA
INTRODUCTION
This self instructional material focuses on providing the medical students with knowledge on how to recognize and assess
patients with errors of refraction. Students are encouraged to apply knowledge they will acquire from this material to clinical
cases they will encounter.
OBJECTIVES
After going through this material, the student is expected to:
1.
Define error of refraction and other related terms.
2.
Identify the various elements in a patient's history and ophthalmologic examination that leads to the formulation of
diagnosis of error of refraction.
3.
Differentiate the various errors of refraction and related conditions.
4.
Based on information given, be able to analyze and interpret provided data to formulate diagnosis.
5.
Discuss the principles of management of refractive errors.
CONTENT
I.
Definition of ametropia or error
II.
Diagnosis of error of refraction
1. rtistor) tacr
2.
Eyeexamirw.
3.
Anallary exa—
of refraction
Dns
III. Classification of errors of refraction
IV. Management of
errors of refraction
Vision 20/20, a proposal for the elimination of avoidable
blindness in the Philippines cited a 1995 University of
the Philippines and Department of Health survey that
showed that there were at least 7.3 million Filipinos with
one or more kinds of error of refraction (EOR) and with a
visual acuity of worse than 20/40 in the better eye. The
same source said that about 30,000 were blind from EOR.
Glasses are sufficient to improve the vision of these people.
In 2002, the Philippine National Survey of Blindness found
that of the main causes of low vision, 53% were due to EOR,
0.15% of children had visual impairment due to EOR, and
that from 1995 to 2002 EOR increased from 1.06% to 2.06%.
The same study showed that EOR is the main cause of visual
impairment of children accounting for 33.9%. Amblyopia,
usually a unilateral decrease in best-corrected vision
without any apparent structural abnormality of the eye or its
nervous pathway, can be caused by significant differences
in refractive errors between the two eyes. High refractive
errors on both eyes can result in bilateral amblyopia though
the condition is not as common. In children suspected of
having amblyopia accurate cyclopegic refraction is critical
for diagnosis and treatment.
There may be differences in the prevalence of errors
of refraction among races. In a study in Singapore. they
found that myopia is 1.5 to 2.5 times more prevalent in
adult Chinese residing in Singapore than in similarly aged
European - derived populations in the United States and
Australia.
I.WHAT IS AMETROPIA OR ERROR
OF REFRACTION?
I his is a condition where the refractive elements of an
eye at rest are unable to focus light rays from 6 meters or
more onto the retina. It may be caused by abnormalities in
length of the eyeball or of the refract veelements of the eye
(mainly the cornea and crystalline lens) or both.
Errors of refraction fall into several categories,. Myopia or
near-sightedness is a condition where parallel light rays
(those from a source more than 6 meters or 20 feet away
are considered as parallel or coming from infinity) are
focused in front of the retina and light from a point at a
finite distance focuses on the retina. In hyperopia or farsightedness, parallel light rays are focused beyond the
retina and can only focus on the retina when the person
accommodates or when convergent lens is placed in
front of the eye. Astigmatism is a condition where
the refractive power of the eye differs in one meridian
compared to another.
II. DIAGNOSIS OF ERRORS OF
REFRACTION
1. HISTORY TAKING IN A PATIENT WITH ERROR
OF REFRACTION
As in any disorder, the patient's history guides the clinician in
arriving at a complete diagnosis, particularly as to the possible
type of error of refraction. Furthermore, the history can provide
the clinician with an idea as to the visual needs of the patient
and the appropriate treatment modality. The clinician should
ask each and every patient suspected to have an error of
refraction the following questions.
A. What is the chief complaint?
The most common presenting complaints of patients with
errors of refraction are blurring of vision for distance, for near, or
both.Clearnearvision but blurred distance vision indicates near
sightedness or myopia. Hyperopes (far-sighted individuals)
may complain of early visual fatigue when performing visual
tasks (especially at near). Headache, especially after prolonged
eye use, is common with hyperopes and astigmatics but is nonspecific and will have to be differentiated from other causes.
As a person loses accommodation (the ability to focus at near)
progressively as one ages, he or she will complain of blurring
at near work. This may start around the age of forty and is
called presbyopia. It is not considered an error of refraction.
B. How long has this problem been going on?
The duration of the problem should be extracted from the
patient. Errors of refraction usually present with a prolonged
historyoftheir complaints. Whether it is recurrent or progressive
should also be noted. As mentioned above, one should be
aware of a condition of middle age called presbyopia where
the lens of the eye gradually loses its ability to focus at near
objects. Sudden blurring of vision seldom results from an
error of refraction except in cases of spasm of accommodation
after prolonged near work or due to exposure to an anticholinesterase like some insecticides.
C. Which eye is involved?
Does the problem involve one eye or both eyes? Significant
difference of refraction between the two eyes may be the
cause of amblyopia or a lazy eye.
D. Are there other associated eye problems?
Elicit from the patient whether or not there is any history of
redness, ocular pain, glare or photophobia, trauma or any
form of eye surgery in the past. These may point to causes of
blurring of vision other than errors of refraction.
5
DISTURBANCE IN VISION I i 6 Errors of RefraLtion
99
E. Does the patient have any prior consultations?
D. Funduscopic findings. Patients with mild to moderate
error of refraction will present with normal findings. In cases
One should be able to determine a patient's previous
correction of his/her error of refraction to help determine the
course of the condition. Frequent increases in the power of a
myopic patient's spectacles may mean a progressive form of
myopia.
where the eyeball is elongated, the fundus and optic nerve
head may exhibit some changes.
F. Other aspects of the patient's history that should be
considered include:
Family History. Is there a history of similar illness in the family?
Genetic factor strongly determine refractive errors of the eye.
Is there any history of any hereditary illness like diabetes?
Changing blood sugar levels may affect a person's refraction
and cause frequent changes in spectacle correction.
Social History. What is the patient's occupation? What are the
patient's usual visual tasks? Prolonged near work may lead to
spasm of accommodation causing blurred vision for far.
Medical History. Has the patient suffered any form of
illness in the past, particularly diabetes? Is she under any
form of medication for any illness? These may affect vision.
Sulfonamides and related compounds for example. may cause
the ciliary processes to swell and cause forward movement of
the lens blurring vision for far.
2. OPHTHALMOLOGIC EXAMINATION
OF THE PATIENT
COMMON OCULAR FINDINGS IN AMETROPIA
3. ANCILLARY EXAMINATIONS
The more commonly requested ancillary procedures include:
A. Retinoscopy is an objective method of measuring errors
of refraction by examining the characteristic of light coming
from the instrument and reflected by the retina. It will reveal
the type and amount of refractive error.
B. The common use of automatic refractors in both tabletop and portable models has made the measurement of errors
of refraction less time-consuming and more convenient.
C. Keratometry. The keratometer is an instrument that can
measure central anterior corneal curvature. It can be used
to check the type and amount of astigmatism. It is also used
in fitting contact lenses, a form of correction for errors of
refraction.
D. Corneal topography is a sophisticated instrument that
produces a color-coded topographic map of the cornea that
shows the pattern of the corneal curvature. It usually functions
as a keratometer as well, measuring corneal curvatures. It
demonstrates irregularities of curvature like keratoconus.
E. Biometry or A scan ultrasonography is a test that
measures of the axial length of the eyeball, a determining
factor of the refractive condition of the eye.
Typically, the patient with error of refraction will present with
the following findings:
A. Visual Acuity. Most patients with an error of refraction will
present with reduction in vision either for far, near, or both.
III. CLASSIFICATION OF
AMETROPIAS
Snellen charts are commonly used for distance vision testing
and Jaeger or Snellen equivalent cards for near vision. If the
vision improves when the patient looks through the pinhole,
the patient most probably has an error of refraction that can
DIAGRAMMATIC CLASSIFICATION
be corrected with lenses.
The emmetropic eye (Figure 1) focuses light rays from infinity
on the retina even at rest or without accommodating.
OF AMETROPIAS
B. Intraocular Pressure. Most patients will typically present
with normal intraocular pressures
C. Extraocular Muscle Movement. The extraocular muscles
are usually not involved in errors of refraction and a majority
of patients will exhibit full movement on all directions of gaze.
or heterotropia are associated
Some forms of heterophoria
with errors of refraction. For example, accommodative
esotropia is associated with hyperopia.
Figure 1. Emmetropic eye
he myopic eye (Figure 2) focuses light rays from infinity in
ont of the retina. An object at a finite distance focuses on
s retina.
In regular astigmatism, the refractive power changes
successively from one meridian to the next and each meridian
has a uniform type of curve.
With the rule and against the rule astigmatism
,figure 2. Myopic eye
hyperopic eye (Figure 3) theoretically focuses light rays
rom infinity behind the retina. It can only focus convergent
ight rays on the retina.
-he
...........
Figure 3. Hyperopic eye
ASTIGMATISM
In astigmatism, the refracting surface (usually the cornea)
is toroidal (like the surface of an American football) rather
than spherical, and therefore the refracting power of the
surface is not the same for all meridians. If retinoscopy
has achieved neutrality in one meridian but is still
or 'against' in another, this indicates different refracting
powers in the two meridians. This is a sign of astigmatism.
In the illustration below, the streak at the 180° meridian is
different in intensity and width than the streak at the 91-'
meridian showing that the refractive power of the cornea
may not be the same in the two meridians (Figure 4).The
cornea may thus be astigmatic.
The term "with the rule" and "against the rule' refer to
the position of the principal meridians. In "with the rule"
astigmatism, the vertical meridian is steepest and a correcting
plus cylinder is located at or near axis 90°. In "against the rule"
astigmatism, a correcting plus cylinder is located at or near
180° and the horizontal meridian is steepest.
IV. MANAGEMENT OF ERRORS OF
REFRACTION
Since an ametropic eye does not focus parallel light rays from
objects on the retina, correction of the errors of refraction entails
focusing those light rays on the retina. This is done to improve
vision or comfort and can be done through glasses or spectacles,
contact lenses and recently, through surgical procedures
collectively called keratorefractive surgery, refractive keratoplasty,
or refractive corneal surgery. Other refractive surgical procedures
include the placement of an intraocular lens (I0L) implant, either
in front of the crystalline lens (phakic 10L) or in place of the
crystalline lens (refractive lens exchange)
The most common means of managing errors of refraction is either
by spectacles or contact lenses. There maybe some situations in
which contact lenses are preferred, e.g. anisometropia, monocular
aphakia, or high refractive errors.
Table 1. Advantages and Disadvantages of using spectacles and
tic e-SeS
Spectacles •
Safe
• Easily adjusted
• Inexpensive
For high errors of
refraction or
anisometropia
• Restricted visual field
t
• marked aniseikonia
Direction of scan
• distortion of image
and prismatic effect
410110
Direction
• heavy weight
e scar
debilitating visually,
cosmetically and
psychologically
with
180°
• Relay safe
Easily adjusted
• suitable for unilateral
aphakia
Figure 4. Astigmatic reflex as seen thru retinoscope
Jim
• patient-parent
compliance
• psychological trauma
frequency of lens loss;:
I complications
Persons with presbyopia can be helped by presbyopic
glasses, presbyopic refractive procedures on the cornea, or
intraocular lens (10Ls) with presbyopic components if they
have to undergo cataract surgery.
5
DISTURBANCE IN VISION I 5 t Errors of Refraction El
FREQUENTLY ASKED QUESTIONS REGARDING
ERRORS OF REFRACTION (FAQ)
FAQ 1: If a child wears glasses early, will it contribute to the
progression of the error of refraction?
Answer 1: No. Major components of an eye's refractive state
are the cornea, the lens, and the length of the eye and their
size, shape and the power are determined genetically.*
FAQ 2: If I use glasses for my astigmatism 0,
astigmatism go away?
RECOMMENDED FOLLOW-UP
It is recommended that the students be given demonstration
sessions on how to properly conduct history taking and
ophthalmologic examination of patients. Following this
exercise, the students should be provided with clinical sessions
to allow them to see actual cases of patients with errors of
refraction.
REFERENCES
1.
Results of the Workshop On Vision 2020 conducted by
ANSWER 2: Depending on the age of the patient. errors of
refraction may change. In young individuals with eyes that
the Department of Health on July 26 to 28, 2000 at the
http://www.yision2020australia.
SEAMEO-INNOTECH,
are still developing, changes in refraction may occur more
org.au/assets/contgent/2168/PHILIPPINES%20-%20
frequently and such conditions as astigmatism may change or
even "go away". In animals, research has shown that there may
be a mechanism that influences the development of the eyes
towards normal or emmetropia.6
FAQ 3: If I wear contact lenses, will the progression of my
myopia decrease compared to wearing glasses?
ANSWER 3: Rigid or hard contact lenses have been shown to
retard or even decrease myopia through the fitting of special
lenses that reshape the cornea that is usually steep in myopes.
National%20PIan.pdf
2_
3_
Ophthalmology/Strabismus Panel 2008
4 TienYin Wong, Foster 1'J, Hee J, Invest. Ophthalrnol. Vis. Sci.
August 2000 vol. 41 no. 9 2486-2494 http://www.iovs.
cogicontent/41 /9/2486.s hort accessed 12 April 2011
5. IlAd_eod SD, Chuck RS, Hamilton R, et al Preferred Practice
fbuerrr Refractive Errors and Refractive Surgery, one.aao.
os9yassetaxd?id=0faa6a59-ef36-42fc-8d80-79b22c...
accessed 12 April 2011
Young11.Metapally R, Shay AE. Complex trait genetics of
adman* errors. Arch Ophthalmol, 2007 ; 125 (1), 38-'18
Opiel. Refraction and Contract Lenses. Basic and Clinical
Sdence Course, Section 2. California: American Academy
FAQ 4: Will I see better after a laser procedure (like LASIK)
than with spectacles?
ANSWER 4: Although a laser procedure such as LASIK ww
improve vision in a large majority of patients, there may be
trade-offs compared to the use of contact lenses or spectacles.
These include some glare especially at night and some loss of
contrast sensitivity.
CONCLUSION
University of the Philippines Manila, Philippine National
Surveyof Blindness, published by UP Manila, Manila, 2004
Arnblyoaia, Preferred Practice Pattern, Prepared by
the American Academy of Ophthalmology Pediatric
8
atOphthalmology, 1990.
Exam
— ROphthalmologic Optics. Manila: Department of
Opfinhairnology &Visual Sciences, 2001.
Head Funk W Ophthalmology, Principles and Concepts,
-1.1osby
and Co., 1986
As medical practitioners, you may, in the future ens
SELF-TEST
patients who will seek consultation for eye problems. One
should bear in mind that many who complain of blurring of /. (
~tstic of a patient with hyperopia
vision may have an error of refraction. It is the most common
A. He will have clear vision for near but not for far.
cause of visual disability. It is therefore your role to be able
R. He may have clear vision for far but easily tires with
to recognize these conditions and differentiate them from
prolonged near work.
permanently disabling visual conditions. Referral to an
C.. He has oTiary spasm.
ophthalmologist is necessary for proper correction through
spectacles, contact lenses, or refractive laser procedures. Early 2. In errors of refraction the presenting symptoms
intervention, especially in children, can prevent amblyopia
•
arm
a.31 S specific
if anisometropia (significant difference in amount or kind of
B. almost always involve sudden visual disturbances
C usually iirtvor^ee vision
refractive error between the two eyes) or severe ametropia is
present.
Intraocular pressure in isolated errors of refraction is
usually
A. normal
B. high
C. low
Errors of refraction
A. show no hereditary pattern since it is caused solel
by the type of visual work a person performs
B. cannot occur in children since the eye is still
developing
C. if significantly different between the two eyes can
lead to progressive loss of vision
Retinoscopy is
A. the same as funduscopy
B. an objective means of measuring errors of refraction
C. a means to take retinal photographs to determine
retinal changes due to errors of refraction
i.
7.
If the poor vision of a patient does not improve when
viewing the test chart through a pinhole
A. the blurring may not improve with corr...
B. there may be error of refraction
C. it is a sure sign of amblyopia
Measurement of refractive errors
A. can not be done for infants and young children
B. is usually very subjective
C. can be performed using automatic refractors
12. A patient can work on a computer without difficulty but
has difficulty reading street signs. What is his refractive
state?
A. I le is probably normal.
B. He may be myopic.
C. l le may be hyperopic.
D. He may have compound hyperopic astigmatism.
13. On visual acuity testing, a 20 year old patient had 6/6
vision but difficulty with reading Jaeger 1 print. What is
the patient's refractive state?
A. presbyopia
B. hyperopia.
C. myopia.
D. no error of refraction
14. If the horizontal meridian of the cornea is steeper than
the vertical meridian, what type of astigmatism does
the patient have?
A. "with the rule"
B. "against the rule"
C.
"natural"
Case 1.
9. In middle age, one may
A. gradually lose the ability to focus for near or develop
presbyopia
B. suddenly lose the ability to read due to ably spasm
C. usually develop hyperopia and thus lose darity of far
vision
9.
11. In astigmatism due to the cornea
The curvature is not the same in all meridians
B. The curvature is flatter than normal
C. The index of refraction of the corneal surface is not
the same in all meridians
D. The curves of the surface are convex
Normal or emmetropic eyes looking at an object
6 meters or 20 or more feet away
A. need to accommodate to c-A:us Fight on the retina
B. need to squint to focus light on the retina
C. should be able to focus light on the retina with the
eye at rest
10. When the image of an object at infinity falls behind the
retina, the patient is
A. hyperopic
B. myopic
C. toric
D. phthisic
A 7 year old pupil's teacher informs her mother that her child
seems unable to copy words from the white-board and squints
her eyes when she looks at the board from her seat. She keeps
books near her face when she reads.
V OU: 20/200 or 6/60 improved to 6/7.5 with pinhole.
Intraocular pressure: soft OU
EOMs: full
FOU: normal
1.
2.
3.
With the given information would it be safe to say
that the patient has an error of refraction?
What type would it be, hyperopia or myopia?
What examination can measure the error and lead to
the prescribed correction?
Casa 2.
1.
A 42 year old employee complains of frequent afternoon
headaches and blurring of vision after prolonged near work.
She has experienced the symptoms for the last ti months. She
has had clear vision for both far and near before this and has
never been prescribed glasses.
V OU: 20/20 or 6/6, Jaeger 1 with difficulty at about 50 cm.
Intraocular pressure: soft, OU
EOMs: Full
F OU: Normal
2.
With the given information would you say the patient
may have an error of refraction?
What information in the history and ophthalmic
examination tells you that this might be part of the
process?
a
Answers to Self-Test on page 221.
6.1 A Clinical Algorithm for the
Diagnosis of the Red Eye
Leo D. P. Cubillan, MD, MPH
INTRODUCTION
The red eye is one of the most frequent clinicaa ocesentationsof ocular disorders.The medical student will be able to differentiate
these disorders from each other by asking certain questions from their patients during history taking and looking for specific
signs when performing the ocular examination_ A rAnical algorithm is presented to help medical students arrive at an initial
impression based on common eye symptoms
OBJECTIVES
After the completion of this learning material, the stucierc sihoulii be able to:
1. Use the algorithm on the differential diagnoses of a sed eye based on the following signs and symptoms: pain, eye
2.
discharge, photophobia and itchiness
complication
Discuss the clinical clues, etiology /pathogenesis.signsandsyrnixorns,chagnostic work-up,treatment, and
of the common causes of a red eye
A.
Viral Conjunctivitis
B.
Allergic Conjunctivitis
C.
Dry Eye
D.
Bacterial Conjunctivitis
E.
Microbial Keratitis
F.
Acute Glaucoma
G.
Uveitis
CONTENT
I.
Differential diagnoses of the red eye
II.
Clinical algorithm for the diagnosis of the red eye
A.
Eye pain
B. Eye discharge
Ill. Discussion of selected causes of red eye
A. Viral conjunctivitis
B.
Allergic conjunctivitis
C. Dry eye
D. Bacterial conjunctivitis
E.
Microbial keratitis
F.
Acute glaucoma
G.
Uveitis
H. Others
I. DIFFERENTIAL DIAGNOSES OF A
RED EYE
Red eye is a common eye symptom Or pal Is with eye
disease. Red eye is seen as a result of dilation of conjunctival
or scleral blood vessels in response to an inflammatory or
infectious process. Another common cause of red eye is
subconjunctival hemorrhage which results from trauma or
injury to the small conjunctival vessels.
The following are the differential diagnoses of a red eye:
1. Conjunctivitis
a. Infectious
i. Bacterial
ii. Viral
b. Non-infectious
i. Allergic
ii. Dry Eye
iii. Toxic or Chemical Reaction
iv. Contact lens use
v. Conjunctival Neoplasm
vi. Foreign Body
2. Uveitis
3. Episcleritis /Scleritis
4. Acute Glaucoma
5. Keratitis
a. Infectious
i. Bacterial
ii. Viral
iii. Fungal
iv. Acanthamoeba
b. Non-Infectious
i. Recurrent Epithelial Erosion
ii. Foreign Body
6. Eyelid Abnormalities
a. Entropion /Trichiasis
b. Lagophthalmos
7. Orbital Disorders
a. Preseptal and orbital cellulitis
b. Idiopathic orbital inflammation
This clinical algorithm is presented to aid the medical student
as well as the primary care physician in the diagnosis of the
more common causes of eye disease presenting as a red
eye. The common symptoms of eye pain, eye discharge,
photophobia and itchiness are used for this algorithm.
A. EYE PAIN
The first step in the algorithm is to determine whether the
patient presenting with a red eye has eye pain or not (Figure 1)
Eye pain may be described as a sharp localized pain, pain
when exposed to bright light or a severe eye pain radiating
to the head. The symptom of eye pain divides the common
dilksential diagnoses of eye pain into two groups: eye pain
"cup and no eye pain group.
Awe 1. Red Eye Algorithm: Eye Pain
1. EYE PAIN WITH EYE DISCHARGE
For patients with red eye and eye pain, the next question will
be the presence or absence of eye discharge. If there is eye
discharge, microbial keratitis or infection of the cornea may be
considered (Figure 2). The presence of abundant nerve fiber
endings in the cornea (CN V) is responsible for the pain when
infection is present
yes
DISCHARGE?
Figure 2
MICROBIAL
KERATITIS
EyeAlgCritttrn: Eye Pain with Eye Discharge
II. CLINICAL ALGORITHM FOR THE
DIAGNOSIS OF THE RED EYE
2. EYE PAIN, NO DISCHARGE,
WITH OR WITHOUT PHOTOPHOBIA
Ophthalmologists are the experts in the diagnosis and
treatment of eye diseases. In the Philippines, however, access
to an ophthalmologist may not be easy. The primary care
physician may still be the first line medical worker in the
identification and initial treatment of eye disease.
If there is no eye discharge in a patient with eye pain, the
next step will be to establish the presence or absence of
photophobia (Figure 3). Photophobia is usually described as
a dull eye pain when exposed to bright lights. This pain due
to the pupillary spasm of an inflamed iris. If photophobia is
present, uveitis or eye inflammation, may be considered. In the
absence of photophobia, acute glaucoma may be entertained.
The eye pain in glaucoma is moderate to severe often with
radiation to the head.
_.111111H MICROBIAL
KERATITIS
CFSC,,ARGE?
PAIN?
I-7
M ACt
inS
2. NO EYE PAIN, WATERY DISCHARGE,
WITH OR WITHOUT ITCHINESS
Patients presenting with watery discharge can be suffering
from either allergic conjunctivitis or viral conjunctivitis. To
differentiate between the two, the presence or absence
of itchiness may be asked. Eye itchiness is very prominent
symptom in allergic conjunctivitis (Figure 6). It is also
worthwhile to note that the watery discharge in viral
conjunctivitis is a symptom that usually presents at the onset
or during the early stages of the disease.
ACUTE
GLAUCOMA
Figure 3. Red Eye Agc-thr-. Eye Pain. No Eye as: - without Photophobia
DRY EYE
7 or
B. NO EYE PAIN, NO EYE DISCHARGE
The second group of differential diagnoses are the red eyes
without eye pain. The presence or absence of discharge is the
next question to ask. Dry eye syndrome may be considered in
patients without eye discharge (Figure 4).
INE! DRY EYE
F
TYPE OF
DISCHARGE?
MUCOPURULENT
ALLERGIC
CONJUNCTIVITIS
ITCHY?
BACTERIAL
CONJUNCTIVITIS
VIRAL
CONJUNCTIVITIS
Figure 6. Red Eye Algorithm: No Eye Pain. Watery Discharge. with or
without Itchiness
III. DIFFERENTIAL DIAGNOSES OF
RED EYE
DISC1-.ARGE ,
A. VIRAL CONJUNCTIVITIS
Figure 4. Red Eye Algorithm. No Be Pair tea Er Di.:
1. NO EYE PAIN WITH MUCOPURULENT DISCHARGE
Red eye patients with no eye pain but with discharge comprise
the conjunctivitis subgroup. The type and character of the
discharge will help one differentiate the possible etiology.
In patients with an initial presentation of mucopurulent
discharge, bacterial conjunctivitis should be the primary
consideration (Figure 5).
CLINICAL CLUES
Viral conjunctivitis or"sore eyes" is the most common cause of
acute onset eye redness (Figure 7). The main feature of this
disease is the presence of watery discharge in the early part
of its course. The most important information in the history
that points to this disease is the history of exposure to other
individuals with "sore eyes" or similar clinical manifestation.
DRY EYE
PAIN?
DISCHARGE?
TYPE OF
DISCHARGE?
MNTERII
MUCOPURULENT
BACTERIAL
CONJUNCTIVITIS
Figure 5. Red Eye Algorithm: Eye Pain, No Eye Pain
with Mucopurulent Discharge
Figure 7. Red eye with watery discharge in viral conjunctivitis
6
RED EYE, TEARING AND DISCHARGE 16.1 The Red Eye
107
ETIOLOGY / PATHOGENESIS
COMPLICATION
Epidemic keratoconjunctivitis (EKC) which is the more
common type of the viral conjunctivitis is caused by adenovirus
types 8, 19, 29 and 37 (Figure 8). Spread is through a direct
contact with eye discharge. The virus may not be neutralized
by alcohol. Proper hand washing is the best way to prevent
In majority of the patients, the disease resolves without sequelae.
In a few cases, subepithelial opacities (Figure 9) may develop in
thecornea that, in turn, lead to blurring of vision.The subepithelial
obes may persist for weeks or months and in some cases may
- dithout scars.
the disease.
F
-
e.
the cornea.
B. ALLERGIC CONJUNCTIVITIS
CLINICAL C
Figure 8. Structure of adenovirus
SIGNS AND SYMPTOMS
Onset of symptoms is acute. Duration varies from few days
to 2-4 weeks. It usually starts on one eye and may become
bilateral after a few days. Symptoms tend to be more severe
in the first eye. During the early course of the disease, the
discharge is watery. In some cases, the discharge may become
mucopurulent when there is a secondary bacterial infection.
ES
Allerg&c
sa cnronic or recurrent eye disease
characterized by eye redness, itchiness and watery or stringy
discharge Pipe 10). Eye itchiness is the most prominent
feature
DIAGNOSTIC WORK-UP
The diagnosis of adenoviral conjunctivitis is arrived at
mainly through the patient's clinical history, character of the
discharge and the presence of follicular conjunctival reaction
seen under the slit lamp biomicroscope. The adenoclone
enzyme immunoassay (EIA) test kit (Cambridge BioScience
Corp, Worchester, MA) may be used to confirm the diagnosis.
However, this test is not readily available.
Figure 111.9rincry cistharge in allergic conjunctivitis
TREATMENT
Hand washing and avoiding direct contact with eye discharge
is the best way to prevent the spread of viral conjunctivitis.
There is no treatment needed. However, antibiotic eye drops
may be given in patients with secondary bacterial infection or
as a prophylaxis for bacterial infection. Mild steroid drops and
cold compress may be given to help reduce inflammation.
-' k
I
ETIOLOGY / PIIIHOGENESIS
The etiology of this disease is immunologic in nature. Often,
it is difficult to identify the specific allergen. The hay fever
type of allergic conjunctivitis is mainly a type I hypersensitivity
reaction to airborne allergens. In atopic keratoconjunctivitis,
the patient has a hypersensitive immune system which reacts
to many antigens. Most patients with allergic conjunctivitis
have atopy or an atopic predisposition.
SIGNS AND SYMPTOMS
Eye itchiness is a prominent feature of the disease. Discharge
is watery, mucoid and distinctively stringy. On ophthalmic
examination, there is a pale papillary reaction on the upper
bulbar conjunctivae. In atopic keratoconjunctivitis, patients
present with a periocular scaly skin with thickening of the
eyelids (allergic shiners).
DIAGNOSTIC WORK-UP
The diagnosis of allergic conjunctivitis is arrived at from an
adequate history and thorough clinical examination. However,
the presence of eosinophils in cytologic studies of conjunctival
scrapings confirms the diagnosis (Figure 11). Often this is
done only in academic institutions.
Figure
12. Cataract
resulting from chronic steroid use.
C. DRY EYE
CLINICAL CLUES
Dry eye disease or keratoconjunctivitis sicca is a common
ophthalmic condition seen among the elderly. It usually
presents with foreign body sensation and mild eye redness.
ETIOLOGY / PATHOGENESIS
The main etiology for dry eye is the decreased tear production
seen among the elderly. Other causes of dry eye include
increased tear evaporation in patients with inability to
completely close the eyelids and unstable tear film in patients
with meibomitis.
SIGNS AND SYMPTOMS
Figure 11. E:s
s in cc- .
TREATMENT
removal of
environmental triggers. Cold compress and mast cell
stabilizers / antihistamine eye drops may help control the
symptoms. In moderate to severe cases, short-term topical
steroids are needed. Oral antihistamines may also be
prescribed to control the symptoms.
Treatment involves the identification and
COMPLICATION
Vernal type of allergic conjunctivitis often occurs in young
children which lasts for several years. In these cases, when
steroid drops are over used, cataract may develop as a
complication of the steroids use (Figure 12). In some patients,
steroid-induced glaucoma may occur.
Patients usually complain of a sandy and gritty sensation
associated with slight eye redness and eye fatigue. The
symptoms are worse with wind and dry climates.
DIAGNOSTIC WORK-UP
Schirmers test with or without anesthesia is done to confirm
dry eye. Standardized strips of filter papers are used to absorb
tears. Consistent measurements of less than 5 mm of wetting
at 5 minutes may indicate a dry eye. Tear break-up time may
also be done. Fluorescein dye is instilled into the eye and the
surface of the tear film is observed for areas of disruption.
Rose bengal stain can also be instilled to identify areas with
devitalized epithelial cells which can be seen in dry eyes
(Figure 13). Normal tear break-up time is generally greater
than 10 seconds.
6
RED EYE, TEARING AND DISCHARGE I 1 The Red Eye
109
Figure 13. Rose Bengal stain on devitalized epit2
TREATMENT
gure 15. Blepharoconjunctivits from Moraxella organism.
SIGNS AND SYMPTOMS
Treatment is mainly topical instillation of aqueous
replacement or artificial tears. For patients requiring tearsubstitute eye drops more than 4x a day, non-preserved
topical eye drop preparation is recommended to prevent
hypersensitivity to the eye drop's preservative. In severe cases,
punctual occlusion may be done using a silicone plug to
increase tear retention.
D. BACTERIAL CONJUNCTIVITIS
CLINICAL CLUES
Conjunctivitis caused by bacteria presents with mucoid to
muco-purulent discharge. In children, it may be associated
with upper respiratory tract infection (URT1).
Most often, bacterial conjunctivitis is unilateral and is acute
in onset. There is a mucoid to muco-purulent discharge
associated with a red eye but no blurring of vision.
DIAGNOSTIC WORK-UP
Conjunarva~~scrapings from children with bacterial
conjunctivkisandURTImight reveal gram negative coccobaci I I i
(charactsistic of Hernophilus organism) (Figure 16). Bacteria
from con#anctivai scraping may also be cultured on a blood
agar plate to further identify the causative organism.
ETIOLOGY / PATHOGENESIS
In children with URTI, the most common etiology is Hemophilus
Among newborns, Chlamydia or gonococcus
influenza.
may be the etiologic agent (Figure 14). In adults, bacterial
conjunctivitis may present as a blepharoconjunctivitis
(Figure 15). Moraxella and Staphylococcus are common
etiologic agents.
Figural& CamSWIM coaxibaciiii.
TREATMENT
Antibiotic eye drops -e used for bacterial conjunctivitis. Oral
antibiotics are aisc a .-..ninistered in patients with Hemophilus,
Chlamydia of oci.rcv:-_,c:34 conjunctivitis.
E. BACTERIAL KERATITIS
Figure 14. Bacterial conjunctivitis in a neonate.
CLINICAL CLUES
Microbial keraLas 6 an accae infection of the cornea associated
with a painful red eye and mucoid to muco-purulent eye
discharge. A white lesion is seen on the cornea (Figure 17).
TREATMENT
Topical antibiotics are the mainstay of treatment. Depending
on the severity of the condition, antibiotic drops may be
applied every 15 minutes to every hour during the first few
days of treatment. In moderate to severe cases, keratectomy
is done.
COMPLICATION
Figure 17. White lesion in the cornea in a patient with
microbial Walls
ETIOLOGY / PATHOGENESIS
In moderate cases, microbial keratitis may result into a corneal
opacity. In severe cases, such as those caused by Pseudomonas,
in a few days, corneal perforation often occurs if the eye is left
untreated. In these cases, corneal transplantation may be
needed to save the eye (Figure 19).
In the Philippines, corneal opacity accounts for 3.4% of all
causes of blindness.
Pneumococcus, a gram positive organism is the most common
cause of bacterial keratitis. Among contact lens wearers,
Pseudomonas is a common and dreaded organism causing
keratitis. In patients with a history of trauma and steroid eye
drop use, fungal etiology may be considered
SIGNS AND SYMPTOMS
Eye redness is mocerate to severe associated with eye pain
often accompanied by mucoid to muco-purulent discharge. If
the lesion is on the central cornea, the patient will also present
with blurring of vision.
DIAGNOSTIC WORK-UP
Corneal scraping is done to determine the etiologic agent
(Figure 18) 3ram stain is used to initially identify the bacteria
but definitive diagnosis is achieved with culture studies
in blood agar-plate and brain heart infusion (BHI) media.
Sensitivity studies are done to determine the most appropriate
antibiotic agent.
Figure 19. After penetrating keratoplasty (corneal transplantation) in a
patient with ruptured microbial keratitis.
F. ACUTE GLAUCOMA
CLINICAL CLUES
The most prominent feature of acute glaucoma is a red painful
eye associated with headache. There is blurring of vision and
occasionally, patients complain of seeing rainbow haloes
(iridescent vision).
ETIOLOGY / PATHOGENESIS
The eye pressure is abnormally elevated (intraocular pressure
greater than 23 mm Hg) due to an acute obstruction in the
outflow mechanism of aqueous humor. Most often this
is secondary to angle closure (Figure 20). Angle closure
glaucoma may be more prevalent among Asians including
Filipinos, because Asians may have genetically narrower iridocorneal angle.
Figure 18. Gram positive cocci. Corneal scraping in a Pneumococcal
keratitis.
6
RED EYE, TEARING AND DISCHARGE
I I The Red Eye Milill
Figure 20. Diagram of an angle closure
SIGNS AND SYMPTOMS
peripheral vision.
When the eye pressure is acutely elevated, the patient
will experience sudden onset of eye pain associated with
headache. With the elevated eye pressure, the cornea becomes
edematous resulting in iridescent and blurred of vision.
DIAGNOSTIC WORK-UP
Applanation tonometry is done to measure the intraocular
pressure. A gonioscope lens is also used to visualize and
evaluate the angle structure. Automated visual field (AVF)
examination and optical coherence tomography (OCT) are
done to determine the extent of damage to the nerve fiber
layer of the optic nerve.
TREATMENT
Acetazolamide or hyperosmotic oral solutions may be used
to facilitate immediate lowering of the eye pressure. Topical
ocular hypotensive agents are also used. Laser iridotomy is
the definitive management. Surgical iridectomy may be done
in the absence of a laser machine. AVF and OCT are used to
monitor response to treatment as well as progression and
control of the disease.
Figure 22. leaume rrt gut nerve cupping in chronic glaucoma.
G. UVEITIS
CLINICAL CLUES
Uveitis is an ocular inflammation characterized by eye redness
around the cornea (ciliary injection) associated with sensitivity
to bright lights (photophobia).
COMPLICATION
ETIOLOGY / PATHOGENESIS
When glaucoma becomes chronic or is left untreated, there
is damage to the optic nerve causing initial blurring of vision
of the peripheral fields which eventually leads to blindness
(Figures 21and 22).
Almost haif of the uveitis cases are idiopathic. In some cases,
the condition is associated with systemic disease such as
Vogt-Koyanagi-Harada, Bechet's and collagen vascular disease.
Others may be infectious in nature such as those caused by
Herpes virus and Mycobacterium tuberculosis.
SIGNS AND SYMPTOMS
Most patients complain of eye redness associated with
photophobia. On slit-lamp biomicroscopic examination,
keratic precipitates are seen on the inner surface of the cornea
which indicates an inflammatory reaction in the anterior
chamber of the eye (Figure 23). Iris adhesion to the lens
(posterior synechia) may also be seen.
DIAGNOSTIC WORK-UP
Laboratory work-up is directed to the most likely
associated systemic disease. Although most cases of uveitis
are idiopathic, the identification of an associated systemic
disease will help in the prognostication and treatment of the
disease.
TREATMENT
Steroid is the mainstay of treatment in patients with uveitis.
Topical steroid drops are used for uveitis located in the anterior
part of the eye. Periocular steroid injection is recommended
for patients with uveitis in the posterior pole. In patients
with bilateral disease or when there is systemic evidence of
inflammation, oral steroids are used. Immunosuppresive
agents are also given in moderate to severe cases.
COMPLICATION
Moderate to severe uveitis is a brining disease. Common
complications include cataract and secondary glaucoma.
H. OTHERS
1. EPISCLERITIS / SCLERITIS
Scleritis and episcleritis present with a red eye and eye pain.
Some are associated with collagen vascular diseases. Topical
steroids and oral NS bilDs are 7r"...'" ',7".F. ..'7,ibed for this condition.
2. CONTACT LENS-RELATED EYE REDNESS
Eye redness may be seen among contact lens wearers. This
results from overwear of the contact lenses, which causes
decrease in oxygen supply to the cornea. This condition
resolves with rest from contact lens wear. Antibiotic eye drops
may be given as a prophylaxis for eye infection.
3. CORNEAL ABRASION / FOREIGN BODY
Figure 23. Keratic precipitates in uveitis.
4. ENTROPION /TRICHIASIS
Entropion and trichiasis are seen among the elderly presents
with eye redness due to misdirected lashes that irritate the
cornea. Removal of the misdirected lashes is done as an initial
treatment. Permanent treatment may require cautery of the
root of the eye lashes or surgery of the eyelids.
SUMMARY
A red eye is one of the more common ocular problems that a
primary care physician will encounter. While most cases may
be relatively benign, there are disorders that present potential
threat to vision or in some instances even life-threatening.
Figure 24 summarizes the systematic approach to arriving at
a diagnosis that was presented in this chapter. Basic principles
for managing the various red eye conditions have also been
presented.
The importance of extracting a comprehensive history as well
as performing a meticulous examination of the eye can not
be overemphasized. Recognizing the pattern of eye redness
that a patient presents has also been shown to be helpful in
arriving at a logical diagnosis. Table 1 lists non-trauma red
eye conditions that are potentially threatening to vision.
Recognition of these conditions is essential so that urgent
referral to an ophthalmologist can be done.
An overview of the more common red eye conditions has
been discussed in this chapter. Subsequent chapters shall
focus on a more detailed discussion of selected disorders that
present with a red eye.
Corneal abrasion from trauma presents with sudden eye
pain and eye redness. Topical antibiotics are used to prevent
infection.The condition resolves in 24 to 48 hours because the
corneal epithelium heals rapidly.
6
RED EYE, TEARING AND DISCHARGE 15.1 The Red Eye
(RED EYE
YES
NO
MICROBIAL
K E RAMIS
PHOIOPHOBIA?
ACUTE
GLAUCOMA
DRY EYE
TYPE OF
DISCHARGE?
YES
MUCOPURULENT
UVEITIS
BACTERIAL
CONJUNCTIVITIS
YES
ALLERGIC
VIRAL
CONJUNCTIVTTIS COINUUNCTIVITIS
Figure 24. L- ec..sc-
anving at a dag-css
e.e -esew
Table 1. Serious Non-Trauma Related Vision Threatening Red Eye Conditions
CHARA4
Condit
Redness
Glaucoma
Daiisa! most
prominent around
the limbus
Anterior LIveitis
Diffuse: most
prominent around
11.1111111
.11.1
1111
)
.„,.,.,.
10P
up!
Pain
Vision
Moderate
to
severely reduced;
iridescent vision
Mild to moderately
reduced
Moderate to severe.
Mid-dilated;
- on-reactive to
to moderate;
photophobia
Moho; irregular
shaped: poorly
reactive to light
May be affected
often with headache
and vomiting
ght
Mild
the limbus
Keratitis
Diffuse; more
prominent around
Moderate to
severely reduced
Moderate to se iere
the limbus
Scleritis
Focal or diffuse with
purple-tinged color
Endophthalmilis Diffuse
yes r
adidlorts
=LSE
Normal to mildly
reduced
usually bonder
Moderately to
Moderate to wow-.
severely reduced
Moderate b serer
associated
normal to
hypotonic
generally
not affected
with uveitis
Not affected
••
-
3 -.•7-
Not affectedi
elevated
REFERENCES AND
4.
A 45 year old executive, complained of severe headache
and right eye pain associated with blurring of vision
after watching a movie. Vision of the right eye was
20/200, not improved with pinhole. Upon examination,
she had a hazy cornea with eye redness. No discharge
was seen. What is the most likely diagnosis?
A. Acute Glaucoma
B. Allergic Conjunctivitis
C. Dry Eye
D. Microbial Keratitis
E. Uveitis
5.
Ten nurses in the operating room have eye redness
associated with watery eye discharge suggestive of
adenoviral conjunctivitis. They were not allowed to go
on sick leave. What would be the best advice you could
give to prevent spread of this infection?
A. 1,000 mg of ascorbic acid
B. Daily intake of multivitamins
C. Frequent hand washing
D. Topical antibiotic as prophylaxis
E. Use of alcohol-based hand sanitizers
6.
Two of the ten nurses who had adenoviral conjunctivitis
consulted the ophthalmology clinic 2 weeks later for
blurring of vision. What might be the cause of their
blurring of vision?
A. Corneal opacities
B. Dry Eye
C. Error of refraction
D. Microbial keratitis
E. Toxic keratitis
RECOMMENDED READING
1.
2.
3.
4.
Vaughan DG, Asbury and Riordan-Eva P. General
Ophthalomology. 14th ed. Appleton & Lange: Stamford,
CT. 1995.
Chern K and Zeagans M. eds. Ophthalmology Review
Manual. Lippincott Williams and Wilkins: Philadelphia. PA.
2000.
Tasman W and Jaeger EA. eds. Duane's OphthalmologyLippincott Williams and Wilkins: Philadelphia, PA_ 2011.
Santos E0 and Cubillan LDP. National Survey of Blindness,
Philippines 2002. University of Philippines Manila: Mania.
Philippines. 2004.
SELF-TEST
1. A 35 year old male consulted for eye redness. A group
of medical students were assigned to get the history
of medical illness. Student A asked if the patient
experienced eye pain. The patient answered yes: to
the first question. Student B was not able to elicit any
history of eye discharge. The patient told Student C
that she experienced photophobia. What eye condition
would you consider as your initial impression?
A. Acute Glaucoma
B. Allergic Conjunctivitis
C. Dry Eye
D. Microbial Keratitis
E. Uveitis
2.
A 15-year-old male consulted for recurrent eye redness
associated with watery eye discharge and itchiness.
What eye condition would you consider as your initial
impression based on the history?
A. Allergic Conjunctivitis
B. Bacterial Conjunctivitis
C. Dry Eye
D. Microbial Keratitis
E. Viral Conjuncitivitis
3. A second year medical student consulted for eye
discharge and blurring of vision 3 days prior to consult.
She is a contact lens wearer for several years. She also
complained of eye pain. On gross examination, a white
opacity was seen at the center of the cornea. What is
your initial impression?
A. Acute Glaucoma
B. Allergic Conjunctivitis
C. Dry Eye
D. Microbial Keratitis
E. Uveitis
7. A 5-year-old boy consulted your clinic for mucopurulent discharge associated with cough. He had no
eye pain. What eye condition would most likely explain
these symptoms?
A. Acute Glaucoma
B. Allergic Conjunctivitis
C. Bacterial Conjunctivitis
D. Dry Eye
E. Viral Conjunctivitis
8. An 80-year old grandmother has been treated for
glaucoma over the last 10 years. Eye pressure control
was not very successful. What kind of visual disturbance
would this patient have?
A. Blurring of the central vision
B. Blurring of the peripheral vision
C. Central scotoma
D. Enlargement of the blindspot
E. No visual disturbance is expected
6
RED EYE, TEARING AND DISCHARGE
I ^ 1 The Red Eye OE
9.
A muco-purulent discharge was observed in a newborn
baby. What is the most common etiologic agent
responsible for this disease?
A.
Chiamytha
B. Hemophilus
C. Pneumococcus
D. Pseudomonas
E. Staphylococcus
10. A 60 year old woman came in for a chronic eye redness
of both eyes. Student A asked if she has eye pain.
The patient said that she did not experience any eye
pain but she felt some foreign-body sensation. Upon
examination, no discharge was observed. Using the
algorithm, what would be your initial impression?
A. Acute Glaucoma
B. Allergic Conjunctivitis
C. Dry Eye
D. Microbial Keratitis
E Uveitis
Seeanswers to Self-test on page 221.
6.2 Uveitis and Scleritis
Teresita R. Castillo, MD, MHPEd
INTRODUCTION
This material is intended to serve as supplementan. -ea:..f-o for the students as part of the unit on THE RED EYE and focuses
:fa how to go about recognizing and assessing patients with uveitis
primarily on providing the medical student with knc
7.'1-
and scleritis. Students are however encouraged to
simulated clinical cases that they will encounter durina
. • -owledge that they will acquire from this material to , a
al,a
-otation in the clinics of the department.
OBJECTIVES
Upon completion of this instructional material, the student should be able to:
1. Formulate a working definition for uveitis, scieritis and related terms.
2.
3.
Identify the various elements in a patients history and ophthalmologic examination that leads to the
formula n of
diagnosis of uveitis and scleritis_
Formulate a diagnosis of infiammaTcry conditions involving the sclera and the uvea according to their location and
course.
4.
w' uveitis and scleritis.
Discuss the therapeutic goals of
CONTENT
I. Uveitis
A. Diagnosing uveitis
1. History taking
2. Eye examination
3. Ancillary diagnostic examinations
4. Systemic findings
B. Classification of uveitis
C. Treatment of Uveitis
II. Scleritis and Episcleritis
A.
B.
C.
Episcleritis
Scleritis
Uveitis
I. UVEITIS
Eye redness is a common complaint among patients seeking
ophthalmologic consult. While not all patients with intraocular
inflammation will present with eye redness, the differential
diagnosis for the red eye should include inflammatory eye
conditions involving the uveal tract and the sclera.
DIAGNOSING UVEITIS
Uveitis is a nonspecific term used to denote intraocular
inflammation involving the uveal tract, that is, the iris, ciliary
body and the choroid. Uveitis can involve one eye or both eyes.
Inflammation may not be limited to the uveal structures alone
and may also involve any part of the eye, including the sclera
(sclerouveitis), cornea (keratouveitis), vitreous body (vitritis),
retina (retinitis) and even the optic nerve (optic neuritis).
In order to formulate a diagnosis of uveitis, it is important
that a thorough, comprehensive history is extracted from
the patient and an accurate eye examination be performed.
Information from both history and exam provides the basis
for the generation of differential diagnosis and appropriate
selection of ancillary examinations for the patient. General
systemic examination is done when intraocular inflammation
is suspected to be a component of a systemic condition.
There are four basic elements which should be considered in
the formulation of a diagnosis of uveitis. 12
HISTORY-TAKING IN THE UVEITIS PATIENT
Extracting a comprehensive history from a uveitis patient
can not be overemphasized. The patient's history guides the
clinician in arriving at a complete diagnosis, particularly as
to the possible etiology of the condition. Furthermore, the
history can provide the clinician with an idea as to the patient's
possible response to treatment. The following are important
questions regarding the patient's current illness that the
clinician should ask each and every patient suspected to have
uveitis.
