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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 RED EYE, TEARING AND DISCHARGE
105 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

7 DEVIATION AND DISPLACEMENT OF THE EYE
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

10.3 Step-By-Step Diagnosis Of Ocular Emergencies

241 10.4 Eye Care Rules To Remember

Self-InstTuetional Materials in Ophthalrn010,3y 1 Ztit1ECIII1011

CONTRIBUTORS
Romulo N. Aguilar, MD, PhD Richard C. Kho, MD
Associate Professor Clinical Associate Professor
Department of Ophthalmology and Visual Science Department of Ophthalmology and Visual Science
College of Medicine College of Medicine
University of the Philippines Manila University of the Philippines Manila
Ocular Manifestations of Systemic Diseases Physiology of the Eye; Cataract
Norman M. Aquino, MD Franklin P. Kleiner, MD

Clinical Associate Professor Clinical Associate Professor
Glaucoma Eyelid Malpositions
Teresita R. Castillo, MD, MHPEd Ruben LimBonSiong, MD

Eye Examination; Uveitis and Scleritis ; Disorders of the Cornea
Ocular Manifestations of Systemic Diseases; Types of Red Eye;
Step-By-Step Diagnosis Of Ocular Emergencies; Eye Care Rules to Remember
Leo D. P. Cubillan, MD, MPH Andrea Kristina Monzon-Pajarillo, MD

Clinical Associate Professor Clinical Associate Professor
A Clinical Algorithm for the Diagnosis of the Red Eye Anatomy of the Eye; Eye Symptoms
Raul D. Cruz, MD Juan Ma. Pablo R. Nanagas, MD, MPH, MSNA

Associate Professor Professor
Disorders of the Optic Nerve Errors of Refraction
Rolando Enrique D. Domingo, MD Mary Rose L. Pe-Yan, MD

Retinoblastoma Ocular Pharmacology
Prospero Ma. C. Tuano, MD Marissa N. Valbuena, MD, MHPEd

Professor Professor
Proptosis Anatomy of the Eye; Eye Symptoms ; Strabismus;
Ocular Trauma and Emergencies; Patient Census
Alexander D. Tan, MD Pearl T. Villalon, MD

Clinical Associate Professor Associate Professor & Chair
Tearing Disorders of the Retina, Choroid and Vitreous
Milagros H. Arroyo , MD
Francis Raymond M. Castor, MD
Michelle D. Lingao, MD
Illustrators

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.
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. Cornea
5. Uveal tract - iris, ciliary body, choroid
6. Lens
7. Aqueous
8. Anterior chamber angle
9. 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)