(1) What is the chief complaint?
The two most common presenting complaints of patients
with uveitis include changes in vision and floaters.1 -3 Often,
the patient consults primarily because of blurring of his
vision. Vision changes may come in the form of reduction or
distortion of vision. In addition to blurring of vision, patients
may also complain of photophobia, defined as sensitivity to
light or eye pain in high illumination.'
Floaters on the other hand refer to black or white floating
"objects" that the patients appreciate in their field of vision.'
These are often described by patients as "flies" or "insects"
which move about in their field of vision.
The onset of these changes should likewise be noted, that is
whether or not they occurred suddenly or progressively over a
prolonged period of time.
(2) How long has this problem been going on?
The duration of the problem should be extracted from the
patient Furthermore, it should also be determined whether
or not a similar problem has occurred in the past.
(3) Which eye is involved?
Does the problem involve one or both eyes? If both eyes
are involved, cki the patient experience his or her symptoms
in both eyes simultaneously or did involvement in one eye
precede the involvement in the other eye? If the onset of
symptoms difered between the two eyes, also inquire as to
the interval in the onset of symptoms between the two eyes.
(4) Are there otherassociated eye problems?
Elicit for the presence of ocular symptoms aside from the chief
complaint of the patient_ Aside from the symptoms previously
mentioned (redness. floaters, vision changes, photophobia),
patients with melds may also present with history of ocular
pain, eye trauma or ocular surgery. Each symptom should
be further c+a-actierized, particularly in terms of the temporal
onset to the patient's chief complaint and
relation of 7presence c' = . -ssion (improvement or worsening) of the
symptoms.
(5) Has the patient consulted previously? If so, were
medications prescribed and used by the patient?
-7 consultations made by the patient
Inquire as -.=
:a Des given to the patient. Gather data
and treatme-:
on how the pa: -1- -: responded to previous treatment as this
will provide valuate information for purposes of determining
prognosis.
(6) Other aspects of the patient's history that should be
considered include:
Family history. is -_-T
a nistory of any similar illness in the
family? Is there any - story of any hereditary illness?
Social History Does the patient have any exposure to pets?
Inquire also as to the patient's diet (ingestion of raw foods), any
history of alcohol intake, smoking, drug intake or travel.
Medical History. Has the patient suffered any form of illness in
the past? Inquiry as to the presence of any systemic symptoms
such as joint pains, oral and skin ulcers, hearing problems,
gastrointestinal or genitourinary problems to name a few,
should also be made.
Corneal Abnormalities. The cornea may lose its normal
luster and clarity in anterior segment inflammation.
Patients typically present with deposits of
inflammatory cells on the corneal endothelium
Keratic
called keratic precipitates (Figure 2).
precipitates are characterized according to their size,
distribution and pigmentation as these provide clues
as to the particular type of uveitis the patient has.
Although more often confined in the inferior portion
of the cornea, they may also be diffusely distributed
in certain forms of uveitis. Large keratic precipitates
would point to a granulomatous type of uveitis while
small to medium-sized keratic precipitates are more
commonly associated with the non-granulomatous
type. The presence of pigmentation, on the other
hand, would generally indicate that the condition
is chronic while non-pigmented keratic precipitates
would indicate a more acute inflammation.' 3
Sexual History. The presence of a history of any sexually
transmitted disease should likewise be elicited from the
patient.
EYE EXAMINATION OF THE UVEITIS PATIENT
The basic eye examination is performed after extracting the
history of the patient. Common ocular findings in uveitis
patients are listed below.
(1) Visual Acuity. Vision is frequently compromised in
patients with active inflammation.' Reduction in vision
can also occur as result of complications of chronic
inflammation. As with most eye conditions, accurate
recording of vision is important as this may serve as an
indicator of improvement or deterioration of the patient's
condition.
(2) Gross Findings.
Ocular adnexae generally remain
normal for uveitis patients. Generally, only patients with
inflammation involving the anterior uvea wi exhibit
abnormal findings on gross eye examination_
•
Ciliary Injection or Peri-limbal Rush. Patients with
inflammation of the anterior segment may present
with eye redness generally of the cfary congestion
type called ciliary injection or pen-timbal fkish. This
is characterized as redness of the eye that is more
marked in the area around the Embus and decreases
towards the fornices of the eyes Rpm 1). The
redness results from congestion tithe deeper ciliary
blood vessels and therefore does not blanch with
pressure or diminish with the use ofvasoconstrictors.4
Figure 2. Medium sized to large keratic precipitates which are
commonly seen in granulomatous type of uveitis (A) front view, (B) as
viewed thru slit lamp
In cases where patients develop secondary glaucoma,
the cornea may appear cloudy due to the elevation
of the IOR Patients may also present with localized
opacified areas of the cornea when the cornea
becomes involved in the inflammatory process.
Band keratopathy which represent deposits of
calcium in the Bowman's layer of the cornea, may
occur as a result of chronic inflammation. These
lesions often start at the corneal periphery but
may eventually cover the visual axis of the patient
(Figure 3) and may need to be surgically removed.
Pupil abnormalities. Patients with anterior uveitis
present with constricted irregularly shaped pupils
•
Figure 1.
because of the presence of posterior synechia which
are adhesions between the iris and the anterior
capsule of the lens (Figure 4).L23 In some instances,
ciliary iniection. Note that redness or congestion is
accentuated in the limbal area, hence called perilimbal flush as well. This
type of redness is more commonly seen in uveitis and glaucoma
6
RED EYE, TEARING AND DISCHARGE 16.2 Uveitis and Scleritis
119
Figure 3. Band keratopathy covering visual axis of patient's eye. Its
presence is usually indicative of a chronic anterior uveitis
an inflammatory membrane may also cover the
pupil (Figure 5). When posterior synechia is present,
despite intact sensory and motor arms of the light
reflex, the pupil will fail to exhibit normal pupil
responses (direct and consensual).
Anterior Chamber abnormalities.
Protein leakage
from iris blood vessels that become affected by the
inflammation would affect the clarity of the anterior
chamber. This is referred to as flare. One may also
Flume S. Eye roil small pupil and an overlying pupillary membrane.
Waft peierce or oiary injection and diffusely distributed large nonfoiAcn-faU keratic precipitates. There is also a localized area
al irisMap" (ghee arrow)
note the presence of inflammatory cells in the anterior
chamber as a result of the inflammation. If the number
of inflammatory cells within the anterior chamber
becomes large, the cells accumulate and settle
inferiody, assuming a level referred to as hypopyon
(Figure 6).
Iris changes. The iris may become thinned out and
subsequently appear "moth-eaten". Nodules may
also be present in the iris, either within the stroma,
cared Busacca nodules or in the pupillary margin,
referred to as Koeppe nodules (Figure 7). These
nodules are composed of chronic inflammatory cells
(lymphocytes, plasma cells) and are reliable indicators
of granulomatous type of anterior uveitis.'
Figure 4. Posterior synechia (adhesions between iris and lens (white
arrow). Pupil dilation can break these adhesions and leave pigments on
the anterior surface of the lens (pink arrows)
Figure 6. iniammatry cells sett* and form a level in the inferior aspect
dile arena cherber lo form hypopyon
Illig
Self-Instructionl
Materials in OUrat107101011Y I 7nr1 Frlirinn
sheathing or narrowing or obliteration of the retinal
blood vessels
•
Granulomatous nodules -composed of inflammatory
cells, which present as creamy white nodules along
the vitreous base or in the retinal pigment epithelium
Retinal Pigment Changes - generally represent areas
of inactive inflammation; these lesions are typically
referred to as retinal scars
Retinal Detachment - may come in the form of diffuse
serous detachment of the retina or as multifocal areas
of detachments
Figure 7. Ins nodules seen in cases of granulomatous
(A) Koeppe nodules (located at pupillary area),
(B) Bussaca nodules (located at stromal area of the iris)
(3) Intraocular Pressure. Uveitis patients would typically
present with very soft or hypotonic eyeballs. This
results from reduced aqueous humor production as a
consequence of involvement of the awry body in the
inflammatory process. Patients with chronic uveitis may
however present with elevated intraocular pressure due
to secondary glaucoma either from the development
of complications from the inflammation or as a result of
prolonged used of steroids.'
(4) Extraocular Muscle Movement. Inasmuch as the
extraocular muscles are usually not kwohred in the
inflammatory process, patients would exhibit full
movement on all directions of gaze Limitation of EOM
movements is however, a halknark of endophthalmitis
which is used to differentiate it from tweitis.
(5) Fundus Examination. ?atients with uveitis may exhibit
-tgs depending on the anatomic area
varying fundus
of the uveal tract that is involved in the inflammatory
process.
If the inflammation is confined to the anterior segment,
patients would have nomial funduscopic findings. Patients
with intermediate or peripheral uveitis may present with
vitritis or haziness of the vitreous. Fundus examination
may further reveal the presence of cellular aggregates
in the vitreous ("snowballs') or in the periphery of the
retina referred to as "snowbanking" (Figure 8). In cases
wherein the posterior segment of the eye is involved,
more frequently encountered findings in patients are
listed below: (Figure 9):
•
•
Cystoid Macular Edema - seen as dullness or absence
of the foveal reflex on direct ophthalmoscopy
Vasculitis - often comes in the form of perivascular
Figure 8. (A) Vitreous snowballs. (B) Snowbanking in peripheral
retina. Both findings consist of aggregates of inflammatory cells. These
are findings commonly seen in patients with intermediate uveitis
ANCILLARY OPHTHALMIC DIAGNOSTIC
EXAMINATIONS
Additional examinations may be requested to aid in the
diagnosis of some conditions. The more commonly requested
ancillary procedures include:
(1) Ultrasound of the Eye. In most cases of uveitis, a view of
the posterior portion of the eye is compromised due to the
presence of anterior segment pathology (cataracts, pupil
membranes, etc) or vitreous pathology. Ultrasonography
gives the clinician a picture of the posterior segment and
assists in the documentation of presence or absence of
6
RED EYE, TEARING AND DISCHARGE I 2 Uveitis
and Scleritis
abnormalities of the vitreous (vitreous condensation),
retina (retinal detachment, masses) and the choroid
(choroidal thickening).5
(2) Fluorescein Angiography. This diagnostic procedure
focuses on the evaluation of blood flow in the vasculature
of the posterior segment of the eye. It is used to
demonstrate the presence of leakage from retinal vessels
and from the optic nerve. It also provides a method for
detecting problems in the choroid and the retina. Some
posterior segment inflammatory conditions may present
with typical fluorescein findings such as retinal edema,
irascufois. retinitis and areas of focal retinal detachment.'
Doc disc as well as macular findings may also be
encountered in these patients.
(31 indocyanine Green Angiography. Indocyanine green
„ _4—an
is often utilized as an adjunct to
angiogram studies. Due to its higher plasma
Wang properties, which prevents its leakage
Mind and choroidal blood vessels, indocyanine
been found to be better in evaluating choroidal
ICG is the examination of choice to confirm
inflammatory process involves the choroid 6
7
been utilized to evaluate disease activity in a
numitev ciforms of uveitis .°
(4) Optical Coherence Tomography.
This procedure
non-invasive assessment of the retina,
and
useful in determining the presence
Or absence of macular
edema which is a common
complication of uveitis. It has also been found to
be
useful in assessing response to therapy in patients with
uveitis.
pr000e.s
SYSTEMIC FINDINGS IN THE UVEITIS PATIENT
There are a number of systemic conditions that may
present with uveal tract inflammation. Examples are various
arthritic conditions, parasitic conditions and immunologic
conditions. These diseases may present with mucocutaneous
abnormalities, e.g. oral/genital sores, vitiligo, erythema
nodosum; joint inflammations; pulmonary involvement or
gastrointestinal pathologies to name a few. '.35,8
CLASSIFICATION OF UVEITIS
Various classification methods have been employed in
formulation of the diagnosis in uveitis patients. This material
focuses primarily on two aspects: location and duration of the
inflammation.
Figure 9. Posterior segment findings in uveitis (A) Vitreous haze with
macular edema in a patient with Behcet's Disease, (B) Vasculitis as
evidenced by perivascular sheathing (white arrows), (C) Posterior pole
granuloma obscuring clear view of the optic disc, (D) Retinal pigment
changes in a patient with serpiginous choroidopathy
In 1987, the International Uveitis Study Group (I USG) developed
criteria based on the anatomical location of the inflammation.
In 2004, the Standardization of Uveitis Nomenclature (SUN)
classification for onset
working group added criteria for
duration and course of the disease.9
Based on the primary anatomical structure involved, uveitis is
classified as anterior, intermediate, posterior or diffuse/panuveitis
(Table 1, Figure 10) As implied by the term, anterior uveitis, this
type of inflammation primarily affects the anterior segment of
the eye. It can also be called iritis when inflammation primarily
involves the iris. Usually, both the iris and ciliary body becomes
inflamed and this is called iridocyclitis. Intermediate uveitis refers
to inflammation involving the ciliary body, anterior vitreous,
peripheral retina and the pars plana (middle portion of the
globe). Posterior uveitis is the term used when the inflammatory
Table 1. Anatomical Classification of Uveitis
Classificati°n'41111
Anterior Uveitis
anterior segment
iritis
iris
cyclitis
ciliary body
iridocyclitis
both iris and
Intermediate Uveitis
pars
an
Posterior Uveitis
posterior secrnerr_
retinitis
'
•
c.
retina
process primarily involves the choroid and/or retina. Specific
terminology such as "choroiditis" and "retinitis may be used if the
choroid or retina is inflamed respectively. If both structures are
involved in the inflammatory process, this may be referred to
as "chorioretinitis" or letinochoroiditis", depending on whether
it is the choroid or retina that is the primary location of the
inflammation. Aleuroretinitis refers to posterior uveitis wherein the
optic nerve is also involved in the inflammatory process. When
ail weal structures (iris. ciliary body, choroid) becomes inflamed,
this is caled ponuveitis or diffuse uveitis. Most cases of anterior and
totermedhate uveitis are idiopathic in nature while most posterior
aid diffuse uveitis have an identified etiology or constitute a
presentation of a systemic condition.
Mother method by which uveitic conditions are classified
is based on the course of the condition (Table 2). As can
be seen from the table, acute cases are differentiated from
recurrent or chronic type by their generally sudden onset
and limited duration (often less than 3 months). When the
irdlammatory process persists beyond three months, these
me labeled as recurrent or chronic depending on presence of
periods of reactivity between periods of exacerbation. Cases
with periods of inactivity are labeled as recurrent while those
without are labeled as chronic cases?
choroiditis
retinochoroiditis
chorioretinitis
Diffuse
UveitislPanuveitis
7-0—Je •221tr
.
—cr-1.1
Table 2. Climikaim of Live& based on Course of the Disease
-;
Jorix1 7BC*
•
•
Sudden onset and limited duration
acute anterior uveitis presents with many
•
cells and severe flare
cells generally smaller in size and flare is
conspicuous
3t:
Recurrent
~~
repeated attacks of inflammation separated
by periods of inactivity without treatment of
at least three (3) months
Cr-on ;..•
~~
persistent inflammation with relapse within
three (3) months after discontinuation of
treatment
•
cells may be absent but flare usually present
Table 3 presents a pathologic classification of uveitis
differentiating them to either granulomatous or nongranulomatous. Generally, granulomatous cases present as
panuveitis and are chronic while non-granulomatous cases
often present with an acute course, generally just involving
the anterior segment.
C
Diffuse/Panuveitis
Figure 10.
5E--s `_v
or veitis is based on localization of
the infiamma::- (A) Anterior Uveitis :nmary site is the anterior
segment, (B) Intermediate uveitis - solves the anterior vitreous,
peripheral retina and pars plena. (C) Posterior uveitis. involves
the retina andlor choro: When all three areas are involved.
Lastly, the various uveitides can be classified based on the
etiology of the inflammation as presented in Table 4. Etiology
is often arrived at after conducting laboratory investigation.
With the aid of careful and thorough medical examination,
one can request for the appropriate laboratory examinations
that can confirm the etiology of uveitis.
uveitis is classified as diffuse or panuveitis.
6
RED EYE, TEARING AND DISCHARGE I
Uveitis and Scleritis
Table 3. Pathologic Classification of Uveitis and Corresponding Features
Features
Nongranulomatou
Granulomatous
Structures
involved
usuail entire uveal
tract
usually anterior
segment only
Onset
insidious
sudden
Course
often chronic
acute with
exacerbations and
remissions
TREATMENT OF UVEITIS
Characteristic Features
keratic
precipitates
large greasy (mutton
fat)
fine or small
posterior
synechia
forms during acute
inflammation. often
at location of
nodules
less likelihood of
synechia formation
iris nodules
frequently present
generally absent
posterior
segment
with granuloma
frequently spared
Table 4.
Etiology of welt s
Group
Etiology
Bacterial
•
Tubercul:,
~~ Syphilis
Viral
•
•
•
Fungal
•
Histoplasmosis
•
Coccidiomycosis
•
•
•
Toxoplasmosis
Toxocariasis
Onchocerciasis
Parasitic
Immunologic
Systemic
•
Lens induced iridocyclitis
Sympathetic ophthalmia
•
Reiter's Disease
Sarcoidosis
Collagen Disease
Rheumatoid arthritis
Multiple sclerosis
Vascular Disease
•
•
•
•
•
Reticulum sarcoma
Neoplastic
Lymphoma
Miscellaneous
•
•
Aim.
Herpes simplex
Herpes zoster
Cytomegalovirus
•
Heterochromic iridocyclitis
Pigmentary syndromes
A complete diagnosis of uveitis should generally include all
these (anatomic involvement, duration and course, etiology)
as well as the level of activity of the inflammatory process. For
purposes of this manual, however, the latter classification shall
not be discussed.
=gm
As with any oisease condition, therapeutic intervention should
be based on a thorough clinical evaluation of the patient and
sound therapeutic guidelines. Therapeutic goals in the uveitis
patients indude (1)control of inflammation; (2) prevention and
treatment of vision-threatening complications; (3) alleviation
and relief of the patient's symptoms; and (4) treatment of the
underlying cause
Inflammatory coneoltakes into consideration both immediate
and long-term caned since adequate inflammatory control
is also the key it minimizing the development of unwanted
complications of the inflammatory process. Drug classes that
are well suited fur immediate control may not be appropriate
for long-term usedue to the side effects that accompany their
prolonged use.
Corticostexids are the mainstay in inflammatory control of
non-infectious welds. Their use in uveitis secondary to a
probable infectious cause should be started only when the
underlying infection has been adequately addressed. While
ideal for iminnediaseinflarnmatory control, the long-term use
of this class of dogs is not encouraged due the unwanted
systemic andeaslartdeeffects that accompany them when
taken for prolonged periods- Steroid-sparing therapies in
the form of non-soesoidal anti-inflammatory drugs (NSAIDs)
and immunoinodulalosy drugs should be considered if it
becomes apparent that therapy will be required for more
than three months. Table 5 lists some of the various drugs
currently in use for the control of inflammation in uveitis
patients. The choice of which specific agent to be used is
based largely on its efficacy and tolerability in a particular
patient situation.
Cycloplegic agents are used to prevent adhesion of the iris to
the anterior lens capsule (posterior synechia formation), which
can lead to pupillary block and elevated intraocular pressure.
They are also used to break recently formed posterior synechia
and to stabilize the blood aqueous barrier and therefore
prevent further protein leakage (flare). The shorter acting
agents (tropicamide and cyclopentolate) play a role in
preventing new posterior synechia formation as their shorter
duration of action keeps the pupil relatively mobile.
Two more common complications of uveitis requiring attention
and cataract formation.
and treatment would be 10P elevation
either
the inflammation
may
result
from
Both conditions
Selection
of 10P lowering
itself or prolonged steroid use.
of
glaucoma.
When
on
the
mechanism
agents would depend
Table 5. List of Commonly Used Anti-Inflammatory Agents used for Uveitis Cases
I.Corticosteroids
•
•
•
•
Inhibition of cyclo-oxygenase and
lipooxygenase pathways
Decrease complement levels
Decrease migration of lymphocvies
Decreased production of vasoactise amines
and interleukins
Decreased circulating monocOes
Decreased macrophage act*
Topical
•
•
•
•
Periocular
•
•
•
•
•
•
•
•
•
■
■
■
■
■
•
•
■
•
elevation of 10P
cataract
exacerbation of infection
corneal or scleral thinning/
perforation
Same as topical
Ptosis
Scarring of Tenon's capsule
Scleral perforation
Hemorrhage
Abscess
Same as topical
Weight gain
Fluid retention
Electrolyte disturbances
Peptic ulcer disease
Osteoporosis
Aseptic necrosis of hip
Hypertension
Impaired glucose tolerance
Mental status changes
Impaired wound healing
Menstrual irregularities
■
•
bone marrow suppression
terratogenicity
increased risk of infection
•
•
•
•
Hepatotoxicity
Gastrointestinal upset
Pneumonitis
Stomatitis
•
•
Gastrointestinal upset
Hepatitis
Systemic
II. Immunosuppresive
Medications
-7-77'e--e.S. NZ'
All
Z.P.A. sratess a-c x4.. a,
A. Antimetabolites
Methotrexate
!rj-Dloiate reductase
Azathiopnne
;ter!.
Mycophendez
rtrubis .rre sprrne&s
•
Diarrhea/
•
Nausea
•
•
•
•
Lymphotoxicity. cross-links DNA
Hemorrhagic cystitis
Sterility
Increased risk of malignancy
■
•
■
■
Renal toxicity
Hypertension
Hirsutism
Tremor
■
•
•
•
•
Renal toxicity
Hypertension
Neurotoxicity
Hepatitis
Diabetes
L. Alkylating Age
Cyclophosphanide
B.T-cell Inhibitors
6
RED EYE, TEARING AND DISCHARGE 1 6.2 Uveitis and Scleritis
medical intervention fails, patients are advised to undergo
surgery. Cataract surgery is likewise advised for patients when
the degree of visual disturbance warrants it.
Table 6. 7 =e-e-t 2', c- between Scleritis and Episcleritis
Specific therapy is also directed towards the relief of eye pain
and photophobia which are common symptoms of acute
anterior uveitis. Topical instillation of mydriatic/cycloplegic
agents relieve pain by immobilizing the iris. Longer acting
agents such as atropine and homatropine are ideal for this
purpose.
Episcleritis
redness
severe, radiating eye
pain
bright red
bluish red
rare
present
4" to 5th decade
zIth to 61h decade
frequently females
frequently females
ZZ:g
111111hkess
Tenderness
Gender
In cases where the underlying cause for the inflammatory
process is identifiable, specific treatment for the underlying
condition should be instituted. This is particularly important in
instances where there may be an infectious process involved.
Scleritis
of cases
50% of cases
EPISCUMITIS
The choice of specific treatment also takes into consideration
the degree/severity and location of the inflammatory process.
Administration via the topical route is useful primarily in
patients who have anterior uveitis, as topically applied drugs
poorly penetrate the posterior segment. The periocular
route is effective for administering anti-inflammatory agents
to patients who have intermediate uveitis, posterior uveitis,
or cystoid macular edema, particularly if the condition is
unilateral. It may also be beneficial in patients who have
severe anterior uveitis found to be unresponsive to topical
therapy. Periocular injections may be given via various routes:
subconjunctival, subtenons or retrobulbar. The selection
of the location for the injection would depend on the site
where higher concentration of the anti-inflammatory agent
is desired. Periocular injections of corticosteroids should
be avoided in cases of infectious uveitis (e.g.toxoplasmosis)
and should be used with caution in patients who have a
history of corticosteroid-induced 10P elevation. Intravitreal
injections may also be given in cases where the primary site of
inflammation is the posterior segment.
Episcleritis is a benign inflammatory disease characterized
by edema and celkilar infiltration of the tissue between the
conjunctiva and sclera, the episcleral tissue. It is a self-limiting
condition usualy lasting for one to three weeks. Episcleritis
usually occurs in the fourth to fifth decade, with females
being more affected by males. Eye redness in this condition
is commonly confined to the interpalpebral area and would
blanch on pessuie or topical instillation of vasocontrictors like
phenylephrinE Patients often complain of mild discomfort,
described as sWit adze, feeling of heat or irritation in the
involved eye_ Male commonly unilateral, the condition is may
be bilateral in one thiud of cases.1°
Episcleritis is trite- &wit:led into two clinical types: simple
diffuse and nodiaiar Rpm 11). Table 7 summarizes the
various lean/ES Cif tl'ese Nrio types.
Other factors influencing the choice of specific treatment
would be the age and general health status of the patient,
and the patient's reliability, preferences and understanding
of his/her condition. It is important for a clinician to provide
the patient with information he would require to have a better
understanding of his illness, its treatment and prognosis.
II. SCLERITIS AND EPISCLERITIS
The terms scleritis and episcleritis refer to conditions where
inflammation involves the sclera and the episcleral tissues
respectively. As with the uveitic conditions, inflammatory
diseases involving the sclera and episclera are further classified
based on their clinical presentation. It is important to distinguish
between these two conditions for purposes of management and
determination of prognosis. Table 6 lists the different criteria
used in distinguishing the two conditions from each other.
Figure 11. Episderis alien pieserts as a localized area of redness (A).
At times, a nodule may also be present (B).
Table 7. Types of Episcleritis with Corresponding Characteristics
-ffignuivr
Feat
e Episcleritis
Frequency
more common
Course
often self-limiting (2-19 days
Nodular Episcleritis
. :a(es longer to resolve (4-6 weeks)
Characteristic Features
-
injection of invoier; a-ea
-
often without disccr7‘art
may be recurrert teccrres
frequent in 3 to 4 yea's
Since majority of episcleritis resolve spontaneously, these
patients frequently do not seek consultation. However,
since it is an inflammatory condition, patients who come in
for discomfort may benefit from a regimen of topical antiinflammatory agents and lubricants.
Systemic associations are found in about one thild of patients
with episcleritis. This is however not correlated to the type.
laterality or chronicity of the disease. Systemic conditions
associated with episcleritis include connective tissue ciseases
(rheumatoid arthritis, SLE, relapsing polychonckitisk 827associated conditions (spondyloarthropathits, inflammatory
bowel disease); vasculitic diseases (polyarteritis noclosa.
Behcet's disease, Wegener's granulornatosis, giant cell arteritis,
Cogan's syndrome); infections (herpes, bacterial, fungal,
parasitic) and some miscellaneous conditions ( atom. rosacea.
gout). 10,11.12
-
, _
with movable non-tender nodule
:: :3 , -:re painful
-3
associated with systemic
Tne primary sign of scleritis is redness which is gradual in
onset and has a characteristic bluish-red tinge that may be
best observed under natural light (Figure 12). Such redness
fails to blanch with local instillation of vasoconstrictors.
Unlike episcleritis, patients affected with this condition
often present with severe, boring ocular pain which may
also involve the adjacent head and facial regions. Pain is
described as severe and penetrating with radiation to the
forehead, brow, jaw or sinuses. It can be severe enough to
keep patients awake at night and may be exacerbated by
touch. Analgesics provide only temporary relief of the pain.
Aside from these, patients may also present with tearing,
photophobia and at times decreased vision which results
from extension of scleritis to adjacent ocular structures
leading to keratitis, uveitis and sometimes even glaucoma,
cataract and fundus abnormalities.1°
Patients with episcleritis general/ do not develop ocular
complications,
although (heti% peripheral comeal
inflammation and glaucoma may occur in a small percentage
of cases. There have also been reports on a small number of
these patients progressing Mt sdaritis.
SCLERITIS
Scleritis is a severe ocular inflammation which if left untreated,
may become progressively destructive. Unlike episcleritis,
patients affected with this condition are usually in their fourth
to sixth decades of life. Females outnumber males to a small
degree. The condition has been reported to occur bilaterally
and is recurrent in about one third of cases. 1"
Scleritis is commonly assnriated with systemic autoimmune
disorders, induding rheumatoid arthritis, systemic lupus
erythematosis, spondyloarthropathies, Wegener granulomatosis,
polyarteritis nodosa and giant cell arteritis. Scleritis may even
precede other symptoms associated with these systemic illness.
Diagnosing scleritis. As with uveitis, a thorough and
complete history is essential in making a diagnosis of scleritis.
Aside from the patient's major complaint and history of present
and past illness, investigate as to any history of infection, injury
or surgery. A thorough review of systems will also assist in
determining if the ocular disease is related to any systemic
condition.
Figure 12. Typical redness seen in patients with scleritis showing
characteristic bluish-red tinge (best seen under natural light).
of Scleritis. Based on the location of the
inflammation, scleritis is classified into anterior and posterior
type." Figure 13 shows representative photographs of
Classification
various types of scleritis. Rarely, a patient may present with
both anterior and posterior scleritis.
1. Anterior Scleritis. Anterior scleritis can be diffuse,
nodular, necrotizing with inflammation (necrotizing),
and necrotizing without inflammation (scleromalacia
perforans). The most common clinical forms are
diffuse scleritis and nodular scleritis. Necrotizing
scleritis with or without inflammation is much less
6
RED EYE, TEARING AND DISCHARGE 1 6.2 Uveitis and Scleritis
frequent, more ominous, and frequently associated
with systemic autoimmune disorders.
Diffuse anterior scieritis is the most common
type of scieritis. It is of insidious onset and
may develop over a 5 to 10 day period. Often
misdiagnosed as episcleritis, it is associated with
the best visual prognosis as ocular complications
rarely occur. It is also least associated with a
a.
systemic disease.
b.
Nodular anterior scleritis occurs less
frequently than the diffuse anterior type but is
more common than necrotizing scleritis. The
inflammatory process is localized to a nodule(s)
'Mach is immobile, firm and tender to touch.
M in the diffuse anterior type it is of insidious
onset In terms of severity of the disease, it is
inimmeciate between that of the necrotizing
type and posterior scleritis.
Neaotizing scleritis with inflammation is
the most severe and destructive form. It is
characterized by the presence of white avascular
areas surrounded by swollen inflamed sclera.
More than half of patients with this condition
haw associated systemic conditions such as
rheumatoid arthritis, Wegener's granulomatosis
and relapsing polychondritis. It is also the most
frequently associated with ocular complications
SuCh as peripheral corneal thinning or stromal
Iceratitis, uveitis, cataract, and glaucoma.
d.
Neaotizing scleritis without inflammation or
Sderomalacia perforans is painless condition
cr,oracterized by the appearance of yellowgray nodules that gradually develop a necrotic
slough or sequestrum without surrounding
inflammation of the sclera. The necrotic tissue
eventually separates leaving the choroid bare,
covered only by the conjunctiva. Spontaneous
perforation rarely occurs, although traumatic
perforation can easily occur. This condition
is almost always associated with rheumatoid
arthritis.
2.
Figure 13. Four types of anterior scleritis: (A) Diffuse Sdentis, (B)
Nodular Scleritis, (C) Necrotizing scieritis, (D) Scleromalacia perforans
showing choroid
,rif
Fe-111-1,r1
Posterior sderitis has the lowest incidence among
these conditions. It occurs twice as often in females
and affects both eyes in about one third of cases.
It may also be associated with anterior scleritis.
Frequently, patients are older than 50 years and
have and increased risk of visual loss. Patients with
this condition complain of periocular pain, pain
with eye movements and decreased vision. Other
eye symptoms include conjunctival chemosis,
proptosis, lid swelling, lid retraction and limitation
of extraocular movements. Fundus examination
may reveal disc swelling, choroidal folds, serous
retinal detachment, uveal effusions and macular
edema. B-scan ultrasonography, the key to making a
diagnosis of posterior scleritis, may show flattening of
the posterior aspect of the globe, variable degrees of
thickening of the posterior coats of the eye (chcand sclera), associated with edema of the retrot
space. Accumulation of fluid in the tenons s:
manifests as the characteristic "T" sign (Figure 14)
seen on B-scan ultrasound:3
Figure 14. Accumulation of lkid in lie lims woe Essissis as toe
characteristic T sign in B son drama
Associated Diseases. Systerric concitiors have been associated
with approximate 5096 of all sderiiis Gases.':-. Table 8 shows a list of
these conditions As with theitt. selection of diagnostic./laboratory
examinations is aimed at confirrring or rejecting suspected systemic
association and, should therefore be guided by information
gathered from the patient's history and physical eamination.
Treatment. In majority of cases, topical anti-inflammatory
therapy is inadequate and would require systemic therapy.
Treatment should be incbvidualized based on the severity
of the disease, prior response to treatment and presence of
associated disease. Non-infectious scleritis is treated with
Table
systemic corticosteroids, nonsteroidal anti-inflammatory
drugs or immunomodulatory drugs. In cases where scleritis
is suspected to have infectious association, anti-inflammatory
therapy should never be started without accompanying or
prior treatment with antimicrobial therapy. 10,11,12
CONCLUSION
It was the primary objective of this self-instructional material to
provide the reader with a guide on how to diagnose patients
with uveitis and scleritis. The importance of a comprehensive
clinical history can not be overemphasized since the etiologic
diagnosis of most of these ocular inflammatory conditions
relies on the history. Secondly, one should be able to recognize
the various ocular signs associated with these inflammatory
conditions.
As medical practitioners, you may, in the future encounter
patients who will seek consultation for eye problems. One
should bear in mind that not all conditions which present with
a red eye is "sore eyes" and a patient may actually be suffering
from another, more vision-threatening condition like uveitis
or scleritis. It is therefore your role to be able to properly
recognize these patients so that immediate referral to an
ophthalmologist for further evaluation and management can
be done. By doing so, early intervention can be facilitated and
permanent visual impairment may be avoided.
RECOMMENDED
FOLLOW-UP ACTIVITY
It is recommended that the students be given demonstration
sessions on how to properly conduct history-taking
and ophthalmologic examination of patients with
ocular inflammation. Following this exercise, it is further
recommended that the students be provided clinical sessions
to allow them to see actual cases of patients with uveitis and
scleritis.
8. Systemic Diseases Associated with Sderitis
rheumatoid arthritis (RA)
systemic lupus erythematosus
B27 spondyloarthropathies
inflammatory bowel disease
relapsing polychondritis (RP)
Wegener's granulomatosis
viral (herpes zoster, simplex, mumps)
bacterial (tuberculosis, syphilis.
Pseudomones, Hemophilus, Borellia)
fungal
parasitic
polyarteritis nodosa
rosacea
gout
Behcet's disease
chemical injury
giant cell arteritis
Psoriatic arthropathy
Psoriatic rash
Cogan's syndrome
6
RED EYE, TEARING AND DISCHARGE 16.2 Uveitis and scleritis
129
REFERENCES
2.
1.
Smith, Ronald E. and Nozik, Robert A. Uveitis: A Clir
Approach to Diagnosis and Management. Williams a- s:
Wilkins:Baltimore, 1983.
2. httpi/www.preventblindness.org/uveitis. Accessed May
12, 2011.
3. Nussenblatt, RB, Whitcup, SM and Palestine, AG. Uveitis:
Fundamentals and Clinical Practice. Mosby:Baltimore. 2nd
4.
Shown are representative pictures of eye redness.
Which of these pictures best corresponds to that found
in patients with uveitis?
ed. 1996.
The Red Eye in: Basic Ophthalmology for Medical Students
and Primary Care Residents. Berson, FG. Exec ed. San
Francisco: American Academy of Ophthalmology. 1993.
57-74.
5.
Pleyer, U and Foster, SC (eds). Essentials in Ophthalmology:
Uveitis and Immunological Disorders. Berlin Heidelberg:
Springer-Verlag. 2007.
6. Huang, 11 and Gaudio, PA (eds). Ocular Inflammatory
Disease and Uveitis Manual: Diagnosis and Treatment.
Philadelphia: Lippincott Williams and Wilkins. 2010.
7. Agarwal, Amar. Fundus Fluorescein and Indocyanine Green
Angiography. Slack Incorporated. 2008. downloaded
through
httpi/www.r2library.com.proxy.lib.umic.edu/
marc_frame.aspx?ResourcelD=83.Accessed November
17, 2010.
8. Foster, SC and Vitale, AT. Diagnosis and Treatment of Uveitis.
Philadelphia:W.B. Saunders Co.lbert T. Philadelphia, W.B.
Saunders Co. 2002.
9. Zierhut, M, Deuter, C and Murray P. Classification of Uveitis
- Current Guidelines. European Ophthalmic Review. 2007;
77-78. Manfred downloaded through http://www.
touchbriefings.com/pdf/2945/zierhut.pdf Accessed Dec
9, 2007.
10. Pleyer, U and Mondino B (eds). Essentials in Ophthalmology:
Uveitis and Immunological Disorders. Berlin Heidelberg:
Springer-Verlag. 2005.
11. Sainz de la Maza M. Scleritis in http://emedicine.medscape.
com/article/1228324. Accessed May 13, 2011.
12. Sainz de la Maza M, Jabbur NS, Foster CS. Severity of
scleritis and episcleritis. Ophthalmology 1994; 101(2): 38996.
13. Biswas J et.al. Posterior scleritis: Clinical profile and
imaging characteristics. Indian J Ophthalmol 1998; 46:195202.
SELF - TEST
1.
Inflammation involving any portion of the uveal tract
(iris, ciliary body, choroid) is collectively referred to as
A.
B.
C.
conjunctivitis
keratitis
neuritis
D.
uveitis
3. The most frequent complaint of patients with uveitis is
A. disturbance in .
B. eye pair
C. eye rec
D. itchiness
4.
Signs that would lead to a working impression of uveitis
would be
A. ciliary injection, irregularly-shaped reactive pupil,
normal OOP with enlarged cup to disc ratio
B. ciliary injection, mid-dilated unreactive pupil, corneal
edema, high 10P and pale optic disc
C. ciliary injection, small constricted irregularly shaped
poorly reactive pupil, low lOP with normal fundus
D.
findings
diffuse eye redness, central corneal opacity, high lOP
with limitation of EOMs
5. 8-scan ultrasound findings that support presence of
posterior uveitis
A.
B.
C.
D.
E.
6.
Inflammatory cells can present as any of the following,
EXCEPT
A.
B.
C.
D.
E.
7.
calcific deposits in the vitreous
choroidal detachment
choroidal thickening
funnel-shaped retinal detachment
vitreous hemorrhage
"snowballs"
flare
Keratic precipitates
Koeppe nodules
Posterior pole granuloma
See answers to Self-Test on page 222
PRACTICE CASES
Case 1. 50 year old female presents with a history of threemonth duration of blurring of vision and redness in the left
.e. She denies any other associated symptoms but claims to
and off eye redness in the past year. Ophthalmologic
2 - 3n revealed the following findings:
Best Corrected %%ionIntraoake = s a
Ws
_rduscapy:
OU: full
00 - essentialy normal funduscopic findings
- no ROR noted due b a very hazy media
Characteristics of granulomatous uveitis
A.
B.
C.
D.
E.
acute onset
diffusely distributed fine keratic pre(
often involves both eyes
often involves the entire uveal tract
tend to present with hypopyon
_ : 1-.Jt
.:.,-=
EOM'S
9.
histoplasmosis
toxopolasmosis
tuberculosis
typhoid
A patient presenting with localized eye reckless of four
days duration associated with eye pain is shown in the
photo. Upon instillation of topic .
f!' ctors, yo u
did not note any blanching of the .esse
s patient is
most likely to have
A. conjunctivitis
B. episcieritis
C. scleritis
D. uveitis
10. Systemic condition more frequently associated with
scleritis
A.
hypertension
B.
allergy
Right Eye
Left Eye
6/21
Soft
Full
6/30
Soft
Full
c-retscopi
(+)ROR- sightly hazy
merle, distinct disc
borders, CD 0.3, AV
2:3, no hemorrhages,
no exudates, slightly
dull fovea reflex
(+)ROR, slightly
hazy media,
distinct disc
borders, CD
0.3, AV 2:3, no
hemorrhages, no
exudates, slightly
dull foveal reflex
Sit Late
Findings
Clear cornea, formed
anterior chamber,
(+) medium to large
non-pigmented KP's,
(++)cells,(++) flare (+)
Bussaca nodules
Clear cornea,
8. Uveitis may be associated with bocteriai ilections.
Common bacterial infection that may ~rifest it the
eye as uveitis
A.
B.
C.
D.
00 = 6/21 OS = 3/60
OD = soft OS = hypotonic
(+) large nonpigmented KP's, (+)
cells, (+)flare, (+)
Koeppe nodules,
moth eaten iris
Slit Lamp Findings:
OD - dear cornea, no cells or flare, no keratic precipitates, normal appearance
of the iris, (+) lens opacity
OS - clear cornea (+) peri-limbal flush, (+) cells/(+) flare. (+)fine. pigmented and
non-pigmented keratic precipitates. (+) posterior synechiae. (+) lens opacity. (+)
vitreous condensation
1.
Based on the given information, how would you
classify the patient's condition on the basis of disease
activity?
2.
Assuming that this patient has normal funduscopic
findings in the left eye, what is the anatomic
classification of this patient's uveitis?
3. What ancillary procedure may be useful in
determining the presence or absence of posterior
segment inflammation?
C. rheumatoid arthritis
D. hyperthyroidism
6
RED EYE, TEARING AND DISCHARGE I 6.2 Uveitis and Scleritis
Case 2. 54 year old male presents with a chief complaint of
bilateral blurring of vision. History reveals that the patient first
experienced eye redness in the left eye about one year prior
to consultation that was associated with photophobia and
blurring of vision. Consult was done at that time and symptoms
allegedly resolved with unrecalled topical medication. About
1 month prior to consultation, the patient noted recurrence of
symptoms in the left eye and a week later, experienced similar
symptoms in his right eye. He also noted the presence of oral
ulcers. The rest of the history was unremarkable.
Ophthalmologic examination at time of consultation revealed
Visual Amity
Right Eye
Left Eye
6/6
6/7.5
Rosacea facies; normal pupillary reflexes; normal eyelids
Gym Elam
10P
BOBIS
ROIIIIIIIIN
clamp
Fib
15mm Hg
12 mm Hg
Full
Full
normal
normal
essentially normal
localized redness
findings
temporally (pls. refer to
picture below)
the following findings:
1.
What parts of the uveal tract is involved in the
inflammatory process? Based on your answer, how
will you classify the patient's condition?
2.
Is the disease condition chronic, recurrent, or acute?
3.
Based on the above findings, is the disease condition
granulomatous or non-granulomatous in nature?
4.
What ancillary procedure will you request to determine
the extent of inflammation?
Case 3. A 43 year old female presents with a 6-month history
of red painful left eye. She had a previous episode of corneal
ulcer in the same eye. Her past medical history was positive
for sinusitis, rosacea, photosensitivity and pneumonia. She
also had a hysterectomy about 2 years ago. Her family history
was positive for glaucoma (grandfather), diabetes mellitus
and tuberculosis (grandmother). The rest of her history was
unremarkable.
Ophtha Exam revealed the following findings:
1. iE
'--,,
,
L
2.
pa-Jent's history and eye findings, what are
mmentud diagnoses?
oil you differentiate one condition from
_itilier?
Answers tr, liactice Gases on page 222.
6.3 Tearing
Alexander Dy Tan, MD
INTRODUCTION
Tearing is a common symptom of many ocular and sometimes even systemic &names. A thorough understanding of th
lacrimal apparatus, tear film and lacrimal drainage system is necessary an order to determine the cause of a patient's tearing.
Tearing is often classified into two entities: lacrimaIon or the excess production of tears, and epiphora which is the overflow of
tears due to blockage of the lacrimal drainage sys:ern.
OBJECTIVES
Upon completion of this instructional mater4. ~cKaieras snout' be able VD
oelveen laairnation and epiphora).
1.
Define the symptom of tearino
2.
3.
Enumerate the common conditions -.not aaealssing
Describe the different clinical erarnirataces and diagnostic tests used to determine the cause of tearing.
4.
Describe the principles of manaoernerst
axon= GiiuseS dftearing.
CONTENT
I.
I NCREASF_D TEAR PRODUCTION ILACRIMATION )
DECREASED TEAR DRAINAGE (EPIPHORA)
Tearing or "watery eyes" is a common ocular symptom
with numerous causes (Appendix). Chronic tearing can
be a debilitating complaint which may be a nuisance (due
to constant need to wipe off the tears), and a source of
embarrassment and discomfort for the patient Tearing is
either due to increased production (lacrimation) or from
10-15mm
impaired drainage (epiphora).
The tear film has unique characteristics (Table 1). It is
composed of three layers: an outer oily layer (oily secretions
from Meibomian and Zeis glands), a middle aqueous layer
produced by the lacrimal gland and glands of Krause and
Wolfring, and an inner mucinous layer secreted by the goblet
cells of the conjunctiva. The superficial oily layer functions to
prevent the evaporation of the aqueous layer_ The mucous
layer is important for proper wetting of the cornea The pH of
tears averages 7.4
- 12mm
R. antrum
5mm
.;:41
fl... - 1_ Lacrimal drainage system (1=valve of Rosenmuller, 2=valve of Hasner
'polars at inferior meatus underneath the inferior turbinate)
toseign bodies, misdirected lashes, corneal ulcers, etc. Tearing
in these situations is the body's attempt to wash out the eye
of thefrritanr
Table 1. Characte- os of the Tear Film
Thickness
Number of Layers
3
Thickness of the Aqueous Layer
6 5 Li-
Tear Volume
6 - 8 pi MA
Tear Production
1.2
;es
The lacrimal drainage system begins at the punctum leading
to the canaliculus to the lacrimal sac down to the nasolacrimal
duct. The duct opens at the inferior meatus under the inferior
turbinate (Figure 1).
The amount of tears in our eye is dictated by three factors:
production, evaporation and drainage. Conditions that
increase production and impair drainage will result in a surplus
of tears in the eye, while increased evaporation (decreased
humidity, prolonged reading, eyelid retraction, etc) will lead to
a relative lack of tears.
Therefore, when seeing a patient complaining of tearing,
the doctor, through history taking and ocular examination,
determines if there are potential causes of increased tear
production (foreign body, conjunctivitis, eyelid malposition).
Once this is ruled out, he may consider the tearing to be due to
impaired drainage (nasolacrimal duct obstruction, canalicular
obstruction, etc).
I. INCREASED TEAR
PRODUCTION (LACRIMATION)
Tearing is more commonly caused by increased production. It is
important to get a thorough history and physical examination
in order to determine the cause of tearing. Ask for: history
of trauma, eye redness, use of medication, photophobia,
and blurred vision. Patients who complain of foreign body
sensation can have conditions such as corneal or conjunctival
Note that patients with dry eye can also manifest with tearing
-ems wing). Generally, patients with mild to moderate
ry eye may complain of tearing which is mostly a reflex
mechanism to compensate for the 'lack of tears Slit lamp
examination
show an abnormal tear meniscus. Decreased
production af ters may be confirmed
by doing the Schirmers
*estllmeed Doty).
HISTORY TAKING IN PATIENTS
WITH LACRIMATION
irriporiara questions to oe asked in a patient's history include
the following
History of trauma is asked to rule out conjunctival or corneal
foreign bodies. corneal abrasions. Individuals engaged in
certain occupations (Le. carpenters, construction workers,
etc) are more peecksposed to foreign bodies in the cornea or
conjunctiva. Lacerations may involve the lacrimal gland or
any part of the drainage system which can affect the amount
of tears present in the tear lake. Canalicular lacerations should
be suspected when there is a lid margin laceration within 5
mm of the medial angle of the palpebral fissure. Associated
ocular symptoms such as discharge, redness, eye pain, blurring
of vision, foreign body sensation, itchiness should be asked.
Exposure to someone with similar "red eyes" may suggest a
form of viral conjunctivitis, while allergies are often associated
with itchiness.
Previous consults with a doctor, medications used, and history of
ocular surgery should also be asked. This may suggest a chronic
process or that tearing may be a result of prior intervention or
surgery. It is important to establish a timeline of consultations,
surgeries, and medications used in order to figure out when the
symptoms started and how they responded to therapy.
Onset and duration of tearing is asked. Tearing that worsens
during prolonged reading or exposure to low humidity
conditions may indicate a "dry eye While reading or working
with the computer, we tend to blink less often which results
in increased tear evaporation that, in turn, signals the lacrir- gland to produce more tears. These situations uncover t- presence of dryness or tear instability. Dry eyes are mc - ,
common in the elderly. Both dry eyes and nasolacrimal duct
obstruction are more common in women.
History of medical problems particularly allergies and/or sinus
disease should also be asked.
EYE EXAMINATION IN PATIENTS WITH
LACRIMATION
A thorough ocular examination (visual acute gross
examination, EOM's, tonometry and funduscopi) is necessary
to determine the cause of a patient's tearingTheeiamination
of patients with lacrimation should foas on the anterior
segment. Any injury or inflammation invoking the lashes.
cornea, conjunctiva, anterior chamber and iris nil res.* in
some form of tearing. Ectropion (outward turning of the ids)
and entropion (inward turning of the ids) may cause ocular
irritation that also leads to tearing.
DIAGNOSTIC TESTS FOR PATIENTS WITH
LACRIMATION
Schirmers Test I Tnis
reflex tearing. A specially designed Whamonfilierpaper called
a Schirmers strip is placed at the junction &the lateral and
middle third of the lower eyelid viithout anesthetic The patient
can keep the eyes either dosed or open. The strips are then
gently removed after free minutes. The demarcation between
the dry and wet part of the strip is noted and xs dunce from
the folded edge of the strip is measured in mihmeters. Wetting
of 5 mm or less in 5 minutes would support a diagnosis of dry
eye (Figure 2).
11111111111111r
Basal Secretion Test: Schirmers Test may be performed
with topical anesthetic (such as proparacaine). This test
measures the amount of tear production without the reflex
component (basal secretion).
MANAGEMENT OF LACRIMATION
Management of lacrimation is generally directed to
address the underlying cause of tearing. Management will
range from antibiotic eyedrops for patients with bacterial
infections, removal of foreign bodies for patients with
conjunctival or corneal foreign bodies to eyelid surgery for
patients with misdirected lashes, entropion or ectropion.
Correction of these conditions will result in the resolution
of the patient's tearing.
II. DECREASED TEAR DRAINAGE
(EPIPHORA)
Tearing due to blocked tear drainage can be a very
bothersome symptom. Patients frequently carry along
boxes of tissue paper in order to constantly wipe off
overflowing tears. Chronic epiphora can sometimes be
caused by or lead to infections of the lids and lacrimal sac.
Any point of the lacrimal drainage system can be blocked:
from the punctum to the canaliculus, lacrimal sac, and
the nasolacrimal duct. Punctal stenosis can be visualized
directly or with the use of a slit lamp. Canalicular stenosis
can be confirmed with probing while a lacrimal apparatus
irrigation is often necessary in orderto diagnose nasolacrimal
duct obstruction. Blockage may be due to scarring from
inflammation or topical medication, from injury (canalicular
transections), or from dacryoliths or lacrimal sac tumors.
Punctal ectropion associated with lid laxity can
contribute to decreased outflow of tears. Conditions
such as Bells palsy or weakness of the CN VII may also
cause physiologic pump failure of the lacrimal drainage
system.
Functional obstruction or lacrimal pump failure should be
suspected in tearing patients with normal anterior segment
examination, and anatomically patent nasolacrimal duct (as
confirmed by probing and lacrimal apparatus irrigation).
Epiphora, seen in patients with CN VII weakness or eyelid
laxity, is due to failed evacuation of tears caused by lacrimal
pump failure. This condition is managed by correcting the
underlying lid laxity through a lid tightening procedure.
Figure 2. Schirmer's test
6
RED EYE, TEARING AND DISCHARGE
I
HISTORY TAKING IN PATIENTS WITH
EPIPHORA
Nasolacrimal duct obstruction (NLDO) should be suspected
in patients with tearing who have normal anterior segment
examination (i.e. no abnormal finding that can explain the
patients tearing). Patients often have a long standing history of
on and off tearing of the involved eye, with or without history
of infection (mucoid discharge, conjunctivitis, dacryocystitis).
Patients with dacryocystitis often present with history of
swelling of the medial canthal area which when exacerbated
results to pain, swelling and erythema (acute dacryocystitis)
Primary acquired nasolacrimal duct obstruction is more
common in elderly females.
Dye Disappearance Test (DDT): This assesses the presence or
ce of adequate lacrimal drainage. Fluorescein is instilled
on the cul de sac of both eyes. Asymmetric clearance of the dye
within 5 minutes indicates relative block in the side with dye
retention. Retention of dye beyond five minutes in one eye is
also indicative of blockage (Figure 4). DDT does not distinguish
between mechanical blockage and functional blockage.
Infants with history of tearing shortly after birth should be
suspected of having congenital nasolacimal duct obstruction_
DIAGNOSTIC TESTS FOR PATIENTS WITH
-is L. Cloyantill nasolacrimal duct obstruction with dye retention in
Isanoearance test
-
EPIPHORA
Probing : a fine blunt probe can be inserted through the
punctum and canaliculus in order to determine the patency of
the upper lacrimal drainage system. Probing may also confirm
the presence of canalicular transections in patients with
history of trauma (Figure 3).
Figure 3. A gauge 25 lacrimal irrigating cannula is inserted through the
punctum (exits at the distal cut end of the canaliculus), confining presence of
canalicular laceration
Lacrimal Apparatus Irrigation: This involves the irrigation of
normal saline solution through the punctum and canaliculus.
Presence of fluid reflux (either thru the upper canaliculus or
lower canaliculus) would indicate an obstruction.
Palpation of the lacrimal sac area: Applying pressure on a
distended lacrimal sac may result in mucoid reflux and confirm
the presence of nasolacrimal duct obstruction. Note that
obstructions involving the canaliculi or puncta will not result in
distension of the sac since the tears will not be able to reach the
sac.
MANAGEMENT OF EPIPHORA
Management d nasolacrimal duct obstruction is surgical. A
daarcynollinostomy (DCR) is performed for adult patients
with sysnoingsk and complete nasolacrimal obstruction.
It involves a *nuking procedure, connecting the lacrimal
car to the nasal mucosa. The surgery is performed under
general anre5iia Dacryocystorhinostomy can be done
thru several approaches: external approach through the skin
(External IX* sanscanalicular using a YAG or Diode laser
(TransGanalcullar VAG or Diode Laser DCR) ; and lastly it may
be done ihmigh the nasal approach (Transnasal Non Laser
EndosagicOOkliar6nasal Laser Endoscopic DCR).
Management of uncompricated congenital nasolacrimal duct
obstruaion
nosigns of infection, dacryocystitis) is lacrimal
sac rnassaget Remislient cases are managed with therapeutic
probing (rupetring the membrane at the Valve of Hasner)
which is usually performed at 12 months of age. Patients
who have undergone failed probings are managed with
bicanarratar titubation with silicone tubes or by performing a
dacryocystorhinostorny.
Epiphora in patients with CN VII nerve weakness or eyelid laxity
is managed by correcting the underlying lid laxity through a
lid tighteniv procedure.
19. Stimulation of some cortical areas - thalamus,
hypothalamus, cervical sympathetic ganglia, or
the lacrimal nucleus
a. encephalitis
b. diencephalic epilepsy syndrome (Penfield
syndrome)
c. Giant cell arteritis (temporal arteritis)
d
Hypothalamic tumors
e Meningitis
f.
Page syndrome
g
Pseudobulbar palsy for Parkinson syndrome
•
Sluder syndrome
i Tic douloureux
various senile dementias
ji
APPENDIX
I.
HYPERSECRETION OF TEARS
A.
Primary (disturbance of the lacrimal gland)
B. Central
1. Central nervous system lesions
2. Corticomeningeal lesions
3. Emotional states
4. Hysteria
5. Physical pain
6. Voluntary lacrimation, such as when acting
C. Neurogenic
1. Ametropia, tropia, phoria and eyestrain and
fatigue
2. Caloric, lacrimal and reflex tearing - biatecal
lacrimation when syringing the ear with warm
or cold water and during Tension testing
3. Crocodile or alligator tears - unilateral profuse
tearing when eating
a. Congenital, often associated with ipsiaieral
paresis of lateral rectus muscle
b. Acquired with onset in way gage of
facial palsy Welts paby) or sequefia riots
parasympathetic fibers to the aic gangicin
growing back into superficial primal nem
c. Duane retractio4. Bells palsy
5. Marin-Amat Syndrome .dram ea
Jaw winking phenomenon)
6. Mel kersson-Rosenthai syrwhorne OMeacersson
idiopathic fits° edema)
7. Drugs: atenoidt, ciprallokacin. dexamelhasone.
diazepam, ketarnine, heflaran. inorPhine,
=-7
n ifed i pi ne. naloomme
8. Exposure to
9. Glaucoma
10. Horner sync:troy 11. Inflammation o
_
uvea, cornea, orbit.
12. Lesions aliectirig *E
a. ptosis
b. entropion/ ectropion
c. facial paralysis
d. trichiasis
13. Morquio-Bradsford syndrome (MPS W)
14. Myasthenia Gravis - afternoon ectropion
(Erb-Goldflam syndrome)
15. Ophthalmorhinostomatohygrosis syndrome
16. Parkinson's disease
17. Reflex, such as vomiting and laughing
18. Sjogren syndrome
Gradenigo syndrome (temporal syndrome)
21. Raeder syndrome (paratrigemial paralysis, cluster
headaches)
22 Retroparotid space syndrome (Villaret syndrome)
23. Rhabdomyosarcoma
24. Rothmund syndrome (telangiectasiapigmentation-cataract)
25. Thermal burns
D. Symptomatic
1. Bee sting of cornea
2. Tabes
3. Thyrotoxicosis (Basedow syndrome)
INADEQUACY OF LACRIMAL DRAINAGE SYSTEM
A.
Congenital anomalies of the lacrimal apparatus
1. Absence or atresia of lacrimal drainage apparatus
2. Amn iotocele
3. Fistulas of lacrimal sac and nasolacrimal duct
4. Waardenburg syndrome (lateral displacement of
the medial canthi with lateral displacement of
puncta and lengthening of the canaliculi
5.
Obstruction of nasolacrimal drainage system
B. Complications from diseases such as pemphigus,
Stevens-Johnson syndrome and lupus
C. Dacryocystitis
D.
Distended canaliculi with obstruction, such as in
Actinomyces israelii , papilloma or dacryolith
E.
Drugs such as: acyclovir, silver nitrate,
triflourothymidine, neostigmine,
fluorouracil, etc
F.
Punctal eversion
G. Goltz syndrome
6
RED EYE, TEARING AND DISCHARGE I 6.3 Tearing EN
H.
Inadequacy of physiologic lacrimal pump
I.
Traumatic
J.
K.
2.
3.
determine the level of obstruction in patients witt canalicular stenosis
B. differentiate an upper from lower nasolacrimal du:system obstruction
C. dilate a stenotic canalicular system
D. dilate a stenotic punctum
remove foreign bodies in the canaliculus
A.
lesions of the lacrimal drainage system
Tumor obstruction
Nasal disease
1. Sinusitis
2. Hypertrophic rhinitis
REFERENCES
1.
6. Probing is most useful in tearing patients to:
Roy, F. Ocular Differential Diagnosis, 8th Edition, Fep
International, 2009
Adler FH, Hart WM (Ed), Adlers Physiology of theEye.
Mosby 1992
Nesi FA, Levine MR, Lisman RD , Smith's Op- Plasctic and Reconstructive Surgery, Mosby, I
SELF-TEST
For questions 1-5 . What is the mechanism of tearing in the
following conditions?
Possible answers are
A: increased production
B:decreased drainage
1. canalicular transaction
2. facial nerve palsy
3. after cataract surgery
4. uveitis
5. trichiasis
7. Most common location of blockage in acquired NLDO is at:
canaliculus
3. intraosseus portion of NLD
C. punctum
D. valve of Hassner
valve of Rosenmuller
8.
Definitive management of patients with NLDO:
A. atropine eye drops
8 botulinum toxin injection
C. probing and irrigation
a stewed antibiotic eyedrops
E. surgery
77_
'f Test on page 222.
7.1 Strabismus
Marissa N. Valbuena MD, MHPEd
INTRODUCTION
Ocular motility problems are among the common ccnditions die medical students will encounter in the out-patient din'
A clear understanding of the anatomy and pnysiolcqf ollribbasaibbdar muscles. knowledge and skills in history taking and
physical examination of patients with motility proolenmaimillasbibmiedge of the chnical manifestations of these conditions
will help the student in his interactions with the pains&
OBJECTIVES
After going though this material, the s7udent iscootiedbx
1.
Enumerate the extraocular inuscies,lkeirmigin, is
2.
Given an extraocular musde. identify Ns springs:. antagonist and yoke.
3.
Given a patient with ocular croft problerok be able to eictracca relevant medical history, and be able to perform a
innenabon. and actions_
complete ocular examination. irrickams basic moollity examination (extraocular muscle movement, corneal light reflex
test and cover tests)
4.
-
Discuss the most common
'estations and principles of management.
CONTENT
L.
ANATOMY AND PHYSIOLOGY OF EXTRAOCULAR MUSCLES
and action of extraocular muscles
1. Osigin. insect:on, ,enervation
Motor physiology
A. Sherrington's law of reciprocal innervations
•
^g's law
II. BINOCULAR VISION
Ill. A hi BLYOPIA
IV. STRABISMUS
3n of strabismus
1.
2.
3.
4.
5.
6.
7.
Types of strabismus:
Examination of the patient
Common types of strabismus
Systemic illness associated with strabismus
Psychosocial impact of strabismus
Principles of management of a strabismic patient
I. ANATOMY AND PHYSIOLOGY
OF EXTRAOCULAR MUSCLES
The extraocular muscle is a specialized form of skeletal muscle
with several fiber types. At one extreme is a slow tonic type
resistant to fatigue and active in holding gaze straight ahead.
At the other extreme is a muscle type adapted for participation
in extreme gaze. The high ratio of nerve fibers to eye mus =
fibers (1:3 to 1:5) allows for more accurate control of muss
movement compared to other skeletal muscles. The ratio ir
other skeletal muscles ranges from 1:50 to 1:125.
only 15° to 20° -from primary position before head
Occurs.
movement
Walk 1 summarizes the origin, insertion, actions and
innervation of the extraocular muscles.
MOTOR PHYSIOLOGY
A. AXES OF FICK, CENTER OF ROTATION, LISTING'S
PLANE AND MEDIAN PLANE
The axes of Fick are X, Y and Z. (Figure 1). The X axis is a
transverse sods passing through the center of the eye at the
civatior;volutary vertica I rotations of the eye occur at this axis.
ORIGIN, INSERTION, INNERVATION AND
Z axis is a vertical axis; voluntary horizontal movements
ACTION OF EXTRAOCULAR MUSCLES
occur at this axis_ Listing's equatorial plane passes through
the center of rotation and includes the X and Z axis. The Y
There are six extraocular muscles controlling eye movement
axis 6 perpendicular to Listing's plane; involuntary torsional
the four recti muscles and the two obliques. The lateral
rnowernerts occur at this axis.
rectus muscle is innervated by the abducens nerve (CN
the superior oblique by the trochlear nerve (CN IV) and the
remaining muscles by the oculomotor nerve (CN Ill).
The primary position of the eye is defined as being that when
the eye is directed straight ahead with the head also straight
The primary action of a muscle is the major effect on the
position of the eye when the muscle contracts while the eye
is in primary position. The secondary and tertiary actions are
additional effects on the position of the eye in primary position.
The eye can usually be moved about 50'in each direction
from the primary position. Ordinarily however, the eyes move
Rom 1_ .des
Table 1. Extraocularmusdes
-- - Origin
Wow
Medial rectus
Insertion
Annulus of Zinn
5.5 mm from medial limbus
Annulus of Zinn
6.9 mm from lateral limbus
Annulus of Zinn
7.7 mm from superior
limbus
Drre=,-
ction from
any Position
Innervation
Cranial Nerve
(MR)
Lateral rectus
(LR)
Superior rectus
(SR)
Inferior rectus (IR)
Annulus of Zinn
6.5 mm from inferior limbus
Superior oblique
(SO)
Orbit apex above
Annulus of Zinn
(functional origin at
trochlea)
Posterior equator at
superotemporal quadrant
Inferior oblique
(10)
Behind lacrimal
fossa
Posterior to the equator in
infero-temporal quadrant
Atilictan
:1
Depression
Extorsion
Adduction
51Z
51*
Torsion
Depression
Abduction
E rc
III
aton
Lbduction
The median plane is a sagittal plane passing antero-posteriorly
through the body, bissecting the head into symmetric parts.
Table 3. Agonists with Their Respective Synergists and Antagonists
B. POSITIONS OF GAZES
1.
2.
3.
4.
the agonist. Table 3 shows the agonists with their respective
synergists and antagonists.
Primary position - straight ahead
Secondary positions - straight up, straight down,
right gaze, left gaze
Tertiary positions - four oblique positions of gazes: up
and right, up and left, down and right, down and left
Cardinal positions - Right and left plus the tertiary
positions (up and right, up and left, down and right,
down and left)
Medial Rectus
Superior rectus
Inferior rectus
Inferior oblique
for obriclue
tenor oblique
Inferior rectus
'Abla
Superior oblique
gliOr oblique
Superior rectus
Inferior oblique
Mer:.a rectus
Table 2. Action of Extraocular lAusoles From The Primary Pawky
Medial rectus
Superior rectus
Inferior rectus
C. PRIMARY, SECONDARY AND TERTIARY ACTIONS
When the eye is in primary position, the horizontal
purely horizontal movers along the Z axis and have only a
primary action. The vertical recti have a direction of pull that
is primarily vertical. However, the angle of pull from
to insertion is 23° inclined to the visual axis, giving ftorsion and adduction. The obliques are incli-ed
visual axis, giving rise to torsion as their prima- .
some vertical and horizontal rotations as we Table 2 - actions of the extraocular muscles.
Lateral rectus
Superior oblique
nie-or
'ectus
Inferior oblique
rectus
Superior rectus
Superior rectus
Superior oblique
Lateral rectus
Inferior rectus
Sherrington's law of reciprocal innervation states that an
_
and contraction of a given extraocular
musde accor-- aniedbya reciprocal decrease in innervation
— action of its antagonist. For example, as the right eye
—edial rectus receives increased innervation
= -: a:e - ai rectus receives decreased innervation.
Vessions (Conjugate binocular eye movements )
Medial rectus
Lateral rectus
Abduction
Yoke muscles are two muscles (one in each eye) that are
Superior RecL.s
E
Inferior rectus
Depression
.
of their respective eyes in a given direction of
gaze For example, as the eyes move to the left gaze, the right
medial rectus and the left lateral rectus are simultaneously
innervated and contracted.
Superior Oblique
Inferior Oblique
cc
Euclidean:10r
:-
Excycioductkn
Eresancr
D. EYE MOVEMENTS
Each extraocular muscle in one eye has a yoke muscle in the
other eye. Figures 2 and 3 show the six cardinal positions of
gaze and the yoke muscles whose primary actions are in that
1. Monocular eye movements (Ductless)
field of gaze.
Ductions are monocular rotations of the eye. Adduction is
movement of the eye nasally, vihie abduction is movement
of the eye temporally. Elevation is upward totation of the eye.
depression is downward movement of the eft. Incydoduction
(intorsion) is nasal rotation of the superior portion of the
vertical corneal meridian. Excydoduction (extorsion) is
temporal rotation of the superior portion of the vertical
L
R
corneal meridian.
An agonist is the primary muscle that is moving the eye in
a given direction. The synergist is the muscle in the same
eye as the agonist that acts with the agonist to produce the
same movement. The antagonist is the muscle in the same
Figure 2. Cardinal Positions of Gaze and Yoke Muscles
eye as the agonist that acts in the direction opposite to that of
7
DEVIATION AND DISPLACEMENT OF THE EYE I
RSR
LIO
RLR
LMR
RIR
LSO
Sup Recti & Inf Obliques RIO
PRIMARY POSITION RMR
I nf Rect & Sup Obliques
RSO
LSR
LLR
LIR
Figure 3. Cardinal Positions of Gazes And Yoke Muscles
Hering's law
states that equal and simultaneous
innervation flows to the yoke muscles concerned in the
desired direction of gaze. Ordinarily, a patient with a weak
muscle in one eye will use the contralateral eye to fixate.
If he will be forced to fixate using the eye with the weak
muscle, the increased innervation needed to maintain that
eye at the center will be transmitted to the yoke muscle,
causing increased amount of deviation in the normal nonfixating eye.
II. BINOCULAR VISION
The eyes are spaced 50 to 65 mm apart. The slightly different
image originating from each eye is fused in the brain as a
stereoscopic image. Each eye must be directed simultaneously
to the same object.
The visual axis is an imaginary line that connects an object in
space with the fovea. In a person with normal ocular, sensory
and motor systems, the visual line in each eye intersects at the
object in space and there is binocular fixation. If visual lines
are not directed at the same fixation point, fixation is by one
eye only.
Normal development of stereoscopic vision requires binocular,
simultaneous use of each fovea during the critical time that
occurs early in life.
III. AMBLYOPIA
Andijapia is a condition in which there is a unilateral or
bilateral decrease in visual acuity that is not fully attributable
to organic claim abnormalities. Table 4 shows the diagnostic
criteria for amblyopia.' It is usually caused by opacities in
the media. high refractive errors, anisometropia (difference
in refractive errors of the 2 eyes) or ocular misalignment or
strabismus during visual immaturity' (Table 5). Amblyopia
is a risk factor for the development of strabismus and
reduction of binocularity, and strabismus is a risk factor for the
development of amblyopia.
is diagnosed and properly treated,
The earlier an
the better the chance of visual acuity recovery. However, all
children should be considered for treatment regardless of age.'
Amblyopia usually results in lifelong visual loss if it is untreated
or insufficiently treated in early childhood.
The prognosis for attaining and maintaining essentially normal
vision in an amblyopic eye depends on many factors, including
the age of the patient at diagnosis, the cause and severity of
amblyopia, the history of previous treatment, the duration of
amblyopia, and compliance with treatment.
There are two principles in treating amblyopia. The first is
to present a dear retinal image to the amblyopic eye by
eliminating causes of visual deprivation (e.g. cataract, ptosis)
and correcting visually significant refractive errors. The second
principle is to make the child use the amblyopic eye by
patching the better eye, or in mild to moderate amblyopia, by
penalization with atropine eye drops.'
TYPES OF STRABISMUS:
Table 4. Diagnostic Criteria For Amblyopia'
11•111111111111r"'
FindieMPOW
-
Unilateral Amblyopia
Fixation preference
Unequal fixation behavior
Preferential looking
2-octave difference*
Best corrected visual
acuity
2-line interocular difference
4
U
A. According to direction of deviation:
. Horizontal - esodeviation, exooe\
2. Vertical - hyperdeviation, hypodeviation
3. Torsional - excyclodeviation, incyclodeviation
B.According to age of onset:
Congenital, infantile - documented prior to age 6
Bilateral Amblyopia
Best corrected visual
acuity
*2-octave difference is a 4-card difference in the set of Tee 4:41r."
Cards, which is equivalent to multiplying or dividing the visual arse
by 4
months
Acquired
2.
Vision less than 20/40 ear" eye
C According to fusion status (whether the deviation
can be controlled by fusion mechanism)
Phoria - latent deviation, controlled by fusion
mechanism so that under binocular condition, the
Table 5. Causes of Amblyopia
minvompepr- triple
Refractive
Myopia
Hyperopia
Astigmatism
Visual Deprivation
Strabismus
Bilateral Amblyopia
eyes remain aligned.
MEI
2.00 D - 2.50 C difference. dece- :
1.50 D - 2.50 C
difference. deQemci-r:.
2.00D-2 50 D
differerce _>:e-6n; 7 NA
fmacro
Ptos is c
eTiturp.kie
catarac4.
2.
3
not present.
D.
gaze or fixating eye.
Exam* AMMON
E.
Myopia
3 X 2 - X 2 3...e.1.11-ig :r 33e
Hyperopia
SS_:-
Astigmatism
2:c2-312 3erie-bric r aoe.
733e
Bilateral ptosis
Sewell! Diet
Bilateral corneal
7trartarternit =153 2rir1:C.
opacities
MESSES 111101207C sr
Scaadc. aulasorral dominant.
era -a.-iassve
I ncom itant - deviation varies with direction of gaze or
fixating eye. Most incomitant strabismus is paralytic.
According to fixation
1. Alternating - There is spontaneous alternation of
fixation from one eye to the other and there is no
2.
Visual Deprivation
Bilateral cataract
According to variation of deviation with gaze position
or fixating eye
1. Comitant - deviation does not vary with direction of
2.
Es::-:_cc-xra *Nice-me
Refractive
Intermittent phoria or tropia - fusion control present
part of the time
Tropia - manifest deviation in which fusion control is
preference for one eye for fixation.
Monocular - There is preference for fixation with one
eye.
EXAMINATION OF THE PATIENT
A.
Historytaking: information should be obtained about
the following
1.
Chief complaint
DEFINITION OF STRABISMUS
2.
3.
4.
5.
6.
7.
8.
Strabismus means ocular misalignment of whatever cause.
When the eyes are not aligned or are "dissociated': strabismus
9.
10.
Age of onset - document onset with photographs
Direction of deviation
Constant or intermittent
Alternating fixation or monocular fixation
Magnitude of deviation
Associated eye complaints - diplopia, blurring of vision
Antecedent or concurring illness - seizures , diabetes,
hypertension, thyroid disease
Trauma
Previous consultation, treatment - patching, glasses,
surgery
Maternal and birth history - maternal infection,
prematurity
Developmental history
Family history
Bilateral
hemorrhage
IV. STRABISMUS
is present.
Orthophoria refers to the ideal condition of ocular balance, so
eyes are aligned in all directions of gazes at all distances even
after occluding one eye.
11.
12.
13.
7
DEVIATION AND DISPLACEMENT OF THE EYE 1 7.1 Strabismus
103
B. Ocular examination
3.
1. Visual acuity
Children often pose a difficult assessment problem.
Various tests are available for visual acuity determination
(Table 6). The method of evaluating visual acuity varies
according to the child's age and level of cooperation. For
verbal and cooperative children, charts using tumbling
E or pictures can be used. The child's fixation pattern
will give a clue as to the comparative vision of the two
eyes. For example, a strabismic child who can alternate
fixation in his two eyes will probably have equal visual
acuity. Another strabismic child who prefers one eye to
fixate probably has a better vision in that eye compared
to the fellow eye.
Tests for ocular alignment
A. Corneal light reflex test (Hirschberg method)
(Figure 4)
a. Ask the patient to sit facing you with head
straight and eyes directed in primary gaze.
b. Hold a penlight in front of the patient's eyes
at a distance of about 2 ft, directing the light
between the patient's two eyes. Instruct the
patient to look directly at the light.
c. Compare the position of the light reflex and
record the estimated degrees of deviation.
lit3ORTHOPHORIA
Table 6. Visual acuity testing in children
150 ESOTROPIA
Pre-verbal children
(less than 24
months)
Clinical methods ability to follow moving
target. presence or absence of fixation
preference. presence or absence of
nystagmus
300 ESOTROPIA
CSM I central. steady and maintained
Preferential looking techniques (Teller
acuity cards)
Verbal children
( 3-5 years)
Lea symbols (shapes) from 36 months of
age.
Literate children
Snelier, chaos (letters or numbers)
2. Ocular motility examinations
The following clinical protocol may be used to assess
ocular movements:
a.
b.
c.
d.
450 ESOTROPIA
HOTV chart (four-letter shapes), tumbling
E chart
Sit facing the patient. Hold your finger or a
small fixation target 10-14 inches in front of the
patient, with the patient in primary position
(straight ahead).
Ask the patient to follow target as you move it
into the six cardinal positions. When examining
down gaze, elevate upper eyelid with a finger of
your free hand.
Note whether the amplitude of eye movements
is normal or abnormal in both eyes. Rate
amplitude for all fields of gaze by considering
normal amplitudes as 100%, and rate lesser
amplitudes accordingly. To record relative over
or underaction, designate normal as 0, that
is, no over or underactions are present. Use 4
to designate maximum over or underaction.
Underactions are rated -1 to -4 while overactions
are rated +1 to +4.
Note any nystagmus and if present record its
direction and amplitude in specific field of gaze.
Figure 4 :7-'63 Light Reflex (Hirschberg method)
B. Prism Test ( Krimsky Test) (Figure 5)
Was test is usually performed in patients unable to
-- er with both eyes because of poor vision in one
in uncooperative patients.
a
b.
c.
Ask the patient to fixate on a light.
Place increasing amount of prism on the straight
eye until the corneal reflex on the deviating eye
is centered.
In patients with incomitant or paralytic
deviations, it is preferred to place the prism in
front of the deviating eye.
C Cover tests
The validity of a cover test depends upon the
patient's ability to maintain constant fixation on
an accommodative target. Each eye must be able
to move adequately when fixating. The coveruncover test is done to establish the presence of
either a manifest deviation (heterotropia) or a latent
deviation (heterophoria). The alternate tests are then
performed to measure the deviation.
C. 1. Cover-uncover test
a. Ask the p =nt to look at a distance fixation. The
examiner should be seated slightly to the side of
midline, facing the patient and at an arm's length
to the patient
4. Ophthalmoscopy
.:onormalities
'--7..4 us i- c—d be noted such
as abnormal cp: z = 3: maz... ar lesions, macular
displacement, macular ass or scar and retinopathy of
prematurity.
5.
Refraction
a"-it to kroe, '-= refractive state of the patient
aCycloplegia, the state in
= 37
3 - 7 accommodation is
- -?.'-action in children.
it has a rapid onset
procsuces _
7 3. 7
•oximates the effect of
with a shorter duration of
=
7:: _a atropine may be necessary
r_
,5g a.
COMMON TYPES OF STRABISMUS
A. COMITANT STRABISMUS
T.
Figure 5. Krimsky Prism Test
b.
c.
d.
e.
g.
Cover the fixating eye wit— 3- 3=44.0e,
ar'!I
your hand and observe the =ler
movement. Note its direction_
tr
Uncover the eye and allow al a.>: 3 sec,
both eyes to be uncove-ed
=c-senie its tilos 4:Ir
Cover the other eye
any movement
arc
After about one second, xii..„..re• 7.-te
observe it for any mmemere..
Repeat the test fix near using a neer '783.-.or
point.
cat_ents
-ear
Repeat the
eyeglasses. if apcic.-ac.ie
C. 2. Alternate cover test ,prism and cover test)
at a
a. With the
- 7-3
distance" .Y
7
2:
from one e,e
t.allowing any periodd ".." 7
should be seated siright 7: 7- 7
facing the patient and at ar a -- 3
patient
b. Place a trial prism over one eye
- 7 - ng
to shift the cower from one etit 7: 7. --E other_
Orient the prism apex to...ie:
. : 7 - 7.- 'ection
of the deviation_ Choose the st-e
of the
initial prism to approximate t-e aeviation
estimated by the Hirschbera's test
c. Continue to place pris— i := c - 2 .:-. ,assiyely higher
power unt ^ o me
:ted in either eye
(neutraliza:
d.
Esotropia or Infantile Esotropia
nwaro aeviation of the eye usually
-c
or up to 6 months of age. The
constant (Figure 6). Cross fixation
,5oceAation is t z
:irfart. 1.5es rioht eye to look at left visual field and left eye
: may be present. There may be over
. 7ueS (Figure 7), causing elevation
a_-:..c.-2
=IE.-action is usually appropriate for the
=If
3--E-ss than +2.0 D). Non-alternating esotropia can
::: 3, Aside from the esodeviation, the patient is
_ -3se normal. The child is best treated with surgery
5.3 months.
2. Refractive Accommodative Esotropia
accommodative esotropia usually starts at age
2 ;ears. The child has a significant hyperopia (+3.00 to
+10.00 diopters). In order to see clearly, he accommodates.
Accommodation is however accompanied by convergence
of the eyes. Esodeviation is moderate in magnitude
approximately 30 prisms diopters. Convex or plus lenses are
prescribed to correct the hyperopia (Figure 8). Constant nonalternating accommodative esotropia can cause amblyopia
and should be treated. Patient should have regular cycloplegic
refraction and spectacle lenses should be changed if needed.
Figure 6. Congenital Esotropia, left eye
Repeat tes: ;:' e3"
7
DEVIATION AND DISPLACEMENT Or THE EYE 1 7.1 Strabismus lila
Figure 7. Overacting inferior obliques. Elevation of the adducting eye.
parent :a-- use either eye for fixation (Figure 9). Amblyopia
wih intermittent exotropia and significant refractive
errors should be prescribed spectacles. The decision to do
surgery iiintermittent exotropia is based on patient's control
of the esouppia. Treatment for constant exotropia is surgical.
Figure 8. Accommodative Esotropia; (A) Esotropia of the right eye,
(B) Eyes aligned with eyeglasses
3. Sensory Esotropia
An esodeviation occurs in a patient with monocular or
binocular condition that prevents good vision (e.g. corneal
opacity, cataract, retinal scars, inflammation, tumors, optic
neuropathy, anisometropia). Treatment consists of the
following: attempt to correct the cause of the poor vision, full
cycloplegic refraction, muscle surgery to correct the deviation.
4. Intermittent Exotropia
Exotropia is an outward deviation of the eye. It usually starts
out as intermittent and becomes manifest when patient is
fatigued, sleepy or inattentive. The patient closes one eye
when exposed to bright sunlight. The frequency and the
duration of deviation may increase as the patient grows
older. The exotropia can later become constant. Usually, the
Figure 9.
(A) Left eye fixating, (B) Right eye
5. Sensory Exotropia
seewell for any reason may turn outward.
An e E._-nent
of sensory exotropia are the same as
Princip e. - ei-.'
that of sensory esouopia.
B. INCOMITANT STRABISMUS.
1. Paralytic Strabismus
There is limitation of action of the involved muscle. The deviation
is bigger when the involved eye is fixating and in the direction of
action of involved muscle. Lateral rectus is the most frec _
involved muscle as a result of abducens nerve palsy. The
should have a neurologic and systemic evaluation to
any underlying cause. Patients may have diabetes me
or hypertension.
2. Strabismic Syndromes
Motility disorders may demonstrate typical feature of a paroailar
syndrome. Examples are Duane syndrome, Brown syndicate,
Mobius syndrome and congenital fibrosis syndrome
Duane syndrome (Figure 10) is a congenital mcf.Tity disadec
usually unilateral, characterized by limited abduc-.
ar Imaged
adduction or both. The globe may retract and
e
may narrow on adduction. There may also be
.:1downshooting of the eye. There may be a face 7_-7- -17
-patient to use both eyes together. Muscle
correct significant face turn or a significa —
gaze.
Brown syndrome is caused by restriction of 7"
-7...tendon sheath, limiting elevation in acc_.7.
in abduction. It may be congenital or acquinillieviiiessiciltas
trauma or systemic inflammatory comic,: -
Congenital fibrosis syndrome is a demo,
eone or more extraocular musdes williasixamaapice7
fibrous
tissue
muscle fibers with
SYSTEMIC ILLNESS ASSOCIATED
WITH STRABISMUS
Right Gaze
mote prescribed to aleviate
If strabismus persists, surgery
may be done during the otiescent phase of the disease.
Diabetes meatus
metaboric ease involving small vessels
and causina widespread damage to tissues, including the eyes.
Patents — E. - 77- -77 777_7e onset diplopia due to infarction of a
aanial nerd a-c
S C*1an extraocular muscle.
The attducens
'ectus are most often
Aimed ithe =Jammu nerve
. c ved, the pupil is usually
vend Recovery of oaten
- ;unction usually happens
sdiiiirs6rnanthr. Patching of one eye or use of prisms can relieve
the dolma& Muscle surgery may be necessary if the deviation
oersigH s beyond six tar Rtn.
C- Illyasdieria
' gravis
littiastrene grans a cnaracterized by abnormal fatigability of
miliedumusides which improves after rest. Presenting complaints
ands and diplopia from involvement of one or more
_
should be evaluated and treated by
D. Pieurcriogic conditions
Cereolowasaaar disoroers arc INS space occupying lesions may
nusas one °fele c nical presentations.
PSYCHOSOCIAL IMPACT OF STRABISMUS
Mobius syndrome is caused by a combir
nerve palsies, producing mask-lice 66E'
sometimes accompanied by adduction
A. Thyroid disease
Grave's ophthaimpa .the extraocular muse:
orbital connective tiss..
orbital
ophthalmoplegia are some of the dinical findings. Limitation
of elevation because of inferior rectus restriction is the most
common motility finding. Patients complain of diplopia that is most
serge r upgaze The thymid disease should be treated. Prisms
'ectng
- Js and
— os
and
is may result in a negative impact on a child's self- image.
• can cause embarrassment in children especially when they are
was associated with significantly
- eased by their peers. Strabismus
orse
general
health-related
quality
of life in preschool children.'
w
Studies on the impact of strabismus have been conducted in
both children and adults. By means of simulation photographs,
strabismus was found to play a significant role in the selection of
playmates by children', influencing decisions on inviting children
to a party and in partner selection by adults.'
Adults with strabismus may also suffer from discrimination
in seeking employment A study among Swiss headhunters
Primary Gaze
Figure 10 T._
Left Gaze
3n
7
in both eyes. There is
DEVIATION AND DISPLACEMENT OF THE EYE 1 7.1 Strabismus
147
showed that in Switzerland strabismic persons are perceived
less favourably by a potential employer, and therefore have more
difficulties in finding a job 8
PRINCIPLES OF MANAGEMENT OF A
STRABISMIC PATIENT
AIMS OF STRABISMUS TREATMENT:
1.Good vision
2. Binocularity
3. Good alignment
1.Enhance vision. Patients should be prescribed spectacles for
significant refractive errors. If present, treat amblyopia by patching
the better eye. An alternative to patching in certain types of
patients may be instilling atropine eye drops to the better eye.
2. Manipulation of accommodation. Esodeviations are treated
with anti-accommodative therapy (plus lenses for hyperopia)
and exodeviations by stimulating accommodation (overcorrect
myopia and under correct hyperopia).
3.Prisms. Incorporation of prisms in spectacles may be useful in
patients with acute onset of strabismus and diplopia and those
with small deviations.
4. Surgery. Muscles are chosen depending on the type and
amount of deviation in the various directions of gaze. Recession
is a muscle weakening procedure whereby a muscle is detached
from the eye, freed from its fascial attachments and then sutured
to the eye at a measured distance from the original insertion
(Figure 11). A muscle is strengthened by resection, a shortening
procedure. A measured amount is cut from the muscle which is
then sutured back to its original insertion site (Figure 12).
SUMMARY
Under normal binocular viewing conditions, the eyes
are aligned and the image of the object of regard falls
simultaneously on the fovea of the two eyes. One of the eyes
may be misaligned (strabismus), so that only one eye at a time
viewsthe object of regard. Constant strabismus at an early age
can Result amblyopia. In addition, any condition which can
resuk rl pooreision can lead to strabismus. It is important that
a physician is able to detect strabismus at an early age so that
early teatimes can be instituted. Early treatment improves
a patient% domes for good vision, binocularity and good
alignment.. Iliimoveledge of anatomy and physiology and skills
in exam maps! cif the extraocular muscles as well as skill in
history takingisfa motility patient are important in diagnosing
and treat-csorabSmus patients.
REFERENCES
1. American Academy of
Ophthalmology Pediatric
Ophthainology/Strabismus Panel. Preferred Practice
Parrern•Guideines.Amblyopia. San Francisco, CA: American
Academy cif Ophthalmology; 2007. http://www.aao.org/
Figure 11. Muscle recession
PPP2. Pediatric Eye Disease Investigator Group. Randomized trial
of treatment ciamblyopia in children aged 7 to 17 years.
Arch Ophthalknol X05;123:437-47.
3. The Pediatric Eye Disease Investigator Group, A
Randomized TiW of Atropine vs Patching for Treatment
of Moderate Panblyopia in Children, Arch Ophthalmol.
2002;1 20.268-2781
4. Wen, G. McKean-Cowl', R., Varma, R. et.al. on behalf
of the Muki-ethnic Pediatric Eye Disease Study Group.
General Heatt-Related Quality of Life in Preschool
Children withStrabismus or Amblyopia, Ophthalmology
2011;11 8:574-580-
5.
Johns HA, Manny RE, Fern KD, Hu YS. The effect of 5. Prism measurement of exotropia is done with the
strabismus on a young child's selection of a playmate.
prism's base oriented
Ophthalmic Physiol Opt 2005;25:400 -7.
A. in
6. Mojon-Azzi SM , Kunz,A, Mojon DS, Strabismus and
B. out
discrimination in children: are children with strabismus
C up
invited to fewer birthday parties? Br J Ophthalmol 2011;
D
95:473-476.
7. Mojon-Azzi SM, Potnik W, Mojon DS. Opinions of dating 6. When the angle of deviation is equal in different
directions of gaze the strabismus is
agents about strabismic subjects' ability to find a partner.
Br J Ophthalmol 2008;92:765-9.
-8. Mojon-AzziSMandMojonDSStrabismusandemploymetr-.
the opinion of headhunters Acta Ophthalmol. 2004 .784-788.
9. Riordan-Eva, P, Whitcher, J. Vaughan and Asbury Gene.
x After removing the cover in one eye, the recently
Ophthalmology. Lange Medical Books : New York,
Empowered eye moved outward. The patient is
10. Wilson, F.F. ed. Practical Ophthalmology. 1996. Maar- = =
__
: : -
: American Academy of Ophthalmology.
SELF -TEST
1.
The agonist in elevating the left eyes
A. left lateral rectus
B. left superior rectus
C. left superior oblique
D. right inferior oblique
2.
The superior division of the oc...
the superior rectus and
A. superior oblique
B. inferior oblique
C. orbicularis oculi
D. levator palpebrae
3.
4.
This test will disting u is ,
A. cover uncover tei:
B. alternate cover test
C. prism cover test
D. modified Krimsky test
es
&
Accommodative esotropia is best treated
9_
When doing the corneal light reflex test, and the light
falls at the center of the pupil, the eye is
-.E.h„ zotropic
a hypertropic
E aligned
B..
C
• .:
Example of incomitont sqi.int is
A. congenital es :-•
B. intermittent =.-. C. accomm:::?.D. lateral recs pa
1 0. Choose the correct statement about exotropia.
-,termittent exotropia resolve spontaneously as the
B.
C.
child grows older.
Exotropia is best treated with spectacle correction.
Intermittent exotropes close one eye on exposure to
bright sunlight.
D.
Intermittent exotropes usually have amblyopia.
Answers to Self-Test on page 222.
7
DEVIATION AND DISPLACEMENT OF THE EYE I
7.1 Strabismus
149
7.2 Proptosis
Prospero Ma. C. Tuario, MD
INTRODUCTION
In the real clinical setting there are several ways that the eye wil exhibit a disturbance prompting the patient to seek consultation.
One of them is proptosis or a bulging eye.This self-instructional material is designed to guide the student in evaluating a patient
with proptosis.
OBJECTIVES
Upon completion of this unit of instruction, the medal silkier( snood be able to recognize a bulging eyeball and explain the
reasons for its presence. Specifically, he should be abletoc
1.
recall the relevant anatomy of the adult human orbit
2.
define proptosis
3.
4.
5.
recognize a bulging eye
differentiate between a true proptosis and pseudoproptosis
evaluate the bulging eye in terms of measurement, direction. and dynamics
6.
7.
enumerate the common orbital disorders among adult
discuss the various clinical examinations that are utilized in the evaluation of proptosis
CONTENT
I.
Anatomy of the adult orbit
II. Proptosis
1. Direction of proptosis
2. Measurement of proptosis
3. Dynamics of proptosis
4. Clinical evaluation of proptosis
5. Ancillary examinations
III. Orbital disorders
patients
I. ANATOMY OF THE
The globe is located in the anterior portion of the orbit such
that lesions surrounding the globe will necessarily disturb the
position of the globe. Anterior displacement of the globe,
either axial or off-axis is the most common result of lesions
in the orbit It is possible, though quite infrequent, for orbital
lesions to retract the position of the globe.
ADULT ORBIT
A knowledge of the anatomy of the bony orbit and its
contents is essential in order to gain a firm understanding
of a bulging eye. The bony walls define the limits of the
orbital volume. Within this space is found not only the globe The normal position of the globe in the orbit is marked by a
but also its supporting structures including nerves, blood fine &awn from the superior to the inferior orbital margin. The
vessels, glandular tissue and connective tissue, all of which straight fine theoretically lies tangential to the most anterior
are potential origins of neoplastic growth and inflammatory portion of the globe, namely the cornea. This position may
reactions. The bony walls are surrounded by the brain, sinuses vary within 10 mm anterior or posterior to this line (Figure 2). 3
and soft tissues of the face. Lesions from these structures may
extend and become secondary sources of pathology in the
orbit. Any disturbance of these structures can influence t`=
eventual displacement of the globe.
The orbit is described as a 4-sided bony cavity Ic sides of the nose. It serves as a socket for the passage for nerves and blood vessels which supply and the periocular adnexa. The orbit is shaped Be a r
whose orbital margin serves as the base and the optict:
as the apex. The globe, occupying one -fifth of the
volume, appears 'connected- to the orbita
nerve before the nerve enters the optic c
;schematic diagram of the adult orbit viewe
the roof removed.'
Figure 2. Normal position of the globe in the socket
II. PROPTOSIS
Proptosis is the hallmark of orbital diseases. While there are
obviously other manifestations of orbital diseases, such as
visual loss and diplopia, it is the protrusion of the eyeball that
is most unique to the orbit and most striking to the clinician
(Figure 3A).
Figure 1.Asche-3:
Stewart B and Goi::erg RA.'
--- - --- J,
The orbital cavity is tightly sunounded by bony walls on four
sides. The medial walls are parallel to one another and are
separated by the ethmoid sinuses~~(a width of 25 cm). The
lateral walls, which have the same length as the medial walls
(around 4.0 — 45 cm), are directed laterally and outwards,
subtending an angle of 45° (Figure 1, aqua arrow) from the
medial walls or the median sagittal plane (green arrow).
Interestingly, a hypothetical posterior extension of both lateral
walls makes them perpendicular to each other. The orbit also
exhibits a lateral and outwards and downwards direction,
approximately 22.5° (Figure 1, red arrow) from the medial
sagittal plane, simulating the same direction of the optic
The forward displacement of the globe is also termed
exophthalmos. Most physicians use these two terms
interchangeably, but some prefer to reserve the term
exophthalmos for the description of prominent eyes
secondary to endocrine disorders, such as thyroid-related eye
disease (Figure 3B).
Proptosis may be real or apparent. On the initial encounter
with a patient with a bulging eye, the first concern of the
clinician is to determine whether the prominence of the globe
is a true proptosis or a pseudoproptosis.
nerve.
7
DEVIATION AND DISPLACEMENT OF THE EYE I 7.2 Proptosis
First, lid changes may lead to asymmetry of the lids. Quite
often, the presence of a unilateral lid retraction in thyroid eye
disease may give the impression of an ipsilateral proptosis
(Figure 5A). On the other hand, a long-standing unilateral lid
drooping in Horner's syndrome may present a contralateral lid
retraction (and apparent proptosis) through the principle o Hering's law.
Figure 3. Proptosis (A) secondary to a mass in the orbit, (B) secondary
to thyroid eye disease
Ram i Pstragroposis as seen in (A) a patient with unilateral lid
milleclik Ma pollen pith Crouzon's Disease
PSEUDOPROPTOSIS
There are four general eye conditions that may manifest as
pseudoproptosis (Figure 4). One may be able to eliminate the
possibilities through the help of an accurate history and ocular
examination, documentation of a previous ocular trauma or
inflammation, explicit information regarding past medical
histories and treatments, as well as imaging studies.
Secondly. a huge globe may be misinterpreted as a
proptosedetc_Itisfrequently observed among high myopes
(near-sighted persons) and among pediatric patients with
congenital 9auoorna_ Awareness of the spectacle history
and/or perfooming refraction may detect the presence of
mr: --clatter displays a huge globe or a longer axial
Pseudoproptoses
Lid fissure
asymmetry
alINSIMIIIIIMMII=C
•
Unilateral lid
retraction
•
Contralateral
Homer's
syndrome
Globe size
asymmetry
Coreraimal
enophittairms
Shallow orbit
I
Enlarged globe
• High myopes
• Congenital
glaucoma
Small globe
• Unilateral
microphthalmos
•
Phlhisisbulbi
Old blow-out
fracture
Scirrhous
adeno CA of the
breast, kings rx
stomach
Figure 4. Differential diagnosis of pseudoproptosis. Adapted from Laws ER Jr.'
Craniosynostosis
diameter with an axial diameter > 24.0 mm. An elevated
intraocular pressure in an "expandable" pediatric eyeball, as
in congenital glaucoma, may likewise lead to an enlarged
globe. On the other hand, the presence of an abnormally
small globe (microphthalmos) in one side may give the
impression of a prominent contralateral eye.