Frontal N, Lacrimal N, Superior oculomotor N
Superior Ophthalmic V Levator M
1. Roof : frontal bone, lesser wing of the sphenoid bone Superior rectus M
Trochlear N
2. Lateral wall : greater wing of the sphenoid bone, Abducens N
Superior oblique M
zygomatic bone Oeulomotor foramen
Optic N
3. Floor : maxillary
bone, zygomatic bone, palatine bone
4. Medial wall : ethmoid, lacrimal bone, frontal bone, Medial rectus M
Lateral rectus M
Nasociliary nerve
maxillary bone, sphenoid bone
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 Supraorbital
notch
vessels to the eye and all the extraocular muscles except the
inferior oblique. (Figure 2). There are openings through or in
Optic Canal Supenor orbital
between bones in the orbit through which several structures 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
Infraorbital
that lies outside the annulus of Zinn: superior ophthalmic groove Inferior orbital
fissure
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 Infraorbital
foramen
nerve and abduscens and nasociliary nerves. The optic nerve
and ophthalmic artery pass through the optic canal which also Figure 3. Anterior view of the bony orbit showing fissures, canal and foramen
2. Bulbar conjunctiva — is loosely attached to the orbital
BLOOD SUPPLY
septum in the fornices and is folded many times. This
A. Arterial Supply : Ophthalmic Artery (branch of allows the eye to move and enlarge the secretory
internal carotid artery) conjunctival surface.The semilunar fold is a thickened
fold of bulbar conjunctiva at the inner canthus and
1. Central retinal artery- supplies the retina corresponds to the nictitating membrane of lower
2. Lacrimal artery — supplies lacrimal gland and upper animals.
eyelid
3. Muscular branches to the muscles — continue to form The conjunctiva has the following layers:
the anterior ciliary arteries and supply the sclera,
episclera, limbus and conjunctiva and contribute to 1. Conjunctival epithelium — consists of 2-5 layers of
the major arterial circle of the iris stratified columnar epithelial cells. The superficial
4. Long posterior ciliary arteries — supply the ciliary epithelial layer consists of mucous secreting goblet
body. The 2 long posterior ciliary arteries anastomose cells. The basal epithelial cells are deeper and may
with each other and with the anterior ciliary arteries contain pigments near the limbus.
to form the major arterial circle of the iris. 2. Conjunctival stroma has an adenoid (superficial)
5. Short posterior ciliary arteries — supply choroid and layer and a fibrous (deep) layer. The adenoid layer
part of the optic nerve contains lymphoid tissue and 'follicle-like" structures
6. Medial palpebral arteries to both eyelids 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
B. Venous Drainage :
is loosely arranged over the globe. The accessory
lacrimal glands (glands of Krause and Wolfring)
Blood drains to the superior and inferior ophthalmic veins, located in the stroma resemble the lacrimal gland in
into which drain the vortex veins, anterior ciliary veins and the structure and function.
central retinal vein. The ophthalmic veins communicate with
the cavernous sinus. The conjunctival arteries are derived from the anterior ciliary
and palpebral arteries and anastomose freely. Conjunctival
The blood from the skin of the periorbital region drain to the veins follow the arterial pattern. The conjunctival lymphatics
angular vein, and to the supraorbital and supratrochlear vein together with the lymphatics of the eyelids form a rich
branches of the superior ophthalmic vein. This provides a lymphatic plexus. The conjunctiva is innervated by the
direct communication between the skin of the face and the ophthalmic (first) division of the trigeminal nerve.
cavernous sinus.
2. TENON'S CAPSULE
Clinical Pearl:
Cavernous Sinus Thrombosis The Tenon's capsule is a fibrous membrane covering the
globe from the limbus to the optic nerve. At the limbus,
The direct communication between the ophthalmic the conjunctiva, Tenon's capsule and the episclera are fused
veins and the cavernous sinus may potentially cause together. Posteriorly,the inner surface of theTenon's capsule lies
a posterior and intracranial spread of infection from against the sclera and the outer aspect lies in contact with the
an orbital abscess or cellulitis. It is thus very important orbital fat and structures within the extraocular muscle cone.
to monitor patients with these disorders for rapid At the point where Tenon's capsule is pierced by the tendons
progression of proptosis and any neurologic signs or of the extraocular muscles, it sends out tubular reflections
dysfunction. 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
B. EYEBALL 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:
The sclera is the fibrous outer layer of the eye consisting
1. Palpebral conjunctiva — lines the posterior surface of mainly of collagen. It is dense and white and continuous
the eyelid and is adherent to the tarsus.
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
Clinical Pearl:
(0.3 mm); elsewhere it is 0.6 mm thick. The outer layer of the Herpes Simplex Corneal Ulcer
anterior sclera is covered with a thin layer of fine elastic tissue,
the episclera, which contains blood vessels that nourish the Ihe Herpes simplex virus (HSV) commonly affects
sclera. the trigeminal ganglion which is the main source of
sensory nerve supply to the cornea.
4. CORNEA
Corneal sensation may be tested by light touch - tul
example, using a strand of cotton. When a patient has
I he cornea is a transparent tissue inserted to the sclera at the
a corneal ulcer caused by HSV, the cornea exhibits
limbus. It is thicker at the periphery (0.65 mm) than at the
hypoesthesia at the ulcer site. This is one characteristic
center (0.52 mm). Its horizontal diameter (11.75 mm) is slightly
of an HSV corneal ulcer that helps differentiate it from
bigger than its vertical diameter (10.6 mm).
other types of corneal ulcers.
There are 5 layers of the cornea : (Figure 4)
1) 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
portion of the stroma. the choroid. It is the middle vascular layer of the eye and
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
polyglycans in association with the keratocytes that iris lies in contiguity with the anterior surface of the lens,
produce the collagen and ground substance. dividing the anterior chamber from the posterior chamber,
4) Descemet's membrane : basal lamina of corneal both of which contain aqueous humor. Within the stroma of
the iris are the sphincter and dilator muscles.The 2 pigmented
endothelium
5) Endothelium : single layer of cells ; responsible for posterior layers of the iris represent anterior extensions of the
maintaining the deturgescence of the cornea and neuroretina and the retinal pigment epithelium (RPE).
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
with minimal capacity for cell division. from fibers of the ciliary nerve.
The cornea gets its nutrition from the vessels of the limbus, the The pupil controls the amount of light entering the eye.
aqueous and the tears. The superficial cornea gets most of its The pupillary size is determined by the balance between
oxygen from the tears. The sensory nerves of the cornea are constriction due to parasympathetic activity via the
from the ophthalmic division of the trigeminal nerve. oculomotor nerve and dilation due to sympathetic activity.
The transparency of the cornea is due to its uniform structure, B. CILIARY BODY
avascularity, and deturgescence.
The ciliary body consists of 2 zones
1. Pars plicata: 2 mm wide; The ciliary processes arise

Epithelium from this zone. The ciliary processes are composed
Bowmans mainly of large fenestrated capillaries and veins
membrane
that drain to the vortex veins. The 2 layers of the
ciliary epithelium are the internal non- pigmented
— Strome
layer (representing the anterior extension of the
Descemet's neuroretina) and the external pigmented layer
membrane (representing the RPE). The ciliary processes produce
Endothelium the aqueous.
2. Pars plana - 4 mm ; flattened posterior zone
Figure 4. Cross section of cornea
The ciliary muscle is composed of longitudinal, circular The lens capsule (Figure 7) is a semi-permeable membrane
and radial fibers. (to water and electrolytes). A subcapsular epithelium is present
1. Circular fibers: contraction and relaxation of the anteriorly.The lens nucleus is harder than the cortex. With age,
zonular fibers alters the capsule of the lens thus giving the subepithelial lamellar fibers are continuously produced,
variable focus for far and near objects of fixation. gradually making the lens larger and less elastic.
2. Longitudinal fibers : insert to the trabecular
meshwork, influencing its pore size The lens consists of 65 0/0 water and 35% protein and minerals.
3. Radial fibers 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
Conjunctival vessels
Retinal vessels
Choroidal vessels
Major arterial circle of iris Long posterior ciliary a
Short posterior ciliary a
Central vessels of the retina
Vessels of ciliary body
Figure 5. Blood supply of the eye
Lamellar lens
C. CHOROID Lens capsule fibers
The choroid is the posterior portion of the uveal tract, located Lens epithelium
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
Bruch's membrane Figure 7. Magnified view of a section of the lens showing lens capsule
ChorlocepiNerls
and epithelium
Larger choroidal
vessels 7. AQUEOUS
SCAM The aqueous is a clear fluid that fills the anterior and posterior
.tir•
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/
Figure 6. Cross section of the choroid
min. Its composition is similar to plasma except for higher
concentrations of ascorbate, pyruvate and lactate and lower
6. LENS concentrations of protein, urea and glucose.
The lens is a biconvex, avascular clear structure, which Aqueous is produced by the ciliary epithelium. From the
is 4 mm thick and 9 mm in diameter. The lens, together with posterior chamber, the aqueous passes through the pupil to
the cornea, are the main refractive components of the eye. It go to the anterior chamber and then drains into the trabecular
is suspended behind the iris by the zonules which connects it meshwork, to the Schlemm's canal and into the venous system.
with the ciliary body. Anterior to the lens is the aqueous and
Some aqueous passes between the bundles of the ciliary body
posterior to it is the vitreous.
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 The retina is a thin, semi-transparent, multilayered sheet of
peripheral cornea and the root of the iris. Its main anatomic neural tissue that lines the inner wall of the posterior 2/3 of the
structures are Schwalbe's line, trabecular meshwork (which eye. It extends anteriorly as the ora serrata. The outer surface of
overlies the Schlemm's canal) and the scleral spur. (Figure 8) the retina is apposed to the retinal pigment epithelium (RPE).
Except at the disc and the ora serrata, the retina and RPE are
The Schwalbe's line corresponds to the termination of the easily separated to form a subretinal space, such as occurs in
corneal endothelium. The trabecular meshwork is triangular retinal detachment. The inner layer of the retina is apposed to
in cross section with the base directed to the ciliary body. the vitreous.
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 Clinical Pearl: Retinal Detachment
insert into the trabecular meshwork. The scleral spur is an
inward extension of the sclera between the ciliary body and In some forms of inflammation, such as in uveitis, fluid
the Schlemm's canal, to which the ciliary body and the iris are may leak out of the retinal vessels and accumulate in the
attached. subretinal space separating the retina and RPE, causing
exudative retinal detachment
Antenor chamber angle