Table 2. Classification of orbital tumors
Primary
Cystic
Vascatar (tumors/anomalies)
Mesenchymal (adipose/ fibrous/ osseous/
cartilaginous/ myxomatous)
Ez
Thirdly, a normal-sized but retracted globe (enophthalmos)
may put on the appearance of a prominent contral&e -a.
These conditions are caused by an old blow-out fraz:_ -e : a metastatic tumor to the orbit from a primary scirrho_
adenocarcinoma of the breast, lungs or stomach respective.
intraocular
Extraocular (lids)
From adjacent non-ocular structures
Nasopharynx/ paranasal sinuses/
cranium
Metastatic
Lastly, a shallow orbit causes a normal-sized globe to
This is exhibited in a craniosynostosis syndrome _
Crouzon's disease (Figure 5B).The characteristic'_
as well as imaging studies are able to identify the air,:—
diseases wal orbital manifestations
Hematopoietic
Histiocytosis
Phacomatosis
TRUE PROPTOSIS
The causes of true proptosis may be simply cavegtiviaed iltb
inflammatory and non-inflammatory diseases of die obi.
(Table 1) The inflammatory causes are furthersabdabledirao
infectious (e.g. orbital cellulitis) and non-ifeamitasa Noninfectious inflammation, thyroid eye &seam is (Mika as
specific because there is an etiology apipendedseisbdeajair.
namely a disturbance of the immune soon le Me Ovoid
disease
and the extraocular muscles. The abler
to
is idiopathic and non-specific because &
any causal agent. s
al (lacrimal gland)
adjacent ocular structures
The various entities that affect the orbit may appear
Ovisivdselmig but a systematic evaluation procedure which
includes an orbital as well as an ocular examination may
nawow down the possibilities further. The following orbital
evakiation is initiated to determine the etiology of the
pep osier It describes the direction, measurement as well as
die dynamics and clinical behavior of the proptosis.
DIRECTION
Table 1. Classification of orbital cleseasei
Infectious
Orbital cellidis
Non-infectious
Soesic
Congenital
kiwag of me time a discussion on proptosis is readily presumed
to be an axial displacement of the globe in the anterior
direction. This is not always the case. Because orbital lesions
are varied in location within the orbital cavity, the globe may
be pushed towards an off-axial direction.
The direction of the proptosed globe is predicated on the
knowledge of the four surgical spaces within the orbit (Figure 6).
Tumors
Trauma
0 - Central space
• - Tenon's space
• - Peripheral space
O - Subperiosteal space
The orbital tumors are further cassias rep primary, secondary
and systemic diseases with (Aid mankstatiOns (Table 2). 6
Primary tumors may original* from am tissue noun,* found
within the orbit (blood vessel nerve% connedive liSSUeS
and glandular tissues). The secondary tiNTIOIS wise from
structures outside the Orbit 'AfliCb include metastasis from
distant primary neoplasms. Systemic diseases. like leukerria
and histiocytosis, may present in the orbit simultaneously or
eventually reach the orbit anytime during the course of the
disease. Certain diseases like lymphoma may appear initially
in the orbit much earlier before making their presence
detected elsewhere unless they are totally eradicated on initial
Tenon's capsule
Lateral rectus
treatment.
Figure 6. Surgical spaces of the orbit
7
DEVIATION AND DISPLACEMENT OF THE EYE 1
7.2 Proatcs s
Egg
1.
2.
central surgical space or muscle cone — space within
the four recti muscles
peripheral surgical space — bound by the four recti
1. A WYROwiri
111111111
muscles and the periorbita
by the
3. Tenon's space — a potential space bound
4.
Figure 8. Luedde Exophthalmometer
Tenon's capsule and the outer coat of the eye
the
subperiosteal space- a potential space bound by
periorbita and the bony orbital walls
Figure 7 shows a proptosis that is off-axis. The globe is
displaced forward, slightly medially and downward-The orbital
mass is located opposite the direction of the proptosis. The
mass must be located superiorly, laterally and posteriorly and
outside the muscle cone. Clinical deduction tells us further
that the orbital mass is a lacrimal gland fossa lesion, most fielly
a tumor derived from the lacrimal gland. Other examples of
orbital pathology in relation to direction of globe displacement
are presented in Table 3.'
Figure 9. Hertel Exopthalmometer
two eyes.The Luedde and Hertel exophtalometers both utilize
as the bases of measurement the most anterior part of the
cornea and the lateral orbital margin. The examiner stands in
front of the patient and places the instrument on the lateral
orbital margin_The image of the cornea is reflected on a mirror
on the instrument Above this mirror is a millimeter ruler used
to measure forward globe displacement (Figure 10).
Figure 7. Patient with Lacrimal gland tumor
Table 3. Orbital lesions based on the direction of globe displacement
Axial
Non-axial
Enlarged extraocular muscles
Mass in central surgical space
Optic nerve tumor
Lacrimal gland fossa tumor
Mucocoele from sinuses
Subperiosteal abscess
Sphenoid wing tumor
(meningioma)
MEASUREMENT
An exophthalmometer is used to quantify the amount of
proptosis. There are several types. A Luedde exophthalmometer
(Figure 8) is similar to a millimeter ruler. It measures the globe
position individually. The clinician stands at the side of the
patient, places the recessed end of the instrument on the
lateral orbital margin and measures the displacement of the
globe by reading the millimeter markings on the instrument.
The procedure is repeated on the opposite eye.
.--,,,s,..rement of proptosis using the Hertel exopthalmometer
A novel instrument that measures not only the anterior
displacement but also the vertical position of the globe is
the Naugle exophthalmometer (Figure 11). It has vertical
fixation bars that are rested on the superior and inferior orbital
rims rather than the lateral orbital rim. It is useful for patients
with irregular or absent lateral orbital rims resulting from
maxillofacial trauma. 8
The more common instrument used is the Hertel
exophthalmometer (Figure9). Unlikethe previous instrument,
it measures the displacement of the two globes simultaneously
and thus facilitates the comparison of proptosis between the
Figure 11. Naugle exoophthalmometer. From Karcioglu
In order to determine the presence of a proptosis clinically
without the benefit of an exophthalmometer, the examiner
stands behind a seated patient and looks over the head of the
patient. From this position behind the patient the examiner
lifts both upper lids. The examiner observes and compares
from above the head of the patient the degree of protrusion
of either cornea (Figure 12).
RESILIENCY
It is normal to be able to retrodisplace the globe by applying
your thumb over the eyeball (Figure 13). In the absence
of any orbital pathology, one can easily push the eyeball
posteriorly because of the compressibility of the orbital tissues
such as orbital fat In the presence of a solid retrobulbar
lesion. the globe is prevented from being pushed backward
tovsards the orbit This is reported as negative resiliency. It is
more practical to push the globes simultaneously in order to
Whose comparison of the two orbits.
Figure 12. A clinical method to detect the presence o' p xecs-s
The normal exophthalmometry values amc - = = - 7. r
measured and compared with Caucasians (Table
Mare
orbtstliuttii
is the asymmetry between the left and right
important than the actual measurement A dikeremue et nue
than 2 mm between the two sides is considered Want
-
Table 4. Normal exophthalmometry values
Aver. No
Measurement
Filipinos
Caucasians
13.5
16.0
a
DYNAMICS OF PROPTOSIS
In evaluating the dynamics ofproci-:-._.
are considered:
1. resiliency
2. intermittency
3. clinical behavior / pulsating por-c,...1..,
4. duration
5. clinical course
"K":21-5
Form 13. tr ae r. 7 . r ?obe
ireenninent proptosis refers to varying degrees of eye
probusicxi as a function of change in the immediate
eriviionment ofthe patient A stimulus may be internal such as
a systemic infection; or external, like a change in head posture
or positionlhe proptosis is noted to increase in size followed
bya spontaneous resolution after the stimulus is removed.
The proptosis in a child with capillary hemangioma may
increase noticeably fast when he is crying but resolves soon
after (Figure 14). Another instance is an adult patient with a
mix or abnormally expansile venous channels. The proptosis
esacerbates when he bends forward into a prone position or
strains during a Valsatva maneuver.
Information regarding these features may provide valuable
hints in the identification of the orbital chsordec They ai
eventually narrow down the choices in the Memorial
diagnosis and provide a working impression from which a pbri
of work-up and management shall commence.
Rgure 14. Cambric hemarigioma
7
DEVIATION AND DISPLACEMENT OF THE EYE 1 7.2 Proptosis
Figure 15. Lymphangioma in a 10 year old child (A) shows the child upon initial consultation with a proptosed right globe with extensive conjunctival chemosis,
(B) shows spontaneous resolution after two weeks, (C) shows complete resolution of proptosis and periorbital swelling. Adopted from Wilson ME, Parker PL and
Chavis RM.1°
Certain vascular tumors, like a lymphangioma, may produce
a sudden exaggerated eye protrusion in the presence of an
upper respiratory tract infection. This expansion is caused
by increased vascularity in the tumor followed by bleeding
within the lymph channels of the tumor, leading to the
formation of "chocolate cysts". The lymphangioma is expected
to resolve spontaneously within a few months of conservative
management (Figure 15).
DURATION
Duration of the orbital disorder is important in the clinician's
formulation of differential diagnoses. It may be described as
acute, chronic or subacute. An acute onset is accompanied
by a short history prior to consultation. It implies a rapidlyevolving disease entity like a malignancy or an inflammatory
condition such as an orbital inflammatory disorder or an
orbital cellulitis (Figure 17).
CLINICAL BEHAVIOR / PULSATING PROPTOSIS
Pulsating proptosis, characterized by rhythmic pulsations of
the globe, may occur in cases of carotico-cavernous fistulas
of high-flow quality. An abnormal communication between
the cavernous sinus and the intracavernous part of the
internal carotid develops several months after a head trauma.
"Arterialization" of the venous channels of the orbit ensue
and the globe exhibits dilated and tortuous cork-screw-like
episcleral vessels (Figure 16). Pulsating proptosis may also
be exhibited by congenital bony defects in the orbital roof of
patients with orbital neurofibromatosis. The pulsations reflect
the same cadence as the peripheral arterial pulsations.
Figure 17. Orbital cellulitis
On the other hand, a chronic condition spanning years of
clinical history before clinical consultation may allude to the
possibility of a benign tumor. The most common primary
benign tumors of the orbit include a cavernous hemangioma
and a pleomorphic adenoma of the lacrimal gland.
There are subacute orbital conditions that are neither acute
nor chronic. These include orbital disorders like dysthyroid
orbitopathy, lymphomas and some metastatic carcinomas.
They have an insidious presentation prior to a more rapid
progression in the later stages of the disease.
Figure 16. Arterio-venous fistula with dilated & tortous
episcleral veins (corkscrew vessels)
CLINICAL COURSE
The clinical course describes the growth characteristics of the
tumor. It also provides information on the rate and direction
of evolution of the mass from the time it is first noted by the
patient up to the time when the clinician starts to observe the
disease process. The clinical course may be described as slowly
progressive, rapidly evolving, almost stationary or at times
On the other hand, there are tumors which may spontaneously
regress. A capillary hemangioma grows rapidly during the first
year of life, then stops and continues regressing until the early
teens (Figure 20)_
spontaneously regressing.
Many benign orbital tumors, such as cavernous hemangior-,a
(Figure 18) and pleomorphic adenoma of the lacrimal gianc
are slowly progressive. Some benign tumors, like optic nerve
sheath meningiomas and optic nerve gliomas, may
stationary or at the very least, are slowly progressive
inowle111.
Fie 2e moues of a female child with capillary hemangioma from
the tine teas detected at 6 months of age up to 10 years old. There are
lc es= t-nicaled by the white arrows) one on the left upper lid and
ate term Ire scalp. The regressing size of the lesion on the left upper
C 5 VINMI as te patient grows older.
CUNKAL EVALUATION
Figure18. 56-year old male viih a imortima -erwripoinait dm* um
noted 17 years prior b ileac ccnsulatria.
Most malignant tumors, like thabCtr-teCsar--Irea
3- 104
cystic carcinoma of the lacrimal gland yes hawri; a short
duration of history of less than a "east.
A faster and more explosive course of
rapid progiession.
'Flat a steel& 6 seen
in orbital cellulitis. Occasionally. the berms clinical course
of thyroid eye disease may proceed ttu IGNOC r1101:40515 after
radioactive iodine therapy or surgital thponeCtorny. in as
these conditions, the sudden resultant mouse can damage
the integrity of the cornea Mime
The patient with a true proptosis undergoes a thorough
dnical evaluation. Utilizing the same routine eye examination
appied to any eye patient, certain special considerations are
emphasized For instance, in the gross examination, there is
focused on lid and conjunctival changes.
and/or lid lag are almost pathognomonic of
particular attention
Lid retraction
thyrOid-related eye disease (Figure 21). Pupillary reaction
is also doubly appraised because of optic nerve dysfunction
secondary to compression by a tumor or enlarged extraocular
muscles.
11It
Figure 19. 19 year old female ctiagnosedw i alluse toxic goiter Her
rapid proptosis of less than one month duration has resumed n severe
bilateral lagophthalmos and intunous exposure Manges b the cornea
Figure 21. Bilateral lid retraction in thyroid eye disease
7
DEVIATION AND DISPLACEMENT OF THE EYE 17.2 Proptosis
gag
Venography and arteriography have remained part of the
history of orbital radiography. They are still both useful but
limited in use for particular diseases with vascular dynamics.
For instance, the management of carotico-cavernous fistulas
demands the localization of the fistula through selective
angiography before embolization treatment can be planned.
Other non-radiographic tests are available to augment the
information already derived from the previous examinations.
They are essential in identifying the disease process so that
the proper management can be instituted. In some cases, they
may be used to monitor the progress of the disease in order to
achieve proper timing of intervention.
sk.
Figure 22. Auscultation of the orbit
A novel maneuver such as auscultation over the periorbital
areas of a proptosed eye may reveal conditions such as
arteriovenous fistulas. In such cases, bruits may be heard by
the examiner (Figure 22). In addition, delicate palpation of
the same area may actually reveal rhythmic pulsation
CLINICAL METHODS OF ORBITAL DIAGNOSIS
1.
Gross Examination
2.
Palpation
3.
4.
Auscultation
Routine Eye Exam
5.
6.
7.
Color vision
Cranial nerve function Systemic examination
iio and conjunctival
abnormalities
pulsation, resiliency,
anteriorly-located mass
Vision, extraocular
muscles, intraocular
pressure,
ophthalmoscopy
pupil, corneal reflexes
RADIOGRAPHIC METHODS OF ORBITAL EXAMINATION
1.
2.
3.
5.
Venography
Arteriography
Plain film
Computerized tomography (CT scan)
Magnetic resonance imaging (MRI)
Radiography is an essential tool among orbital patients. There
is an absolute need to visualize the concealed structures
of the orbital cavity. The usefulness of radiography was not
evident with the first available machines for plain X-ray film
because only the bony walls were readily seen. The advent
of computerized tomography revolutionized the diagnosis
and treatment of orbital diseases because it was able to
view and distinguish the soft tissues within the orbit. Further
enhancement of the visualization was achieved with magnetic
resonance imaging which offered a discriminating picture
of the orbital apex. Plain radiography has been relegated to
detection of bony abnormalities such as fractures and bony
growths.
1.
2.
3.
4.
5_
Ocular ultrasonography
Visual field examination — for optic nerve evaluation
in thyroid eye disease, arteriovenous fistula, and optic
nerve tumors
Electrophysiology — for optic nerve evaluation
Laboratory exams — thyroid function tests
Tissue biopsy
III. INCIDENCE OF ORBITAL
DISORDERS
After a thorough clinical evaluation using the present and
past history, an orbital and ocular examination, and relevant
radiographic and laboratory examinations, there is still room
for epidemiological data in order to narrow further the
diagnosis of the orbital disorder.
Depending on which institution conducts the survey, certain
orbital diseases stand out. Local efforts by different authors
spanning four decades have revealed the predominance
of certain tumors like dermoid cysts, lacrimal gland tumors
and angiomatous new growths. The frequency of tumors is
explained by the fact that these studies were conducted on
histologically-proven specimens. 11,12
A more recent survey compiled all the available clinical records
in the Orbit Section of the Department of Ophthalmology
and Visual Sciences in the Philippine General Hospital. The
usefulness of the following epidemiologic data is depicted
in the occurrence of orbital disorders in certain ages. The
differential diagnoses of pediatric and adult patients do not
share many diseases in common. (Table 5) shows that the
overall most common orbital diseases are inflammatory in
nature, specifically thyroid eye disease. 13 In children less than
12 years old, vascular tumors, such as capillary hemangioma,
are more commonly encountered 14
Table 5. Incidence of Orbital Disorders by Age Group"
(arranged in decreasing order)
1111
11111.1b7dren (<12 years
• Thyroid eye disease
• Orbital inflammatory disease
• Secondary tumors (from the
paranasal sinuses
• Vascular tumors (cavernous
hemangioma)
• Lacrimal gland tumors
• Neural tumors (meningioma)
• Systemic disease with
orbital manifestations
(orbital lymphoma)
• Cystic tumors
• Vascular tumors (capillary
hemangioma)
• Cystic tumors (dermoid cysts
• Orbital infections (orbital
cellulitis)
• Systemic disease with orbital
manifestations (leukemia)
• Trauma
• Rhabdomyosarcoma
• Neural tumors (opt< new
glioma)
• Orbital inflammatory Jsease
SUMMARY
Proptosis is an ocular complaint and manifestation
occurs rather infrequently in comparison with ot*-ie, correrion
complaints such as headache, redness and biaTirg of
vision. Despite its relative rarity, the complaint mint be
evaluated because it is peculiarly an orbital commicAant. Ike
most important value of learning the flange and behavior of
proptosis is the knowledge that this manifestation cormanaes
its own share of problems to the well-being of theeye
There is difficulty in identifying the lesion because it ernes
behind the eyeball where it is InratisiditetD mane eye
examination. As such, the clinician needs 1D COndila not anily
the routine eye examination but also cdrer recominended
steps in a systematic evaluation of the tedlgingepe
It is important to determine if the peopiosis is red ix not The
differential diagnoses of pseudopiopsomis include unilateral
myopia, lid fissure asymmetry and oontodaterafenopluhaimos,
True proptosis, should undergo further dried evaluation,
' or clinical
namely, measurement, direction and dynamics
behavior. In general, the clinical considerations indude lesions
that are inflammatory or non-fir_
Clinical examination is folosved bg the use of ancillary
procedures such as CT scan or MN of the skull and orbit_
Other laboratory eluminatinns indude visual field tests,
biopsy procedures on accessible tumors. ultrasonography.
e I ectrophysiology and selective carotid cinigiugaphy.
REFERENCES
1.
2.
Rootman J, Stewart B, Goldberg RA. Orbital Surgery a
Conceptual Approach. Philadelphia: Lippincott — Raven.
1995 p79.
American Academy of Ophthalmology. Basic and Clinical
Science Course Sec 7 Orbit, Eyelids and Laaimal System, 2003.
3.
Zuckerman J. Diagnostic Examination of the Eye.
Philadelphia: JB Lippincott. 2nd edition 1964 p73.
4. Laws, ER Jr. (ed). The Diagnosis and Management of Orbital
Tumors. New York: Futura Publishing Co.1988, pp153155_
5_ Jones IS and Jakobiec, FA (eds). Diseases of the Orbit.
Maryland: Harper & Row, 1979. Chap 12.
6. Hogan MJ, Zimmerman LE (eds). Ophthalmic Pathology
an Atlas and Textbook. Philadelphia: WB Saunders Co 2nd
edition 1962. pp739-40.
7_ Nerad JA, Krachmer JH (eds). Ocuplastic Surgery The
Requisites in Ophthalmology. St. Louis Missouri: Mosby.
2001, p 355.
Karcioglu ZA (ed). Orbital Tumors Diagnosis and Treatment.
New York: Springer Science + Business Media Inc, 2005,
pp 51-60.
3_ Fajardo RV, Aquino MV. Exophthalmometric
measurements among Filipinos, Philipp.lofSurg
Specialties 22:1967.
Kt Wilson ME, Parker PL, Chavis RM. Conservative
managementof childhood orbital lymphangiomas.
Ophthalmology ,1989; 96:484-90.
IL Lim GD. Symposium: unilateral exophthalmos
ophthalmologic aspects. Trans Phil Acad Ophthalmol
Otolaryngol 3:0P-5, 1973.
12 Vergara M. I ntraorbital tumors. MD Journal, 10:811, 1961
13_ Tuano PC, Remulla HD. A survey of orbital diseases
in the UP-PGH Department of Ophthalmology 1991
(unpublished).
14. Sy RT, Remulla HD, Tuano PC. A review of 75 cases of
orbital tumors in children at the orbit clinic, Philippine
General Hospital from 1980-1991. Transactions
Department of Ophthalmology UP College of Medicine 2:1
December 1994 pp 66-74.
SELF-TEST
1.
The bony orbit is directed forwards and
A. laterally and upwards
B. laterally and downwards
C. medially and upwards
D. medially and downwards
2.
The volume of the orbit is:
A. 30 cc
B. 35 cc
C 40 cc
D. 50cc
3.
In which bone does the lacrimal gland fossa lie?
A. trontal
B. lacrimal
C. maxillary
D. zygomatic
7
DEVIATION AND DISPLACEMENT OF THE EYE I
2 Proptosis
159
4.
The normal range of exophthalmometry measurements
among Filipinos is:
A.
B.
C.
D.
9.0 - 14.5 mm
10.0 - 19.5 rnm
the same as Caucasians
still unknown / unreported
9.
A globe with negative resiliency and positive
intermittency may indicate the presence in the orbit of:
A. lymphangioma
B. orbital floor fracture
C. inflammatory pseudotumor
D. cavernous hemangioma
5.
One of the landmarks in measuring proptosis using the
Hertels exophthalmometer is the
A. bridge of the nose
B. lateral orbital rim
C. pupil
D. lateral canthus
10. One suspects a lacrimal gland tumor if the globe is
proptosed forward,
A. powrivvaras and medially
B. upwards and medially
C. downwards and laterally
D. upwards and laterally
6.
Pseudoproptosis is evident in the following situation:
A. ipsilateral Horner's syndrome
11. A vascular orbital tumor which spontaneously stops
growing and even regresses is exemplified by a:
A. cavernous hemangioma
B. capillary hemangioma
C. lymphangioma
D. varix
B. pseudotumor
C. axial myopia
D. elevated intracranial pressure
7. Acute proptosis (rapidly-progressive proptosis) of the
globe is noted in the following, EXCEPT:
A. cavernous hemangioma
B. thyroid-related eye disease
C. inflammatory pseudotumor
D. rhabdomyosarcoma
8. A proptosis which increases after a Valsalva maneuver
is probably due to:
A. a cavernous hemangioma
B. a capillary hemangioma
C. a thyroid eye disease
D. an inflammatory pseudotumor
160
Self-Instructional Materials in Ophthalmology I 2nd Edition
12. CT scan of the orbit is most needed in a:
A. proptosis with positive resiliency
B. proptosis with unexplained ophthalmoplegia
C. proptosis accompanied by palpable lid masses
D. exophthalmometry difference of 2.0 mm
Answers to Self-Test on page 222.
8.1 Retinobla oma
Rolando Enrique D. Domingo, MD
INTRODUCTION
This self instructional material is designed to pry. 3e neisegicarisINOrmar. oirenliev. of the life threatening eye disease known
as retinoblastoma. Although it provides basic informil.suldsammillositiisalso meant to encourage the student to further
reading. Knowledge acquired from this material+iil
i
paclioe as ad as further training in Ophthalmology.
OBJECTIVES
After reading and understanding this
1.
Identify through history taking and
dues, signs and symptoms leading to a diagnosis of
retinoblastoma.
2.
Recognize and differentiate zxstlikinvilildimerpesentimiti signs and symptoms similar to retinoblastoma.
3.
Develop an appropriate sense atimiliiiiramarficedivih a patient potentially suffering from retinoblastoma.
4.
Enumerate the therapeutic -reditisawilablirma patient with retinoblastoma.
CONTENT
I. BACKGROUND
III. HISTORY
Retinoblastoma is the most common intraocular malignancy
of childhood. Its incidence is approximately 1:18000 live births';
however some series have reported an increased incidence
in the last few decades. There is no known sexual or racial
predilection. In non-Caucasian populations wherein uveal
melanomas are rare, retinoblastoma is the most common
primary intraocular malignancy in all age groups.
In a child suspected to have retinoblastoma it is important
to ask about the birth and maternal history. Factors such
as preterm birth, birth weight, family history of metabolic
disorders, childhood blindness and early death are important.
Occasionally, a complete history is enough to rule in or rule
out retinoblastoma.
In our country with a very high birth rate, it is logical to expect
many new cases annually. Local tumor registries in Manila
and Rizal show an incidence of 7.7-8.9 (1983-1995) per million
children aged 0-14 years.' In the tertiary referral center setting
of the Philippine General Hospital (PGH) around 80-100
new patients are seen every year. Studies have shown that
the number of retinoblastoma cases in PGH increased from
40/100,000 new eye case per year (1%7-1977) to 237/100,000
new eye cases per year (1997-2001).3
II. GENETICS
The development of retinoblastoma can be traced to
mutations on chromosome 13. The retinoblastoma gene (RB
gene) is one of the best-studied genes in the human genome.
It is a tumor suppressor gene whose presence (even of a single
allele) protects against the development of the tumor.
Most cases of retinoblastoma are sporadic mutations. This
means that one single retina cell suffers a mutation on one
allele of the RB gene, then after some time suffers another
mutation on the remaining allele. The loss of the tumor
suppression from both alleles then allows that particular cell
to multiply uncontrollably (Knudson's Two Hit Hypothesis).'
In around 30% of cases, the condition is heritable. In this
instance the child inherits a normal chromosome 13 from
one parent and a mutated chromosome 13 from the affected
parent.Therefore, all the retina cells (in fact, all cells in the body)
have one mutation at birth. Retinal cells are very metabolically
active and are constantly exposed to light energy and in most
instances these children will develop a second mutation in
one or more retina cells producing retinoblastoma.
Although the average age for the diagnosis of retinoblastoma
is 18 months, patients with sporadic mutations develop
tumors later (mean age at diagnosis 24 months5) because two
hits are needed on a single cell. Sporadic cases are unilateral.
Children with the heritable variety are diagnosed earlier at a
mean age of 12 months, because only a second hit is needed
after birth and all retinal cells are at risk. These cases are usually
bilateral with multiple tumors on both eyes. Clinically, heritable
retinoblastoma behaves as an autosomal dominant trait with
marked penetrance. Retinoblastoma is very rarely seen after
the age of six.
The most common presenting symptom of retinoblastoma is
leukocoria (white pupil) also called cat's eye reflex or"matang
pusa", in Filipino. This is seen in two thirds of retinoblastoma
patients with intraocular tumors (Figure 1).
Figure 1. Leukocoria in the right eye of a child with retinoblastoma
If the tumor is located in the posterior part of the retina then
the leukocoria may be constant. However, if it is located in the
periphery, the cat's eye reflex might be seen only on certain
directions of gaze.
Retinoblastoma may occasionally present as strabismus,
inflammation or mimic infection. Sometimes tumor cells
seed into the anterior chamber and settle inferiorly giving the
appearance of pus (hypopion) .When the tumor grows it may
cause glaucoma and, later, buphthalmos or enlargement of the
eye. Advanced tumors that grow beyond the confines of the
globe (extraocular extension) may present with exophthalmos
and an orbital mass6 (Figure 2). At this stage, intracranial
extension via the optic nerve and hematogenous metastasis
become more likely.
IV. PHYSICAL EXAMINATION
A complete ocular and physical exam on a child suspected to
have retinoblastoma is imperative. Unilateral visual loss usually
goes unnoticed and must be tested in a child.
Gross examination will usually show a white pupil. Great care
must be taken to ascertain the cause of the leukocoria, as this
may be caused by opacities in the cornea, lens or vitreous
other than a tumor.
A dilated ocular funduscopy will show a yellow, white or pink
mass. Indirect ophthalmoscopy gives more panoramic and
three dimensional views (Figure 3) compared with a hand
held direct ophthalmoscope examination.
V. DIFFERENTIAL DIAGNOSIS
There are several conditions that may present with leukocoria
other than retinoblastoma7. A white pupil may be due to a
comeal scar or opacity in the lens such as a developmental
catarac (Figure 4) Cataracts may be congenital or may
develop
grows. A careful examination is usually
ide- -.he lens as the cause of the white reflex.
Awe
Figure 2. Re:
extraocurir earscr
A firm eye and one that is larger than the fellicvi erealesgsof
an enlarging tumor. An extraocular tumor. andle
the gas
appearance of exophthalmos might also vest* in emmocular
muscle restriction and extraocular movement &soden. In
these cases a systemic and neurologic evahmtiOn &the diikl
should be done to detect signs of metastase.
:..e:e -act presenting with leukocoria.
^ollogies posterior to the lens may also cause a cat's
may be more difficult to differentiate
A condition commonly mistaken for
nobly _
s retinopathy of prematurity or ROP. In
atIvrrec = = 7 - e retina may become detached, disorganized
: • --= ke structure causing leukocoria. A history of
Pine- 7
._•=5, than 28 weeks gestation and birth weight
less
S- •= and/or a stormy clinical neonatal course will
point the
an in the right direction.8
Persistent hyperplastic primary vitreous (PHPV) is another
condition which mimics retinoblastoma. The leukocoria
s : -went at birth and the affected eye is usually smaller
-:halmia). There is a fibrous plaque behind the lens
through a stalk to the optic disc. This is an anomaly
ccogenesis which is otherwise benign.
off e
Coats 7: ease manifests as telangiectatic changes in the
of c- ::ren_ The blood vessels leak and cause subretinal
-E..aation, retinal detachment and scarring. Although patients
7.h Coats' Disease can present with leukocoria, particularly if
e
7 - affected portion of the retina is large enough, a distinct
retinal mass would not be seen on funduscopy. These patients
are also usually older than those affected with retinoblastoma.
Other more unusual diseases such as retinal dysplasia, parasitic
endophthalmitis and tuberculosis may present with signs and
symptoms suggestive of retinoblastoma. In all cases the need
for a good history and thorough physical examination can
never be overemphasized.
8
SPECIAL TOPICS I C.1
Retinoblastoma
163
VI. ANCILLARY TESTS
Although a complete ophthalmologic exam including
indirect ophthalmoscopy leads to an accurate diagnosis of
retinoblastoma in the great majority of patients, ancillary
tests might be useful in the few equivocal cases. An ocular
ultrasound (B scan) is readily available in most eye centers
and can easily demonstrate the presence of a distinct mass
(Figure 5) in cases where there is doubt especially if there is
an opacity in the cornea or lens occluding the view.
It should be noted that even with a thorough expert
examination and after performing diagnostic procedures
in many cases making a definitive clinical diagnosis of
retinoblastoma may still be difficult. Foreign studies show
that 10-20% of eyes enucleated for suspected retinoblastoma
turn out to be pseudoretinoblastomas. In the local setting,
a review done at the UP-NIH Institute of Ophthalmology
revealed that 8% of submitted eyeballs with a clinical diagnosis
of retinoblastoma turned out to be other benign lesions.'
These were blind, leukocoric eyes in young children with a
suspicious intraocular mass wherein it was more prudent
to remove the eye instead of risk the possibility of leaving a
malignant tumor untreated.
VII. MANAGEMENT
Once a patient is diagnosed with retinoblastoma the situation
must be treated as urgent. Visual loss is a very serious
consideration but the threat to life is of utmost importance
because untreated retinoblastoma is almost uniformly fatal.
Figure 5. Ultrasound photo showing a solid mass at the center.
By far, the most useful ancillary procedure in the diagnosis of
retinoblastoma is a CT scan.9 One particular characteristic of
retinoblastoma is that calcification is seen in more than 90% of
tumors and the CT scan easily demonstrates this (Figure 6). On
the other hand, all other childhood eye pathologies very rarely
calcify before the age of seven. Therefore, a child less than six
years old with an intraocular mass showing calcifications on
CT scan is almost certainly suffering from retinoblastoma.
The most important objective of treatment is to save the
child's life. The secondary aim is to preserve as much vision as
possible without increasing the risk for metastasis. The tertiary
goal is to make the patient's cosmetic appearance as near
normal as possible to minimize any negative psychological
impact the condition might have on a growing child.
The management of retinoblastoma is performed by a team
primarily consisting of an ophthalmologist, a pediatrician and a
radiologist. Small and medium sized tumors (Figure 7) may be
successfully treated using conservative eye sparing methods.
A deadly characteristic of retinoblastoma is its propensity to
invade the optic nerve, and in the advanced stage spread
directly into the brain.The CT scan is also useful in documenting
this and guides the physicians in treatment planning.
Figure 7. Regressed small sized intraocular retinoblastoma after laser
treatment
The small tumors may be treated with laser, thermotherapy,
brachytherapy or cryotherapy depending on the size and location.
Medium sized tumors may be treated with chemotherapy
combined with the previously mentioned modalities. External
radiation therapy is also sometimes used, either alone or in
combination, to save an eye with retinoblastoma."
Figure 6. CT scan showing intraocular tumors with calcification.
Larger tumors occupying more than half of the eye and with no
hope for vision are enucleated. It is imperative for enucler_ez:
eyes to undergo histopathologic examination to look for sigrs
of extraocular spread. Tumors with extraocular extensicr
have higher rates of metastasis and result in worse pica-cs
Extraocular extension is an indication for chemothe---__D.
operatively.
In recent years there has been a focus on the uses -et:adjuvant chemotherapy to prevent recurrence in
enucleation patients with intraocular retinoblastoma strwing
high risk histopathologic characteristics. These factor_ rtzu3e
invasion of the scleral coat, post laminar optic nerve r"..-cr
and massive choroidal involvement.12
Patients with large tumors involving the orbit have rite sicrg
prognosis. They are treated with chemotherapy anc —foe
extensive surgery.The newer chemotherapeutic chrLr_.5 s-c".as
the platinum compounds are increasing the survika -ems of
these patients. Medical therapy may be done in ccr-oraelor,
with radiation treatment.
Retinoblastoma patients must be closely follow,:
sgins
of recurrence or development of new turno-s -lentabe cases
are especially at risk and have been reportec 3E'setIC drier
malignancies in later life.'3 Genetic courseirc b adkaed
families planning to have more children is as;. -mewl
SUMMARY
Retinoblastoma is a life threatening eye dose r ditties
that usually presents as leukocoria_ It is imper-arc e-leran
a high index of suspicion and differentiae t flaw tub
conditions at the first consult. A =wine lislay and
physical examination combined vitt the digit legs ad lead
to an accurate diagnosis necessary 1c
treatment. Delay in diagnosis and
only loss of vision but, more irrtn7-
3_
RB, De Jesus AA, Valera EC, Mercado, GV,
- piiidemiological pattern of retinoblastoma at the
Philippine General Hospital. Philipp J Ophthalmol , 2004;
29:136-139.
Mclean IW. Retinoblastomas, Retinocytomas, and
Pseudoretinoblastomas. In: Ophthalmic Pathology an Atlas
are Textbook. Spencer WH, editor. Philadelphia, PA: WB
Saunders. 4th edition. 333-1336.
Our , Devron . Clinical Ocular Oncology. New York, NY:
Churchill Livingstone Inc. 1989.
lac Lean IW, Burnier MN, Zimmerman LE, Jakobiec FA.
AVM of the Eye and Ocular Adnexa. Washington, DC:
Mned Forces Institute of Pathology. 1993. 103-105.
Chua CT, Lim MC, Seah LL, et al. Pseudoretinoblastoma in
enudeated eyes of Asian patients. Singapore Med J 2006;
47:617-620.
Kama P, Muttineni J, Angell L, Karmaus W. Retinopathy of
pematurity and risk factors: a prospective cohort study.
&ICPediarr 2005; 5: 18.
9. thosh 5, Mukhopdhyay S, Chattopahyay D, Biswas K.
Diagnostic accuracy in retinoblastoma. J Indian Med Assoc
2010; 108: 509, 512-513.
110 Valenzuela RM, Domingo RED, Ranche, JM, Manganip LE.
A review of retinoblastoma cases at a tertiary hospital.
Philipp J Opthalmol 2010; 35. http://www.paojournal.
oorn/vol35no1/toc.php . Access date: July 24, 2011.
11_ Lumbroso-Le Rouic L, Aerts I, et al. Conservative treatments
of intraocular retinoblastoma. Ophthalmology 2008; 115:
1405-1410.
12. Uusitalo MS, Van Quill KR, et al. Evaluation of
chemoprophylaxis in patients with unilateral
retinoblastoma with high-risk features on histopathologic
examination. Arch Ophthalmol 2001; 119: 41-48.
13_ Draper GJ, Sanders BM, Kingston JE. Second primary
neoplasms in patients with retinoblastoma. Br J Cancer
1986; 53: 661-671.
SELF-TEST
1.
ACKNOWLEDGEMENT
Dr. Allan Joseph L Larona cor
0140839111001s
C Protects a child from retinoblastoma.
D. Is a heritable defect that is passed on
generations.
REFERENCES
1.
2.
Yanoff M and Fre BS_ Oadar Padriagy: A Color
Atlas. Singapore: Gower Medical Publishing rd edition.
1992. 18.5 - 18.11.
Ngelangel CA and Wang EHM, Cancer and the Philippine
Cancer Control Program. Jpn J Gin Oncol 2002; 32
(supplement 1): S52-561.
The presence of the retinoblastoma gene:
A. Causes the development of retinoblastoma.
B. Increases the risk of development of secondary
tumors in later life.
2.
to future
Unless proven otherwise, a child less than five years
old presenting with leukocoria, should be considered
a case of:
Retinopathy of prematurity
B. Retinoblastoma
C Persistent hyperplastic primary vitreous
D. Congenital cataract
SPECIAL TOPICS 1 8.1 Retinoblastoma
165
3. In a child presenting with leukocoria which
accompanying sign is the least associated with
retinoblastoma:
A. Congestion
B. Exopthalmos
4.
C.
Exotropia
D.
Hypotonia
A child born at 26 weeks age of gestation with a birth
weight of 1.4 kg presents with bilateral leukocoria since
3 months of age. The most probable diagnosis is:
A. Heritable retinoblastoma
B. Persistent Hyperplastic Primary Vitreous (PHPV)
C. Retinopathy of Prematurity
E. Coats'disease
5. A one year old child is brought to you for leukocoria
What other finding would lead you to PHPV as a primary
consideration:
A. Bilaterality
B. Microphthalmia
C. Preterm birth
D. Gestational infection
6.
A 3 year old child with leukocoria is presented to you. On
examination the cornea is hazy and the lens is opaque.
What examination would be most helpful in definitive
diagnosis of this patient?
A. CBC and peripheral blood smear
B.
Ultrasound
C. CT scan
D. X-ray of skull and orbits
7.
166
A four year old child with left sided leukocoria and
exotropia is diagnosed with retinoblastoma, the most
likely treatment modality is:
A. Laser treatment
B. Chemotherapy
C. Enucleation
D. External beam radiation
Se-Instructional Materials in Ophthalmology I 2nd Edition
8. Orbital recurrence and metastasis after enucleation is
most likely if the histopathologic report shows:
A. Poorly differentiated retinoblastoma cells.
B. Tumor seeding in the anterior chamber with
glaucoma.
C. Massive invasion of the choroid.
D. Invasion of the optic nerve beyond the margin of
resection.
9. A six month old child underwent enucleation of the
right eye for intraocular retinoblastoma. The other
eye was normal on examination under anesthesia. On
discharge you would advice the parents to:
A. Not worry since the tumor was completely remove
and no further follow up is needed.
B. Bring the patient back for consultation if they nu recurrence at the post-enucleation socket.
C. Bring the patient back every few months to check for
tumors developing on the remaining eye.
D. Consult the pediatric oncologist for post op
chemotherapy.
10. A man who survived bilateral retinoblastoma marries
and the couple decides to have children. Your advise to
them would be:
A. Not to worry because the chance of having children
with retinoblastoma is very small.
B. Bring their children to the doctor once they see
leukocoria or other signs of retinoblastoma.
C. Do routine CT scans on their children every six
months.
D. Take their future children to be seen by an
ophthalmologist the soonest time possible after
birth.
Answers to Self-Test on page 222.
8.2 Ocular Manifestations
of Systemic Diseases
Romulo N. Aguilar, MD, PhD
Teresita R. Castillo, MD, MHPEd
INTRODUCTION
This self-instructional material is designed to he.:
systemic diseases. It aims to emphasize the
earn key concepts regarding eye manifestations of common
rrrnary care physicians in preventing visual loss by appropri te
recognition, treatment and referral to the ot÷t^,a,
Many systemic conditions can present :-
—ar---festations. Certain ocular signs and symptoms may sig
dira gathered from an eye examination can provide the clinic'
presence of serious underlying systemic disc - t..
with clues that may help in the diagnosis ar• —a-zi3e—ert-oitile underlying systemic disease. While some ocular findings may
be non-specific, certain findings ma) be
presence of one or more diseases.
OBJECTIVES
5-c4.40.7. De able
cr
Upon completion of this unit of
the following
-c ccaarlyeai sys,emic diseases, specifically those associated with
1. To recognize charac-:ef,s,
conditions
Diabetes Mellitus
Hypertension
HIV/AIDS
Thyroid Disease
Tuberculosis
•
•
•
•
•
2.
To learn the bas`_ 2.--Ictifes of management of the above conditions
3.
To determine \.%nen
3compliarlberier a patient to an ophthalmologist for consultation or treatment.
CONTENT
Diabetes mellitus
II. Hypertension
Ill. Acquired human immune deficiency syndrome
IV. Thyroid eye disease
V.
Tuberculosis
Anterior segment: tuberculosis, rheumatoid arthritis,
vitamin A deficiency, drug or heavy metal toxicity,
immune-mediated diseases, metabolic diseases
The eye can provide clues to the diagnosis of many systemic
diseases because significant effects of these various conditions
may manifest in the eye. The initial diagnosis of a number of
systemic diseases may therefore be made in the course of
performing a comprehensive ophthalmic examination.
Lens: metabolic conditions (diabetes), steroid toxicity,
Apert syndrome, juvenile rheumatoid arthritis, Wilson
disease, homocystinuria
Evaluation of the ocular fundus is particularly important in
the evaluation of systemic disease since it is the only region
in the body where one can directly visualize manifestations
of macro and microvascular pathology. Nevertheless. various
components of the comprehensive eye examination may help
identify existing systemic disease.' For example
•
Posterior segment: diabetes mellitus, systemic
hypertension, infectious diseases (e.g., acquired
tuberculosis,
syndrome,
immunodeficiency
toxoplasmosis), primary or metastatic tumors,
drug toxicity (ex., hydroxychloroquine, tamoxifen),
cerebrovascular disease, hematologic disorders, brain
tumors
External examination: orbital tumor, thyroid eye
disease, acquired immune deficiency syndrome.
tuberculosis
Pupillary function, ocular alignment and motility:
neurological disorders (e.g., myasthenia gravis,
central nervous system defects, multiple sclerosis,
optic nerve disorders, brain tumors), thyroid eye
disease
An outline of some of the more significant diseases, along with
their ocular presentation, is summarized in Table 1. A review
of the important ocular pathology seen in some systemic
diseases will subsequently be discussed.
Visual fields by confrontation: tumors affecting the
optic pathways
Table 1. Overview of Ocular Manifestations of Common Systemic I>
F
System/Category
Disease
Endocrine
Diabetes mellitus
Thyroid eye disease
Pituitary lesions
Diabetic retinopathy
Thyroid orbitopathy
Field loss
Cardiovascular
Hypertension
Retinal Emboli
Hyperlipoproteinemia
Marian Syndrome
Endocarditis
Hypertensive Retinopathy
Retinal Vessel Occlusion
Corneal Arcus/ Xanthelasma
Lens Dislocation
Roth Spots
Rheumatology
Rheumatoid Arthritis
Scleritis
Keratitis sicca
Uveitis
Keratitis sicca
Anterior Uveitis
Sjogrens Syndrome
Seronegative Spondeloarthropathes
Collagen Vascular Disease
Juvenile Rheumatoid Artnntis
Herpes zoster
HIV, CMV
Candidiasis
Infections
ITS3
rnif
Ocular Manifestation
Syphilis
Uveitis. glaucoma
Retinitis
Endophthalmitis
!ribs, Optic Neuritis, Ophthalmoplegia
Malignancy
Lymphoma
Leukemia
Metastases
Infiltrate, uveitis
Infiltrative retinitis
C"oroidal mass
Neurological
Multiple sclerosis
Giant cell arteritis
Myasthenia gravis
Optic neuritis. uveitis
Ischemic optic neuropathy
Diplopia ptosis
Dermatological
Acne rosacea
Atopy
ler::: !is oa!aract
I
rs 1 _1
.:cose is thought to damage retinal (and renal)
-,ne following ways:
I. DIABETES MELLITUS AND
DIABETIC RETINOPATHY
1.
3f
Diabetes Mellitus (DM) is associated with a
complications. These include cataracts, extra-ocular muscle
palsies (Cranial Nerves Ill, IV, VI), diabetic optic neuropathy.
neurotrophic keratitis and diabetic retinopathy Among these.
diabetic retinopathy is the most common and may lead to
permanent loss of vision if not properly attended ta
Based on the 2002 Third National Survey of Phippine
Blindness', the overall prevalence of visual irnpairment was
4.62%, which roughly translates to 3,673.070 Ripinos The
crude prevalence of bilateral blindness a—oing Filipinos was
Whet inducted
0.58% or, about 461,121 Filipinos. Re: of tandness.
diabetic retinopathy, was the 4th lea: following cataract, error of refraction 3 = 2: aUCOMel tr ',sad a
iipines.
prevalence of 0.11%, affecting about
Also in 2002, the World Health Organization (10101egrnated
that there were 37 million cases of blindness due to raying
eye diseases.' Diabetic retinopathy was the 5' leading cause
of blindness after cataract. glaucoma. age-relmed macular
degeneration and corneal opacities and accourred for 4.8%
or, roughlyl.8 million persons. The pooperion at blindness
due to diabetic retinopathy rangedtfoom newly Air
Africa, to 3-7% in much of South-East Asia whicii recce
Philippines, and the Western Paw. to 5-17%c it*
affluent regions of the Americas, Europe and the
Pacific.'
Studies have shown that at any one erne
diabetic population will have diabetic rear p~ .
time, 90% of diabetics will eventually &Nem tr€
3.
ca:
. basement membrane thickening,
''ary pericytes and,
brea.....:L...^; of the blood-retinal barrier.
As a result of these processes (Figure 1), the blood vessels
weaken and form saccular dilatations called microaneurysms
rigor. 2), which can leak, resulting in hemorrhages
(Figure 3) and exudates (Figures 4 and 5) in the retina.
Vascular remodeling takes place resulting in capillary
telangiectasie :3:led intraretinal microvascular abnormalities
beading (Figures 6 and 7). Because
ORIAAs a- 7 •
age, vessels eventually close and cause
of struct-L.- Lretina, usually manifested as cotton-wool
ischemia of
spots or patches (Figure 4). These ischemic areas are thought
to produce a special growth chemical (vascular endothelial
growth factor or VEGF) which is known to be responsible
*x new blood vessel growth (Figure 8). When this occurs,
Proliferative diabetic retinopathy develops.
.41'Permeability
*COW
Oodala
was
t
am=
Capillary
occlusal
lAcmussaiar
erdotelopolls
avacee-matane
Retnopathy
Necuasadanzatoo —
1
*•
4=C-swam
8amassica lylc,ns7..iar Mammal
',soma=
—>
or-ogo
Figure 1. ,:it'-k.Ayerriesiz, of
Rehoopothy
, ,:c Retinopathy
--_ _ :-
The prevalence of diabetic retinopaihy has bee.- bun:: ;2E
related to the duration of the systemic condocr^: (Table 2)
Table 2. Prevalence of Deter RelinapiftimildlinapDimios ri
the Disease
Duration
111111111111111111111111111111
to- 15 yrs
16-2C yrs
30+ yrs
1111111111111111Mml
Figure 2. Microaneurysms are the earliest clinically visible changes
of diabetic retinopathy. They are localized capillary dilatations which are
usually saccular (round). They usually appear as small red dots in clusters
although they may also be isolated (arrows).