The 10 layers of the retina (Figure 9), from the inner aspect are
Schlemm's canal
the following:
Anterior chamber
Trabecular meshwork 1. internal limiting membrane

2. nerve fiber layer — ganglion cell axons passing to the
optic nerve
3. ganglion cell layer
4. inner plexiform layer — connections of the ganglion
Posterior chamber cells with the amacrine and bipolar cells
5. inner nuclear layer — cell bodies of the bipolar,
Figure 8. Anterior chamber angle amacrine and horizontal cells
6. outer plexiform layer — connections of the bipolar
and horizontal cells with the photoreceptors
Clinical Pearl : 7. outer nuclear layer — cell nuclei of photoreceptors
8. external limiting membrane
Acute angle closure glaucoma
9. photoreceptor layer — rod and cones inner and outer
segments
The eye's natural response of dilation to environmental or
10. retinal pigment epithelium (RPE) — The inner layer
chemical stimuli which can result to apposition and contact of the Bruch's membranes is actually the basement
between the lens and the iris is called pupillary block. In membrane of the RPE
addition, the forward-most surface of the lens is anterior
to the plane of the iris insertion into the ciliary body. As The retina is 0.1 mm thick at the ora serrata and 0.56 mm thick
a result, aqueous flow from the posterior chamber to the at the posterior pole. In the center of the posterior retina is
anterior chamber is obstructed or altogether blocked. the macula (Figure 10). It is clinically seen as a 3 mm area of
The increasing pressure in the posterior chamber causes yellowish pigmentation (due to xanthophylls pigments) and
the iris, particularly its peripheral region, to bow forward bounded by the temporal vascular arcades. In the center of
(iris bombe). Iris bombe further closes the already narrow the macula is the fovea, clinically seen as a depression and
angle and compromises aqueous drainage, thus increasing corresponds to the "foveal reflex". It corresponds to the retinal
intraocular pressure (10P). 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
GANGLION CELL 3 - GANGLION CELL LAYER
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
500µm ILM
Muller cells in
#ifi —lie is al inner nuclear
layer
Iczry %II.
XLM
AllligiNglainal
es, UM W
- r, ' •," , , RPE
Capillary
arcades 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. choriocapillaris — supply outer third of retina, from
outer plexiform layer to RPE
2. 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
Figure 11. Histophotograph of the retina at the area of the macula blood-retinal barrier lies at the level of the RPE.

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 1. EYEBROWS
lens, retina and optic disc. The hyaloid membrane, the outer
surface of the vitreous is in contact with the posterior lens I he eyebrows are tolds of thickened skin covered with hair.The
capsule, zonules, pars plana epithelium, retina and optic nerve glabella is the hairless prominence in between the eyebrows.
head. The base of the vitreous maintains a firm attachment
throughout life with the pars plana epithelium and the retina 2. EYELIDS
immediately behind the ora serrata. The attachment to the
lens capsule and the optic nerve head is formed early in life I he upper and lower lids (palpebrae) are folds of skin that can
but soon disappears. close to protect the anterior portion of the eye. Blinking helps
spread the tear film, keeping the cornea and conjunctiva wet.
The vitreous is 99% water. Collagen and hyaluronic acid make
the vitreous gel-like because of their ability to bind large Layers of the eyelids (Figure 14)
amounts of water.
1. Skin — thin, loose, elastic, few hair follicles and no
EXTRAOCULAR MUSCLES subcutaneous fat.
2. Orbicularis oculi muscle — Circular muscle fibers
Eye movement is facilitated by its six extraocular muscles surround the palpebral fissure which functions to
consisting of four recti and two oblique muscles. The four close the eyelids. It is innervated by the facial nerve.
recti muscles originate from the annulus of Zinn at the apex 3. Areolar tissue — under the orbicularis oculi,
of the orbit and are named after their insertion at the sclera on communicates with the subaponeurotic layer of the
the medial, lateral, superior and inferior aspect of the eye. The scalp.
superior oblique, which also originates from the orbital apex, 4. Tarsal plates — dense fibrous tissue layer ; main
is the longest and thinnest of the extraocular muscles. The support of the eyelids
inferior oblique originates from the nasal side of the orbital 5. Palpebral conjunctiva — adheres firmly to tarsal plate
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. Frontal Sinus
Figure 13 shows the spiral of Tillaux, which connects the
points of insertion of the four recti muscles to the sclera. Levator palpebrae muscle
Orbital fat
Gland of Krause Orbicularis oculi muscle
The blood supply to the extraocular muscles comes from the
Gland of Wolfring -Orbital septum
muscular branch of the ophthalmic artery. The lateral rectus Levator palpebrae aponeurosis
and inferior oblique are also supplied by the branches from Superior tarsal muscle
the lacrimal artery and infraorbital artery respectively.
Conjuctiva Melbomian gland in tarsal plate
SR Eyelash
• f.
— Lower eyelid retractors
10.6
Spiral of Interior oblique muscle
Tillaux
4 Figure 14. Cross section of the eyelid

103 mrs.
Clinical Pearl : Eyelid swelling
The thin, loose skin and the absence of subcutaneous

fat makes the eyelid vulnerable to swelling, such as
g.g in accumulation of fluid in allergy or infection and
blood in trauma.
IR
Figure 13. Spiral of Tillaux, showing the insertion of the recti muscles to the sclera
Table 1.
Muscle Origin Insertion Direction of Action from Innervation

pull Primary Position Cranial Nerve
Medial rectus Annulus of Zinn 5.5 mm from medial limbus (,(1 Adduction 111
(MR)
Lateral rectus Annulus of Zinn 6.9 mm from lateral limbus 90' iAt)rilk;tio!I \11
(LR)
Annulus of Zinn 7.7 mm from superior 23° Elevation III
Superior rectus
(SR) limbus Intorsion
Adduction
6.5 mm from inferior limbus 23° Depression III
Inferior rectus (IR) Annulus of Zinn
Extorsion
Adduction
51° Intorsion IV
Superior oblique Orbit apex above Posterior equator at
Annulus of Zinn superotemporal quadrant Depression
(SO)
(functional origin Abduction
at trochlea)
51° Extorsion III
Inferior oblique Behind lacrimal Posterior to the equator in
(10) fossa infero-temporal quadrant Elevation
Abduction
Plica semilunaris Lacrimal lake 1. Anterior margin

Lacrimal caruncle
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 Posterior Gray Orifices of
punctum lid margin lid margin line Me ibomian
glands 3. ORBITAL SEPTUM
The orbital septum is the fascia behind the portion of the

Figure 15. Lid Margin (medial portion of the eyelids). Adopted from Riordan
E, Whitcher, J.2 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.

Superior canaliculus
Common canaliculus
Superior punctum
‘,."— Lacrimal sac
Interior canaliculus Nasolacrimal

duct
Inferior punctum
Figure 16. Lacrimal drainage system
B. Accessory lacrimal glands of Krause and Wolfring

Clinical Pearl: - located in the substantia propria of palpebral
conjunctiva
Preseptal and Orbital Cellulitis
C. Canaliculi
D. Lacrimal sac
An infection which causes inflammation of the eyelids
E. Nasolacrimal duct- drains out to the nasal cavity
and periorbital structures is termed preseptal cellulitis if
the orbital contents are not involved, since the orbital The lacrimal drainage system is illustrated in Figure 16. Tears
septum serves as the barrier between the eyelids and drain thru the superior and inferior puncta to the superior
the orbit. and infertior canaliculi, then to the common canaliculus, to
the lacrimal sac, nasolacrimal duct and out through the nasal
lo determine if the cellulitis is preseptal or orbital, we meatus.
need to check extraocular muscle function, pupillary
reaction and visual acuity. Restriction of ocular motility, Fhe lacrimal gland receives its blood supply from the lacrimal
abnormal pupillary reaction and decreased visual acuity artery and venous blood drain to ophthalmic vein. Lymphatics
suggest involvement of the cranial nerves in the orbital drain into preauricular lymph nodes.
apex and would mean that the cellulitis is already orbital
and would necessitate aggressive and immediate Nerve supply to the lacrimal gland is by
management. a. lacrimal nerve (sensory), a branch of the trigeminal
first division
b. great superficial petrosal nerve (secretory)
c. sympathetic nerves
4. LID RETRACTORS
The lid retractors are responsible for opening the eyelids; have
striated and smooth muscle components E. OPTIC NERVE
A. Upper lid
1. Levator palpebrae superioris The trunk of the optic nerve consists of about 1.2 million axons
2. Muller's muscle (superior tarsal muscle) arising from the ganglion cells of the retina and has four parts
(Figure 17)
B. Lower lid
1. Inferior rectus muscle 1. intra-ocular portion - optic nerve head ; 1.5 mm in
2. Inferior tarsal muscle diameter, 1 mm long
2. orbital portion - 3 mm in diameter, 25-30 mm long,
5. LACRIMAL COMPLEX located within the muscle cone
3. intra-canalicular portion — 4-9 mm long
4. intra-cranial portion - 10 mm long, and with the
A. Lacrimal gland - has orbital portion and palpebral
opposite optic nerve joins to from optic chiasm
portion
self-Instructional Material, in Ophthalmcdmiy 12nd EdITIOn