Although the likelihooc
between Type I and Typ=
apathy varies
= T_s, :=_- - efaily, the risk of
retinopathy increases with
Dn c- --e disease. Almost
100% of Type I patients will dew. -etir c c athy after 15 years
of diabetes. The more severe form of proliferative diabetic
retinopathy does not appear at all until disease duration of at
least 10 - 15 years.:
8
SPECIAL TOPICS
1 8.2 Ocular Manifestations of Systemic Diseases
169
Eh
Figure 3. Intraretinal Hemorrhages may be 'dot' or' blot' shaped (termed
'dot/blot hemorrhages: arrow) or flame shaped (arrow head) depending
upon their depth within the retina. The capillary network in the posterior
retina is found in two layers; a superficial one in the nerve fiber layer and
a deeper one within the inner nuclear layer. Hemorrhage within the nerve
fiber layer tends to be flame shaped. following the divergence of axons. In
the inner layer. hemorrhage is aligned at right angles to the retinal surface
and is consequently viewed end-on when using an ophthalmoscope; these
hemorrhages appear dot or blot shaped.
Figure 4. Cotton-wool spots are grayish-white patches of discoloration
in the nerve fiber layer which have indistinct (fluffy) edges. They are the
result of local ischemia which leads to disruption of axoplasmic flow.
Figure 5. Hard exudates are distinct yellow-white intra-retinal deposits
which can vary from small specks to large patches. They may evolve
into rings known as circinates and form large confluent plaques. Hard
exudates are composed of lipid deposits. In this respect, they are also
considered "true exudates."
Figure 6. Venous beading (arrow heads) is a sign of changes in the
hemodynamic characteristics of blood flow among diabetics. (Image
source: http://www.glostruphospital.dk/menu/Afdelinger/Oejenafdelingen/
Oculus/EURODIAB.htm)
Figure 7. (IRMA) Intraretinal microvascular abnormalities are areas
of capillary telangiectasia or dilatation. They are often seen in severe
non-proliferative diabetic retinopathy. IRMAs can be mistaken for
neovascularizations (NVEs) but, unlike NVEs, IRMAs are intra-retinal.
(Image source: http://www.glostruphospital.dk/menu/Afdelinger/
Oejenafdelingen/Oculus/EURODIAB.htm)
Figure 8.
from (A) the
importance of
or new vessel lorostor ar74.. 1
re 're ,ear-es -ore Wthemic. New blood vessels may arise
so
or, (B) else/bee it Pe mrire-. 3 re "mrri,
--ese
..seks are fragile and bleed easily. hence the
'waive retitimpatry.
Table 3 presents a summary of the various s--Laig -retinopathy and its hallmark characteristics. Awes show representative photograre's ci each stage
Table 3. Class''c.a-:'-
=
Disease Stage
-tatInary Cfaractie-&,
Non proliferative Diabetic z.
Mild
Moderate thow-ers's
Hard ex-cw1=4
1A3o-ter
In —I a -e—cr—a3m
Severe
Figure 9. 'A r `c,r -oiirferative Dooetrc Reonopathy with microaneurysms.
Ira--rers-rs ../..inceIntra-scra et A., da,=.
-
t.-J.2Sava:r
Cr
Proliferative Diabetic Retinopathy
Neovasallarzator ,/ re lsc Tot•?:.
Neovasc....ar-.mcr meanest
r
retina
Fbrora...Jar stia
Tracsona Reim Deactrierc
The primary goal in
prevention of visual loss
=,
of diabetic retinopathy
condition. Patients wit- deper
(IDDM ,Type 1 diabetes r- 7-s
be
ophthalmologic COIISLP.. 7-*
is of five yea•
already. All patients Cis. csed tc nave non
=c :ent
diabetes mellitus
Type 2 diabetes -re 7_:
:.` be
referred to an ophthalmologist at the time of 7 :7-,
a• OSiS.
Diabetic patients who complain of any vis..s
should be referred immediately to an eye spec s =r ;:' proper
evaluation. Pregnant women with history of c-ac-F.es should
Figure 10. Moderate Non-proliferative Diabetic Retincoany with typical
trims of multiple cotbn wool spot. had exudates and intra-relinai
11)1-
likewise be referred to an eye specialist for proper monitoring
of her ocular status for the duration of her pregnancy.°
Foremost in the management of patients with any stage
of diabetic retinopathy is strict blood sugar control."i°
Management of the eye condition will depend on the stage of
the retinopathy. Patients classified to have mild to moderate
8 SPECIAL TOPKS 1 82 Ocular Manifestations of Systemic Diseases
Eig
Figure 11. Severe Non-proliferative diabetic retinopathy with multiple
microaneurysms, soft exudates and diffuse intraretinal hemorrhages.
Figure 14. Grid Laser Treatment
sok
Figure 12. Proliferative Diabetic Retinopathy with new vessels (arrows)
at the disc and retinal periphery.
Figure 15. Focal Laser Treatment
Fiume 13. runduo Photograph* with tthetherthndino Ph nrocroin Anrurv!ra —
ti
non-proliferative diabetic retinopathy (NPDR) should have
regular fundus examination and fluorescein angiography6
(Figure 13). Grid or focal laser photocoagulation (Figures
14 and 15) should be considered for patients with severe
NPDR and/or clinically significant macular edema (CSME)."32
Panretinal photocoagulation (Figures 16 and 17) is the
treatment of choice for patients with proliferative diabetic
retinopathy.13 Complications such as vitreous hemorrhage and
traction retinal detachment (Figures 18 to 20) are managed
by vitreoretinal surgery.14
I
/
Figure 16. Panretinal pholumagulation
Fives 18. Vireos hemorrhage (arrows) can give rise to profound
(11 aeon the macula is obscured. Only a small amount of bleeding
espied since blood dissolved in the vitreous produces a haze effect
WWI =pan vision (and ophthalmic assessment).
Figure 17. Laser Saws seconds/ le iteerleellmet.
Medical management of diabetic setincipattle consists of
controlling the following risk faLlt.in, (1) blood SUgar interlSiVe
glycemic control lowered the risk of peogiession of diabetic
retinopathy to 17.1% from 49.29k" 0 blood pessuie tight
control of blood pressure (<15&85 nm Hg) led to /educed risk
of retinopathy progression's; (3) serum ipidT elevated levels
of serum cholesterol was associated with increased severity
of retinal hard exudates severity of hard exudates associated
with decreased visual acuity'607 and, (4) anemia: there was an
increased risk of high-risk PDR with decreasing hematocrit."
Figure 19. Subhyaloid hemorrhage (arrows) refers to accumulation of
*eels blood in areas of locaized detachment. Blood accumulates between
the retina and the vi re= and is often described as boat-shaped.
8 SPECIAL TOPICS I 8.2 Ocular Manifestations of Systemic Diseases LW
Figure 21. Macular Star - hard exudates at the fovea.
Figure 20. Retinal fibrosis and fibrc...as:_
a consequence of bleeding from tr'e -e...
traction on the retina, consequent ret,a
loss of vision.
-
.
as
-
II. HYPERTENSION AND
HYPERTENSIVE RETINOPATHY
Systemic arterial hypertension is one of the most common
diseases worldwide. More than half of the population over 60
years has hypertension's. Based on the 2004 International Data
base of the US Census Bureau'', there were an estimated 15.9
million people affected by hypertension in the Philippines (in
a population of approximately 86 million). In addition, there
may be another 4.8 million undiagnosed cases of hypertension
in the Philippines.19
Arteriosclerosis occurs as a result of intimal layer hyalinization,
medal layer hypertrophy and endothelial hyperplasia.
this presents as focal narrowing and straightening of
ine retinal arterial walls. Arteriovenous (AV) crossing changes
occurs as the condition progresses.'s
Gracing systems for hypertensive retinopathy have beer
preserved by various authors. The Keith Wagener Barke
(KWB) aassification26 was published in 1939 which classifies
the condition into four stages (Table 4).
Table 4. I i Wag en e r Barker Classification of Hypertensive Retinopathy
CHARACTERISTICS
Slight or modest narrowing of retinal arterioles,
..thAVratio>_ 1:2
The changes leading to primary systemic arterial hypertension
is multifactorial.'s In the elderly, an increase in basal smooth
muscle tone occurs as a result of sympathetic activity,
renin-angiotensin overactivity, cell membrane changes and
progressive architectural alterations in the vessel walls. Other
factors which contribute to this are salt sensitivity, volume
depletion and orthostasis.27.1s
Both prevalence and incidence of retinal microvascular
changes in hypertension varies widely from 2-15%.20-24 The
ocular picture is directly related to status of retinal arteries and
the rate of rise and degree of systemic blood pressure. Arterial
sclerosis occurs in the normal aging population (involutional
sclerosis) as well as in long standing hypertension.'s
Retinal manifestations of hypertension include vascular
constriction, leakage and arteriosclerosis.25'738
Vasoconstriction manifests as generalized or focal arteriolar
narrowing.2,18,25 Leakage occurs due to abnormal vascular
permeability and manifests as a variety of clinical signs: flameshaped hemorrhages, retinal edema, hard exudates and
optic disc edema (in cases of malignant hypertension) 2'7 '8
The presence of hard exudates in Henle's layer of the fovea
presents in a star-like configuration referred to as the"macular
star"5.25 (Figure 21).
Modest to severe narrowing of retinal arterioles
(focal or generalized), with AV ratio < 1:2 or AV
nicking
Ill
Above changes plus bilateral soft exudates or
ame-shaped hemorrhages
ly
Above changes plus bilateral optic disc edema
Scheie, in 1953, proposed a different grading system which
incorporated changes due to arteriolar sclerosis." This is
shown in Table 5 and Figures 22 to 24.
Vision threatening complications of hypertension include the
following (Figure 25):
1.
2.
3.
4.
Central retinal vein occlusion (CRVO)
Branch retinal vein occlusion (BRVO)
Central / branch retinal artery occlusion (CRAO / BRAO)
Anterior ischemic optic neuropathy (AION)
Recent studies have demonstrated an association between
hypertensive retinopathy and cardiovascular morbidity and
mortality.28 This is shown in Table 6.
Table 5. Scheie Classification for Grading of Hypertehs'.e Rs
GRADE
•-
Blood Vessel Changes
Arteriolar Reflex Changes
AV aossing changes
-•
I
broadening of the arter
II
obvious broadening of the airclar Igrc
III
copper-wire artenc es
IV
silver-wire artero es
Figure 22 Scree Classification based on Hyperte-s - (A )
artenotar narrowing. nerve fiber layer infarcts and blot Herr•,;--^age
changes
—_= - . - _
'''ierfr.
_ -anges
=SS-Ng changes
(B) Grade II: (C) Grade III; (D) Grade IV showing swollen optic nerve, retinal
8
SPECIAL TOPICS 18.2 Ocular Manifestations of Systemic Diseases GE
(C)
Figure 23. Arteriolar Reflex Changes: (A) normal: (B) broad light reflex or 'copper wiring;"
A
'silver wire"
B
C
Figure 24. Blood Vessel Changes: (A) Normal: (B) Tapering (C) Banking
A
Figure 25. Vaso-occlusive Diseases: (A) CRVO (B) CRAO
Table 6. Association of Hypertensive Retinopathy to Cardiovascular Morbidity and Mortality
Retinopathy
Mild
(KWB Grade I — II)
Moderate
(KWB Grade III)
Description
One or more of the following signs:
Generalized arteriolar narrowing, focal arteriolar
narrowing. AV nicking, arteriolar wall opacity
(silver wiring)
Weak associations with stroke, coronary
heart disease and cardiovascular mortality
Mild retinopathy with one or more of the
following signs:
Strong association with stroke, congestive
heart failure. renal dysfunction and
cardiovascular mortality
Retinal hemorrhages (dot/blot. flame-shaped).
microaneurysms, cotton- wool spots, hard
exudates
Accelerated
(KWB Grade IV)
Systemic Associations
Moderate retinopathy signs plus optic disc
swellingi maybe associated with visual loss
onal Materials in Ophthalmology 12nd Edition
Associated with mortality and renal failure
No
Hypertensive
Retinopathy
titer
Patient with
Hypertension
Medical
history,
examination,
appropriate
laboratory
investigation
and
management
fileimpolig
Retinal
Examinato"
•loireesige
zeircestor
Rooms Care
HI
• Routine Care
• Closer monitoring of vascular risk
• Exdude diabetes
• Closer monitoring of vascular risk
• Posible indication for treatment of
hypertension and other risk factors
Urgent hypertension treatment
• Consider ophthalmology referral
in selected patients (e.g., borderline
hypertension with other target
organ damage, patients with diabetes,
patients with visual symptoms)
Figure 26. Proposed Flow Chart for the Itrapeitca' WINNOIsisime
Hypertensive retinopathy has also ee glamor ti be
associated with:
1.
2.
3.
Diabetic retinopathy - hoiVerVirsOn tortmed
progression of DR
Age-related macular oeoere•atccr - .14wrierision
increases the risk for Al0C--: Seaver err ,E-se, Study'
Glaucoma - Hypertensor r"..w Arcliesset~e, risk and
development of glaucoma-I`
The primary management of OC.1.7(
1550Cialled
with hypertension is adequate brood pais..re. control
-
Homosexuals and bisexuals
Health workers
Prevalence of HIV infection in the Philippines remains low at
less than 0.1% of the adult population.3° Data gathered in 2009
estimated 8,700 people living with HIV/AIDS. As of 2010, the
Department of Health has reported 315 AIDS-related deaths.
While the Philippines is perceived as a low-HIV prevalence
country, incidence had increased by 25% from 2001 to 2009.
From 2007, the number of reported cases has doubled every
two years, suggesting that two new cases of HIV/AIDS are
reported daily (DOH, 2009)."
Figure 26 shows the summed .nanage.7-e
—rti:r ryzeetensive
retinopathy.
For complications such as vascular occiLsors, Dose follow-up
by an ophthalmologist is reconvneno= - .user treatment is
performed whenever indicat-?,-.!
III. ACQUIRED IMMUNE
DEFICIENCY SYNDROME
Infection with the numan drirnonooeuciency virus ( HIV) causes
immune system suppression of patient which subsequently
allows opportunistic infections and neoplastic conditions to
affect the eye. Individuals at risk of acquiring this infection
include the following
•
People receiving transfusions
•
IV drug users
•
•
•
•
Healthy sex partners of infected patients
Babies born of infected mothers
Hemophiliacs
Prostitutes, sex workers
Ocular manifestations of HIV/AIDS include the following:
•
•
dry eye
retinal microangiopathy often manifested as cottonwool spots
opportunistic infections commonly presenting as
Cytomegalovirus (CMV) retinitis
tumors like Kaposi's sarcoma of the lids or conjunctiva
neuro-ophthalmologic lesions
Cotton wool spots (Figure 27) are the most common finding
in these patients. It is found in 100% of HIV infected patients.
Cotton wool spots may be associated with retinal hemorrhages
and microaneurysms. Patients are usually asymptomatic and
these lesions may disappear spontaneously. It is proposed
that this occurs as a result of immune complex deposition
and/or HIV infection of retinal vascular endothelium.
Cytomegalovirus (CMV) retinitis (Figure 28) affects 40% of
patients with AIDS. Its presence signifies severe systemic
S SPECIAL TOPICS 1 82 Ocular Manifestations of Systemic Diseases El
Figure 27. Cotton wool spots (arrows) in a patient with HIV infection.
Figure 29. Kaposi's Sarcoma of the conjunctiva
(http://www.itg.be/itg/distancelearning/lecturenotesvandenendene/
imagehtml/ppages/cd_1082_084c.htm)
thyroid dysfunction." Aside from Grave's ophthalmopathy or
orbitopathy, this autoimmune eye condition is also known as
•
•
•
•
Figure 28. CMV retinitis in a patient with HIV infection
involvement. This condition may however occur in other
immunodeficiency states.
Kaposi's sarcoma (KS) is a tumor caused by human herpes
virus 8 (HHV8), also known as Kaposi's sarcoma-associated
herpes virus (KSHV). It was first described in 1872 by Moritz
Kaposi (KA-po-she), a Hungarian dermatologist .31 AIDSassociated Kaposi sarcoma or KS-AIDS presents with skin
lesions that typically start as one to several red to purple-red
macules, rapidly progressing to papules, nodules, and plaques.
Unlike the classic form of Kaposi sarcoma, KS-AIDS is often
seen on the head, back, neck, muscular palate and the area of
the gingiva" (Figure 29).
Since ocular manifestations often imply severe systemic
involvement, management should be closely coordinated
with an infectious disease expert.
IV. THYROID EYE DISEASE
It was Robert Graves, in 1835, who described signs of thyroid
disease, including exophthalmos. His name has since
become an eponym for an eye condition associated with
Thyroid Related Eye Disease (TRED)
Thyroid Eye Disease (TED)
Thyroid-associated orbitopathy (TAO)
Dysthyroid orbitopathy / ophthalmopathy
While most patients with this condition present wit h
hyperthyroidism and eye signs simultaneously, the oculz
involvement may lag behind or even precede the endocrin e
manifestations. In some instances, the eye condition ma y
even present in the absence of any evidence of thyroi d
dysfunction."
Among patients with thyroid disease, thyroid eye disease
occurs in 37.5% (25% — 50%). Severe eye disease develops in
3-5%. Women are affected five times more often than men.
Smoking is a significant risk factor in the development of
thyroid eye disease.34 Ocular involvement may be unilateral or
bilateral. Symptoms may include excessive redness, tearing,
itching, pressure, puffiness and pain.
The pathophysiology of the eye findings of Grave's disease
remains obscure although it is widely accepted to be an
autoimmune disorder. For still unknown reasons, the body's
host inflammatory cells attack tissues around the eye,
specifically, the orbital fat, the directional eye muscles, and the
muscles in the eyelid."
Unilateral or bilateral lid retraction (Dalrymple's sign) is the
most common sign ofTED.2,5" As a result of lid retraction, the
upper lid margin is at or above the superior limbus. This may
be due to sympathetic overdrive affecting Mullers muscle,
fibrosis of the muscles elevating the lid, or hypotropia.'
TED is the most common cause of unilateral or bilateral
proptosis in adults.2-5 Proptosis is due to inflammation of the
extraocular rnueidesand orbital fat, causing anterior protrusion
of the globe and sometimes, optic nerve compression in the
relatively confined bony space of the orbit. However, signc
optic nerve compression can still occur without mar.
3proptosis.' Proptosis or exophthalmos can be measur,
an exophthalmometer. Although exophthalmometry
proptosis can be determined by viewing the patient°. Digital palpation through the patient's closed eyed
used to estimate orbital compliance.
Lid retraction together with exophthalmos ones riseiovahr
s7
._ §
often referred to as the "Thyroid Stare' (Koc'Ner
Other common signs of TED are lid lag
Graefe's sign), injection over the recti
In scesotropia and hypotropia.25"5
Figure 31. Soft tissue involvement = Class 2
extraocular muscles may enlarge resuitito limited motility of the eye. Thyroid eye
affects the medial rectus and fallen:
accounting for the appearance of esonoc
Initially the muscles are swollen and dw
over the recti insertions. Later the rnindm
Figure 32. Proptosis = Class 3
__
The severity of thyroid eye diseasecan
to the "NO SPECS" classificatiork dereteeed tar livalerer*
(Table 7 and Figures 30 to 35
Table 7. Classification of Thyroso Cr: ::atv
Figure 33.- Extraocular Muscle Involvement = Class 4
2
Solt tissue
involvement
3
Proptosis
eibillorat torizeitelf
call Web=
Otsti tteetisia•
PIWCW
Table 8. Clinical Assessment Score for Thyroid Eye Disease
some
4
EXtra0CuiF
Pain
involveTe-:
5
Corneal invotverervt
6
nerve imiaved
Disease activity is assessed using the Clinical Assessment
Score (CAS) of Mouritsr (Table 8). For every criterion met,
one point is assigned. A CAS of 3 or less responds poorly to
immunosuppressive therapy, indicating that these patients
have passed the stage of active inflammation. A CAS of 4 or
more responds well to corticosteroid therapy.38
•
Stanng vlMtt fluoresce n
Ulceration. infiltrate.
certration
Pain on attempted movement over the last 4
weeks
Redness
:
•
iecease
:ss
7e valor
Pain at rest on or behind the eye over the
past 4 weeks
•
Redness of one or both eyelids
Diffuse conjunctival congestion involving at
least 1/4 of eyeball
Swelling
•
Swelling of one or both eyelids
•
Chemosis
Swollen caruncle
Proptosis increasing .? 2 mm over past 1-3
months
Loss of
Function
8
•
Reduced eye movements 5° in any
direction over 1-3 months)
•
Decreased pinhole visual acuity by
on Snellen's chart over 1-3 months
1 line
SPECIAL TOPICS 1 8.2 Ocular Manifestations of Systemic Diseases
179
may present even when the patient is in an euthyroid state.
Extraocular muscle involvement may be documented using
radiologic examinations which will reveal extraocular muscle
enlargement."
It is common for thyroid eye disease to fluctuate within the
first few years of the disease. Beyond this time, the disease
usually attains a stable condition. The disease may however
continue to progress even when the patient's thyroid status
is controlled.
Figure 34. Corneal Involvement = Class 5
Treatment of congestive phase include local therapy with tear
substitutes and lubricants to help to protect the surface of the
eye from drying. Head elevation particularly while sleeping
reduces swelling around the eyes.'
Double vision can be troublesome if it affects straightforward
and down-looking positions. Special lenses called prisms
may be used to relieve this. In some instances, patients may
also benefit from strabismus surgery.s•'•35 Steroids are used
in selected cases. Since steroid use may cause a number of
undesirable side effects with chronic use, they are only given
as a temporary measure. Radiation is also utilized to reduce
swelling of periocular tissue and subsequently decompressing
the optic nerve?•34.35 When vision is threatened, early lid
or orbital decompression surgery may be necessary.7•34.35
Otherwise, surgery is usually reserved for stable, inactive
or the cicatricial phase of the disease with the following
possible complications: abnormal staring appearance; severe
protrusion of the eyes; disturbing double vision not relieved
by prism glasses and drooping or sagging of tissues around
the eyes.
Because of its complexities, thyroid eye disease is best managed
with a team approach consisting of an endocrinologist and an
ophthalmologist.
V. TUBERCULOSIS
Figure 35. Sight Loss = Class 6. Usually due to compression of optic
nerve by swollen muscles (arrow).
Less serious complications of TED are tearing, foreign body
sensation, lid and conjunctival edema / chemosis. More
serious complications include exposure keratitis, diplopia,
ophthalmoplegia and loss of vision.57
Loss of vision usually results from compression of the optic
nerve by swollen tissues surrounding the eye. Urgent
treatment is required otherwise visual loss can be permanent.
Other complications include glaucoma and exposure of the
anterior surface of the eye resulting from the inability to
completely close the eyelids5•'
There is no single laboratory examination that will confirm the
presence of thyroid eye disease. As was mentioned earlier,
the condition is not related to thyroid hormone levels and
According to the World Health Organization (WHO) report
201039, one-third of the current world population is infected
with the tubercle bacillus. Five to ten percent of these
eventually get sick. In 2008, the largest number of new TB
cases was found in the Southeast Asian region, accounting for
35% of all new cases."
In the Philippines, the incidence ofTB was reported to be 284.8
per 100,000 population in 2008.4°
Ocular involvement in tuberculosis can be caused by either
direct invasion of organism, or as a result of hypersensitivity
reaction to tuberculoprotein.18 Ocular involvement is more
common in patients with miliary tuberculosis, although, it
may also be seen in patients with no evidence of pulmonary
disease.
T
Figure 37. Other Manifestations of Ocular TB: (A) choroidal tubercle
(B) phlyctenulosis (C) retinal periphlebitis
Figure 36.
(B) Busacca -cc..
(A) •cera::
(C) KDezoe -oc es
8
SPECIAL TOPICS I 8.2 Ocular Manifestations of Systemic Diseases
181
The most common manifestation of TB in the eye is
granulomatous uveitis (anterior and/or posterior; (Figure 36).18
Other manifestations (Figure 37) are:
Phlyctenulosis — conjunctival condition featuring a
phlyctenule, which is a small pinkish white nodule
near the limbus, believed to be a non-specific delayed
hypersensitivity reaction
•
Vitritis — inflammation of the vitreous
REFERENCES
2.
3.
Retinal periphlebitis — inflammation of the retina~~
•
venules
4.
Choroidal tubercles — choroidal masses believed to
contain tubercle bacilli. Histopathologically, they
represent caseating granulomas'
5.
Panuveitis — inflammation of the entire weal tract
choroid, ciliary body and iris
6.
The ocular inflammatory condition associated with TB is
usually treated with topical and/or systemic corticosteroids. 7.
It is however, imperative that patients be treated with the
appropriate anti-TB medication prior to institution of the
anti-inflammatory regimen to avoid exacerbation of the
8_
systemic infection.
SUMMARY
The importance of being able to recognize ocular signs,
symptoms and complications of many systemic diseases is a
vital part of good medical practice. It is therefore necessary
for the primary care physician to be able to perform a
thorough eye examination, particularly that of the fundus.
Early diagnosis of the conditions earlier discussed, in
particular diabetic retinopathy is crucial in the ultimate
outcome of treatment.
This instructional material is by no means complete. Only
conditions that are more commonly encountered in local
practice have been emphasized. Additional reading is
recommended to supplement the information provided.
RECOMMENDED READING
Other systemic diseases with ocular manifestations:
•
Sickle-cell Retinopathy
•
Collagen-vascular diseases:
Rheumatoid Arthritis (RA), Systemic
Lupus
Erythematosus (SLE), Polyarteritis Nodosa (PAN), etc.
•
Blood dyscracias
Leukemia, anemia, hyperviscosity states
Others:
Sarcoidosis, Herpes Zoster, Leprosy
9.
American Academy of Ophthalmology Preferred
Practice Patterns Committee. Preferred Practice
Pattern® Guidelines. Comprehensive Adult Medical Eye
Evaluation. San Francisco, CA: American Academy of
Ophthalmology, 2010.
Ka nski JJ. Clinical Ophthalmology:A SystematicApproach,
ed 3. Oxford: Butterworth-Heinemann, 1994.
Cubillan LDP, Olivar-Santos EO. Third National Survey
on Blindness. Phil J Ophthal 2005; 30 (3): 100-114.
http://vision2020.org/main.cfm?type=WIBDIEBETIC.
May 18, 2011
Tang RA, Coleman AL, Wilkins JK, Brown J, Newman
SA, Skootsky S, Whitcup SM: Ocular Manifestations of
Systemic Disease: A Slide-Script Program. San Francisco:
American Academy of Ophthalmology, 1996.
American Academy of Ophthalmology Retina
Panel. Preferred Practice Patterns Guidelines. Diabetic
Retinopathy. San Francisco, CA: American Academy of
Ophthalmology; 2008
Federman JL, Gouras P, Schubert H, Madison Slusher M,
Vrabec TR. Retina and Vitreous, in Podos SM, Yanoff M
(eds): Textbook of Ophthalmology, Vol 9. London: Mosby,
1994.
Diabetes Control and Complications Trial Research
Group. The relationship of glycemic exposure (HbA1c)
to the risk of development and progression of
retinopathy in the Diabetes Control and Complications
Trial. Diabetes 1995;44:968-83
Diabetes Control and Complications Trial Research
Group. The effect of intensive treatment of diabetes
on the development and progression of long-term
complications in insulin-dependent diabetes mellitus.
N Engl J Med 1993;329:977-86.
10. Diabetes Control and Complications Trial Research
Group. The effect of intensive diabetes treatment on
the progression of diabetic retinopathy in insulindependent diabetes mellitus. The Diabetes Control and
Complications Trial. Arch Ophthalmol 1995;113:36-51.
11. Early Treatment Diabetic Retinopathy Study Research
Group. Photocoagulation for diabetic macular edema.
Early Treatment Diabetic Retinopathy Study report
number 1. Arch Ophthalmol 1985;103:1796-806.
12. Early Treatment Diabetic Retinopathy Study Research
Group. Treatment techniques and clinical guidelines
for photocoagulation of diabetic macular edema.
Early Treatment Diabetic Retinopathy Study report
number 2. Ophthalmology 1987;94:761-74.
13. Diabetic Retinopathy
Study Research Group.
Indications for photocoagulation treatment of diabetic
retinopathy: Diabetic Retinopathy Study report number
14. Int Ophthalmol Clin 1987;27:239-53.
14. Diabetic RetinopathyVitrectomy Study Research Group.
Early vitrectorny for severe vitreous hemorrhage in
diabetic retinoperhy_ Four-year results of a randomized
15.
16.
17.
18.
19.
trial: Diabetic Retinopathy Vitrectomy Study report 5.
Arch Ophthalmol 1990;108:958-64.
UK Prospective Diabetes Study Group. Tight blood
pressure control and risk of macrovascular and
microvascular complications in type 2 diabetes: UKPDS
38. BMJ 1998;317:703-13.
Klein R, Klein BE, Moss SE, et al. The Wisconsin
Epidemiologic Study of Diabetic Retinopathy. IX. Fouryear incidence and progression of diabetic retincipathy
when age at diagnosis is less than 30 years. Arch
Ophthalmol 1989;107:237-43.
Klein R, Klein BE, Moss SE, et a I.The Wisconsin Epcierniaiolic
Study of Diabetic Retinopathy. X. Four-year incidence and
progression of diabetic retinopathy when age at diagnosis
is 30 years or more. Arch Ophthalmol 19619007:244-9.
Schachat AR Murphy RP (eds). Medical Rank in Ryan. Si
(ed): Retina, ed 2. St Louis: Mosby, 199k
atshttp://www.cureresearch.com/h/hyper
country.htm. May 22, 2011
20. Klein R, Klein BEK, Moss SE. The relation of systemic
hypertension to changes in the veinal mouse
Sac
the Beaver Dam Eye Study. Trans Ass
1997;95:329-48.
21. Wang JJ, Mitchell P, Leung H. et atitvenissitesetinall nal
signs in a general older population the ire Mountains
Eye Study. Hypertension 20014Z53,11-41
22. Wong TY, Hubbard LD, Klein 111„ et allleand alba.
sarcoma May 22, 2011
33. httpi/www.thyroid.org.aunhySociThySocTED.html May
21,2011
34_ Cawood T, Moriarty P, O'Shea D. Recent developments in
thyroid eye disease. BMJ 2004; 329:385-90
i sea se May
htflx//eirmitipeciaorg/wikinhyroid_eye_d
35.
21,2011
36. Werner SC. Modification of the classification of the eye
changes of Graves' disease: recommendations of the Ad
Hoc Committee of the American Thyroid Association. J
Qrr Endocinol Metob 1977;44:203-4.
37_ Mounts MR Koornneef L, Wiersinga WM, Prummel
Berghout A. van der Gaag R. Clinical criteria
for the assessment of disease activity in Graves'
ophthalmopathy: a novel approach. Br. J. Ophthalmol.
1989; 73,639-644
38 Mounts MR Prummel MF, Wiersinga WM, et al. Clinical
activity score as a guide in the ma nagement of patients
with Graves' ophthalmopathy. Clin Endocrinol (Oxf)
1997;47:9-14.
39_ httpJ/www.who.int/med iacentre/factsheets/fs104/
en/ May 21, 2011
40. http://www.tradingeconomics.com/philippines/
incidence-of-tuberculosis-per-100-000-people-wbdatahtml May 21, 2011
41. Helm CJ, Holland GN. Ocular tuberculosis. Sury
0ohthalmol 1993;38:229-56
abnormalities and blood pressure is older
the Cardiovascular Health Sind, ft .1 Ophr-
2002;86:1007-13
23. Klein R, Sharrett AR, Klein BE. et al. Ise reinal artier,:
24.
25.
26.
27.
abnormalities related It) allhandlerosis?
Atherosclerosis Risk in Commingles SIN* Anelosder
Thromb Vosc Biol 20002a1644-50
Couper DJ, Klein Ft, Hubbard L. et at Illelabilty of retinal
photography in the assessment of retinal miamescular
characteristics. The Atherosclerosis Illsk M Communities.
Study. Am J Ophthalmol 200Z13:178-416
Yanuzzi LA, Guyer, DR, Green.ViR AreMinaAtkli
St Louis:
Mosby, 1995.
Keith NM, WagenerHP,BarkerMACSomediferent types of
essential hypertension: their course and prognosis
' . Am J
Med Sci 1939; 197: 332-43_
Scheie HG. Evaluation of ophthalmoscopic changes of
hypertension and arteriosderosisArdr Ophthalmo/ 1953;
SELF-TEST
_a:
of func....s pictures.
Picture 1. Identify the encircled lesions. Give a
diagnosis.
v\70 -612,1iAcontosh R Hypertensive
retinopathy signs as
risk
indicators of cardiovascular momidity and mortality
Br Med Bull 2005;73 and 7457-70
29. Mitchell
P, Lee AJ, Rochtchina E, Wang IL Open-angle
glaucoma and systemic hypertension: the Blue Mountains
eye study. J Glaucoma
2004; 13: 319-26
30. http://www.usaid.gov/our_work/g
loba l_hea Ith/a ids/
Countries/asia/philippines _profile.pdf May 21,2011
31. http://en.wikipedia.org/wiki/Kaposi%27s_sarcoma
May
22,2011
32. httpi/en.wikipedia.org/wiki/AIDS-associated_Kaposi_
a SPECIAL TOPICS 182
Ocular Manifestations of Systemic Diseases
183
Picture 2.
Using Scheie Classification, give the stage
In order to prevent diabetic retinopathy from becoming
the world's leading cause of blindness, the following
should be done:
1.
of hypertensive retinopathy
A.
regular and proper eye examination for individuals at
risk
B. aggressive oral hypoglycemic therapy for type II
diabetics
C. aggressive insulin therapy for type I diabetics
D. proper diet and exercise for the elderly population
2. A 4 year old male consults for a small pinkish white
nodule near the limbus. You will order for:
A.
B.
Fasting Blood Sugar and HbA1 C
Chest X-ray and PPD
C. HIV test
D. T3 and T4 determination
3.
Picture 3. In what disease condition is this fundus
picture associated? What are the abnormal findings?
A 45-year-old male consulted a doctor for a bulging left
eye. He was advised to undergo an MRI. Because of the
expense involved, he decided to seek a second opinion
from you. You will:
&
B.
C.
D.
4.
Routine eye examination of a 57 yr. old hypertensive
"Idle patient revealed exudates and hemorrhages all
over the fundus with distinct disc borders and an AV
ratio of 1:3. This patient will have:
A. An early cataract
•
C.
D.
Picture 4. In what disease condition is this fundus
picture associated? What are the abnormal findings?
orcer a CT scan instead
go on with the MRI
order a T3 &T4 determination
order an HIV test
Concomitant diabetic retinopathy
A strong association with stroke and cardiovascular
mortality
Renal failure
S. In the management of diabetic retinopathy, the
folrowing will apply:
aaloetics of > 2 years duration should be
referred to an ophthalmologist
A diabetic maintained on oral hypoglycemic for the
past 8 years should be referred to an ophthalmologist
as soon as possible
C. Panretinal photocoagulation should be considered in
background retinopathy
D. Type 2 diabetics of > 5 years duration should be
to an ophthalmologist
B.
6.
A 68-year-old male has had a history of BPs ranging
from 170-200 100-120. On ophthalmoscopy one would
commonly expect to find:
constriction
:
=per-vile venule
.-
hernorrhage
7.
On routine ophthalmic examination, an asymptomatic
28 year old guest relations officer (GRO) was found
to have a small, solitary whitish lesion with binned
margins on the left fundus. You will order for:
A. T3 &T4 determination
B. fasting blood sugar
C. serum cholesterol
D. HIV test
9. In the progression of Grave's ophthalmopathy the
following may be encountered:
"thyroid stare" resulting from the combination of lid
lag and lid retraction
B. a "frozen" eyeball
C. sudden, painless loss of vision
D. consistently abnormal thyroid hormone levels
A.
10. Mild nonproliferative diabetic retinopathy is best
8.
A 50-yr old female who has had Type 2 diabetes farthe
last 10 years consults for blurred vision. Yon nought
A.
B.
look for vitreous hemorrhage
a ierrai
order ultrasound examination tc
detachment
C. examine for corneal defects wrtr a ocrlicr:.- xre
D. do a thorough retinal examination
managed with:
A.
B.
:17
D.
panretinal photocoagulation and strict blood sugar
control
vitreoretinal surgery and endolaser treatment
control of risk factors and regular fundus fluorescein
angiography
pulse insulin therapy and regular eye exams
Answers to self-test on page 222.
8 SPECIAL TOPICS 1 8.2 Ocular Manifestations of Systemic Diseases
185
8.3 Eyelid Ma' positions
Franklin P. Kleiner, MD
INTRODUCTION
This self-instructional material is designed to help tne student learn the basic concepts of eyelid malpositions, their classificatior
pathophysiology, diagnosis and management
The eyelids are important accessory structures that give support and complement the proper functioning of the eye. Every
student of ophthalmology should be able to recognize eyelid malpositions, and know theoretically their pathophysiology arc
management.
OBJECTIVES
Upon completion of this unit of instruction, the student should be ate to recognize the four basic eyelid malpositions and knov,
the basic concepts of their diagnosis and management. Specifically they shouici be able to:
1.
2.
3.
4.
5.
Define and recognize the four basic lid malpositions: Ectropion, Enbopion, Ptosis and Lid Retraction.
Discuss the pathophysiology of the different types of Ectropion. E—tropion, Ptosis and Lid retraction.
•e.--action
Classify the different types of Ectropion, Entropion, Ptosis and
Discuss the diagnostic maneuvers performed to evaluate the feu- malpositions
Discuss the principles of management of each of the four lid rnalcostions.
CONTENT
I.
Anatomy of the eyelid
II.
Basic Lid Malpositions
A. Ectropion
B. Entropion
C. Ptosis
D. Lid retraction
I. ANATOMY OF THE EYELIDS
The eyelids are important accessory structures that give
support and complement the proper functioning of the eye
They provide protection, support and lubrication for the eye
to enhance its proper functioning, particularly vision_ Ai
abnormality or irregularity of the position of the eyelids can
have drastic effects on the eye and its function.
To understand the malpositions of the eyelids, a short 'edam'
of the anatomy and physiology of the eyelid retractors and
protractors and other pertinent eyelid structures (Forms 1.
2) is helpful.
The eyelid can be divided into two layers. the artErizr
which consists of the skin and orbicularis and the posperior
lamella which consists of the tarsus and the cony :Acme
orbital septum and lid retractors are structures bertneenne-ye
two lamella.
reflex closure while the periorbital portion is responsible for
.•oluntary closure_
-evator Palpebrae Superior's
".'r•Jr.m Sulam
=ni-wieuratc
Muller s Muscle
Accra-mos
Rpm 11.-Asestsi d re Eyelid Schematic cross section of upper eyelid
The levator muscle originates from the annuiliscfZevt. 510*
above the superior rectus muscle. It is in dote, asspowcir wre-grr., t
the superior rectus muscle almost throstpout
held up and supported by the Whitnallt liga-rert. arc
the eyelid its muscle fibers terminalleillo a broad ieriircts
sheet, the levator aponeurosis, which ir-sers ruc
portion of the anterior surface of the 1:35.5 Ber- ^^e e, and superior rectus muscles are inne-ia.L-t1
branch of the 3-3 cranial nerve. and its fr-rincr- s r ape''
eyelid.
Closely associated with ti-e
i'.^-oattielic nerves. f
This is a lid retractor 7h5
angirialEs from
function is eyelid open:- a as v
the underside of the belly of the reeler mi..sdie and inserts on
the superior tarsal border_ tt ies between Me *valor muscle
above it, and the palpebral conjunctivae below, it_ It can be
recognized by the vertical oriel-upon ales muscle fibers, and
the superior palpebral arcade of blood vessels which wave
on top of it, along the superior tarsal Nyder.
The protractor of the eyelid is the orbicularis tint'' muscle,
which is responsible for eyelid dosue It is the antagonist of
the levator muscle. It is a circidat skier musde vbilich
beneath the skin of the eyelids ad originates from the rn..:
canthal tendon_ It has three portions the pretarsall preseptal
and periorbital portions The pietarsal portion forms the
innermost circle, and overlies the tarsus of the upper and lower
lids. The preseptal portion forms the middle circle and overlies
the septum. The outermost circle is formed by the periorbital
portion, which overlies the orbital rim and bone The orbizulais
muscle is innervated by the facial nerve (N VII).The
anal and
preseptal portions are responsible for involuntary c
F.. -
Merlon tarsal muscle
biension of retractors to
iideriog fornix
Lockwood's
ligament
Inferior rectus
muscle
Capsulopalpebral
head
Swan
Orticeilirts oaf
wmescie
Figure 2. Anatomy of
Inferior oblique
muscle
the Eyelid Schematic cross section of lower eyelid
II. BASIC EYELID MALPOSITIONS
-here are four basic eyelid malpositions: ectropion, entropion,
blepharoptosis or ptosis, and eyelid retraction.
A. ECTROPION
Ectropion is the outward turning of the upper and/ or lower
eyelid margin. It can be easily recognized in patients due to
the everted position of the lid margin, which creates a space
or gap between the palpebral conjunctiva and the globe.
In severe cases, this eversion leads to visualization of the
palpebral conjunctiva. If the ectropion is carried medially, one
may even visualize the punctum, which is normally not visible,
since its normal position is in apposition with the globe.
8 SPECIAL TOPICS 18.3 Eyelid Malpositions
Etiologic classification of ectropion is as follows:
1. Senile involutional ectropion
2. Paralytic ectropion
3. Cicatricial ectropion
4. Congenital ectropion
5. Mechanical ectropion
SENILE INVOLUTIONAL ECTROPION
As we age, our tissues tend to stretch out and become lax.
Patients who constantly rub their eyes can hasten this process.
The eyelid tends to stretch out and lengthen, especially at the
canthal tendons. Excessive eyelid laxity can result in ectropion
Figure 5. Eyelid distraction test
(Figure 3).
Signs and symptoms are tearing due to the interrupted flow
of tears from the lateral to the medial canthus, interruption of
the tear meniscus and lacrimal pump, and at times even due
to an everted punctum (see medial ectropion). In more severe
cases.. reflex tearing occurs due to irritation from dry eye or
exposure keratitis. Patients may also present with superficial
portraits keratitis and corneal opacification. Irritation and
dryness of the conjunctiva is common.
Figure 3. Senile involutional ectropion of the right lower eyelid
Eyelid laxity can be tested with the snap back test
(Figure 4). This is done by pulling the eyelids downward
toward the orbital rim, then letting them go. Normally, the
eyelids snap back to their original position, even without the
blinking. However, if there is laxity in the patient's eyelids, the
lids do not snap back, but instead go back up slowly. The lids
may return to their original position, however, in instances
when they have become very lax, they may stay everted and
return to their original position only upon blinking.
Sende involutional ectropion is best treated by a horizontal
eyelid tightening procedure. Examples are lateral tarsal strip
operation and id shortening procedures such as a wedge
resection tithe tarsus. Figure 6 shows a patient with senile
involutional ectwopion before and after surgical correctior
with a tarsal strip procedure.
Figure 4. Snap back test
Another test is the eyelid distraction test (Figure 5) wherein
the eyelid is pulled away from the globe to see how far it can
stretch out. Stretching of 6 mm or more confirms the presence
of laxity.
Flume t him air Senie Involutional Ectropion of both lower lids.
(A) shims lie port st.rgery Note that ectropion of left lower lid is
wasetitsetihteflsle iqt (B) snows the same patient after tarsal strip
procedget.
_. ___I •
I 11-tri Frlitinn
PARALYTIC ECTROPION
When the orbicularis oculi becomes paralyzed in affectations
of the facial nerve (CN VII), there is loss of eyelid tone. This
is reversible in temporary cases such as Relitlolley_ Set
prolonged cases, such as a stroke, or CN VII palsy or paresis,
atrophy of the muscle can occur resulting in more per— =
laxity of the eyelid (Figure 7).
of
earopion is done by checking on the
ughtness of the ulterior lamella, checking while the patient is
in upgaze or with the mouth open.
huger ent invokies lengthening of the existing anterior
lamella. Depereing on the severity of the condition,
lengliening d the anterior lamella may be done by scar
endtkiliand zunlasty or skin grafts (Figure 8).
In temporary conditions, lubrication with articial 115114
ointments, and in worse cases, goggles or moist dwi:
may be beneficial. Punctal plugs may be inserted as
Patient's eyelids may need to be taped togedieratbedifirr
avoid corneal exposure.
If corneal exposure is expected to be
period of time, tarsorrhaphy or suturing of may be done to effect closure. Another oc of a gold weight in the upper lid of a
ectropion. The implanted gold weigr
due to gravity.
77--4"r7-
Figure 8. Patent with Cicatriciai Ectropion prior to surgery (A) and
timing skin grafting procedure (B).
CONGENITAL ECTROPION
This is a form of cicatricial ectropion, usually due to shortage
of anterior lamella since birth. The condition usually occurs in
conjunction with some other congenital conditions such as
blepharophimosis.
MECHANICAL ECTROPION
kaki lower Id (A)_ Nose
Figure 7. •7-a:e--: eirr ,;:ezra.fsc
patient's inabilitytolidedimillselellegekts (B)
Tie presence of a mass or iump in the lower eyelids may weigh
down on the lid and make it ectropic. Management in these
cases is excision of the mass, whenever possible.
CICATRICIAL ECTROPION
In the normal eyelid there is a balance between the anterior
lamella and the posterior lamella_ If there is shortening of
the anterior lamella (skin and orbicularis muscle), cicatiical
ectropion can occur. Some conditions that can cause this are
scarring of the eyelid skin due to trauma, healed lacerations.
thermal and chemical burns, healed infections or abscesses,
and longstanding chronic infections of the lid
B. ENTROPION
Entropion is the inward turning of the eyelid margin (Figure 9). This
inward rotation of the eyelid margin results in loss of visualization
of the lid margin. The lashes are also turned in and rub against
the globe. There is frequent irritation, redness and possibly
discharge of the eye. Patient complains of constant irritation and
frxeign body sensation caused by rubbing of the lashes against
8
SPECIAL TOPICS I c.3 Eyelid Malpositions
189
Conservative management includes the use lubricants
and ointments to prevent rubbing of the lashes against
the cornea and taping of the eyelid in an everted position.
Surgical intervention is needed for definitive management of
entropion.
Entropion can be classified into the following types based on
their etiology or cause:
Figure 9. Entropion of the lower lid
the cornea. In severe cases, corneal abrasion and scarring
may occur, subsequently causing decrease in visual acuity.
Entropion can also result to infections of the cornea or corneal
ulceration, which if left untreated can lead to rupture of the
eye.
One should also examine the lid margin under slit lamp for
conjunctivalization of the lid margin. Its presence signifies
chronicity of the condition. One may even detect the mildest
of entropions with this technique.
The normal mucocutaneous junction along the lid margin lies
posterior to the meibomian glands. If the mucocutaneous
junction looks like it has advanced to the level of the meibomian
glands, or even more anteriorly, to the gray line, or the lash line,
this implies that the posterior portion of the lid margin is in
apposition with the globe, making the posterior portion of the
lid margin conjunctivalized. One should also examine the lid
margin under slit lamp to check for its conjunctivalization. This
is a telltale sign of chronic entropion.
Entropion must also be differentiated from trichiasis (Figure 10)
which is the inward turning of lashes and from distichiasis
which is the presence of extra row of lashes, usually from the area
of the meibomian gland orifices.
1.
2.
3.
4.
Cicatricial entropion
Senile involutional entropion
Congenital entropion
Spastic entropion
CICATRICIAL ENTROPION
Cicatricial entropion is caused by scarring of the posterior
lamella of the eyelid, the conjunctiva and tarsus. This scarring
causes a deformity of the tarsus, causing it to rotate inwards
permanently. Frequent causes of scarring are chronic infection
of the eyelids, trauma, chronic irritation from artificial eye
use in the anophthalmic socket, inflammatory conditions of
the conjunctiva such as pemphigus, pemphigoid or Stevens
Johnson Syndrome and systemic diseases such as leprosy.
Cicatricial entropion, being caused by a permanent deformity
of the tarsus, is best managed by surgical correction.
Depending on the severity of the entropion, management
may be a wedge resection of the eyelid, a lid margin rotation
procedure such as a tarsotomy or a grafting procedure to
replace the severely deformed tarsus.
SENILE INVOLUTIONAL ENTROPION
Senile involutional entropion is caused by aging and laxity of
tissues. There are four factors that come into play causing the
inward turning of the eyelid margin:
1. lid laxity
2_ preseptal orbicularis overriding the pretarsal
orbicularis
1 detachment or dehiscence of the lower lid retractors
4 involutional enophthalmos
Detactwrent or dehiscence of the lower lid retractors
to the instability of the lower border of the
- -n combined with lid laxity and overriding
ai rag orcitza:-Ls muscle, causes the eyelid to flip inwards.
1111111111111Menophthalmos is not always present, but may play
Figure 10. Trichiasis (red arrow heads)
~~cicatricial from senile involutional
• ng test: Press on the lower lid to return
position. If upon releasing it, the
entropic
pfl
into an entropic position, the entropion
_
If.
however, the eyelid stays in its normal
- - _
:
n:--=- -_: resting position after releasing the lower lid, and
only turns inward when the patient blinks or closes then the patient has senile involutional entropion_
C. PTOSIS (BLEPHAROPTOSIS)
laroptosis is drooping of the eyelids below the normal
position. This is commonly referred to as just ptosis (drooping).
The normal position of the upper eyelid is two mm below the
superior limbus. If the upper eyelid position is any lower than
this, ptosis is present (Figure 12).
E
There are several surgical procedures used to correct
involutional entropion. Tarsal strip with retractor reinsertion is
the preferred procedure for this condition as it adcliessesthree
factors causing the entropion, namely lid laxity. lid serracsor
dehishcence, and orbicularis overriding.
CONGENITAL ENTROPION
Congenital entropion is present in nevAxen chilerten arc
may persist up to early childhood. It more ',ewer* 'ism
the lower lid, but may affect the up
caused by a prominent or hypertrop skin or epicanthal fold which rotates the toward the eye (Figure 11)
Figure 12. Ptosis of right upper lid
If lash touch to the eyes is mild, lubricarrisandpertiodictolb*
up will suffice. This type of entropion is hammer opened
es~~the
to resolve spontaneously. As the dulds toe ssassier
nasal bridge grows higher, and the medal eyelid sib macts
leading to resolution of the entropion.
I n moderate to severe cases, or in instances shaesponsarreous
resolution does not occur, surgical couectirtse womanted
This involves removal of the cress skin ad hypersophic
muscle with concomitant use of everting eyelkl susses.
Eye conditions may simulate ptosis and they are called
pseudoptosis. When an eye is deviated downward
(hypotropia), the eyelid may follow the eye mimicking a ptosis.
Dermatochalasis, a condition where there is overhanging skin
from the upper eyelid, may simulate a ptosis. Enophthalmos
may also simulate a ptosis.
A complete eye examination for ptosis should start with the
basic eye examination. In addition to this, one should also
check the following:
1.
2.
Test for degree of ptosis
A. palpebral fissure height
B. Marginal Reflex Distance (MRD)
Test for levator function
Measurement of the palpebral fissure height
With the patient looking straight ahead, measure the palpebral
fissure height by recording the distance between the upper and
lower lid margins with the aid of a millimeter ruler (Figure 13).
Measurements taken for each side are recorded and compared.
Normal palpebral fissure height is 10 mm. In cases of unilateral
rincic. a difference of 2 mm between the 2 eyelids means a 2 mm
otosis, a difference of 3 mm means a 3 mm ptosis and so on.
SPASTIC ENTROPION
This type of entropion may occur due to the constant
squeezing of the eyelids and spasm of the orbicularis. The
presence of irritative conditions oldie eye in association with
constant foreign body sensation causes the patient to squeeze
his eyelids frequently. This is also observed in conditions
such as blepharospasm. Relief of the spasm by relieving the
irritative condition will usually resolve this type of entropion.
In bilateral ptosis cases, comparing the two eyelids is not
practical. In these cases, one can judge the level of ptosis by
observing the level of the eyelid. Since the normal position of
the eyelid is 2 mm below the limbus, a 2 mm ptosis would
mean that the upper lid margin is located 4 mm below the
limbus; a 3 mm ptosis would mean that the upper lid margin is
located 5 mm below the limbus and so on.
However in chronic cases such as blepharospasm, botulinum
toxin may be used.
II
SPECIAL TOPICS 18.3 Eyelid
Malpositions 111111
Figure 13. Measuring Palpebral Fissure Height in a patient (A) Patient is asked to look straight ahead, (B) shows measurement of
9 mm in the right eye, (C) shows measurement of 11mm for the left eye
technique may be subject to misinterpretation in
cases of hypertropia or hypotropia, and extra caution should
be exerted in interpretation of these cases.
The MRD
Marginal reflex distance method (MRD)
marginal reflex distance (MRD) is defined as the distance
between the lid margin and the central corneal reflex. This is
taken by shining a light onto both corneas, and measuring
the distance between the lid margin and the corneal light
reflex. MRD1 is the margin to reflex distance of the upper lid,
while the MRD 2 is the margin to reflex distance of the lower lid
(Figure 14). For MRD1, the measurement is expressed in + mm
if the upper eyelid margin is above the reflex or — mm if the lid
margin is below the light reflex. For MRD2, the measurement is
expressed in + mm if the lower eyelid margin is below the reflex
or — mm if the lid margin is above the light reflex.
The
2
Measuring levator function
Levator function is measurement in millimeters of the
amount of excursion of the upper eyelid from extreme
downgaze to extreme upgaze while immobilizing the
frontalis muscle. This is done by laying one hand on the
patient's forehead and using the thumb to prevent the
motion of the eyebrow. The patient is then instructed to
look down or up as far as he can without moving his head.
The difference in the palpebral fissure height on upgaze
and downgaze is measured and recorded (Figure 15). The
test is repeated on the other eye.
2
- 5 mm
0
1
cm
A
6 mm
0
B
Figure 14. (A) MRD1 is the margin to reflex distance of the upper
lid (+5 mm) (B) MRD2 is the margin to reflex distance of the lower lid (+5.5 mm)
cm
Malmo Damps
Maximum Upgaze
Figure 1S. liceurement of levator function showing 6mm difference in
palpebral foram begfrit mit pmt at maximum downgaze and upgaze.
CLASSIFICATION OF PTOSIS
A. ACCORDING TO ETIOLOGY
1.
Neurogenic ptosis is caused by a paralysis or paresi6 _
the third cranial nerve. The levator muscle may be soe
involved, or in the case of complete CN Ill palsy, thew
is involvement of the other extraocular muscles aswe
In the latter case, aside from ptosis, the e), e
= soto_.
deviated downward and outward. Double elevator
palsy is a condition wherein the levator a _
rectus muscles are both affected by the pa--3 ,.sis or
paresis of the superior branch of the CN IIL
2.
Myogenic ptosis is generally caused by aticx+v
or weakening of the levator muscle. Inadeqt..::- ,
development or death of muscle fibers lead to try
replacement by fibrous or fatty tissue. An
this type of ptosis is congenital ptosis.
3.
Ptosis due to myasthenia gravis is aisc
under this type since the uncienying pa&.: on the muscle fibers as well. Myas-. -e-gradual weakening of muscles due
the neuromuscular junction, involvirc
production and sensitivity of the _ acetylcholine_ Weakness may any:
well, such as the extraocular rnusc- diplopia. Eyelid height may be nor— ,
droopasthetilaypeopessm
morning but may begin to
with full blown ptosis and fatigue in ihraillestotans.
.
ation of the condition is do- - _- _tensilon test, which resto-e
4.
:
Aponeurotic ptosis G3USed by
-_
levator aponeurosis rrom the tarsus.
_
-:
may be good or normal Majority& ac4—re
under thrs type.
5.
_
Traumatic ptos is s caused by trauma to the *valor
l•
6.
Mechanical ptosis _ ...sed by the Asighing down of the
unoer lid by a mass or wow&
B. ACCORDING TO TIME OF ONSET
1.
Congenital ptosis ptosis
:-.. -esent at birth. This
2 2 ---ore commonly associated with a weak
e and absence of the lid crease. As the
child ge-.5 :el; the noriunctional or atrophic muscles
become r_:: 8ced with fibrous or fatty tissue. The eyelid
fails to ope- .vell due to the lack of muscle fibers, and,
they also fail to dose well due to the rigidity of the fibrous
tissue. This can be easily identified on downgaze, when
the patient's ptotic
=
:ally higher
than the opposite eye (Figu re 16 and 17)
-_
levator
Figure 17. Congenital ptosis
2. Acquired ptosis refers to ptosis that is acquired
after birth. This type of ptosis is more commonly
associated with a strong levator muscle whose
aponeurosis has detached from its tarsal attachment.
This is commonly manifested by a comparatively
higher lid crease in the affected eye compared to
the opposite eye. This difference is best seen when
the patient is asked to look down. Upon asking the
patient to look downwards, the ptotic eyelid will
be lower than the opposite side, due to the levator
detachment from the tarsus (Figure 18).
8
SPECIAL TOPICS 18.3 Eyelid Malpositions
193
SURGERY FOR PTOSIS
Aside from the severity of ptosis and the levator muscle
function, other factors listed below should be taken in
consideration in planning for surgical correction for ptosis.
1. Bells phenomenon - The Bells phenomenon is the reflex
action of the eyes to turn upwards when the eyes are closed.
This protects the globe when the patient is asleep. Ptosis
surgery in a patient without or poor Bells phenomenon may
result in exposure keratitis.
To test for Bells phenomenon, ask the patient to close his eyes
as if sleeping, then gently lift the upper lid with your fingers
and note the position of the eyeball. If the eye is elevated, he
has the Bells phenomenon (Figure 19).
Figure 18. Acqu red c:os s
C. ACCORDING TO SEVERITY OR DEGREE
Ptosis may be classified as mild, moderate or severe based on
MRD1 and palpebral height drop/lid drop (Table 1).
d rop
I
1.66 fo the amount of drop or droop from the normal position
of the upper lid. The upper lid covers around 2 mm of the
superior limbus. In cases of unilateral ptosis, the contralateral
(unaffected) upper lid may be used as the basis for normal lid
position.
Table 1. Severity of ptosis based on MRD1 and Palpebral Height Drop
Se
Figure 19. Bell's phenomenon
2. Orbicularis tone - Orbicularis tone has to be evaluated in a
patient whose eyelids will be raised, to check if the patient has
enough muscle tone to cause adequate closure of the eyelids.
of Ptosis 11011.1D 4111111111111.1111
Mild
Moderate
Severe
> 1 mm
2 mm ptosis
1 mm
3 mm ptosis
0 or less
4 mm ptosis
This is done by asking the patient to squeeze his eyelids
forcibly. Now using the thumb and forefinger, try to forcibly
open the patient's eyes. One should feel the forceful closure of
the eyelid against the fingers, and one can gauge the strength
of the orbicularis muscle.
D. ACCORDING TO STRENGTH OF LEVATOR
FUNCTION
Ptosis may also be classified based on the strength of the
levator muscle.Table 2 shows classification for levator function
strength.
Table 2. Classification of Levator Function
Classification
Levator Function
Measurement (mm)
Poor
0-4
Fair
5-7
Good
8-10
Very Good
11 - 12
Excellent
13- 15
3. Tear production - In a procedure that will raise the eyelids,
acequate tear production to ensure proper
e.e
lubrication df the corneal surface. One would not want to
expose a patient with dry eye to a ptosis operation which
would cause further exposure and drying of the cornea.
This can be done by performing the Schirmer's test (Figure 20).
Put the folded end of the Schirmer's strip in each lower eyelid,
with the strip hanging out, and observe for 5 minutes.The strip
with the corner cut off is traditionally placed in the right eye.
* It may remain open, or closed, whichever
The eyes of the patter
is more comfortable. After 5 minutes, one must measure the
amount of tears absorbed by the Schirmer's strip using a
millimeter rule( Dry er is suspected if the result is less than 2
s visible above the limbus (superiorly) or below the limbus
--ncericovi 1s (Amer."
sder-41
CAUSES OF LID RETRACTION
1_ Tnyrord Opritnaimopathy - The most common cause
of lid re
eon is thyroid eye disease In the acute stage,
id tettaction may be due to inflammatory changes in
the eyelid and eyed muscles, particularly the eyelid
tesotiots. Stimulation of the Mullet's muscle by circulating
osiecholamines may cause it to contract resulting in lid
Eniagement and hypertrophy of the levator
mode map cause hither lid retraction. In the chronic
Figure 20. Schirmer's test
sum fibrosis
' and scaring of the muscles and septum may
Another test would be the fluorescein dye test.
set I% making the id retraction permanent. Lid retraction is
of fluorescein in each eye, or using a fluoreseingliffillillaidle imquendy accompanied by proptosis, and this may further
tip in each inferior fornix until some dye has comertiffillillidie coniteute to the appearance of a retracted lid, however
conjunctiva. Examine the cornea under the
diem 2 ainditions should be differentiated from each other.
:a1 n. F.3-04* lliewarilkt. A Mend flare may frequently accompany the lid retraction of
light. One may see if there is any superfv.present due to dry eye.
liwoirlophdialmopathy (Figure 21).
4. Corneal sensation -Ina patient undo
corneal sensation will serve as the alarm
him that his cornea is in danger of
_
patient with poor corneal sensation will IDexaggerated drying and exposure of thE- undergo ptosis surgery.
This is performed with the patient seated aid inanarmeo look upwards. One may use the twisted iipolapieteaftim, pa per, or a cotton wisp to touch the comeaasende side As".
the patient to grade how much of die GM= p he felt
against his eye using a scale of 1 to 10 fl-kiwest 110-lict+est
The goals of surgical procedures for ptosis reC-a •
follow,1.
2.
3.
To elevate the eyelid above -.-
_
to see
To elevate the eyelid high
properly and cover the corn€.
To maintain proper cosmetic-
the p
-Figure 21. Lid retraction in thyroid opthalmopathy
era
sat" it to dose
e eyelid
for perisis bickides itarsomullerectomy and
levator resection for good Immix function ptosis or fascia lata
2. Anterior Lamellar shortening - This may be caused by
cicatricial changes of the skin, such as in trauma or burns, or
excessive removal of skin during blepharoplasty.
3. After muscle surgery - Patients who undergo recession
of the rectus muscles may occasionally develop lid retraction.
Surgical repair
sling procedure fix poor legator function ptosis.
D. LID RETRACTION
Lid retraction is the abnormal displacement of the eyelid
toward the orbital rim, resulting in exposure of the sclera
above or below the limbos (Rgure21).
Upper lid retraction may result in retraction of the eyelid
above the superior limbus, while lower lid retraction results in
retraction of the eyelid below the inferior limbus. Sclera which
4. Idiopathic- In some cases, no known cause can be identified
TREATMENT OF LID RETRACTION
All cases of iia retraction must be worked up for their etiology.
Thyroid ophthalmopathy must be ruled out by requesting
for the pertinent laboratory examinations: serum T3, T4 and
thyroid stimulating hormone (TSH) levels. Axial and coronal
views of an orbital CT scan will also help to determine the
presence of thyroid induced hypertrophy of muscles. To
minimize effect of exposure of the globe, topical lubricants
may be given. Taping of the lids may also be done at night.
8
SPECIAL TOPICS 1 8.3 Eyelid Malpositions
195
Surgical management for severe retraction may be necessary.
Examples of surgery performed are tarsorrhaphy, recession of
3. Entropion may cause significant decrease in vision by:
A. increased tearing
B. corneal abrasions from the lashes
C. corneal scarring from keratitis
D. none of the above
levator-Muller's muscle complex in upper lid retraction and
use of spacer grafts.
SUMMARY
The four basic eyelid malpositions — ectropion, entropion,
ptosis and lid retraction - their definition, classification,
pathophysiology, recognition, diagnostic maneuvers, and
management were discussed. It is important to recognize that
these conditions, if uncorrected wil adversely affect the eye
and may ultimately affect the patien*vision. Early recognition
and management can save the eye and sight of the patient.
4.
A. canthal tendon laxity
B. eyelid inflammation
C. mass on the eyelid
D. tarsal shortening
5. Entropion can be easily recognized by:
inward turning of the eyelid margin
inward turning of eyelashes, rubbing on the cornea
superficial punctate keratitis on the cornea
due to lashes
D. all of the above
A.
B.
C.
ACKNOWLEDGEMENT
Dr. Catherine Vigo-Matic provided some of the pictures.
6.
Kersten RC (editor) et al. Basic and Clinical Science Course
2003-2004 Section 7 Orbit Eyelids and Lacrimal System,
American Academy of Ophthalmology, San Francisco,
USA, 2003.
2. Beard C. Ptosis, 3rd edition, CV Mosby, St. Louis, 1981
3. Hatt M. Ophthalmic Plastic and Reconstructive Surgery,
Georg Thieme Verlag, Stutttgart, 1986.
4. Collin, JRO. A Manual of Systematic Eyelid Surgery,
Churchiull Livingstone, 1983.
5. McCord Jr. CD. Chapter 5 Surgery of the Eyelids, Duane's
Clinical Ophthalmology, Volume 5, TD Duane, ed, Harper
and Row, 1984.
6. Kersten RC, Kleiner, FR Kulwin DR. Tarsotomy for the
treatment of cicatricial entropion with trichiasis, Arch
Ophthalmol 1992: 110:714-717.
The following can cause ptosis EXCEPT
Cranial nerve III paralysis
Horizontal upper lid laceration 20 mm above the lid
margin
C. Hypotropia
D. Myasthenia gravis
A.
B.
REFERENCES
1.
Senile involutional ectropion is commonly caused by:
7.
The following will predispose a patient undergoing
ptosis surgery to post-operative complications EXCEPT
A. absence of Bells phenomenon
B. corneal anesthesia
C. epiphora
D. spasm of the orbicularis oculi
8.
Identify the picture with lid retraction:
SELF-TEST
1. The following are the factors that contribute to
involutional entropion EXCEPT:
A. detachment of lower lid retractors
B. enophthalmos
C. lid laxity
D. overriding of pretarsal over preseptal orbicularis
2.
Cicatricial entropion is more commonly caused by:
A.
B.
acute blepharoconjunctivitis
scarring of the anterior lamella
C.
scarring of the lid margin
D. scarring of the posterior lamella
Answers to S64---e
223.
8.4 Ocular Trauma
and Emergencies
Marissa N. Valbuena MD, MHPEd
INTRODUCTION
The medical student, either a clinical clerk or an r- l-- —..af De 71e first medical personnel to see a patient in the emergencyI
room. After ruling out any life threatening cz,-:-.. -,,-.)- 7re swell( should assess the patient's ocular condition, perform eye
examination without further harming the
ee riacient to the ophthalmologist.
OBJECTIVES
At the completion of this study material, t.-)e ...,..rtlentsnoulid be able to
1.
extract a relevant medical history Arena-nen ant,* =Kona patient
2.
perform the necessary ocular exar-trugion when Oren an eye trauma patient
3.
recognize the conditions which needpitsgproefergatto the ophthalmologist.
4.
discuss the principles of manactementahhetninirnon ocular emergencies.
CONTENT
L
Dour and orbital trauma
Evakkatcr of patient with trauma to the eye and/or orbit
2.. infiries to the lids and adnexa
I Orbital fracture
4_ injaaries to the globe
S. Chemical bums
I.
lion-traumatic ocular emergencies
1_ Acute angle closure glaucoma
2.. Central retinal artery occlusion
3. Corneal ulcer
4. Endophthalmitis
5. Orbital cellulitis
I. OCULAR AND
ORBITAL TRAUMA
Any patient who comes to the emergency room
possible eye injury or condition should be evaluated k possible life-threatening conditions. If the patient is sta.= -a,
an initial assessment of the eye should be ma.-Je
any of the two true eye emergencies: chemical bum
and central retinal artery occlusion. In
appropriate management should be initiated
and concurrently with history taking and ocular e •
Immediate referral to an ophthalmologist is manca:ory_
EVALUATION OF THE EYE TRAUMA PATIENT
If the globe is undamaged, the lids, palpebral conjunctiva and
fomices can be more thoroughly examined.
INJURIES TO THE LIDS AND ADNEXA
1. ECCHYMOSIS OF THE EYELIDS
Orbital contusions due to blunt trauma may cause localized
tissue damage like lid eccymosis (Figure 1) with minimal
disability. Blunt trauma, however, can also cause orbital fracture
and globe injury like hyphema, angle recession, iridodialysis,
retinal edema and retinal breaks.
Treatment of lid ecchymosis consists of cold compress in the
first 24 hours followed by warm compress and analgesics as
needed.
A. HISTORY
When a patient's chief complaint is trauma, the precise time
of onset of symptoms should be determined. The patients
activity at the time of injury and the site where it occurred
should be asked. The history should also include an estimate
of the vision prior to and immediately after the injury. An
intraocular foreign body may be suspected if there is history
of hammering, grinding and explosion. Aside from visual
symptoms, the presence of the following should be elicited
pain, foreign body sensation, bleeding, and diplopia. Previous
treatment given and general medical history should also be
determined.
B. OCULAR EXAMINATION
•
2. LID LACERATION
Despite the need for a complete examination, initial
effort must be directed to prevent further injury to the
eye. An eye shield should be taped to the orbital rim in cis
of lid laceration, foreign bodies or suspected globe rupture.
Physical examination should begin with measurement of
visual acuity. If visual loss is severe, check for light projection,
pupillary reaction including relative afferent pupillary defect
Test for eye movement, palpate the orbital rim and test
for periorbital sensation. If a slit lamp is not available in the
emergency room, a penlight or a direct ophthalmoscope on
+10 D can be used to inspect the anterior segment of the eye.
A:lac&
Figure 2) can be caused by sharp objects,
arias al
blows from a blunt object. Injury to the
globe should be first ruled out before repairing the laceration.
Lacerations ineolving the lid margin and the medial aspect of
the ids should be referred to an ophthalmologist. Cosmetic
and functional success of lid margin laceration repair
depends on precise approximation of lid margin, tarsus and
skin_ Lac ations near the medial canthus may involve the
The bulbar conjunctiva should be examined for hemorrhages.
foreign bodies and laceration. The cornea is inspected for
foreign bodies, abrasions and Iacerations.The depth and clarity
of the anterior chamber are checked. Size, shape and reaction
of the pupil are checked and compared with the uninjured
eye. Obviously, palpation is avoided in cases where there is
laceration of the cornea or sclera. The direct ophthalmoscope
is used to assess the clarity of the media, from the cornea,
to the lens and vitreous and to visualize the optic nerve and
retina.
Figure 2 laced= d te o'er eyelid.
canaliculus and may require intubation of the canalicullus.
Antibiotics, analgesics and tetanus prophylaxis are aisc
to the patient.
Serail conjunctival laceration does not need to be repaired.
_aceraitions bigger than 5 mm should be sutured. Surgical
143air of scieral laceration depends on injury to other ocular
struaures.
ORBITAL FRACTURE
Orbital fracture usually occurs with facia'
-associated with globe injury. When or:.
a blow, compressive forces can fractuie
and inferior walls with prolapse and p^ - 7 - of soft tissues (Figure 3).This is cane-d bioir-cuat fracture
Enopthalmos may develop. Diplop a
damage to the extraocular muscle a of the orbital content or entrap---, —
and inferior oblique within the f-E-.:ecchymosis, epistaxis, orbital emp-,
the ipsilateral cheek and upper lip.
CT scan provides the best assessmert
X-rays may be helpful in the initial
The indications for repair and timing affsepillreilfsibiiilloar
fracture are still controversial_ Genesi/ =WI. iidiallions
for repair include motility disturbaicelikastesfeeraocular
muscle entrapment or enoptualirc
Figure 4. Subconjunctival hemorrhage
Figure 5. Conjunctival laceration
INJURIES TO THE GLOBE
1. INJURIES TO THE CONJUNCTIVA AND SCLERA
Subconjunctival hemorrhage (Figure 4) :ommonly re
from blunt
-ries.the
is reassures
_ompress.
Conjunctival laceration (Figure 5) may result from trauma
from sharp
,
•,
3l or glass. There may be
subconjunctiva =
- olapse of Tenons or fat.
Occult sclera! laceration (Figure 6), especially at the limbus
or just pos:e:.o:
rectus ,nsertion, must be ruled out
Signs to look out for are bullous subconjunctival hemorrhage,
asymmetrical decrease in intraocular pressure, shallowing or
deepening of the anterior chamber, irregularity of the pupil,
and hyphema (Figure 7).
Figure 6. Semi Isceraion
SPECIAL TOPICS 18.4 Ocular Trauma and Emergencies
199
2. INJURIES TO THE CORNEA
Corneal foreign bodies (Figure 10) and abrasions can
cause pain in eye on eyelid movement. Metallic foreign bodies
may leave a rust ring. The manner of removal of the corneal
foreign body depends on the material and depth in the
cornea. Superficial foreign bodies are removed using sterile
gauge 25 needle after instillation of topical anesthetic eye
drops. It is important to assess visual acuity before applying
any medication to the eye.
Figure 7. Scleral laceration with oyes! prolapse. Hole blood in the
anterior chamber (hyphema)
Conjunctival foreign bodies (Figures 8 and 9) can cause
acute pain. If the conjunctiva as well as the retained foreign
body are not easily movable over the sclera, or if the foreign
body appears to be fixed to deeper structures, sclera! injury
should be suspected_ A foreign body adherent only to the
conjunctiva can be easily removed with a forceps or cotton
pledget after applying anesthetic eye drops.
Figures 10. Corneal foreign body (white arrows)
Figure 8. Foreign body on bulbar conjunctiva
Suspect corneal abrasions (Figure 11) in contact lens
viewers
ng of severe eye pain or among welders
who do not wear protective face or eye gear when working.
Foreign body in the upper palpebral conjunctiva should be
suspected when there are linear corneal abrasions.
Figure 9. Foreign body on palpebral conjunctiva. From Lightman S and
McCluskey
When the corneal epithelium is abraded or denuded, the
superficial corneal news are exposed, causing pain, tearing
and phoeophobia. The usual smooth glistening tear film is
disrupted Using the sit lamp will confirm depth and extent
the of abrasionlhe insulation of fluorescein dye on the eye
surface and the use of a cobalt blue light source will delineate
the abrasion More 11 B). Small abrasions can be treated
with topical allthelliCS. Bigger abrasions may require eye
patch or bandage contact lens.
•E
may also be disinserted on its root lridodialysis). This is
by polycoria or the appearance of multiple pupils.
".'auma causing tear in the anterior ciliary body is the
:ommon cause of hyphema (blood in the anterior
3-terior chamber is totally
ai—oef) (Figure 13). V.
and
increase in intraocular
e.d with blood (Figure 14)
may
result. The treatment
ng
- .assure is present. cornea
n
controversial.
Among the
7
hypherna is yea:: =
.
alization,
bed
rest,
sedation,
suggested treats-1-,
medications, antianti-glaucoma
eye patch, cycle:
:al evacuation.
fibrinolytic agents
B
Figure 13. Partial hyphema
Figure 11. (A) Corneal abrasion. (B) Cram swami Moat Ohm
with fluorescein dye in cobalt blue fight.
Penetrating corneal injury may ne
7.‘ g-arp or
blunt
trauma. Corneal lacerations (Rpm= may be acxompanied
' war deperxis on
by injury to trie ins, tens arra retina. Sts
involved eye structures aside from the cornea.
Figure 14. Total hyphema
4. INJURIES TO THE LENS
Figure 1 2_.Corree lacaraiiy- as rxiiciaisid by uhie antra_ Adopted torn
Atlas of
3. INJURIES TO THE IRIS
Blunt eye trauma can cause injury to the iris sphincter muscle,
causing traumatic nos (constriction) followed by traumatic
mydriasis (dilation). Associated ciliary spasm or paralysis
may cause blurred vision especially for near tasks. Signs of iris
injury are constricted or dilated pupils, iris sphincter tears, and
inflammatory or pigment cells in the anterior chamber.
Penetrating corneal injury can result to rupture of the lens
capsule and cataract. Blunt trauma resulting to cataract
and/or lens subluxation is often associated with posterior
segment sequelae. Complete rupture of the zonules results
in a free-floating lens in the anterior chamber (Figure 15) or
in the vitreous (luxated or dislocated lens). Partial severance
of the zonules result in a subluxated lens (Figure 16).
Management of subluxated lens depends on the severity,
presence of cataract and of glaucoma.
8
SPECIAL TOPICS 1 8.4 Ocular Trauma and Emergencies
201
Choroidal and chorioretinal rupture (Figure 17) occurs when
a greater force hits the eye, causing distortion of the globe and
stretching of the choroid. Involvement of the macula results in
greater visual disability.
Optic nerve head avulsion results when a small blunt object
hits the globe from the inferotemporal area and compresses
the nerve against the orbital roof.There is sudden loss of vision.
Generalized retinal ischemia ensues. There can be retinal and
pre-retinal hemorrhages and retinal edema.There is no known
effective treatment for this condition.
Figure 15. Lens dislocated in the anterior cnamber.
Figure 17. Choroidal rupture (white arrowhead)
6. INTRAOCULAR FOREIGN BODIES
Figure 16. Lens subluxed superiorly (edge of lens indicated by
white arrows)
Cataract which occurs together with a corneal laceration is
usually removed during the primary corneal repair. Cataract
resulting from blunt trauma may have varying severity. If visual
acuity is not decreased and inflammation and glaucoma are
absent, observation is the preferred management.
5. INJURIES TO THE POSTERIOR POLE OF THE EYE
Severe contusion to the eye can result in a variety of
posterior segment injuries: retinal edema, hemorrhages,
tears, detachment, choroidal and chorioretinal ruptures, and
avulsion of the optic nerve.
Severe eye trauma can cause disruption of axonal transport
in the nerve fiber layer of the retina. When this occurs in
the retinal periphery, it is called commotio retinae and
traumatic macular edema or Berlin's edema when it
occurs in the macula. The retina appears gray.The foveal reflex
is lost if macular edema is present. Intra-retinal and vitreous
hemorrhage may be present. In the absence of other injuries
treatment of commotio rctIrsa
Mild
resolve in a few days but severe cases may result in retinal
atrophy and retinal holes.
One should suspect intraocular foreign bodies (Figure
18) when a patient complains of eye pain and/or blurred
vision with a history of striking metal, explosion or projectile
injury. The anterior portion of the eye should be inspected
for possible site of entry. If possible, direct visualization by
funduscopy should be done. Localization of the foreign body
can be made by orbital x-ray, ultrasound or CT scan. MRI is
absolutely contraindicated for metallic foreign bodies because
the foreign body may move and cause further injury.
Whenever possible, intraocular foreign bodies shoukf be
surgically removed. Iron and copper foreign bodies c case
inflammation and toxicity to the retina and other sr_ .7...,615 in
the eye while organic foreign bodies can cause infer — —mon
and infection. Inorganic foreign bodies like glass
inert.
Complications of chemical burns include corneal scars,
glaucoma, symblepharon (adhesions between bulbar and
palpebral conjunctiva) and entropion.
CHEMICAL BURNS
All chemical burns should be treated as trueopiilmienrc
emergencies. immeoiate tap water
started at the site where injury occurred bet:-i- 7.-e =lent
is transported to the emergency room. A bo-F - s err and
'-ocular examination should be followed by coo.:
won
with
several liters of normal saline solution V-- _ -
tubing. Topical anesthetic and lid retractor rr,al
-ceded in
order to do proper irrigation. The fornices shy De swabbed
for particulate matter. The pH of the oc
snouid be
checked and irrigation continued until
:el.-Aimee., 73 =7.7. Immediate referral to an ophtha
s ---andatory_
Other medications for chemical bums ar-i. =acs c.cbp~egics.
antibiotics and anti-glaucoma drugs. ors a•-aioese,
Alkali penetrates ocular tissue race* .ire
77, do
damage long after the inciting inFrit Accs bre:-_c -F. 7 _sue
protein which serves as a barrier icr
,
on.
Chemical injuries can occur frcr- ro....ta a_==-old
accidents and from che— :a being
r:Arn to
the face. Examples of aliK
_de lime
aster,
drain cleaner, oven clea—.a.
-Imre. fragr-es.
in sparklers. Examples
car
ac
inoude
battery fluid, bleach. Figure 19
acid burns or' z
eyes
of varying severity. The paies
conitanct~.
arly the
area around the limbus, the more
Figure 20 shows add bum resuiting
, _ = Lal burn.
..:3:ion of the
corneal epithelium
Figure 20. (A) Aad bums
::.)— ea
Figure 19. Acid burns of both eyes. OD has very cloudy cornea and
pale chemotic conjunctiva. OS has very hazy cornea and moderate
chemosis
epithelium. (B) The area devoid of epithelium stains with fluorescein dye when viewed
blue kit*
8
SPECIAL TOPICS
I 4 C - .rar Trauma and Emergencies
203
II. NON-TRAUMATIC OCULAR
EMERGENCIES
CENTRAL RETINAL ARTERY OCCLUSION
Measures to decrease intraocular pressure should be
initiated. These include topical anti-glaucoma medications,
acetazolamide, intravenous mannitol and glycerine. Patient
should also be given analgesics. Definitive management is
laser iridotomy or surgical peripheral iridectomy. Fellow eye of
these patients should also undergo iridotomy if the angle is
found to be narrow and occludable.
Central retinal artery occlusion (CRAO) is a true eye
emergency. Patients will have sudden, severe, painless
blurring of vision. Previous transient visual loss (amaurosis
fugax) may be present. Visual acuity ranges from counting
fingers to light perception at the time of examination. Relative
afferent pupillary defect (RAPD) is observed. On funduscopy,
the retina appears edematous and grey in color except at the
macula, which may appear red (cherry red spot) (Figure 21).
Twenty five percent of patients with CRAO have cilioretinal
artery and thus may have residual central vision
t fee, \tit i
L
Figure 22. Acute angle closure glaucoma
sc
CORNEAL ULCER
Consider a corneal ulcer in a patient with painful red eye, eye
discharge and a corneal opacity (Figure 23). There may be a
history of contact lens wear, minor trauma or foreign body to
the eye, or self medication with topical steroids. Patient should
undergo corneal scraping for Gram staining and culture and
sensitivity studies so that appropriate antibiotics can be given.
Figure 21. Central retinal artery occlusion, with cherry red spot
on macula.
The Retina, Vitreous and Choroid chapter of this SIM discusses
the pathophysiology of CRAO. Irreversible retinal damage
can occur within 90 minutes of onset of CRAO. Measures to
decrease intraocular pressure and to increase retinal artery
perfusion include the following: inhaling oxygen-carbon
dioxide mixture by breathing in and out in a paper bag, anterior
chamber paracentesis, and administration of intravenous
acetazolamide. Patients should be evaluated for systemic
diseases like hypertension, arteriosclerosis, collagen disease,
hematologic disorders and diseases that may predispose tc
embolic and thrombotic phenomena.
Figure 23. Comeal ulcer
ACUTE ANGLE CLOSURE GLAUCOMA
ENDOPHTHALMITIS
Patients with acute angle closure glaucoma (AACG) present
with acute eye pain and/or headache, associated with
blurring of vision and red eye. Some patients may have
vomiting. Ocular examination will show red eye, hazy or
cloudy cornea, mid-dilated pupil, shallow anterior chamber
and firm eyeball on palpation (Figure 22). Tonometry will
show increased intraocular pressure.
Endophthalmitis is an intraocular infection which manifests as eye
pain that worsens on eye movement, blurred vision, eye redness
and sweing. It can occur after an intraocular surgery, tra uma, from
a leaking glaucoma filtering bleb or from endogenous source like
an intravenousine_ Prompt referral to an ophthalmologist should
be made Management will include vitreous culture, vitrectomy
and intravitreal systemic and topical antibiotics.
ORBITAL CELLULITIS
Orbital cellulitis is the most common cause of proc
in children. It can also occur in the elderly and in imrcompromised patients. It can be preceded by trauma o'
be associated with infection in the paranasal sinuses.
Appendix 10.3 illustrates a step-by-step diagnosis of ocular
erne gencies which can serve as a guide to primary care
--.L.Th-F:fa.ns in the emerce^7% 'oom
-
ACKNOWLEDGEMENT
Carrnvia Quito anti Dr. Jonn Alfred Lim provided some of
Patient will present with pain, lid swelling and
It is important to differentiate preseptal caul orbital cellulitis because they can both pres-?
swelling, redness and tenderness of the eye
leucocytosis. Proptosis, chemosis, limitation of
eye movement and blurring of vision points to a
cellulitis. Extension of the infection to the cavern.,
can cause bilateral CN II—VI palsy and high levet C:
corn plications are meningitis and brain abce,
REFERENCES
As soon as nasal, conjunctival and blood GAEL
the patient should be started on intravenous
antibiotics. CT scan or MRI are helpful in dIF septal from orbital cellulitis, for localizing an
foreign body and identifying sinusitis.
SUMMARY
Doctors working in the emergency Koos oboold be farnirar
with the clinical presentation and 111111111111111111 dose injuied
eye and its adnexae. He should be compolloot iii powiding
immediate treatment while widening kodoaribjuties so the
Illion-ilaumatic
patient. He should likewise be ''salt
emergencies like central retinal army 00:6111011 and &axe
angle closure glaucoma. He should lotogrdie the conditions
that require referral to the ophthalmologist 101 defirlitiVe
treatment Table 1 classifies ocubr emegenoles to true
emergency, urgent condition a-7 F.e—f-lageit concitirxi_
Table 1. Classiicalon of OctibrEmer-L.
Therapy should be
• Cherrica
instituted witrtin menuaes . cerra
Therapy should be
•
instituted with,' one to
several hours
•
•
•
a: '
oceiar - - E-.
• --a-rnatC
Therapy should be
days
(whe- e .
Adap:ec
•
•
•
•
Mule exophta6nT,s
Attila ribs
Acute rer.
Bkrii-:•
7_
4_
4loiclan-Eva P, Whitcher, J.P.. Vaughn and Ashbury's
.;eneal Ophthaknology , 16th Edition, New York: Lange
Medical Books/ McGraw Hill, 2004, pp 371-379
Nelson LB. 01rtsicy SE Harley's Pediatric Ophthalmology, 5th
5Ation. Philadelphia : Lippincott Williams & Wilkins, 2005 ,
pp 508-525
Piefenrd practice Pattern for Acute Angle Closure
20/0031710. American Academy of Ophthalmology.
2005. www.aao.org
Lightrnan 5, McCluskey P, Handbook for Medical Students
leaning Ophthalmology, International Council of
Ophthalmology, 2009
5_ Webb LA Manual of Eye Emergencies, Diagnosis and
Management. Edinburg: Butterworth and Heinman, 2004
6_ Selected pictures from the files of External Disease
Service ,Retina Service and Glaucoma Service of the
Department of Ophthalmology and Visual Sciences,
University of the Philippines Manila, College of Medicine
and Philippine General Hospital.
7. http://www.sarawakeyecare.com/
Atlasofophthalmology/anteriorsegment/
anteriorsegmentpicture7cornealaceration.htm
accessed October 24, 2011
8. Ocular Urgencies and Emergencies, downloaded
from www.opt.uab.edu , accessed last August 2011.
SELF-TEST
1.
A true ophthalmologic emergency:
A. Central retinal vein occlusion
B. Chemical burns
C. ntra-ocular foreign body
D. Retinoblastoma
2.
A patient has a conjunctival laceration. What will make
you suspect an underlying scleral laceration?
J unctival laceration is more man 10 mm long.
B. Conjunctival laceration is located
3 mm from the
limbus.
C. There is bullous subconjunctival hemorrhage around
the conjunctival laceration.
D. Vision is 20/25.
• Optc ne-'
a- . gexaes a:4 Emergencies. from wvivr.optuab.edu
8
SPECIAL TOPICS 13.4
,,,,4
3.
This condition can cause severe eye pain:
A. Central retinal artery occlusion
B. Conjunctival laceration
C. Corneal abrasion
D. Subconjunctival hemorrhage
4.
The most important management of chemical burns is
A. Analgesic
B. Anti-glaucoma medication
C. Copious irrigation of saline solution to the injured
eye.
D.
5.
6.
Topical anesthetic
A machinist comes to the ER because of eye pain and
foreign body sensation he felt after working on metal.
You suspect a corneal foreign body. What must you do
first before instilling topical anesthetic?
A. Measure visual acuity
B. Measure intraocular pressure
C. Do funduscopy
D. Examine extraocular eye movement.
The definitive management of acute angle closure
glaucoma is
A. Laser iridotomy
B. Intravenous mannitol
C. Topical anti-glaucoma medications
D. Acetazolamide
7. The following clinical finding is suggestive of central
retinal artery occlusion
A. intraocular pressure of 30 mm ng
B. Pale and grayish retina on funduscopy
C. Pale optic disc
D. Visual acuity of 20/40
8. One should expect visual recovery from this type of
injury EXCEPT
A. Conjunctival laceration
B. Corneal abrasion
C. Optic nerve avulsion
D. Subconjunctival hemorrhage
9.
The patient felt foreign body sensation while walking in
the sidewalk on a windy day. Upon reaching home, he
got a basin of water, submerged his face with his eyes
open. Because of the persistent eye pain which was
worse when he blinks, he went to the emergency room
for consult. The resident on duty saw linear abrasions
on his cornea. The foreign body is most likely located in
the
A. Bulbar conjunctiva
B. Cornea
C. Limbus
D. Palpebral conjunctiva
10. The following eyelid laceration needs to be repaired by
an ophthalmologist
A. Horizontai laceration, 10 mm in length, located 10
mm inferior to the lower lid margin
B. Horizontal laceration, 20 mm in length, located 1C
mm inferior to the lower lid margin
C. Vertical laceration, 10 mm in length, located 5 mm
below lid margin
Vertical
laceration, 5 mm in length, located 5 mm
D.
from the medial canthus, involving lower lid margin
Answers to Self-Test on page 223.
8.5 Ocular Pharmacology
Mary Rose Pe Yan MD
INTRODUCTION
While pharmaceutical agents are often needed 'ix tne dorms arid reatinent of most ophthalmic diseases, it may not be as
clear and straightforward in some situations.
or asymptomatic patients. Patient compliance
education and simple reassurance may be sufficient for mild conditions
be Arced
the cost of the drug. pate-7 understanding of various
characteristics of the drug, and patient wilFngnessio mar trie inconvenience of applying the cwith patients the cost, dosage, side effects. anC
must discuss
Vices in order to achieve bette- c.-:.-r,ance and successful
treatment.
OBJECTIVES
At the end of this unit of instruction, the —eisaf male* shoutd beagle to
used for the eye and adnexae.
1. Discuss the various ways in whiciwn.qsaammitsebtxtit, with specific emphasis on drugs
2.
3.
Discuss the diagnostic and theraoeuticsiiesdaphtharndogic medkations.
adn i+iseeddingsaoaaularfl%Xlion.
Discuss the effects of syste—
CONTENT
~~ Phamicodimmics
R. Plharumawallimieties
1. Ocular structures and pharmacokinetics
Faciors affecting drug penetration into ocular tissues
•
O,
is drug delivery
IV. Ocular pharmacothera peutics
1. Local anesthesbcs
2 Analgesics
3. Mydnatics and mydriolytics
4. Cydopiegic3
5. Ocular hypotensive drugs
6. Anti-infective drugs
7.
8_
9.
Anti-inflammatory drugs
Anti-allergy drugs and decongestants
Drugs for dry eye and ocular surface disease
I. PHARMACODYNAMICS
Pharmacodynamics or mechanism of action refers to the
biological and therapeutic effect of the drug. A drug is
an agonist or antagonist if it binds at the receptor level
(e.g.neurotransmitters); and is an activator or inhibitor if it
binds at the enzyme level (e.g. hormone receptors).
total volume of the conjunctival cul-de-sac of 30 microliters.
The excess is either drained by the lacrimal drainage system
or is blinked out of the eye by the eyelid. Increasing the drop
size, therefore, does not increase drug absorption through
the cornea; rather, there is an increase in systemic absorption
resulting from increased volume drained through the punctum
of the lacrimal drainage system into the mucosa of the nasal
cavity and later swallowed.
II. PHARMACOKINETICS
The effect of drugs on the eye is dependent on specific
pharmacokinetic properties, namely:
The normal rate of unstimulated or "basal tear flow" is 0.5 to
2.2 microliters per minute. Tear flow is decreased with age
and is increased by ocular irritation caused by many ocular
medications. The available drug in tears for ocular absorption
is inversely proportional to tear flow rate.
Absorption - Drug absorption depends on the
CORNEA, SCLERA, AND CONJUNCTIVA
molecular properties of the drug, the viscosity of
Absorption of topical medication is primarily by the cornea. For
its vehicle, and the functional status of the tissue
certain substances like hydrophilic drugs, however, the cornea
forming the barrier to penetration.
acts as the major functional barrier for ocular penetration.
2. Distribution - Drug distribution affects absorption The cornea is an avascular structure, allowing a direct route
over time. Bioavailability of the drug at the site of
of ocular drug penetration without systemic absorption. The
action is affected by the compartments and barriers
comeal epithelium, which is the outermost layer of squamous
of the eye.
cells, is lipophilic and resists the penetration of hydrophilic
3. Metabolism - Metabolic enzymes may convert
drugs like sodium fluorescein, an anionic diagnostic agent. An
"prodrugs" to its active form, or may transform drugs
epithelial break will allow penetration of hydrophilic drugs into
to an inactive form in order to lessen side effects.
the corneal stroma. For effective corneal penetration, a drug
Metabolism plays an important part in eliminating
must have both hydrophilic and lipophilic properties.
drugs.
4. Elimination or excretion- This refer to elimination of
the substances from the body or accumulation of the The sclera, which is continuous with the cornea at the limbus,
drug in body parts. Rates of drug clearance can be is opaque and vascular. The conjunctiva overlying the sclera
is likewise vascular. Together, the conjunctiva and sclera
computed.
constitute less than one-fifth of drug absorption to the iris and
ciliary body.The conjunctiva may function as a major depot for
OCULAR STRUCTURES AND
subconjunctival injections, allowing the active drug to dissolve
PHARMACOKINETICS
slowly and be gradually released to the tears.
1.
TEARS
The tear film over the cornea is composed of 3 layers:
1.
Oily layer - An outermost lipid monolayer is produced
mainly by the meibomian glands in the eyelid. It
functions to stabilize the underlying aqueous layer
and retard evaporation.
2. Aqueous layer - More than 95% of tears is aqueous
secreted by the lacrimal glands. The layer is
approximately 7 microns thick over the cornea and
conjunctiva, and is inherently unstable, thinning
centrally at the end of each blink.
3. Mucinous layer -The inner thin hydrophobic coating,
composed of glycoproteins secreted by the goblet
cells, functions to cleanse the tears of particulate
debris.
MIS
The iris has sphincter and dilator muscles for pupillary
constriction and dilation, respectively. The iris functions to
regulate the amount of light reaching the retina, and contains
pigment to absorb light. The pigment granules of the iris
also absorb lipophilic drugs and act as a depot or reservoir of
some drugs, concentrating then re-releasing drugs for longer
periods. Drug response may vary depending on amount of iris
pigmentation_
CILIARY BODY AND AQUEOUS HUMOR
Tne recn cecr or capillaries of the ciliary body constantly
generates aqueous humor, which occupies the anterior and
posterior chambers. In the anterior chamber, aqueous exits
thee)edvough the trabecular meshwork at the angle formed
by the cornea and iris, enters the Schlemm's canal, goes to
episderal vessels and then on to the general circulation. The
ciliary body is the main source of metabolizing enzymes in the
The normal volume of the tear film is 8 to 10 microliters. A single eye for drug destufication and drug removal.
drop of medication is about 50 microliters, exceeding the
LENS
UPID SOLUBILITY
The lens is thick and flexible, and is composed of densely A ngner lipid solubility increases drug penetration through
packed cells with clear proteins or crystallins. Anteriorly and **epithelial cell membranes.
posteriorly, the lens has an outer basal lamina or capsue_ The
epithelium of the anterior capsule is the most metabolically 1111111FACTANTS
active and is thus, the most prone to damage by tort Surbaants, like benzalkonium chloride (BAC), alter the cell
substances. The lens is a barrier for the rapid penention inenbranes in the cornea and increase drug permeability.
of drugs from the aqueous to vitreous hump( Lipcchic
drugs can penetrate the lens slowly, but large proteins and PEI
hydrophilic drugs cannot be absorbed by the lens from tie Same drugs formulated in acid solution are more stable than
aqueous humor. Surgical lens removal changes the kineticsa Vulkane pH because of increased protonation and decreased
degradation. A change in the normal pH of 7.4, however, can
the aqueous and vitreous humor.
causeoadar irritation and increased lacrimation. This results in
lammed tear flow, decreasing available drug concentration
VITREOUS
The vitreous, which constitutes about 80% of the ocufair gess. andldeceasing drug penetration.
is a gel-like or viscoelastic connective tissue that contains
diffused small particles and high molecular weight substance% 1111111111110NICITY
such as glycosaminoglycans (e.g. hyaluronic acidlardpioleins Theognolarity of tears is 290 mOsm, equivalent to 0.9% saline,
(e.g. collagen). It serves as a major reservoir cf drugs ad as andisthetonicity of most ocular and intravenous medications.
a temporary storage depot of metabolites. Substa-Iraseased tonicity relative to tears causes osmotic water
molecular weight can freely diffuse from the oiar
—italement from the eyelids and eye, resulting in immediate
the vitreous. However, systemic administration o 311ition of drug solution.
drugs, such as gentamycin, does not readily crosi retinal barrier. For drugs to reach the vitreous. MOLECULAR WEIGHT AND SIZE
be injected intravitreally, introduced by iontccr
E-a.ar weight polymers and additives increase the
surgically implanted intraocularly. The major rouse of fit is wit amity of the drug formulation, decreasing tear film washout,
arid increasing bioavailability of the drug.
through the lens zonules, into the aqueous. and through
aqueous outflow pathway.