The optic nerve sheath is continuous with the meninges.
Figure 18 shows the cross section of the optic nerve.
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
intraocular
peripapillary choroidal vessels. At the region of the lamina
intraorbital
cribrosa, the blood supply comes from the short posterior
ciliary arteries. The retrolaminar portion receives blood from
intracanalicular branches of the central retinal artery.The rest of the intraorbital,
intracanalicular and intracranial portions are supplied by pial
intracranial
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
An understanding of the anatomy of the eye, ocular adnexae,
Fibers of the
optic nerve consist of
orbit, visual pathways and the cranial nerves is important in
1. visual fibers — 80%, synapse in the lateral geniculate
the proper diagnosis of ocular diseases and other disorders
body on neurons whose axons terminate in the visual
with ocular manifestations.
cortex of the occipital lobe
2. pupillary fibers — 20% , bypass the geniculate body
en route to the pretectal area. REFERENCES
The ganglion cells of the retina and their axons are part 1. Duane, Thomas and Jaeger, Edward. Clinical
of the central nervous system and as such, do not Ophthalmology, Philadelphia : Harper and Row, 2006
regenerate if severed. 2. Riordan-Eva, Whitcher, John. Vaughn and Ashbury's General
Ophthalmology, 17th Edition, New York: Lange Medical
Books/ McGraw Hill, 2007
Dura
3. Scheie, Harold, Albert, Daniel. Textbook of Ophthalmology,
Philadelphia : W.B. Saunders Co,
Subdural space
Central
retinal vein Arachnoid
SELF-TEST
Subarachnoid space
1. An anti-glaucoma drug which decreases aqueous

Central Pia
retinal artery production acts on the epithelial cells of the
A. Pars plicata
Nerve bundles
divided by septa B. Choroid
C. Iris
D. Pars plana
Figure 18. Cross section of the optic nerve
Choroid 2. The rectus muscle tendon that inserts on the sclera
r
---- Posterior Ciliary A
nearest to the corneal limbus belongs to the
Retina-6\ Dura A. superior rectus
Arachnoid B. inferior rectus
Subarachnoid C. medial rectus
space
Optic Disc D. lateral rectus
Pia
( Central
3. Paralysis of this cranial nerve will result in inability to
Retinal Vein
close the eyelid
Central Retinal
Artery
A. Ill
B. IV
Figure 19. Blood supply of the optic nerve
C. V
D. VII

4. The following structures are part of the medial orbital 8. In order to ensure good vision, the following structures
wall, EXCEPT must maintain their clarity, EXCEPT
A. ethmoid bone A. Cornea

B. lacrimal bone B. aqueous
C. maxillary bone C. lens
D. sphenoid bone D. vitreous
E. choroid
5. Layer of the retina that receives its oxygen supply from
the choriocapillaris is the 9. Axons comprising the optic nerve come from which cells
A. ganglion cell layer in the retina?
B. nerve fiber layer A. amacrine cells
C. photoreceptors B. bipolar cells
D. inner nuclear layer C. ganglion cells
D. photoreceptor cells
6. Which of the following statements regarding the cornea
is FALSE? 10. Which muscle is an abductor?
A. The corneal endothelium is important in maintaining A. medial rectus
corneal dehydration. B. lateral rectus
B. The water content of the cornea is less than that of C. superior rectus
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
A. PHYSICAL OPTICS
index of refraction.
Light is the basic stimulus for vision. The wavelength that is
visible to the human eye comprises only a small portion of the The Index of Refraction or Refractive Index (n) is a constant,
electromagnetic spectrum of energy: depending on the material; it determines the angle of
deviation. It is simply a relative unit compared to air.
air = 1.0
Ymillion mp kilometer
water = 1.33
X-rays UV Infra Hersian glass > 1.40
Cosmic red waves
rays
Radium Radio - TV
rays Radar As light passes from one medium to another with a different
invisible V 130Y
Invisible refractive index and at a certain angle, there is bending of light,
visible
i.e., light is refracted (Figure 2).
Figure 1. The electromagnetic spectrum. Adopted from Espiritu RB.'

AIR
GLASS
This small portion, called the visible spectrum, is the ONLY AIR
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 Figure 2. Refraction of light as it passes from one medium to another (with a
different refractive index)
wavelength of each color increases as it moves toward the
direction of infrared rays (Figure 1).
There are three important physical characteristics of light: PRISM
1) Velocity or Speed Any media whose two sides are not parallel will refract light
-remains constant in vacuum , 3 X 1010 cm/sec rays. Light is deviated towards the base of the prism. (Figure 3)
-slower in clear air and in denser media.
APEX
2) Wavelength
-size determines color; with violet (380p) the shortest, and
red (760p) the longest. 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 Lenses can be viewed as a certain arrangement of prisms
optics, encompasses events that occur from the moment light (remember that light is deflected towards the base of the
strikes the eye and eventually gets focused on the retina. Its prism). A converging lens (positive lens) can be thought of as
principal basis is the transmission and bending of the direction two prisms joined at the base, while a diverging lens (negative
of traveling light rays, i.e., refraction. 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
Myopia, commonly known as "nearsightedness", is a condition

wherein parallel light rays focus at a point in front of the retina
CONVERGING DIVERGING
(Figure 6). It can be axial (eyeball longer than average) or
Figure 4. Converging and diverging lenses 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. Figure 6. Myopia: Light is focused IN FRONT of the retina
A +4.00 diopter lens will converge light rays at 25 centimeters
(0.25m), i.e., 4D = 1/(0.25m).
To correct myopia, one would need a divergent lens ("negative"
or biconcave lens to neutralize the convergent effect of the
The power of the lens depends on its curvature and the myopic eye) in order to focus light rays on the retina (Figure 7).
difference in its refractive index relative to air.
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. Simple Myopic - one image on the retina, one image

Figure 8. Hyperopia: Light is focused BEHIND the retina in front of the retina (Figure 11)
7. Simple Hyperopic - one image on the retina, one
image behind the retina (Figure 12)
To correct hyperopia, one would need a convergent lens 3. Compound Myopic - both images in front of the
("positive" or biconvex lens) in order to focus light rays on the retina (Figure 13)
retina (Figure 9). 4. Compound Hyperopic - both images at the back of
the retina (Figure 14)
5. 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 Figure 12. Simple hyperopic astigmatism One image on the retina, other image
without astigmatism) (Figure 10). To correct astigmatism, one behind the retina
would need cylindrical lenses (lenses each with power in two
different meridians/axes)
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
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
Figure 14. Compound hyperopic astigmatism. Both images at the back of the retina 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
The human retina is a thin, semi-transparent, multilayered

sheet of neural tissue that lines the inner aspect of the posterior
Figure 15. Mixed astigmatism. One image in front of the retina, one image at the 2/3 of the wall of the globe. The young, adult retina contains
back of the retina approximately 120 million rods, and about 6 million cones.
The human retina is capable of perceiving the following visual

senses:
CORRECTION OF AMMETROPIA
• Light sense
• Form sense
1. Spectacles
• Color sense
2. Contact lenses
• soft, rigid gas permeable, hard, etc.
• multifocal LIGHT SENSE:THE ROLE OF VISUAL PIGMENTS
3. Refractive Surgery
• photorefractive keratectomy (PRK) For the eye to perceive light, the latter has to be converted
• radial keratotomy (RK) into the biochemical energy of the visual nerve impulse. First,
it must be absorbed by the visual pigments located at the
• laser-assisted in situ keratomilieusis (LASIK)
outer segments of the rods and cones. These visual pigments
• implantation of phakic lenses
(rhodopsin, lodopsin, etc.) are lipid-protein complexes of a fat-
• refractive lens exchange surgery
soluble aldehyde of Vitamin A, plus a protein called opsin.'
2 PHYSIOLOGY OF THE EYE El

These two lights subserve an angle at the nodal point of the
Vitamin A is present only in animal tissue. A molecule of its
precursor (beta-carotene) derived from plants, is split into eye called the minimum visual angle.'
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 MINIMUM VISUAL ANGLE
trans-retinal structure. Only the cis-retinal isomer combines
with opsin to form rhodopsin.' Experimentally, the smallest detectable line subtends one
minute of arc (Figure 17). The big "E" on the Snellen Chart
PHOTOCHEMISTRY OF VISION subtends an angle of 5 minutes
When light strikes rhodopsin, it is split into cis-retinal (cis-retinene)

NODAL POINT
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.
1 minute of arc
Trans-retinal is reconverted to cis-retinal by the action of the

retinene isomerase enzyme with energy provided by the Figure 17. Minimum visual angle
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).'
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
1
amount of separation between two light sources at a given
distance from the eye so that they can still be seen as two.
Figure 18. The Snellen "Big E" and its corresponding visual angles
Light energy
nerve impulse
orange
intermediates
cis-retinene + opsin
Opsin
isomerase * energy
cis-retinene
1
DPN - H2.4\ trans-retinene
\•• (Dehydrogenase)
DPN
Figure 16. The photochemistry of vision. Adopted from Espiritu RB '
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 — Deuterdnornalous (green anornuly)
angle when viewed at distances of up to 200 ft (Figure 19). Protanomalous (red anomaly)
- Trianomalous (blue anomaly)
• In Dichromats, there is total loss of one color pigment
1 minute 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
5 minutes color blind
60 meters
1111 I I B. NEURO-OPHTHALMIC OPTICS
0 20 40 80 80 100
200 feet
distance from eye BASIC CONCEPTS
Figure 19. Construction of the Snellen Chart for consistency

Monocular vision, seen in lower vertebrates, is a less-advanced
form of visual function wherein visual impressions from one
One usually measures visual acuity at 20 ft (6 m) and is side cross-over to the contralateral cerebral cortex completely
recorded as two numbers: The numerator represents the (there is complete decussation)'. (Figure 21)
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 Lett half Right half
(emmetropic) eye can read at 40 ft.
COLOR SENSE: A FUNCTION

OF THE CONE PHOTORECEPTORS
White light or sunlight is a composite of different colors

complete decussation
corresponding to each wavelength in the visible spectrum
(Figure 20).
Left cortex Right cortex
—4g
RED
Figure 21. Visual pathway in monocular vision. Adopted from Espiritu RB.'
ORANGE
YELLOW
In binocular vision, there is nasal (partial) decussation of fibers
GREEN
from the two sides (Figure 22). As a result, both retinas send
BLUE
INDIGO
the same visual impressions to the visual cortex.
VIOLET
Left half Right half
Figure 20. The Color Spectrum
COLOR BLINDNESS
"Color blindness" occurs in about 10% of all males and about nasal decussation
1% of all females. It has a sex-linked, recessive pattern of
Left cortex Right cortex
inheritance. True color blindness (total absence of one type
of photo pigment or color-sensitive cone) is rare. Most of
Figure 22. Visual pathway in binocular vision. Adopted from Espiritu RB.'
the time, all photo pigments are present except for a relative
deficiency of one color----an "anomaly".'
2 PHYSIOLOGY OF THE EYE 19

This partial decussation of fibers at the optic chiasm is the • Eyes (retina)
basis for single binocular vision in humans. Stereopsis or depth • Optic Nerves (CN II)
perception is possible only with binocular vision. • Optic Chiasm
• Optic Tracts
• Lateral Geniculate Nuclei (LGN)
NEURO-ANATOMIC PATHWAYS Optic Radiations
o Parietal Lobes
These are structures which perceive, relay, and process visual Corresponds to inferior visual fields
information. From the external world, all the way to its end (superior retina)
terminal (occipital lobe), the following are its components': o Temporal Lobes
Corresponds to superior visual fields
(inferior retina)
Striate Cortex (Occipital Lobes)
Temporal Fields 4111 Nasal Fiekis