RETINA AND OPTIC NERVE
The blood-retinal barrier resembles the blood-boin bowie
in form and function, with both the retina ad bait beinc
derivatives of the neural tube. Most hydooptdrc dugs an:
metabolites and toxins of high molecular wieiglitull not ernethe inner blood-retina barrier formed by theendothellal cells
of retinal capillaries. On the other hand Ilpoplac drugs cross
the barrier easily in either direction. Some S)clismic drugs can
be toxic to the retina a^-_'
=
FACTORS AFFECTING DRUG PENETRATION
INTO OCULAR TISSUE
III. OPHTHALMIC DRUG
DELIVERY
TOPICAL ADMINISTRATION
Most ophthalmic drugs are applied topically because it is
simple, convenient, non-invasive, and can be self-administered
by the patient. Topical medications do not typically penetrate
the posterior structures of the eye in useful concentrations,
and are therefore of no therapeutic benefit for diseases of the
posterior segment.
1. SOLUTIONS AND SUSPENSIONS
DRUG CONCENTRATION AND SOLUBILITY
The rate of
C.7
Law, is linearly dependent On the ccr
_
fference
between the compartments on either side c- -- e barrier. A
higher drug concenuation improves drug penetration.
VISCOSITY
is a function of molecular weight and
Molectha:
concentration_ Addition of an "ophthalmic vehicle' to the
active ingredient and preservative complements drug action
by providing proper tonicity, buffering, and viscosity to the
formulation_ Vehicles such as methylcellulose and polyvinyl
alcohol are water-soluble viscosity enhancers with both
hydrophilic and lipophilic sites.
Eyearop soiutions and suspensions are the most commonly
used form of topical administration. Eye drops, however are
an inconsistent and imprecise method of drug delivery.
Compared to ointments, eye drops are easier to instill and
cause little interference with vision. However, eyedrops have
less contact time, have increased risk for contamination, and
may cause ocular injury from careless instillation.Traditionally,
one drop is SO microliters, which exceeds the volume of the
conjunctival cul-de-sac of 30 microliters.
Standard colors for drug labeling help lessen confusion: red
for mydriatics and cycloplegics, green for miotics, pink for
steroids, brown or tan for anti-microbia Is, teal for prostaglandin
analogues, yellow or blue for beta blockers, and orange for
carbonic anhydrase inhibitors.
SPECIAL TOPICS I 8.5 Ocular Pharmacology
209
Instillation of eye drops may be done with the patient looking
down and retraction of the upper eyelid, or with the patient
looking up with head inclined backwards and retraction
of the lower lid. The drop is applied to the exposed bulbar
conjunctiva, avoiding the cornea to minimize a blink reflex.
The dropper is kept away from the globe to prevent contact
contamination and possible injury. The eyelids are gently
5. SOLID DELIVERY DEVICES
Solid delivery devices allow for a more regulated release
of drugs, instead of the pulsed administration of solutions,
characterized by an initial period of over dosage followed by
relative under dosage.
closed without squeezing to retard nasolacrimal drainage and
minimize potential side effects associated with systemic drug
absorption. Nasolacrimal occlusion for 2 to 3 minutes; done by
applying finger tip pressure over the punctum and canaliculi,
may enhance intraocular drug absorption.
2. OINTMENTS
Ointments have the advantage of prolonged ocular contact
time compared to solutions, allowing for less frequent dosing
of the medication. When ointments are applied during the
day patients frequently complain of blurred vision and "oily"
skin around the eye. Hypersensitivity to the preservatives and
certain sensitizing agents in the ointment may occur due to
prolonged contact time.
Administration of ointments is done while asking the patient
to look up with head inclined backwards. While retracting
the lower lid, a 1 centimeter strip of ointment is placed in the
inferior conjunctival cul-de-sac. When applied to the cul-desac, ointments melt immediately and spread to the eyelid
margin, lashes, and skin. Ointment in the eyelid margin acts
as a reservoir and increases drug contact time. An alternative
method of applying ointments is by placing it on a cottontipped applicator and applying it to the upper eyelid margin
and lashes. This method minimizes blurred vision and drug
irritation.
a. Soft contact lenses
Contact lenses with high water content, when placed in
soaking solutions, absorb more water-soluble drugs for
later release into the pre-corneal tear film. However, rapid
loss of drug from the contact lens lessens the significance
of this advantage over topical administration of solutions
and ointments.
b. Collagen shields
Collagen shields are thin membranes of porcine or bovine
sclera collagen, and are similar to contact lenses in shape
and application. They are packaged in a dehydrated state
and are rehydrated with a drug solution before placing on
the cornea. The drug is released as the shield dissolves.
Topical anesthesia is placed into the eye to minimize
discomfort caused by application of the shield.
c. Filter paper strips
Drug-impregnated filter paper strips allow for easy
administration of drugs in amounts adequate for
their intended clinical purpose. The use of filter paper
strips prevents administration of excessive amounts
and eliminates the risk of solution contamination
with Pseudomonas aeroginosa. Three staining agents,
sodium fluorescein, lissamine green, and rose bengal,
are commercially available in filter paper strips. The
concentration delivered to the ocular surface depends on
the strip soak time and technique.
3. LID SCRUBS
Application of a solution, ointment, or detergent, such as baby
shampoo, by lid scrub is helpful in the treatment of seborrheic
or infective blepharitis. This aids in the removal of oil, debris,
and desquamated skin from the inflamed eyelid. Lid scrubs are
also used for hygienic eyelid cleaning.
The drug-impregnated filter paper strip is moistened with
a drop of normal saline prior to touching the exposed
bulbar conjunctiva and conjunctival cul-desac of an eye
with retracted lower eyelid. Separate strips can be used
for each eye to avoid cross-contamination between eyes.
d. Cotton pledgets
Lid scrub involves placing a strip of ointment or several drops
of solution or detergent on a cotton-tipped applicator and
applying it to the lid margin with eyes open or closed.
A pledget is a small elongated tuft of cotton constructed
by teasing the cotton tip of an applicator. The cotton
pledget is saturated with 1 or 2 drops of solution, usually
mydriatics like phenylephrine, and placed into the inferior
4. GELS
Gelling agents transform from gel to liquid upon contact
with the eye, rendering the drug hydrophilic and minimizing
conjunctival cul-de-sac (fornix).
complaints of blurred vision.
Gel-forming agents are applied as eye drops and are converted
by temperature changes into a gel-like viscosity that prolongs
vision or
contact time with the eye without causing blurred
ocular discomfort.
PERIOCULAR ADMINISTRATION
Compare° w topecai administration, local injections into
periocuiar tissues bypass the conjunctiva and corneal
epithelurn. and delver higher concentrations of drugs with
IOW lipid sdubdity such as corticosteroids and antibiotics.
There are four main routes for periocular injections. Selection
of the injection SINP depends primarily on the location of the
target aneet-
1. 5 UBCONJUNCTIVAL INJECTION
Subconjunctivai injections between the conjunctiva arc,
Tenon's capsule allow for higher local drug concert-atcrs
with the use of smaller drug quantities.This eliminates.use
systemic effects of the drug, avoids the need for oca or
systemic drug administration, and minimizes probes we"
INTRAVITREAL ADMINSTRATION
Because of the blood- retinal barrier, there is decreased
penetration into the eye of systemic antibiotics. Intraocular
infections like endophthalmitis can be successfully treated
with intravitreal rather than systemic administration.
patient compliance.
2. SUBTENON'S INJECTION
Compared to subconjunctival injection, subtenon's ripEction
between the Tenon's capsule and sclera offers ktIlle advantage
and may even deliver lower quantities of drug into the
eye, as well as increase the risk of globe perforaton For
certain inflammatory diseases, like severe weird. cystoid
macular edema, and diabetic macular edema. injection of
corticosteroids may penetrate the underlying sclera. and so
the drug must be placed immediately adjacent ID die site of
inflammation.
3. RETROBULBAR INJECTION
Drugs injected into the intraconal space for inside the
muscle cone posterior to the globe) En da& aneghetics.
corticosteroids, phenols, and alcohot. Fletrobulbar ilection of
anesthetics results in rapid onset of anesthesia and akinesia
(or skeletal muscle paralysis) for anterior segment arc
vitreoretinal surgery. The retrobuIbar technique however. is a
blind procedure where a needle is placed ediemely dos-7 the globe while aiming for the roust* cone. vitich c---vital structures like the optic nerve. Potential risks
inadvertent globe penetration. ietrobufbar hemorrhage
direct injury to the optic nerve
4. PERIBULBAR INJECTION
The peribulbar technique invokes one or more injections
around the globe, without directly aiming forthe muscle cone
Anesthetic injected around the globe eyeing,* infiltrates
the muscle cone. Although also a bind procedure, the
SYSTEMIC ADMINISTRATION
1. Oral
2.
Intravenous
3.
Intramuscular
PHOTODYNAMIC THERAPY
Photodynamic therapy involves systemic administration of
a photosensitive drug followed by the application of nonthermal laser to produce a "dynamic' reaction which causes
necrosis of the lesion. This method is used to treat choroidal
neovascularization associated with age-related macular
degeneration. Non-thermal light converts the drug and
produces cell death of abnormal tissues. Unlike conventional
laser procedures, photodynamic therapy produces minimal
damage to normal retinal and choroidal tissues.
IV. OCULAR
PHARMACOTHERAPEUTICS
LOCAL ANESTHETICS
Local anesthetics act on cell membranes to produce
completely reversible conduction blockage of nerve impulses,
resulting in sensory anesthesia and skeletal muscle paralysis
(or akinesia), without structural damage to nerve fibers and
loss of consciousness. Duration of the anesthetic effect is
proportional to the length of time the drug is bound to nerve
proteins, which depends on the chemical structure of the
drug, the drug concentration, the amount of administered
peribulbar technique is safer than the retrobubar technique.
Compared to the retrobutpar technique. penbulbar injection
Of anesthetics provides a simian anesthesia and akinesia, but
drug, and the rate of drug removal by diffusion and circulation.
Local anesthesia containing amide is metabolized primarily by
with less rapid onset.
the liver.
INTRACAMERAL ADMINISTRATION
LINJECTABLE ANESTHETICS
Intracamerai acknirisnation involves directly plating a drug
into the anterior chamber. During anterior segment surgeries.
such as cataract extraction and glaucoma filtering surgery,
substances can be placed in the anterior chamber, like
viscoelastics to prevent damage to the comeal endothelium,
sustained-release pelets to provide high intraocular drug
levels for a longer duration. and unpreserved 1% lidocaine
to anesthesize the iris and diary body and decrease patient
discomfort.
a. Lidocaine
Lidocaine is the M05: frequently used injectable
anesthetic. One percent lidocaine without preservatives
can be injected into the anterior chamber during cataract
surgery to supplement topical anesthesia. Addition
of local vasoconstrictors like epinephrine to lidocaine
decreases the rate of absorption into the systemic
circulation, resulting in longer duration of action, less local
bleeding, and lower risk of systemic anesthetic toxicity.
8
SPECIAL TOPICS 1 85
Ocular Pharmacology MI
b.
B upivacaine
c.
Procaine
d.
e.
Etidocaine
Mepivacaine
2. TOPICAL ANESTHETICS
Topical ocular anesthetics suppress corneal sensitivity.
However, it can cause eye irritation and, if used frequently,
localized or diffuse corneal desquamation.The onset of action
is 10 to 20 seconds and the duration is 10 to 20 minutes.
Moderate stinging or a mild burning sensation immediately
follows instillation, and corneal anesthesia lasts for 20 to 30
seconds. Combining two or more topical anesthetics has no
additive effect and can increase the risk or side effects.
b. Non-salicylate non-steroidal anti-inflammatory
drugs (NSAIDs)
The analgesic effect of NSAIDs is produced by inhibiting
cyclooxygenase. The drug is metabolized in the liver and
excreted by the kidneys. Like salicylates, NSAIDs can cause
GI discomfort and GI bleeding. NSAIDs also interfere with
platelet aggregation, resulting in prolonged bleeding
time.
i.
Although rare, side effects include allergic hypersensitivity,
epithelial keratitis, corneal edema and corneal desquamation
resulting in tear film dysfunction.
a.
b.
c.
d.
Proparacaine
Proparacaine is available as a topical 0.5% solution.
Tetracaine
Benoxinate
Cocaine
ANALGESICS FOR TREATMENT
OF ACUTE OCULAR PAIN
Patients may experience substantial pain from ocular
conditions like corneal or conjunctival foreign bodies (even
after their removal), corneal abrasion, and ocular trauma.
Nociceptors in specialized pain endings of peripheral
nerves, activated in response to trauma, can be found
in the subcutaneous tissues and periosteum of the eye
and orbit. Pain signals are conveyed to the brain through
the trigeminal nerve; in turn, the trigeminal nucleus
sends pain signals to the somatosensory cortical areas in
the brain. Analgesics act as: (1) Peripheral acting agents,
like nonsteroidal anti-inflammatory drugs (NSAIDs), block
the formation of inflammatory and pain mediators at the
cyclooxygenase pathway; (2) Anesthetic agents, which block
nociceptive signals from the peripheral source to the brain or
spinal cord; and (3) Centrally acting agents, like opioids, that
react with specific receptors in the central nervous system.
1. NON-OPIOID (NON-NARCOTIC) ANALGESICS
Propionic Acids
1. Ibuprofen
2. Naproxen
3. Fenoprofen
4. Ketoprofen
5. Oxaprozin
ii. Cox-2 Inhibitors
1. Celecoxib
c. Acetaminophen
The analgesic action of acetaminophen is unclear. It is a
weak inhibitor of cyclooxygenase. Unlike aspirin, it has
no anti-inflammatory properties. Therefore, aspirin is
superior to acetaminophen in treating pain associated
with inflammation. Acetominophen, however, does not
cause gastrointestinal irritation or prolonged bleeding
time from inhibition of platelet aggregation. It can be
used safely during pregnancy and breastfeeding. When
used in patients with chronic alcoholism and pre-existing
liver impairment, acetaminophen can lead to serious liver
toxicity and ultimately death.
d. Non-narcotic combinations
2. OPIOID (NARCOTIC) ANALGESICS
Opioids are natural or synthetic compounds that possess
morphine-like analgesic effects. They are the first drug of
choice for treatment of severe acute pain affecting both
noxious stimulation (pain) and the emotional component
of subjective distress (suffering). Analgesia is produced by
binding to various opioid receptors in the brain, brainstem,
and spinal cord, thus mimicking the effect of endorphins.
The amount of analgesia produced is directly proportional
to dose. with no ceiling effect, thus the potential for abuse
and ackfiction_ It produces a high degree of sedation and GI
Non-opioid analgesics like NSAIDs are the most effective and
safest for short-term use.
a. Salicylates
Acetylsalicylic acid, or salicylate aspirin, has analgesic,
anti-inflammatory, and antipyretic properties. Aspirin
inactivates the cyclooxygenase pathway. The most
common side effect is gastrointestinal disturbance,
particularly increased gastric acid secretion.
a.
b.
c.
d.
e.
f.
Codeine
Oxycodone
Hydrocodone
Propoxyphene
Hydromorphone
Tramadol
:-. a -
MYDRIATICS AND MYDRIOLYTICS
. a - .ng degrees of parasympathetic
=7-E.' muscle produces varying degrees
Adrenergic receptors of the autonomic 'e. Dus system
are targeted by catecholamines, particularli. zradrenaine
and affect
(norepinephrine) and adrenaline (epinephr
various ocular functions like pupil size, pa 1pebra ssuie. bksod
vessel diameter, aqueous flow, and accommoca - 7r_ These
--are two main groups of receptors: a (alpha) and F
___
several subtypes. Adrenergic nerve terminals air
in the ciliary smooth muscle, iris dilator muscle. aid wOrillees
muscle.
Adrenergicagonistsorsympathomimetics causeasympathetic
response (flight-or-fight response), like increase in heart rate
and pupillary dilation. Mydriatics are used to dianeihe Dam
Adrenergic receptor antagonist, anti-ackenergi:3. or
adrenergic-blocking agents block the
Midriolytics are a-receptor blocking agent -.- a - La
constriction (miosis).
1. MYDRIATICS
a. Phenylephrine
Phenylephrine is a selective a-receplotagortist It 6 nxistty
_used clinically for dilating the pupi ugh
dilation at 45 to 60 minutes and cloaricr _-_- 77 77 - =
: -It contracts the iris dilator muscle arc
of the conjunctival arterioles. cau9ing
and blanching of the conjuncLikra corn wasp.: 7 Other effects include widening of the
from sympathetic stimulation tithe Mid& s
decreased intraocular press se bom
5,4ueous
production by the ciliary body_ Because a'
- a^ry local
and systemic side effects of plienylephrim_ ong term
clinical use is unsatisfactory
b. Hydroxyamphetarnine
c. Cocaine
2. MYDRIOLYTICS
Dapip-azole
e is an a-receptor blocking agent in the
iris dilator muscle, re:. 7 - in miosis and decreased
intrao_ 'a c -essure_
is concentratior
dep,
:an
"E
CYCLOPLEGICS
Cycloplegic agents are a E-7
an; - :muscarinics, and cr.:
:• j ace--3
—
the action of acetylchc e on 7s
inre- .
autonomic nerve fibers, and on srr: :71
e cells that la
cholinergic autonomic innervation. Cholinergic innervation
in the eye is seen in the ciliary body, iris sphincter muscle,
agents can increase the intraocular
billydniatic-cycicc
with open angle glaucoma and can
pressure it
precipitate a- attack of acute angle closure glaucoma in
J,"" -?—,W0Cfl.':,1?tde angles.
1. ATROPINE SULFATE
.ective muscarinic antagonist. It is
,s a
potent
mydriatic
and cycloplegic agent, with
:st
ass starting at 12 minutes and lasting up to 10 days,
and cyc = 7. a 7. a starting at 12 minutes and lasting 7 to 12
-- paralyzes accommodation up to 8 days. It is
.:_.• ng cycloplegic refraction of young, actively
- g children with suspected latent hyperopia
and acz: - -odative esotropia. In school-aged children and
adults~~hov.E. er, the prolonged paralysis of accommodation
7 — ear vision, thus a short-acting cycloplegic is
to prevent this inconvenience. The
,
c. -E•
caused by atropine has been used in
.
. as a form of 'penalization" of the eye with
arra:: .
combined with optical overPer
nor-;
a - a :ernative to direct occlusion of the
or
a :-.erapy. In inflammatory conditions,
a-::
better e.-s relieves pain by relaxing ciliary
.
lbs.
atropine
as
formation
of posterior synechiae by
spasm,
prevents
_ide
that prevents iris-corneal touch, and reduces
7--.7- :7
a=_==_a :e a and flare by decreasing excessive permeability
a -led vessels.
Adverse systemic reactions appear to be dose dependent.
Topically applied atropine is absorbed systemically through
the conjunctival vessels and the nasal mucosa. Children
and elderly are more susceptible to anti-cholinergic toxicity,
including depressed salivation, fever, hallucinations,
convulsions, and death. The treatment of atropine overdose
is supportive: preventing hyperpyrexia and dehydration.
Physostigmine, in repeated doses, is reserved for severe and
life-threatening side-effects.
2. HOMATROPINE HYDROBROMIDE
3. SCOPOLAMINE HYDROBROMIDE
4. CYCLOPENTOLATE HYDROCHLORIDE
Cyclopentolate is the cycloplegic agent of choice for
cycloplegic refraction in all age groups due to its relatively
fast onset of about 20 to 30 minutes and short duration of 24
hours. Recovery of accommodation to permit reading is about
6 to 12 hours.
Compared to atropine, cyclopentolate has more CNS side
effects, such as cerebellar dysfunction, visual and tactile
hallucinations.
8
SPECIAL TOPICS 18.5 Ocular Pharmacology MI
5. TROPICAMIDE
Tropicamide is a non-selective muscarinic antagonist. Like
cyclopentolate, the onset is fast (20 to 40 minutes) and the
duration of action is short (6 hours). The mydriatic effect is
greater than the cycloplegic effect, so it is not the drug of
choice for cycloplegic refraction. Unlike atropine, scopolamine,
and cyclopentolate, topical tropicamide absorbed systemically
has little affinity to systemic muscarinic receptors, thus adverse
systemic effects are rare.
OCULAR HYPOTENSIVE DRUGS
The group of diseases collectively known as "glaucoma" is
managed pharmacologically or surgically by lowering the
existing intraocular pressure (10P). Ocular hypotensive agents
each have their unique mechanisms of action, so drugs can be
used alone or in combination.
1. PROSTAGLANDIN ANALOGS
Prostaglandin analogs are the "first-line" treatment for most
patients with open angle glaucoma and ocular hypertension
because of their convenience (once daily dosage) and good
safety profile. The most common side effect is conjunctival
hyperemia. Other side effects include reversible increased
pigmentation to the eyelid skin and iris color, hypertrichosis,
allergy, anterior uveitis, cystoid macular edema, and punctate
corneal erosion. There is no drug tolerance with prolonged
use.
Latanoprost, the first commercially successful prostaglandin
analogue available, decreases l01) by decreasing uveoscleral
outflow. It is most effective when used in combination with
Timolol.
a. Latanoprost
b. Travoprost
c. Bimatoprost
2.11-ADRENERGIC ANTAGONISTS (j3-BLOCKERS)
The ocular hypotensive effect of (3-blockers is from antagonism
of the (32 adrenoceptors,in the ciliary body. With twice daily
dose, 13-blockers decrease the production of aqueous humor,
and have an insignificant effect on outflow. Drug tolerance
has been described with chronic use of (3-blockers, making
prostaglandin analogues better in terms of long-term efficacy
and compliance. Systemic side effects include bradycardia,
systemic hypotension, heart block and failure, bronchospasm,
diarrhea, and amnesia.
a. Timolol
b. Betaxolol
c. Levobunolol
d. Metipranolol
e. Carteolol
3. ADRENERGIC AGONISTS
In the 1920s, epinephrine, an adrenergic agonist, was
documented to decrease 10P after topical application to the
eye. Alpha 2-receptor agonists in presynaptic adrenergic nerve
terminals of the ciliary body decrease production of aqueous
humor and enhance uveoscleral outflow. When administered
thrice daily, it is an effective short term therapy for patients
on maximal medical therapy who still require additional 10P
reduction. It is effective in preventing 10P spikes after laser
procedures like argon trabeculoplasty, YAG capsulotomy, and
YAG peripheral iridotomy.
a. Apraclonidine
Common ocular side effects include conjunctival
blanching, lid retraction, and mydriasis.
b. Brimonidine
Unlike apraclonidine that causes mydriasis, brimonidine
causes miosis. Dry mouth is the most common systemic
side effect. Other side effects include headache,
drowsiness, and fatigue.
4. CARBONIC ANHYDRASE INHIBITORS (CAI)
Inhibition of carbonic anhydrase activity in the ciliary
processes by CAI decreases aqueous production because
carbonic anyhydrase catalyzes the cellular production in the
ciliary epithelium of bicarbonate, an essential component of
the aqueous humor. Systemic CAls, such as acetazolamide
(250 mg capsule every 6 hours), lowers 10P by inhibiting the
activity of carbonic anhydrase throughout the body. CAls are
excreted unchanged by the kidneys. Impaired renal function
may require substantially lower doses of CAls. Oral CAls can
cause hypokalemia; thus, necessitating potassium monitoring
and replacement.
Topical CAls, as a twice or thrice daily dose, have an onset of
action at 2 hours and duration of 8 hours. Topical and oral CAls
do not produce an additive effect, and their combined use is
not indicated in glaucoma treatment.
a.
b.
c.
d.
Acetazolamide (available locally in tablets of 250 mg)
Methazolamide
Dorzolamide ,available locally as a topical eye drop)
Brinzolamide (available locally as a topical eye drop)
5. CHOLINERGIC AGONISTS (MIOTIC)
Cholinergic agonists, also known as parasympathomimetics
or cholinomimetics, are biologically similar to acetylcholine.
They are divided according to their mechanisms of action,
into direct and indirect acting (cholinesterase inhibitor). Direct
acting agents. like pilocarpine, act directly at the neuroeffector
junctions of the iris sphincter muscle and ciliary body, resulting
in pupilary constriction, spasm of accommodation, and
reduction d 10P. Indirect acting agents inhibit cholinesterase,
thereby increasing amounts of acetylcholine available at
cholinergic receptors
a.
Pilocarpine
3oxycycline
Pi 0Cdf pine is a muscarinic agonist that increases aqueous
..e erythromycin, clarithromycin,
outflow through the trabecular meshwork. At a dose of
3:
four times a day, pilocarpine is indicated in acute angleclosure glaucoma. It is also useful in stre-.:"jng ti' iris
common.
prior to laser iridotomy. Ocular side effects
making pilocarpine intolerable to mans -.:..a-Lencs. Side
effects include blurring of vision due to acconignonatiwe
spasm in the young, miosis in the elderly with tracts.
pupillary block with secondary angle-closure glaucoma.
and retinal detachment. Systemic side effec-_--1, assoomed
with the cholinergic activity of pilocarpine are
b.
. :in
col
d.
Inhibiting folk acid synthesis.
- _ amides
it Pyrimethamine
Trirneth C'irT1
e. Inhibition of enzymes DNA gyrase and
topoisomerase IV, which are specific for bacteria.
quinolones (fluoroquinolones) like
Carbachol
7,
c.
ANTI-INFECTIVE DRUGS
-±-e-af,-; starts with obtaining a history
Anti-Infective drugs exhibit selec-u.e towicity.The dilemmas
between the cells of humans and of miC100111111111191115 allow
drugs to kill microorganisms while causing eniirlirnall or no
adverse reactions to the host. "Spectfurn of activity' velars to
whether a drug is "narrow- or broad-spec:rise', diepencing on
the number of species the drug is active against.
1. ANTI-BACTERIAL DRUGS
Bacteria can oe divided into C:i;an Star !maim cell shape and
- = -- pm
7 ?..sing
cell arrangement. Common
Serratia marcescens, Proteus
norficcocin, dprofloxacin, ofloxacin,
a :in, gemifloxacin, levofloxacin, and
ic •-
Echothiophate
are Staphylococcus aureus
Gram-positive, and Neisseria
is seen in:
_
43 ix
_
Estnerthia co&
;sada/Toms aerughosa
".-e patient. A tentative diagnosis
of the causative .--.icroc - :anism is made, which becomes
the basis kw empiric trey- — ent using one or a combination
agents. usually a
.7-spectrum agent that is the least
wick. The route of ad— - stration (topical application, oral
ar injection, intravitreal injection,
administration.
a
intravenous kijection. or a combination of routes) and the
dose are determined. For ocular surface infections, topical
appicaion is preferred. Laboratory culture of tissues or body
kids is used to confirm the clinician's initial diagnosis and
to determine the sensitivity and resistance of the isolated
microorganism to the agents started.
for Gram-negative bacteria.
Reasons for antimicrobial failure include: wrong diagnosis,
Anti-bacterial drugs act against bactertathroucfrvthefollowing
mechanisms:
drug resistance, inadequate dosage, patient non-compliance
and inadequate immune response. Bacteria can mutate to
cause drug resistance by: producing enzymes that inactivate
the ar--.Thiotic, blocking the binding of the antibiotic to the
a. Inhibiting cell wall synthesis of peptidoglycans,
which is necessary for structural integrity of the
bacteria.
:
i.
Pe-
ii.
CephatiSpOriln
iii.
Ba:
recec -.: - site, and preventing antibiotic entry into the bacterial
cell.
2. ANTI-VIRAL DRUGS
;ge
--.erfere with viral replication and
on by in - siting thymidine kinase needed for
nucleic acid synthesis.
N. Ite'
b. Selectively disrupting bacterial cell membranes.
Herpes simplex virus (HSV1) is the most frequent cause
of primary and recurrent eye disease, such as blepharitis,
conjunctivitis,epithelial and stromal keratitis, uveitis, and
retinitis.Treatment of herpes simplex and of herpes zoster viral
infections include:
c.
Selective binding of drug to bacterial ribosomes,
which differ from that of humans in size and
composition, thereby inhibiting bacterial protein
synthesis. s see- :
Armnogrycosides like neomycin, gentamicir
tobrarnycin, and amikacin
a.
Tr ifl u rid ine
b.
c.
d.
e.
Acyclovir
Valacyclovir
Famcyclovir
Gancyclovir
8
SPECIAL TOPICS 1 8.5 Ocular Pharmacology
arif
Admovirusos (serotypes 2, 7, g,19, and 37) cause conjunctivitis
and epidemic keratoconjunctivitis. Currently, no antivirals are
approved for ocular adenoviral infections.
Cytomegalovirus (CMV) retinitis is the most common
opportunistic ocular infection in patients with AIDS and
immune-compromised transplant patients.
3. ANTI-FUNGAL DRUGS
Fungi can infect any eye structure, including the cornea,
conjunctiva, lens, ciliary body, vitreous, retina and the entire
uveal tract. The most common ocular fungal pathogens are
the yeast Candida and the molds Aspergillus, Fusarium, and
Curvularia.
There are four classes of anti-fungals based on mechanism of
action:
a. Polyenes increase cell permeability by binding
ergosterol in the cell membrane. They are fungistatic
at low concentration and fungicidal at higher
concentration. Resistance is relatively rare.
i. Amphotericin B
ii. Natamycin
release in type I (Ig-E mediated) hypersensitivity immune
response; and (4) the inflammatory prostaglandin pathway
by blocking phospholipase A2, which prevents biosynthesis
of arachidonic acid, and production of prostacycline,
thromboxane A, prostaglandins, and leukotrienes. Steroids
decrease capillary permeability and fibroblast proliferation.
They affect the quality of collagen deposition, thereby
influencing tissue regeneration and repair.
Corneal penetration of topical steroids is affected by the
steroid base of the drug. Acetate and alcohol derivatives make
the steroid molecule more liphophilic. Salts, such as sodium
phosphate and sodium hydrochloride, make the steroid
molecule more hydrophilic. Acetate derivatives produce the
highest corneal concentration. The route of administration is
determined by the location of inflammation. The dosage and
frequency of administration are determined by the clinical
experience of the physician, but should be high enough to
suppress inflammation. Short-term, low dose topical steroid
treatment generally does not produce side effects. Longterm, high dose treatment must be gradually tapered and not
discontinued abruptly.
b. Pyrimidines inhibit DNA synthesis by blocking
thymidine kinase. It is fungistatic and drug resistance
can occur. An example is Flucytosine
c. Azoles inhibit fungal growth by increasing cell
permeability through binding ergosterol in the cell
membrane. They are fungistatic. Drug resistance can
occur with their use. Examples are:
i. Ketoconazole
ii. Miconazole
iii. Itraconazole
iv. Fluconazole
v. Voriconazole
d. Echinocandins weaken the cell wall by inhibiting
glycan synthesis.
Caspofungin
i.
Micafungin
iii. Anidulafungin
ANTI-INFLAMMATORY DRUGS
1. CORTICOSTEROIDS
Corticosteroids, particularly prednisolone, are the most
common agents for ocular inflammation. They affect every
tissue in the body and every aspect of the immune system by
inhibiting: (1) neutrophil migration into the extracellular space
and adherence to vascular endothelium at the site of tissue
injury; (2) B-cell and T-cell lymphocytic activity by preventing
Corticosteroids can be classified as short acting
(hydrocortisone, cortisone, prednisolone), intermediate
acting (trimcinolone, fluprednisolone), and long acting
(dexamethasone, betamethasone).
Ocular hypertension and cataracts are the most common
ocular side effects of steroid treatment to the eye by any route.
Steroids can also retard corneal healing and can increase
susceptibility to viral, fungal, and bacterial infection. Other side
effects include paradoxical anterior uveitis, mydriasis, and ptosis.
Systemic side effects include adrenal suppression, peptic ulcer,
hypertension, increased blood sugar, osteoporosis, mental
changes, and activation of tuberculosis and other infections.
2. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
(NSAIDS)
Like steroids, NSAIDs reduce inflammation but without
the side effects of steroids. Topical NSAIDs, however, are
less effective than topical steroids in controlling anterior
chamber inflammation. It blocks the cyclooxygenase arm
of the inflammatory prostaglandin pathway. Ketorolac and
diclofenac reduce pain and discomfort after corneal refractive
surgery.
NSAIDs can prolong clotting time from decreased platelet
aggregation.
3. CYCLOSPORINE A
Cyclosporine A is used to treat keratoconjunctivitis sicca (dry
eye). It is safe and well-tolerated.
mnii 1 - /ALLLKGY DRUGS AND
DECONGESTANTS
antihistamines, such as pheniramine maleate and antazoline
phosphate, are commercially available in combination with
naphazoline, an adrenergic agonist decongestant. Second
The eye, particularly the conjunctiva, eyelids, and cornea, is a
generation antihistamines, such asazelastine, ketotifen, and
olopatadine, also 6?...e ? ?.
stabilizing effect.
common sitefor allergic reactions.The immunesystemprovides
a defense mechanism against antigens, such as pollen
dander. A normal immune response removes ar _ _
with an inflammatory reaction that results in minimum tissue
damage. Hypersensitivity or allergic reactions are exaggerated
immune responses that result in tissue damage. -Twes I and
IV hypersensitivity responses play a significant to,.
=
-_- eye disease. Type I or humoral hypersenolioir
mediated mainly by histamine, involves immetteof B lymphocytes and production of Immo(IgE) that binds to mast cells and basophils
cyclooxygenase arm of the inflammatory p
pathway. Histamine release can result in a vice range of
clinical manifestations, from life-threatening a-azrglapc
ad—T
shock to the relatively benign presentations at
tearing, and conjunctival hyperemia. Histamine aso
hypotension, tachycardia, and decreased atricneiasitular rode
conduction time. Type IV or cell-mediated immune resPorse
is a delayed hypersensitivity reaction involving TIlriphocyles.
Avoidance of environmental allergen=
management. Treatment of ocular allerry.
and characteristics of symptoms.
"P,
3. MAST CELL STABILIZERS
as cromolyn sodium, lodoxamide,
nedocromi, and pemirolast, inhibit type I immune response
and release of mediators of allergic disease by preventing
mast cell degranulation and calcium influx across mast cell
—embr
4. NONSTEROIDAL ANTI-INFLAMMATORY
DRUGS ,NSAIDS)
•etoiciac uoinewomine is the only topical NSAID approved
for beatinent of seasonal allergic conjunctivitis. It inhibits
cydoonygenase, an enzyme needed for the conversion
of asachidonic acid to prostaglandins, an itch-producing
substance in the conjunctiva.
S. 00111TKOSTEROIDS
SterOidS are effective in treating seasonal allergic conjunctivitis
by deaeasing histamine release, preventing degranulation of
mast cells, and preventing formation of various mediators.
PREPARATIONS FOR DRY EYE
AND OCULAR SURFACE DISEASE (OSD)
1. DECONGESTANTS
•ftmphainine.
Ocular decong:__ .ants, such as pherigl pilline.
oxymetazoline, and tetrahydrozoine are sysligicatbenergic
agonists that cause conjunctival Va500311INICNOn iD lessen
hyperemia and edema.
2. ANTI-HISTAMINES
Anti-histamines inhioit tne action of histamine_ They prevent
further release of histamine but usualllydoesnot reverse &mica'
manifestations already present ilia nasal and conjunctival
itching, sneezing. congestion., and maser, aid red eyes. Oral
antihistamines may be sedating (first generation antihistamines
like diphenhydramine and prOmediazine) or non-sedating
(second generation andigarnines
like felarenackne,
loratadine, desloratacine. and catkin?), depencing on their
ability to penetrate the bbod brain bailer, which is affected
by factors like kpophillecity and low molecular weight. Nonsedating second generation antibistamines bind less to
cholinergic and a-adrenergic receptors. resulting in less adverse
effects associated with first generation anti-histamines, such
as CNS depression, dry mouth, blurred vision, and tachycardia.
Oral antihistamines. compared to topical anti-histamines. have
a deeper penetration of ocular tissues, and are therefore more
effective in moderate to severe eyelid edema and chemosis.
Topical administration, with more frequent dosing, provides a
more direct and rapid route of relief. First generation topical
Dry eye syndrome is described as a deficiency in the quantity or
quality of the tears or tear film due to inadequate aqueous tear
production (referred to as keratoconjunctivitis sicca or KCS) or
to excessive tear evaporation. Dry eye causes ocular surface
disease and is associated with symptoms of ocular discomfort
and varying degrees of ocular surface inflammation.
Treatment of OSD involves relieving ocular symptoms, healing
the ocular surface, and preventing serious complications.
Treatment of dry eye can be categorized into: (1) tear
supplementation (seen in artificial tears and lacriserts), (2)
tear conservation (seen in ointment and punctal occlusion),
and (3) tear stimulation (seen in secretagogues and antiinflammatories or immunomodulators).
1. ARTIFICIAL TEARS
arz.t.c.a. tears snould reproduce the metabolic, optical,
3e5
and physical characteristics of natural tears, should have a
long ocular residence time, and should contain therapeutic
additives to treat primary and secondary damage to the eye.
Water-based artificial tears with added polymer are commonly
used to treat dry eye. Polymers, such as methylcellulose (MC),
polyvinyl alcohol (PVA), povidone or polyvinylpyrrolidone
(PVP), dextran, and propylene glycol, enhance viscosity,
lubrication, and retention time, to promote tear film stability.
8
SPECIAL TOPICS I 8.5
Ocular Pharmacology
Ells
2. OINTMENTS
Non-medicated ointments containing esters of fatty acids with
long-chain alcohol, such as petrolatum, mineral oil, lanolin,
and lanolin alcohols serve as lubricants and create a lipid layer
that retard evaporation. Ointments are indicated for moderate
dry eye, especially with lagophthalmos, exposure
keratopathy, or severe corneal epithelial compromise.
to severe
3. SECRETAGOGUES
Secretagogues or lacrimomimetics stimulate lacrimal gland
function to enhance tear production. It includes cholinerg
agents (carbachol, bethanecol, pilocarpine) and mucolytics
(bromhexine and ambroxol).
4. ANTI-INFLAMMATORIES/IMMUNOMODULATORS
Hormonal (like androgens), anti-inflammat:
corticosteroids), or immunomodulatory agents (like
cyclosporine) can suppress cytokine and receptor-mediated
inflammatory process of the lacrimal gland that leads to
decreased tear production and chronic dry eye.
SUMMARY
Successful diagnosis and treatment of ophthalmic
disease require proper drug selection and administration.
Inappropriate, inadequate, or contraindicated drug regimen
may lead to potentially adverse consequences_ Pharmacists
or other qualified drug experts must be consulted when
necessary.
REFERENCES
1.
Bartlett JD and Jaanus SD. Clinical Ocular Pharmacology,
5th edition. St. Louis, MO: Butterworth-Heinemann,
Elsevier, 2008.
2. Flach AJ and Fraunfelder FW. Chapter 3: Ophthalmic
Therapeutics, in Vaughan & Ashbury's General
Ophthalmology 16th edition. New York, NY: McGraw Hill
Companies, 2004.
3. Weitzman S and Caprioli J. Chapter 61, Ocular
Pharmacology of Antibacterial Agents, in Duane's Clinical
Ophthalmology, 2006 edition. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006.
4.
Sutphin JE and Wells JM. Chapter S6: Medical Treatment
of Glaucoma, in Duane's Clinical Ophthalmology, 2006
edition. Philadelphia, PA: Lippincott Williams & Wilkins,
SELF-TEST
Which of the following INCREASES ocular drug
absorption?
A. Increase in age of the patient
B. Increase in hydrophobicity of the drug
C Increase in rate of tear flow
D. Increase in size of released drop from the container or
bottle
2. Which of the following DECREASES ocular drug
penetration?
betweer
concentration
drug
in
, ncrease
compartments of the eye
B. Increase in lipid solubility through the epithelial cel
membrane
C. Increase in pH of the drug formulation
D. Increase in tonicity relative to tears
7.
3.
Which is TRUE about eye drops?
A. Eye drops are easy to instill but causes blurring of
vision.
B. Nasolacrimal occlusion decreases intraocular drug
absorption
C. The bottle of the eye drop precisely delivers 50
microliters with every drop
D. The volume of a drop from the bottle is more than
the volume of the conjunctival cul-de-sac
4. Which of the following statements is TRUE regarding
topical eye drug preparations?
A. Eye drops have a high absorption rate into the
vitreous.
B. Gels are hydrophobic and this leads to complaints of
bluffing of vision.
C. Ointments are most commonly used due to ease of
application and minimal subjective complaints from
patient use.
D. Ointments have prolonged contact time, allowing for
less frequent dosing of medication.
5. Addition of local vasoconstrictor epinephrine to
lidocaine results in which of the following?
A. Decrease in duration of action
B. Decrease in local bleeding
C. Increase in risk for systemic toxicity
D. Increase in rate of absorption into the circulation
2. OINTMENTS
Non-medicated ointments containing esters of fatty acids with
long-chain alcohol, such as petrolatum, mineral oil, lanolin,
and lanolin alcohols serve as lubricants and create a lipid layer
that retard evaporation. Ointments are indicated for moderate
to severe dry eye, especially with lagophthalmos, exposure
keratopathy, or severe corneal epithelial compromise.
3. SECRETAGOGUES
Secretagogues or lacrimomimetics stimulate lacrimal gland
function to enhance tear production. It includes cholinergic
agents (carbachol, bethanecol, pilocarpine) and mucolytics
(bromhexine and ambroxol).
4. ANTI-INFLAMMATORIES/IMMUNOMODULATORS
Hormonal (like androgens), anti-inflammatory (like
corticosteroids), or immunomodulatory agents (like
cyclosporine) can suppress cytokine and receptor-mediated
inflammatory process of the lacrimal gland that leads to
decreased tear production and chronic dry eye.
SELF-TEST
1. Which of the following INCREASES ocular drug
absorption?
A. Increase in age of the patient
B. Increase in hydrophobicity of the drug
C. Increase in rate of tear flow
D. Increase in size of released drop from the container or
bottle
2. Which of the following DECREASES ocular drug
penetration?
A. Increase in drug concentration between
compartments of the eye
B. Increase in lipid solubility through the epithelial cell
membrane
C. Increase in pH of the drug formulation
D. Increase in tonicity relative to tears
3.
SUMMARY
Successful diagnosis and treatment of ophthalmic
disease require proper drug selection and administration.
Inappropriate, inadequate, or contraindicated drug regimen
may lead to potentially adverse consequences. Pharmacists
or other qualified drug experts must be consulted when
necessary.
REFERENCES
1.
2.
3.
4.
5.
Bartlett JD and Jaanus SD. Clinical Ocular Pharmacology,
5th edition. St. Louis, MO: Butterworth-Heinemann,
Elsevier, 2008.
Flach AJ and Fraunfelder FW. Chapter 3: Ophthalmic
Therapeutics, in Vaughan & Ashbury's General
Ophthalmology, 16th edition. New York, NY: McGraw Hill
Companies, 2004.
Weitzman S and Caprioli J. Chapter 61, Ocular
Pharmacology of Antibacterial Agents, in Duane's Clinical
Ophthalmology, 2006 edition. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006.
Sutphin JE and Wells JM. Chapter 56: Medical Treatment
of Glaucoma, in Duane's Clinical Ophthalmology, 2006
edition. Philadelphia, PA: Lippincott Williams & Wilkins,
2006.
Sutphin JE and Wells JM. Chapter 61, Ocular
Pharmacology of Antibacterial Agents, in Duane's Clinical
Ophthalmology, 2006 edition. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006.
218
Self-Instructional Materials in Ophthalmology 12nd Edition
Which is TRUE about eye drops?
A. Eye drops are easy to instill but causes blurring of
vision.
B. Nasolacrimal occlusion decreases intraocular drug
absorption
C. The bottle of the eye drop precisely delivers 50
microliters with every drop
D. The volume of a drop from the bottle is more than
the volume of the conjunctival cul-de-sac
4. Which of the following statements is TRUE regarding
topical eye drug preparations?
A. Eye drops have a high absorption rate into the
vitreous.
B. Gels are hydrophobic and this leads to complaints of
blurring of vision.
C. Ointments are most commonly used due to ease of
application and minimal subjective complaints from
patient use.
D. Ointments have prolonged contact time, allowing for
less frequent dosing of medication.
5. Addition of local vasoconstrictor epinephrine to
lidocaine results in which of the following?
A. Decrease in duration of action
B. Decrease in local bleeding
C. Increase in risk for systemic toxicity
D. Increase in rate of absorption into the circulation
6.
Characteristic of atropine eye drops
A. Is an intermediate-acting cycloplegic agent
B. Is used for amblyopia treatment
C. It can cause blurring of vision because of its miotic
effect.
D. It can cause bradycardia and asthmatic attacks
7. Which of the following statements is TRUE regarding
prostaglandin analogues?
-e-tt ocular
A. First-line drug for open angle c
hypertension
B. Mechanism of action is dec =poi aqueous
production
C. Prolonged use results in drug :ibiera-ce
D. The most common side effe..7 oypettnchosis
8.
9.
Anti-microbial treatment of eye disease
A. Combination of several antibiotics in a single eye
drop preparation is preferred for wide microbial
coverage.
B. Eye drops are given twice daily for ocular infections.
C. Topical administration for ocular surface infection is
preferred.
D. Treatment is started once the results of the Gram
stain and culture are available.
Characteristic of beta biodcers
A.
B.
C.
D.
Dose is once daily
Drug tolerance develops af-L- - Drponged use
Mechanism of action is in
ao_eous outflow.
Miosis is a side effect
Answer to Self-Test on page 223.
8
SPECIAL TOPICS I 8.5 Ocular Pharmacology
219
CHAPTER 1. ANATOMY OF THE EYE
A
1
2. C
3. D
4. D
5. C
6. C
7. C
8. E
9. C
10. B
CHAPTER 2. PHYSIOLOGY OF THE EYE
1. C
2. A
3. True
4. A
5. A-2, B-3, C-1
6. B
7. A
8. C
9. C
10. C
11. B
12. False
13. D
14. C
15. C
CHAPTER 3. EYE SYMPTOMS
CASE 1.
1. When did the blurring of vision (BOV) start?
2. Is the BOV in one eye or both? If one eye, which eye?
3. Is the BOV for distance, near or both?
4. Has the BOV worsened since the onset?Or has there
been some improvement?
5. Is the BOV in the whole visual field or in certain
portions of it only?
6. Are there associated eye symptoms like pain and
redness?
7. Do you squint in order to see better?
8. Have you consulted another doctor for this
problem? What did the doctor prescribe? Was there
10
improvement?
9. Have you worn eyeglasses before? When? Are you
still wearing eyeglasses now? If not why did you
discontinue?
10. Do you have any other illness? Are you taking
medications or have you taken medicatins prior to
ASE 2
1. When did the red eye start?
2. Was there no redness of the left eye?
3. Do you have tearing, discharge, itchiness, eye pain,
BOV?
4. Describe your eye discharge. How much is the
discharge?
5. Are your symptoms worsening, same as during the
onset or improving?
6. Are there family members or friends with red eye
7.
8.
9.
similar to yours?
Do you have allergies?
Do you have previous consultation? If yes, what was
prescribed? What was the response of your eye to the
medications? How are you applying the medications
and for how long?
Have you self-medicated? What did you apply and
what was the response of your eye?
CHAPTER 4. BASIC EYE EXAMINATION
1. B
2. B
3. B,C,D
4. A
5. A
6. C
C,D,F
CHAPTER 5.1. DISORDERS OF THE CORNEA
1. A
2. C
3. A
4. C
5. D
6. C
7. B
8. D
9. C
10. A
11. D
12
Ili
CHAPTER 5.2. CATARACT
2.
3.
4.
5.
D
CHAPTER 5.3. RETINA, VITREOUS AND
CHAPTER 5.5. DISORDERS
CHOROID
OF THE OPTIC NERVE
CASE 1
1. Vitreous hemorrhage OD probably secondary to
Proliferative Diabetic Retinopathy / Non Prokferaiine
Diabetic Retinopathy OS
2.