Temporal Fields
Left t ye 4— Right Eye
Note that the Visual Fields and the

Nasal FlaNes Retina are optically Inverted
Temporal Half, of Retinas Temporal Half,
Lett Retina Right Retina
411--
Optic Nerve
Optic Chiasm
IOptic Tract I
Lateral Geniculate
Nucleus
Geniculo-
calcarine Tract:
•Optic Radiations
Note that the cortex of one side receives
-Parietal Lobes
images from the contralateral visual fields
•Temporal Lobes
of BOTH eyes
•Occipital Lobes
Occipital Lobes
Primary Visual Cortex
Figure 23. The Afferent Visual Pathway

Note that the visual field and the retina are optically inverted, location.This retino-topic organization is preserved throughout
i.e., the right visual fields (both the right field of right eye and the entire visual pathway, and this logical architecture is the
the right field of left eye) are projected to the left hemi-retina basis for localization of lesions in the visual pathway via visual
of both eyes and, retro-chiasmally, the left visual pathway until field testing (perimetry).
its termination in the left occipital lobe (Figure 23). Vertically,
visual field and retinal projections follow a similar pattern Understanding the neuro-anatomy of the visual pathway
of optical inversion. In addition, there is direct one-to-one is the key to effective evaluation, localization, and eventual
correspondence between visual direction in space and retinal diagnosis of many intracranial lesions (Figure 24).
A. Right optic nerve - central scotoma/

generalized depression of the right eye
• LESION
••
B. Optic chiasm - Bitemporal hemianopia
C. Left optic tract - Right homonymous
hemianopia
D. Left optic radiation (temporal lobe) B
- Right Superior Homonymous
Quadrantanopia ("pie in the sky") Cm*
E. Left optic radiation (parietal lobe)
- Right Inferior Homonymous
Quadrantanopia ("pie on the floor")
F. Left occipital lobe (visual/striate cortex)
- Right Homonymous Hemianopia
D
(Temporal Lobe)
E
(Parietal Lobe
Figure 24. Location of Lesion with Corresponding Visual Field Defects

2. Riordan-Eva P, Whitcher JP. eds. Vaughan's and Asbury's
SUMMARY
General Ophthalmology. 16th ed. New York, NY: McGraw
Hill Companies; 2004.
I.THE EYE AS AN OPTICAL INSTRUMENT
3. Spalton DJ, Hitchings RA, Hunter PA. eds. Atlas of Clinical
A. PHYSICAL OPTICS
Ophthalmology. 2nd ed. London: Wolfe Publishing; 1994.
3 properties of light:
4. Goldberg S. Clinical Neuroanatomy Made Ridiculously
1) velocity
Simple. Miami: Medmaster Inc; 1979.
2) wavelength
5. DeMyer W. Technique Of The Neurologic Examination: A
3) frequency
Programmed Text. 3rd ed. New York: McGraw-Hill Book
Company; 1980.
B. GEOMETRIC OPTICS
• refractive index (n)
• prisms
• lenses (converging and diverging)
REFERENCES
• emmetropia
1. Espiritu RB. Ophthalmologic Optics. Manila: Department
• ammetropia
of Ophthalmology and Visual Sciences-UP-PGH Medical
• myopia
Center; 2001.
• hyperopia
2. Riordan-Eva P, Whitcher JP. eds. Vaughan's and Asbury's
• astigmatism
General Ophthalmology. 16th ed. New York: McGraw Hill
simple myopic
Companies; 2004.
simple hyperopic
3. DeMyer W. Technique Of The Neurologic Examination: A
compound myopic
Programmed Text. 3rd ed. New York: McGraw-Hill Book
compound hyperopic
mixed astigmatism Company; 1980.
correction of ammetropia
• spectacles
• contact lenses
SELF TEST
• refractive surgery
1. In the visible spectrum, which of the following colors
has the longest wavelength?
II. THE EYE AS A SENSE ORGAN
A. blue
A. PHYSIOLOGIC OPTICS
B. green
• light sense: role of visual pigments
C. orange
• photochemistry of vision
D. red
• form sense: visual acuity
• minimum visual angle
2. What happens to the velocity of light as it passes from
• testing visual acuity with the Snellen Chart
a medium of low refractive index, to one of higher
color sense: a function of photoreceptors
refractive index?
• color blindness
A. slows down
• Trichromat
B. speeds up
• Dichromat
C. stays the same
• Monochromat
D. is dissipated
• Achromat
3. True or False? A converging (positive) lens can be