For OD: Vitreous hemorrhage because the retina
cannot be seen in OD/ negative ROR. This is probably
due to PDR because the other eye has NMI and she
has been a diabetic for many years with poor s.. -control.
For OS: NPDR because of the ex..:3-f
hemorrhages and microaneurysms ano oecaLse
is diabetic
3.
I would want to know if she has ever been seen by
an ophthalmologist and diagnosed to hake diabetic
retinopathy, if laser treatment has been done for 00.
I would also want to know if blurring of OD started
long before in a milder fours bekwe the sudden
drastic visual loss a week ago. I mil ask 'she has been
seeing her endocrinokvist, because blood sugar
management is necessary_
I will need an ocular ultrasound for OD and a
fluorescein angiogram for 05.
CASE 2
1.
Age related macular degeneration wet type OS,
pseudophakia OU
2.
Because OS has subretinal bleeding , poor vision, and
because she is 77 years old
3.
2_
3. 6
4. D
5. D
B
7. C
8 A
1A
CHAPTER 5.6. ERRORS OF REFRACTION
B
2_ C
3, A
4. C
5. B
-6_ A
7. C
8. A
9. C
10. A
11. A
12. B
13. B
14. B
CASE 1
1. Yes
2. Myopia
3. retinoscopy or autorefraction
CASE 2
No
Patient's age, good vision for distance, patient has to
put reading material 50 cm away to be able to read
'she takes vitamins,
I will want to know ishesretinal problem, if
ar
if she has a famiy history c this has happened to her before, if anyone else in her
famey has the same problem.
1.
CHAPTER 6.1 A CLINICAL ALGORITHM FOR
THE DIAGNOSIS OF THE RED EYE
4.
I will ask for a fundus fluores'.7e^ angiogram -and OCT
CHAPTER 5.4. GLAUCOMA
2.
E.
3.
4.
5.
C
A
E
6.
A
7.
A
8. A
9. D
10. C
2.
3.
=
A
D
4.
A.
5.
6.
7.
8.
9.
10.
A
C
B
A
C
9
ANSWERS TO SELF- TEST
Eg
CHAPTER 6.2. UVEITIS AND SCLERITIS
1
D
2. C
3. A
4. C
5. C
6. B
7. D
8. C
9. C
10. C
CHAPTER 7.1. DEVIATION OF THE EYE
1. B
2. D
3. A
4. D
5. A
6. B
7. C
8. B
9. E
10. C
CASE 1.
1. Chronic uveitis, active or with acute exacerbation, CE
2. Anterior uveitis, specifically iritis or iridocyditis
3. B-scan ultrasound, due to absence of view through
the pupil
CHAPTER 7.2. PROPTOSIS
CASE 2.
1. anterior segment, specifically the iris, possible
involvement of the macula
2. recurrent uveitis - assuming that the patient was
inflammation free during the one year period
3. Granulomatous type based on the slit lamp
4.
findings particularly the presentation of the keratic
precipitates and presence of nodules in the iris.
Fluorescein angiography and OCT can be requester
to determine involvement of the macula
CHAPTER 8.1. RETINOBLASTOMA
E
CASE 3.
1.
2.
2. A
3. A
4. B
S. B
6_ C
7_ A
& B
9. A
10. A
11. B
12. D
nodular episcleritis vs. nodular scleritis
Check the following:
a. Response of the eye to use of vasoconstrictors
and/or pressure. If blanching occurs, it is more
likely that the patient has episcleritis rather than
scleritis.
b.
Presence of tenderness since tenderness
c.
support diagnosis of scleritis.
Check mobility of the nodule. Movable nodule
would support the diagnosis of episcleritis over
scleritis.
A
S.
A
6.
A
7.
8.
B
E
10. D
CHAPTER 8.2. OCULAR MANIFESTATIONS
OF SYSTEMIC DISEASES
EVALUATION OF FUNDUS PICTURES
1 - dot / blot hemorrhages; 2 - hard
exudates
Picture 2:
Scheie Stage 3 hypertensive retinopathy
Picture 3:
Hypertension. Abnormal findings: flameshaped hemorrhages, hard exudates,
altered AV ratio
Diabetes. Abnormal findings:
Picture 4:
pre-retinal hemorrhage, dot hemorrhages,
microaneuryms
CHAPTER 6.3. TEARING
B
2. B
3. A
4.
3. D
4. C
5. B
6. C
7. C
8. D
9. C
Edition
A
B
C
C
B
A
D
8. D
9. B
10. C
1.
2.
3.
4.
5.
6.
7.
CHAPTER 8.4 OCULAR TRAUMA AND
EMERGENCIES
2_
3.
4.
5.
6.
7.
9_
CHAPTER 8.3. EYELID MALPOSITIONS
1.
D
2.
3.
4.
5.
6.
7.
8.
D
C
A
D
C
C
D
C
C
C
A
A
B
C
D
D
CHAPTER 8.5 . OCULAR PHARMACOLOGY
9
ANSWERS TO SELF-TEST
Elm
10.1 2010 Census of the
Department of Ophthalmology
and Visual Science, Philippiney
General Hospital
Marissa N.Valbuena MD, MHPEd
Table 1. Number of Patien:s
OPD Clinics
Number of Patients
OPD Clinic
General Clinic
New
Old
TOTAL
14,506
11,207
25.713
7.695
Refraction Clinic
7,695
Subspecialty C - .:.s
6.542
29,849
36.391
343
413
756
88
156
244
1.292
3,571
4.863
Dry Eye
165
915
1.080
Glaucoma
818
9,650
10,468
11
0
11
Pediatric Optithairboiog), .-a -:
Strabisrr
546
3,181
3.727
Neuro-C - -
176
571
747
Orbit
272
699
971
Plastic Lacrimal
638
1.535
2.173
1,557
4,493
6,050
453
3,619
4,072
183
1,046
1,229
25,444
44,355
69,799
Cataract
Contact Le - s
Cornea-Extemal Diesease
Low Vision
Retina. Med ,_.
--a
Retina. S _
--
Uveieis
TOTAL
Table 2. TO2
Table 3. Top 10 Admissions
Ciric G: cats
n•
NIlrnhAr
134
102
8.5
Sclero-Corneal Perforating injury
79
6.6
R e t n o bl a sto m a
74
6.2
5.5
Angle Closure Glaucoma, Primary (PACG)
69
5.7
5.3
Corneal Microbial Keratitis, ruptured
58
4.8
383
3.4
Congenital Cataract
48
4.0
Dys'..- :• -. -a "ea-
376
3.4
Corneal microbial Keratitis. bacterial
45
3.7
Diabet: =F. -
335
3.0
42
3.5
311
2.8
Nasolacrimal Duct Obstruction. acquire.
complete
Proliferative Diabetic Retinopathy
38
3.2
250
2.2
Rhegmatogenous Retinal Detachment
34
2.8
Cataract
3265
29.3
Corneal Perforating Injury
Error o'
1.664
14.8
692
62
611
Pteryg
594
Nasola:--f-ai Da: Obstructs°.
Conj
Hypee.•:,
f
Presbyoc a
TOTAL NO. OF NEW PATIENTS
11.207
TOTAL NO. oidigissioNs
1,203
)Ppartment of Ophthalmology and Visual Science of the Philippine General Hospital Eli
--•'- -
Table 6. Top10 Diagnosis: Dry Eye Clinic
Table 4. Top 10 ER Consults
Diagnosis
Rank
Diagnosis
Number
Contusion eyeball + commotion retinae ±
orbital wall fracture
512
20.6
Conjunctivitis, viral
380
15.3
Conjunctivitis, bacterial
203
8.2
Corneal Perforating Injury ± cataractous
lens + intraocular foreign body
110
Corneal Foreign Body
Number
1
DTS' mild mixed
39
23.6
2
DTS with MGD, Blepharitis
14
8.5
3
DTS mild evaporative
13
7.9
4
DTS with Tear Instability
11
6.7
4.4
5
DTS with Aqueous Deficiency
10
6.1
101
4.1
6
DTS mild
6
3.6
Comeal Abrasion
73
2.9
7
DTS with Meibomian Gland
Dysfunction
4
2.4
Central Microbial Keratitis
69
2.8
Lid Laceration/Avulsion
64
26
8
DTS with Nasolacrimal Duct
Obstruction
2
1.2
Essentially Normal Findings
61
2.4
No DTS
2
1.2
Subconjunctival Hemorrhage
42
1.7
Mixed Blepharitis
2
1.2
DTS Moderate Evaporative
1
0.6
ETD
1
0.6
TOTAL NO. OF ER CONSULTS
9
2,490
TOTAL NO. OF NEW PATIENTS
165
DTS - Dysfunctional Tear Syndrome
Table 5.Top10 Diagnosis: Contact Lens and Refraction Clinic
Table 7. Top10 Diagnosis: External Disease and Cornea Clinic
Rank
Rank
Diagnosis
1
High astigmatism
2
Number
Diagnosis
No.
10
11.4
1
Comeal Perforating Injury (CPI)
96
7.4
Phthisis Bulbi
9
10.2
2
Central Microbial Keratitis, Bacterial
49
3.8
3
Comeal Scar
7
8.0
3
Pterygium, Recurrent
42
3.3
4
High Myopia
6
6.8
4
Central Microbial Keratitis, Unspecified
37
2.9
5
Surgical Aphakia
5
5.7
5
Central Microbial Keratitis, Fungal
35
2.7
6
Cosmetic
4
4.5
6
Keratitis, Exposure
26
2.0
7
Aphakia secondary to trauma
2
2.3
7
Pterygium, Primary
25
1.9
8
Others
8
Endophthalmitis
24
1.9
9
Central Microbial Keratitis, Pseudomonas
21
1.6
Leukoma, Adherent
21
1.6
Conjunctivitis, Adenoviral
20
1.5
Adherent Leukoma
1
1.1
Anisometropic amblyopia
1
1.1
Contact Lens Related Punctate
Epithelial Erosion
1
1.1
Lenticular Astigmatic Amblyopia
1
1.1
Myopic Astigmatism
1
1.1
Myopia
1
1.1
Traumatic Resorbed Cataract
1
1.1
10
TOTAL NO. OF NEW PATIENTS
1,292
Table 8. Top10 Diagnosis: Glaucoma Dr:
Rank
Diagnosis
1
Open Angle
2
Angle Closure Glaucoma, Primary
Table 10. Top10 Diagnosis: Plastic Lacrimal Clinic
FRank
No.
Primary
1
Orbital Wall Fracture
2
Nasolacrimal Duct Obs•-..
Angle Closure Suspect, Primary
3
3
Glaucoma Suspect
4
Angle Closure, Primary
5
Absolute Eye secondary tc re;
glaucoma
6
Neovascular Glaucoma
7
Secondary Angle Closure f"-..ir-r-a.
8
Angie Closure Glaucoma_ Cfravic
73
28
Open Angle Glaucoma Sear
73
78
9
Pseudoexfoliative
-:
10
Phacomorphic
•
48
No. X
Diagnosis
108
16.9
97
15.2
Lid Mass
31
4.9
4
Dacryocystitis
19
3.0
5
Nasolacrimal Duct Obstruction. Congenital
15
2.4
Ptosis
15
2.4
6
CN VII Palsy
14
2.2
7
Entropion
13
20
8
Periorbital Contusion Hematoma
11
1.7
9
Lid Laceration. unspecified
10
1.6
10
Contusion Eyeball
9
1.4
- Acquired
TOTAL NO. OF NEW PATIENTS
638
TOTAL NO. OF IA Mme! SNI
Table 11. Top10 Diagnosis: Neuro-Opnthalmology Clinic
Ta*9. Top10 Dggr *mararta-ccgi
Rank
maim* MB lit
1
Optic Nerve Atrophy
28
15.9
7_3
2
Optic Neuropathy, post traumatic
18
10.2
7.1
3
Optic Neuropathy. 2° to ethambutol
14
8.0
33
6.0
4
CN VI Palsy
12
6.8
30
5.5
5
Myasthenia Gravis
11
6.3
Optic Neuritis
11
6.3
29
5.3
4.5
27
4.9
Sensory Exotropia
Inter- 7.9^t E.
40
4
Recra.:- • e Pc:: - :/sta Bolo*
te
6
-e
Ne_rx9c Dealers
.
8
Maim Reera
No.
8.6
Error of Reird a..)
1
2
3
5
Diagnosis
Rank
26
24
4.8
6
Optic Neuropathy, Compressive
8
7
Cortical Blindness
6
3.4
Anterior Ischemic Optic Neuropathy
5
2.8
CN III Palsy
5
2.8
Space Occupying Lesion
5
2.8
Intracranial Mass
5
2.8
8
44
TOTAL NO. OF NEW PATENTS 546
CN III. IV. VI Palsy
10
2.3
Multiple CN Palsy
4
2.3
lschemic Optic Neuropathy
3
1.7
Pituitary Adenoma
3
1.7
TOTAL NO. OF NEW PATIENTS 176
10 APPENDIX I 10.1 Patient Census of the Department of Ophthalmology and Visual Science of the Philippine General Hospital
121
Table 12. Top10 Diagnosis: Orbit Clinic
Rank
Table 14. Top10 Diagnosis: Surgical Retina Clinic
Diagnosis
No.
%
Rank
Diagnosis
1
Thyroid Related Eye Disease
64
23.5
1
Proliferative Diabetic Retinopathy
2
Carotico-Cavernous Fistula
29
10.7
2
3
Anophthalmia
28
10.3
4
Orbital Inflammatory Disease
14
5
Lacrimal Gland Tumor
6
101
22.3
Rhegmatogenous Retinal Detachment
89
19.6
3
Vitreous Hemorrhage
68
15.0
5.1
4
Idiopathic Macular Hole
33
7.3
13
4.8
5
Endophthalmitis
24
5.3
Lymphangioma
12
4.4
6
Proliferative Vitreoretinopathy
23
5.1
7
Congenital Microphthalmos
11
4.0
7
Myopic Fundus Changes
20
4.4
8
Neurofibromatosis
10
3.7
8
Dropped 101
15
3.3
9
Phthisis Bulbi
3.3
9
Intraocular Foreign Body
11
2.4
10
Orbital Mass
10
Non Proliferative Diabetic Retinopathy,
Severe
10
22
8
2.9
TOTAL NO. OF NEW PATIENTS 272
TOTAL NO. OF NEW PATIENTS
453
Table 15. Top10 Diagnosis: Uveitis Clinic
Table 13. Top10 Diagnosis: Medical Retina Clinic
Rank
Diagnosis
No.
Diagnosis
No.
1
Hypertensive Retinopathy
214
3.7
1
Anterior Uveitis Acute, Active
16
8.7
2
Proliferative Diabetic Retinopathy
211
13.6
2
Chorioretinitis
14
7.7
3
Non-Proliferative Diabetic Retinopathy
127
8.2
3
Anterior Uveitis, Chronic (unspecified)
11
6.0
4
High Myopia
126
8.1
4
Lens Induced Uveitis
10
5.5
Age Related Macular Degeneration,
Non Neovascular
64
4.1
5
Panuveitis
8
4.4
5
6
45
2.9
6
Anterior Uveitis Chronic
(Non-Granulomatous)
7
3.8
Pathologic Myopia
7
Clinically Significant Macular Edema
32
2.1
7
Nematode Uveitis
6
3.3
Age Related Macular Degeneration,
Neovascular
31
2.0
8
Sclerouveitis
5
2.7
8
9
Endogenous Endophthalmitis
4
2.2
9
Central Retinal Vein Occlusion,
Ischemic
28
1.8
Anterior Uveitis Chronic (Granulomatous)
3
1.6
Central Retinal Vein Occlusion,
Non Ischemic
Fuch's Heterochromic Iridocyclitis
3
1.6
10
21
1.3
Juvenile Rheumatoid Arthritis
3
1.6
Retinoblastoma
21
1.3 „
Posterior Uveitis
3
1,6
Uveitic Cataract
3
1.6
White Dot Syndrome
3
1.6
Rank
TOTAL NO. OF NEW PATIENTS 1.557
10
L
r
I
REFERENCE
1.
No.
Astudillo P. Annual Report of Department of
Ophthalmology and Visual Science 2010
I.-. a.
a.'
-I
• I • 11 I_
1
I
1..‘
e_l• •
TOTAL NO. OF NEW PATIENTS 183
10. 2 Different Types
of Eye Redness
Teresita R. Castillo MD, MHPEd
After extracting a cornpre'-ensive history c-o— a ca.
would be useful to take some time to evali..a:
eye redness that a patient presents with This e.
the clinician with dues as to the underfy redness and assist in determining
-hand requires urgent referral to an L.= - redness can be classified into four main
Subconjunctival Hemorrhage_ %act
:ne v:sio:e vessel meeye _ Ore
to first determine if
---±-iness is clue to
vessels or blood
due to eeding or
r- rod underneath tria
Di of blood foam trk
(Figure 1). Subcor.,,,- :7 • -errerrhage usually
-as a
localized well-defined
-our any
good '.eas
they are concealed by the acc_ — _ ±-ed blood. Attoiougn this
frequently results fro — trait.—.a 7-e eye. it has been found
to occur spontanec5
be due to sudden rise in
pressure within the
Figure 2. Conjunctival injection showing diffuse congestion that is more
prominent at conjunctival fomices
present no threat to vision. The most common etiology for this
pattern of redness is conjunctivitis, a benign ocular infection.
While there may be a variety of causes for conjunctivitis, they all
basically present with this type of red eye.
Ciliary Injection/ Perilimbal flush. When the injection
:ne ,.moal area and diminishes
towards the fornices, this is referred to as ciliary congestion
appears IS pc .oca.zea
Figure 1 E..
Conjunctival Injection, Congestion. - this instance. injection
F:•ea
IS more rnarKeo trie tor= and diminishes as the
t-. . a'
is approached (Figure 2). As it is the superficial cc vessels that are dilated, one will observe blanch - zredness with pressure on the eye. This type of redness also
responds to topical instillation of vasoconstrictors. Conditions
associated with this type of redness are usually benign and
(Figure 3). Since deeper vessels are involved, instillation of
topical vasoconstrictors and exerting pressure on these vessels
and instillation of topical vasoconstrictors will not affect its
presentation. Despite its relatively benign appearance, this
type of redness is frequently associated with vision-threatening
conditions such as keratitis, anterior uveitis and acute
glaucoma. As both these conditions may lead to complications
that are potentially vision-threatening, eye redness of this type
requires urgent referral to an ophthalmologist.
Figure 4. Scleral congestion in a case of diffuse scleritis.
Figure 3. Ciliary congestion in a patient with acute angle closure
glaucoma.
The dilated vessels are deeper in
Sclera! Congestion.
location which gives a characteristic purple-colored tinge
to the affected area (Figure 4). Scleral congestion will not
diminish with pressure, nor respond to topical instillation
of vasoconstrictors or epinephrine. This type of redness is
typical for scleritis, which is also considered as potentially
vision threatening as it involves inflammation of the vessels
(vasculitis) which can cause necrosis of the affected sclera and
possibly jeopardize the integrity of the globe. As such, all cases
of scleral congestion should be referred to an ophthalmologist
for appropriate evaluation and management.
Table 1 summarizes diagnostic characteristics of selected
conditions that present with eye redness.
Table 1. Serious Non-trauma Related Vision Threatening Red Eye Conditions
-sr..
...1111111111111111
CHARACTERISTICS
Condition
Rednei
INN"
Vision
Pain
Discharge
Puriil
10P,,
Acute
Glaucoma
Diffuse; most
prominent around
the limbus
Moderate to
severely reduced;
iridescent vision
Moderate to severe;
often with headache
and vomiting
^j:
Mid-dilated;
non-reactive to
light
elevated
Anterior Uveitis
Diffuse: most
prominent around
the limbus
Mild to moderately
reduced
Mild to moderate:
photophobia
No
Miotic; irregular
shaped: poorly
reactive to light
normal to
hypotonic
Keratitis
Diffuse; more
prominent around
the limbus
Moderate to
severely reduced
Moderate to severe
Yes; if
infectious
cause
May be affected
if associated
with uveitis
generally
not affected
Scleritis
Focal or diffuse with
purple-tinged color
Normal to mildly
reduced
Moderate to severe.
usually tender
No
Not affected
Not affected
Moderately to
severely reduced
Moderate to severe
Yes
Mid-dilated
elevated
Endophthalmitis Diffuse
10.3 Step-by-Step Diagnosis
of Ocular Emergencies
Teresita R. Castillo MD,
Presented is a simplified ap;.-. .:.3ctillistprimorycare physic
may use when confronted with p1110115 ill die Emergency
Room setting. It is assumed t.'- F nallimits seek consult in the
ER primarily for conditions that
-eamItoracte in onse
Initial distinction that is made is
—e presence of a
history of trauma, hence cistr-,-_non-traumatic ocular C0f1CrtiCri Playmate A)
Ocular trauma ;els to arty in*/ to the eye The injury may
be due to mechanical trauma art or penetrating), chemical
agents, or physical agents tarchasiadaboa Summarized are
additional key features arml aoriesponckig management that
each physician should know IMAM conhormed with cases of
ocular trauma.
The two most common complaints of non-trauma patients
seek - eye cor -. on an emergency basis would be acute
visual disturbance (Diagram B) and an acute red eye
(Diagram C) Mese form the basis for further distinction of
_
-.hat commonly confronts a physician. Note
-. 1 -is that generally lead to unilateral visual
c
Discussed inasmuch as bilateral involvement is
a:-.- stable to non-ocular etiology. Furthermore, as
-_ 3ns fre.:;Jently overlap each other, they may fall under
several categories.
Each category of conditions is further discussed in the
subsequent tables. Emphasis is placed on the key points,
initial or immediate management for each case and lastly, the
urgency or need for ophthalmologic consult.
r
(ER CONSULT)
TRAUMA?
YES
NON-TRAUMATIC
NATURE OF
INJURY?
SAME
MECHANICAL?
CHEMICAL?
I
4
1
CONJUNCTIVAL
LESIONS
VISION?
EXTRAOCULAR?
• CHEMICAL
BURN
REDUCED
iC1
CORNEA INVOLVED
GLOBE INJURY
SUPERFICIAL
(1B-1
LENS PROBLEMS
PERIORBITAL
INJURIES
POSTERIOR SEGMENT
10P?
ORBITAL
14C1C4
OPTIC NERVE
FRACTURE
LID LACERATION l•
LID MARGIN I AREA
INVOLVED NASAL
TO PUNCTUM
NORMAL
HYPOTONIC
CLOSE GLOBE
OPEN GLOBE
INJURIES
INJURIES
CONTUSION —4D1
NO
iC3)
1
YES
LAMELLAR
LACERATION/
rTh,
ID2
RUPTURED
GLOBE
ID3
INTRAOCULAR
FOREIGN BODY
ABRASION
1183
HEMORRHAGE
Diagram A. Trauma-related Ocular Emergencies
PENETRATION/
PERFORATION
IC5 )
IE
1E3
I.
OCULAR TRAUMA
IA
Chemical Burns
TRUE OCULAR
EMERGENCY
Extract information on
1.
Nature of chemical (acid vs
2.
alkali)
Any first aid administeivict
OPFITHA REFERRAL
ER NIAIRAGEINEINF
KEY Poem
CONDITION
....•• err
etc 3r45 :"..;
affected epe/eses.
2 wow slier at least 1liter NSS
&meal solution) using cannula_
Irriptibn 6 done wd chemical has
ophthalmologist
been neutaked
3. Evert eyeld and dean eye of any
debris/foreign bodr make sure that
conjunctival fornices are dean by
sweeping them wirh moistened
canon budfpledgets.
AL Complete eye emmlnation. Always
son with testing visual acuity!
IB
1.
Superficial Orbital
Injuries
Includes injury r.. Pecr-Jcal 537
tissues:
•
cher-css
•
COIllt_SOr'S Nenanznra
laceraccrsavascrs
•
L Perla= basic eye exam whenever
possble Always start with visual
acuity tinting prior to doing any
manipulation of the eye_
• Avoid forcing the eyelids open.
• Lid'enactors may be used to
faciNate inspection of the globe.
2. 'Beat uriaxnpficated blunt injuries
rah ice compress. head elevation,
analgesics/anti-inflammatory agents.
Reassure that swelling usually
resolves in 2 - 3 weeks.
3. Primary wound care for simple
lacerations and avulsions; including
Maras prophylaxis.
2.
Orbital fracture
'.- 7-- arc 5orrcan^15
...
•
:ar arC .
'Itsarricm ECIP5. 7_ doope
•
•
>loss
•
:3,,rairri eriogrerair-vc_ ocoe
1_ Complete neurologic and eye exam.
Orel sensation of cheek. upper
Seed's and gums (compare with
conualaterai side}
2 Palpate orbital rim and eyelid (for
cieptus)
3. RequeSt for orbital CThcan4_ Ice pack to the orbit for 24-48 hours.
5. Instruct patient to avoid Valsalva
maneuvers (e.g. blowing of nose,
straining, etc.)
•-partiwit to esodoollebnialsisimi
3.
Lid lacerations
An eyelid Lace+ etpu.i should be
treated as a case of penetrating
eye injury until proven otherwise.
•
kik to assess edent of damage
_id lacerations involving the id
•narcn or those located nasal
to the purictuni will 'equine
ophthalmologic referral (prior
to repaid.
Non-urgent referral
- patients should be
seen within 1-2 weeks
post trauma (evaluate
for persistent diplopia,
enophthalmia)
Refer for following:
1. Examine with magnification to
1. with accompanying
assess for any comeaVconjunctival
globe trauma or if suspect
laceration or penetration. Dilated
intraorbital or intraocular
fundus examination may be required.
foreign body.
2 Would examination - size and
2. full thickness laceration
depth_
or involvement of the lid
3. Superficial lacerations - primary
4_
wound care and repair_
Tetanus prophylaxis.
10
margin
laceration is nasal to
punctum (upper or
lower)
4. extensive tissue loss or
distortion of the anatomy
3.
APPENDIX 1103 Step-By-Step Diagnosis Of Ocular Emergencies
Egig
IC
CONDITION
KEY POINTS
ER MANAGEMENT
OPHTHA REFERRAL
1. Conjunctival
lesions
Vision generally not affected if
conjunctiva alone is involved.
Pain or foreign body sensation,
however, is usually present. This
may come in the form of
laceration
•
foreign body
•
subconjunctival hemorrhage
•
1. Assess extent of wound if
present. Conjunctival lacerations
may be left unsutured if less than
5mm in length. Suturing is done
in cases when length is greater
than 5 mm.
2. Foreign body removal is done
with the aid of moistened cotton
bud or forceps after instilling
topical anesthetic.
3. Give topical antibiotics in cases
of lacerations and foreign bodies.
4. For subconjunctival
hemorrhages, give cold
compress (1" 24 hours)
and reassure patient that
subconjunctival hemorrhages
will resolve in 1-2 weeks.
Refer to ophthalmologist
if wound repair necessary.
Advise patient to see
ophthalmologist if other
symptoms develop,
particularly blurring of
vision.
Injury to the cornea can lead to
reduced vision primarily if the
lesion involves the visual axis of
the patient. Injury may come in
the following forms:
•
abrasions
•
foreign bodies (FB)
•
lamellar lacerations
(see Section ID2)
•
perforating injury
(see Section 1E1)
1. Corneal abrasions
a. Eye patch or bandage contact
lenses for large abrasions.
b. Topical antibiotic to prevent
secondary infection
c. Topical cycloplegic agents
2. Corneal foreign bodies
a. Foreign body removal with
aid of cotton pledget or small
gauged needle (g. 25 or
smaller) after instilling topical
anesthetic
b. Topical antibiotic to prevent
secondary infection
.
Reduced vision
with corneal
Involvement
NOTE: Despite presence of severe
eye pain or discomfort, topical
anesthetics should NEVER be
prescribed to the patient.
3.
Lens problems
Lens involvement comes in
following forms:
•
lens subluxation/dislocation
•
rupture of the lens
•
cataract formation
1. Rule out injury to other ocular
structures.
Treatment of sequelae of lens
injury that may be present
(eq. deleted lOP and severe
intraocular inflammation)
• Referral required in
cases of penetration or
presence of retained FB
particularly if organic in
nature.
• Refer to
ophthalmologist for
follow-up care to check
on progress of healing.
Note that corneal
abrasions should
resolve in 24-48 hours
if area involved is not
large.
• Advise patient to
see ophthalmologist
immediately should
pain or BOV persist
beyond this period.
Urgent referral in
following instances:
• Severe inflammation
(red eye)
• Elevated lOP
Follow-up for possible
surgical intervention.
4.
Posterior
segment
problems
Reduced vision occurs as a resit
of following conditions:
•
vitreous hemorrhage
•
retinal contusion
•
retinal detachment
•
choroidal rupture
Any of the conditions listed
would require referral to an
ophthalmologist for further
evaluation and management.
Urgent referral
5.
Optic nerve
problems
Optic nerve contusion or avulsion
Referral to ophthalmologist
for further evaluation and
management.
Urgent referral for proper
assessment.
may result from orbital trauma/
injury
CONDITION
ID
KEY Pawns
1. Contusion
ER MANAGEMENT
Contusion eyebar! —
various intrack: _ a-
Eyeball
OFHMA REFERRAL
Basic eye examination (to rule out
other injuries)
Referral depends on
extent and nature of
injury.
1. Topical antibiotics to prevent
secondary infection.
2. Topical cycloplegic agents.
3. Watch out for development
of hypotony due to leakage of
aqueous from the wound.
Urgent referral for proper
assessment.
Hyphema
1. Restrict physical activity of
patient.
2. High back rest
3. Topical steroids for inflammation
Follow-up consult with
ophthalmologist within
2-6 days (hyphema should
resolve spontaneously
within this period)
the ccs.-^ea 7:
_
see•
•
•
•
2. Lamellar
Laceration/
Abrasions
Stioccriurictuai he—
-age
Ste sector' C
-ifore—a see Section 03)
;tetra edema' detachment
See Sewn
Diec vier.e
1e,(.450- see Section ICS)
:4.:yriera-rc roves 3c aracterized
.74
re wound.
--e. > 31e= .a....crts when due
"Z Bra:: doe=
ar-elar aceation s a form of
_ _ry injury bekig partial
wounds of the cornea
scera See aso Section 1C2.
3.
Hemorrhage
i -lenar--act a bleeding may
ox-r r anous structures:
S-occrfaxtival hemorrhage
•
see Sera 1C1)
•
-04:rer-a
•
iifIstecus hemorrhage (see
Section C3)
control due to presence of
blood.
4. Topical cycloplegic agents
(controversial)
5. Monitor loP
6. Watch out for re-bleed.
NOTE: Establish level of blood in
the anterior chamber. If completely
filled with blood, watch out for
elevation in 10P which may lead to
permanent corneal damage (corneal
staining)
IE
1.
;Eric/wry rqures are
Penetrating awl
Peristalsis ghee character2ed by the presence of
an enbarce and exit wound. These
injuries
wounds may be accompanied by
injury to ocher structures like the iris
and the lens.
1. Topical and intravenous
antibiotics.
2. Eye shield to protect the eye.
3. Tetanus prophylaxis.
4. Advise patient regarding surgical
repair.
Urgent referral required
in ALL instances where
globe integrity is
compromised.
2.
Ruptured globe
Frequently a result of blunt
trauma, and should be suspected
1. Eye shield to protect the eye.
2. Topical and intravenous
in these patients in presence of
antibiotics.
3. Tetanus prophylaxis.
4_ Advise patient regarding surgical
repair.
Urgent referral in ALL
instances where globe
rupture is suspected.
following:
•
severe conjunctival osmosis
•
bullous subconjunctival
hemorrhage
•
limitation of movement of
EOMs
3.
Intraocular
foreign body
A special category of globe
perforation.
1 Topical and intravenous
E..-- = :7 :S_
2.
d to protect the eye.
3.
prophylaxis.
Urgency of referral
dependent on
accompanying injuries.
4. Advise patient regarding surgical
repair.
0
APPENDIX 1103 Step-Ety-Step
Diagnosis Of Ocular Emergencies
Eigi
NONTRAUMATIC
RED EYE?
VISUAL
DISTURBANCE?
LATERALITY?
UNILATERAL
RAPIDITY?
SEVERITY?
CONDITIONS GENERALLY
PRESENT WITH
SYSTEMIC ASSOCIATION
_I NEUROLOGIC CAUSE
JONCOLOGIC CAUSE
J DIABETES
RAPID ACUTE
PERSISTENT?
VASCULAR
CAUSE
PAINFUL EYE?
JREQUIRES MINIMAL
EVALUATION IN ER
JREFER TO OPHTHA FOR
FURTHER EVALUATION
AT A FUTURE TIME
AMAUROStS
FUGAX
YES
NO
EYE DISCHARGE?
• CENTRAL RETINAL
ARTERY OCCLUSION
VASO-OCCLUSIVE
CONDITIONS
- I1A7
1•••••
CENTRAL RETINAL
VEIN OCCLUSION
YES
/-(11A1
NO
OPTIC NEURITIS
ENDOPHTHALMITIS
CORNEAL ULCER
(11,1/43\4—
illAs
RESEPTAL I
P
ORBITAL CELLULITIS
I1A4 Hi- ACUTE GLAUCOMA
(llA9)
OPTIC NERVE
DISORDERS
ACUTE ISCHEMIC
OPTIC NEUROPATHY
RETINAL
DETACHMENT
)
IlAio
1
4-,11A1
VITREOUS
HEMORRHAGE
11Al2
UVEITIS (POSTERIOR)
IIA13
IIA5 I*- UVEITIS (ANTERIOR)
Diagram B. Non-trauma Ocular Emergencies associated with G
II. NON TRAUMATIC EMERGENCIES
1.
IIA
ER MANAGEMENT
KEY Po 'vs
CONDITION
_
Suspected in t
• Previous intraocuiar gage"
(cataract surgery or ilerirg
operation often less dor one
month prior)
• I mmunocornpronsed parients 2.
Endophthalmitis
--:,rough history and eye
examination with particular
attention to previous ocular
history and general health
status of the patient.
OPIITHA REFERRAL
Urgent reTer'a to
ophthalmologist for
further evaluation and
management.
Broad spectrum topical and
intravenous antibiotics.
In addition to vtaon iloSi patients
may also present mion a earful
red eye_
2.
Corneal ulcer
(keratitis)
1. Thorough history and eye
• Primary considealion in
examination with particular
paiinnes•olih hiMory of conaixt
attention to history of contact
ienswerlens use.
• Palos inairabo poem
1 Broad spectrum topical
Ina kkaorjrafpior suisna
antibiotics.
or bream bodyerweing the
e)e, thanes not plena*
seen bya physidarby
Preseptal!
Orbital cellulitis
Cannonlyanournesed in
Urgent referral to
ophthalmologist for
further evaluation and
management.
aPhillubliblocfist
3.
2.
3.
4.
1.
Acute Glaucc — a • IlluipappensisviehOthet eye
• =laudations indude
• onmareambanal headache
Oviddlogsanieside) and on
minim nausea and vomiting.
2.
5.
Uveitis Antenof
• Pain is precipitated by intense
fight Illumination or sunlight
•
(photophobia).
May have systemic
associations depending on
etiology of the inflammation.
Thorough history and eye
examination with particular
attention to infection of
adjacent tissues
Broad spectrum intravenous
antibiotics.
Referral to pediatrician for comanagement.
Urgent referral to
ophthalmologist for
further evaluation and
management.
Thorough history and eye
examination. Eye Exam shows
• red eye (ciliary injection)
• hazy cornea
• mid-dilated, unreactive
pupil
• elevated 10P
May give patient analgesics
to assist in relieving pain and
headache.
Immediate referral to
ophthalmologist for
further evaluation and
management as this may
lead to permanent loss of
vision if left untreated.
Thorough history and eye
examination. History should focus
on systemic symptoms and illnesses
as well. Eye exam will show
• red eye (ciliary injection)
• irregularly-shaped small,
Urgent referral to
an ophthalmologist
(within 24 hours) for
further evaluation and
management
unreactive pupil
•
6.
Amaurosisfugax
Visual loss usually lasts seconds to
minutes only, but may last up to
two hours. Vision subsequently
returns to normal.
2.
lOP normal or low
Thorough history and eye
examination.
Referral to a neurologist/
cardiologist
10
None provided all eye
exam findings normal.
APPENDIX 1 103 Step-By-Step Diagnosis Of Ocular Emergencies
Egg
Central retinal
artery occlusion
7.
OPHTHA REFERRAL
ER MANAGEMENT
KEY POINTS
CONDITION
Thorough history and eye
examination focusing on exact
onset of the condition. Eye exam
Marked loss of vision of very sudden
onset
Immediate referral to an
will show
•
EMERGENCY
Defect (RAPD)
• Pale retina with cherry red spot
May institute measures to improve
circulation (vasodilation)
9.
Optic neuritis
Thorough history and eye examination
focusing on history of diabetes or
hypertension. Fundus exam shows large
•
diabetic
mew of hemorrhage
•
Loss of vision may occur crier
period of hours to days.
Pain may be noted with eye
movement.
Thorough history and eye examination
which reveals (aside from BOV)
• RAPD
• swollen, edematous disc
Urgent referral to an
ophthalmologist for further
evaluation.
Differs from optic neuritis since
condition is often associated with
systemic findings:
• temporal headaches or sc
tenderness
• generalized muscle pain anckw
Thorough history and eye
emamination.
Referral to a neurologist/
caedolooist
Urgent referral to an
ophthalmologist for further
evaluation.
1
11. Retinal Detachment Most common cause is a pietisposing 1.
retinal defect as seen in high mopes
Patient may present with a hisaory
of flashes or floaters. MstMl defect Es
often described astuilain tie
12.
Vitreous
hemorrhage
More commonly seen it padentsvials
following systemic conditions
2-
1.
1. diabetes
2. hematologic cisordeis
focusing on patient's refractive
Thorough history and eye
examination with particular
attention to previous ocular history
Referral to ophthalmologist
not urgent but patient
and general health status of the
at a future time.
Referral to internal medicine
specialist for systemic evaluation.
more marked effeu on 116110111 MI
comparison to anterior wefts.
Patients may also piesera with
systemic finctings since underiping
1.
Thorough history and eye
examination. History should
focus on systemic symptoms and
illnesses as well.
cause frequently with systemic
2. Eye exam may reveal vitreous
associations.
Urgent referral to an
ophthalmologist particularly.
history as well as accurate onset of
the problem.
Eye examination may reveal
•
RAPD if involved area is
extensive
•
Abnormal red orange reflex
(ROR)
•
Retina may appear pale or
grey with tortuous vessels (in
detached areas)
2.
Problems
Uveitis (Posterior)
Thorough history required,
evaluation and management.
should be advised to consult
patient.
Often accompanied by ocher mind
13.
Urgent referral to an
ophthalmologist for further
Patients predisposed if
• elderly (increasing age:
• hypertensive
•
10. Acute ischemic
neuropathy
management.
Relative Afferent Pupillary
TRUE OCULAR
Central retinal vein
occlusion
8.
ophthalmologist for further
evaluation and institution of
condensations and other retinal
findings such as retinal vasculitis,
macular edema and focal areas of
retinal detachment.
Urgent referral to an
ophthalmologist for further
evaluation and management.
NONI RAUMATIC
1
VISUAL
DISTURBANCE!?
B
RED EYE?
l'AINrUL
RYE?
4
1 yes
NO
I)Itt 11411111110N
ABNORMAL
LIDS?
HI URRED
VISION?
LID INFECTIONS
.. 118 1
L LID MALPOSITION
1vi!; 4-
8
1)InClIA14(41
LOCALIZED
YES 14—
KERAT ITIS
I1A2)4— CORNEAL ULCER
41/—
LID
ABNORMALITY?
SUBCONJUNCTIVAL 1
HEMORRHAGE
CONJUNCTIVITIS 11—
KERATITIS
ULCER
4-- CORNEAL
*
ID3
L NO 14—
0
LID INFECTION
al=1114.
A7=0--
IIA4)-4—ACUTE GLAUCOMA
1
UVEITIS
011104---
1-6
(11AE)46-
UVEITIS
[ NO
SCLERITIS
(iiB2 4--
SUBCONJUNCTIVAL
HEMORRHAGE
1D3)
SCLERITIS
CONJUNCTIVITIS 1-411B3
;
r
N.)
Diagram C. Non-trauma Ocular Emergencies associated with acute eye redness
IIB
1.
Lid infections
and Malpositions
2. Scleritis
Problems involving the lids
associated with red eye are also
generally accompanied by foreign
body sensation. On occasion
infections may present with pain
and discharge. These conditions
can further be subdivided into
1.
Hordeolum (Stye)
2.
Blepharitis
3.
Entropion
4.
Ectropion
5.
Preseptal cellulitis
(see Section iiA3)
6.
Orbital cellulitis
(see Section IIA3)
Redness may be diffuse or
localized; may be accompanied
by nodule.
Usually associated with systemic
conditions, most common of
which is rheumatoid arthritis.
3.
Conjunctivitis
ER MANAGEMENT
KEY POINTS
CONDITION
1.
Pain may or may not be
present.
2.
Classified according to
etiology
•
•
•
•
Bacterial - with
mucopurulent discharge
Viral - generally with
serous discharge
Allergic - associated
with itchiness; frequently
bilateral
Chemical - history of
exposure to specific
substances
OPHTHA REFERRAL
Non-urgent conditions
1. Hordeolum
Ophthalmologic consult
a. Warm compress
for hordeolum only
b. Topical antibiotic ointment
if it does not resolve
(may use steroid-antibiotic
combination)
despite completion of
medication.
c. Analgesics
d. Antipyretic if accompanied by Ophthalmologic consult
fever
for lid malpositions
2. Entropion
for possible surgical
a. Tape lids to evert them
correction.
b. Topical lubricants and artificial
tear preparations
3. Ectropion
a. Tape lids to effect closure
when sleeping
b. Topical lubricants and artificial
tear preparations
1. Thorough history and basic eye
exam. Focus on presence of
systemic conditions that can
cause scleritis.
2. Topical steroid preparations
1. Thorough history assists in
ascertaining etiology. Also ask
about specific symptoms that are
associated with specific types of
conjunctivitis
2. Specific treatment dependent
on etiology. Refrain from
prescribing topical steroid
preparations if infection has not
been ruled out.
Urgent ophthalmologic
referral for further
evaluation and
management.
Non-urgent conditions
Refer to ophthalmologist
if
• mucoid to
mucopurulent eye
discharge present
• recurrent condition
REFERENCES
1.
BMJ Publishing Group. Eye Trauma in Best Practice. June
6.
7, 2011: http://bestpractice.bmicom/best-practice/
2.
monograph/961/ (accessed October 29, 2011).
Classification of ocular trauma, June 21, 2011: httpsi/
vodvos.com/classification-of-ocular-trauma/ (accessed
October 29, 2011).
3.
Eye Emergency Manual An Illustrated Guide, 2nd ed. New
4.
South Wales: NSW Department of Health, May, 2009.
Khare, GD, Symons, DV. Common Ophthalmic
5.
Emergencies. Int J Clin Pract. 2008;62(11): 1776-1794.
Pokhrel, PK and Loftus. SA. Ocular Emergencies. Amer
Fam Physician. 2007; 76(6): 829-836.
Pramanik, Sudeep. Assessment and Management of
Ocular Trauma, June 28, 2008: http://webeye.ophth .
uiowa.edu/eyeforum/tutorials/trauma.htm (accessed
October 29, 2011).
7.
Sherry Eugene. Electronic Textbook Injuries Chapter 23
Eye.
8.
The WorldOrtho Textbook of Orthopaedics, Trauma and
Sports Medicine, 2007: http://www.worldortho.com/dev/
(accessed October 29, 2011).
10.4 Eye Care Rules
to Remember
Teresita R. Castillo MD, MHPEd
1.
Always take and record your petiesies visual acuity
Every effort must be taker __
, _
_
:= a
patient prior to any further
_
This is done regardless of ho,"
- ±- eye
may appear.
If vision improves with patie_ a 2,e,
the patient's blurring of visicr
"•
OUt = aerror of refraction.
2. Pupil examination: Suspect NNW andlilliews for
corresponding findings
pupil sargery
Dilated pupil - Acute gtauarre-ersoe nassv crf
associated with history of heat
•
Constricted pupil - Ir s- Horne- 1•
Relative Afferent P c elect f3i
- fetinal artery
7. Corneal abrasions should heal in 24 to 48 hours.
•
Daily follow-up of patient is ideally done until the
corneal abrasion is completely healed.
Cover patient with topical antibiotic drops to prevent
secondary infection.
8. A penetrating eye injury requires urgent care.
Gentle transport is of utmost importance.
Place an eye shield over the patient's injured eye to
protect it.
If treatment is delayed, give the patient systemic
antibiotics and anti-tetanus injections.
9. Consider the presence of intraocular foreign
bodies if
•
Mechanism of injury is o,e to hammering or nigh-
occlusion; optic •
3.
Irrigate chemical burns.
co
,
_4:rously with water for at least
15 minutes
Instill a local anesthett net and swab the eye
lids.
Immediately refer tc
"7".`
4.
Any sudden onset of Marring of vision requires
prompt investigation.
=--;7.-1- s accompanied by
----
5.
Beware of ungateral eye redness
Trauma
=-.7.,Fr •
velocity in nature.
Presence of a possible entry wound in the cornea or
sclera
10. In the presence of trauma with a black eye, consider
presence of globe rupture unless otherwise ruled
out.'
Consider a ruptured globe if
Patient complains of diplopia or there is
limitation of EOMs
Patient presents with a bullous subconjunctival
hemorrhage
Patient has a hypotonic eye
Anterior chamber is completely filled with blood
Orbital floor fracture should be ruled out if the patient
complains of diplopia or presents with enophthalmia
(sunken eye).
aY
11. Never use anesthetic drops for continued pain
uveitis (Iritis)
7 -_ siromeal ulcer
_
above cases reg._
:::-thalmologTs for fur e _.a
e-r%ent.
6.
7 7.
!72. to
and
Leave some foreign bodies alone.
'•
.-..odies that are deep
central corintra-ocular or intra-orbital. These
cases should be referred to an ophthalmologist.
relief.
Use of topical anestnetic crops snouid be limited to
facilitating examination of painful lesions or as part of
performing a diagnostic procedure.
Anesthetic drops should never be prescribed to
patients.
12- Always advise patientsthat steroids are potentially
dangerous.
5terolus con activate a dormant infection (e.g. Herpes
simplex)
Prolonged use can lead to the following:
Glaucoma
Cataract formation
Steroid should be used with caution if
Any break in the integrity of the globe is
suspected
Patient has an ocular infection
Patient is immunocompromised (e.g. diabetics,
patients on immunosuppressant therapy)
13. Refer all children noted to have squint or eye
deviation.
Squint may be a sign of an underlying lifethreatening or vision-threatening condition such as
retinoblastoma or congenital glaucoma.
Children with poor vision in one eye often develop
deviation of the involved eye. In very young children
it is important to institute measures to correct vision
as this may lead to development of amblyopia.
14. Conjunctivitis is almost always bilateral.
•
Viral conjunctivitis is often accompanied by pre-
15.
Cataract surgery
operation.
is the most common
eye
oavised when symptoms affect a patient's daily
life activities.
It is generally performed as an out-patient procedure
(day surgery) under local anesthesia.
Laser is not a treatment option for cataract surgery.
Yag laser capsulotomy may be used at a later time
for post-cataract surgery patients when posterior
capsule opacification occurs.
Cataract does not recur.
16. Not all red eyes are"sore eyes"(viral conjunctivitis).
Urgent referral to an ophthalmologist is warranted
if patient presents with
Severe eye pain
Reduced vision
Mucopurulent eye discharge
•
Prolonged duration
17. Hospital admission is considered if the patient has
•
Hyphema
•
Hypopyon
•
Penetrating/peforating ocular injuries
•
Severe chemical burns
•
Acute glaucoma
auricular lymphadenopathy.
•
Allergic conjunctivitis is always accompanied
by itchiness which can be relieved by use of ice
compress. Always advise patients to avoid scratching
their eyes as this will just aggravate the itchiness.
•
242
All cases of prolonged conjunctivitis should be
referred to an ophthalmologist.
Self-Instructional Materials in 0ohthalmoloov I Mel Friitinn
REFERENCE
1
Calvin JL• Reich JA. 35 Golden Eye Rules. http://www.eyeandeatorg.au/
EYELectures/35_Golden_Eye_Rules.pdf (accessed August, 2008).