B. PSYCHOLOGIC OPTICS OR NEURO-OPHTHALMOLOGIC OPTICS
thought of as 2 prisms stacked with the bases adjacent.
• monocular vision
• binocular vision
4. Which of the following structures accounts for about
• neuroanatomy of the afferent visual pathway
one third (on average) of the total refracting power of
• lesions and corresponding visual field defects
the human eye (about 20D)?
A. lens
B. cornea
Recommended Reading C. vitreous
D. aqueous
1. Espiritu RB. Ophthalmologic Optics. Manila: Department
of Ophthalmology and Visual Sciences-UP-PGH Medical
Center; 2001.
5. Match the following refractive states in reference to the 10. What stable product results from combination of cis-
location of the image relative to the retina. retinal and opsin ?
A. myopia 1. on the retina A. metarhodopsin
B.hyperopia 2. in front of the retina B. beta-carotene
C. emmetropia 3. behind the retina C. rhodopsin
D. lumirhodopsin
6. Which statement best describes astigmatism?
11. What angle does the entire big "E" in the Snellen Chart
A. The curvature of the lens is spherical.
B. The curvature of the cornea is not the same in subtend?
different meridians. A. 1 min
C. The curvature of the cornea is neutralized by the B. 5 min
curvature of the lens. C. 10 min
D. The convergence of rays in two different axes cancel D. 20 min
each other out.
E. The best type of lens for the correction of 12. True or False? In recording visual acuity, the
astigmatism are prism lenses. denominator represents the distance between the chart
and the patient.
7. To correct myopia, one would need which lens?
A. diverging (negative) lens 13. Which condition is described as having total loss of blue
B. cylindrical lens color?
C. converging (positive) lens A. deuteranope
D. prisms B. protanope
C. trianomaly
8. Which type of astigmatism has both images focused in D. trianope
front of the retina?
A. simple myopic 14. A symmetrically-growing pituitary macroadenoma
B. simple hyperopic impinging on the optic chiasm would most likely
C. compound myopic present with this kind of visual field defect:
D. compound hyperopic A. binasal hemianopia
E. mixed astigmatism B. left homonymous hemianopia
C. bitemporal hemianopia
9. Your neighbor who is an emmetrope develops difficulty D. left superior homonymous quadrantanopia
in reading for near on his 40th birthday and asks for
your casual advice. Which type of eyeglasses would you 15. Which of the following lesions would most likely give
recommend? rise to a right inferior homonymous quadrantanopia?
A. Bifocals to correct both distance and near vision A. left temporal lobe
B. Toric lens with reading adds B. right temporal lobe
C. Reading glasses for near work only C. left parietal lobe
D. Prisms reading glasses D. right parietal lobe
Answers to Self-Test on page 220.

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: Is the visual loss transient or permanent? Transient loss of
vision may be due to vascular disorders anywhere from the
1. abnormalities of vision retina to the occipital cortex.
2. abnormalities of ocular appearance
3. abnormalities of ocular sensation — pain and Is the patient's vision worse or better in some circumstances?
discomfort Patients with error of refraction may have better vision when
they squint their eyes. Patients with presbyopia will read better
These symptoms should always be described according to if they position their reading material further away from their
eyes. Patients with central focal cataracts, such as posterior
a. onset — gradual, rapid or asymptomatic subcapsular cataracts, may have worse vision in bright sunlight.
Example of asymptomatic onset is that the blurring
of vision was discovered only when patient Decline in visual acuity may be due to abnormalities anywhere
inadvertently covered one eye. along the optical and neurologic pathway. Consider the
b. duration — acute, chronic following as possible causes:
c. frequency — continuous or constant, intermittent or
episodic a. refractive error
d. degree — mild, moderate or severe b. ptosis
e. location — focal or diffuse, unilateral or bilateral c. ocular media disturbance (corneal edema, hyphema,
f. progression — worsening of symptoms cataract, vitreous hemorrhage)
d. retinal diseases
Determine if forms of treatment have already been initiated e. optic nerve diseases
or tried. If so, to what extent have they helped to relieve the f. intracranial visual pathway abnormalities
symptoms? Are there circumstances that provoke or worsen
the condition? Is this the first time these symptoms are Clinical Pearl
experienced? Are there associated signs or symptoms?
Determining the characteristics of a patient's symptom is a
valuable tool in helping us direct our investigation towards
I. ABNORMALITIES
a suspected pathology.
OF VISION
,
.777:777:71
1. VISUAL LOSS
Patients can describe visual loss as "nanlalabo',' "maulap Sudden Gradual

ang paningin" "nawawala ang paningin", "hindi makakita" or
"nabulag"
Mild Severe Severe
When a patient reports impairment of vision, the examiner
should determine when it occurred, whether onset was
check cornea Check retina Check refraction Check lens for cataract
sudden or gradual, whether one or both eyes were affected. for dry eye for error of and optic disc for
for CRAO
If both eyes are involved, which is worse, which failed first and refraction glaucoma
how much time has elapsed between the two.
CRAO - central retinal artery occlusion
Actual onset of visual impairment may not coincide with the

time given by the patient. Vision in one eye may have been 2. VISUAL ABERRATIONS
deteriorating over the years, becoming noticeable when the
patient accidentally covered one eye. A. Glare, photophobia
One should distinguish between decreased central acuity Patients may describe this as "silaw" or "nasisilaw"
and peripheral vision. Disturbances in peripheral vision may
be focal such as scotoma, or may involve a bigger area as in Irritative disease of the conjunctiva or cornea especially
hemianopsia. A scotoma is a blind or partially blind area in foreign bodies of the cornea may induce photophobia. Acute
the visual field while hemianopsia is blindness in one-half of inflammation of the iris may likewise make the eye sensitive to
the visual field. Abnormalities in the central nervous visual ordinary light.
pathway disturb the visual field more than the central visual
acuity.
3 EYE SYMPTOMS 1111

Glare may also result from uncorrected error of refraction,
scratches on spectacle lenses, excessive pupillary dilatation Clinical Pearl
and hazy ocular media
Characterizing the particular quality ofvisual aberrations
B. Visual distortion can guide us in formulating a differential diagnosis
Visual distortion manifests as irregular patterns of dimness, Glare/ Photophobia - corneal edema, cataracts
wavy or jagged lines, image magnification/ minification. This Visual Distortion - central serous chorioretinopathy,
may be caused by migraine, optical distortion from strong age related macular degeneration
corrective lenses and lesions involving the macula and optic Flashing/ flickering lights - posterior vitreous
nerve. detachment, retinal detachment
Floating Spots - vitreous condensations
3. FLASHING/FLICKERING LIGHTS Oscillopsia - nystagmus
Patients may describe this as "may parang kidlat", "biglang may

maliwanag", "may kumikislap"
This may indicate retinal traction, posterior vitreous II. ABNORMALITIES OF
detachments or migrainous scintillations or auras.
APPEARANCE
4. FLOATERS 1. RED EYE
"May lumulutang so harap ng mata","may insekto no sumusunod One must differentiate between redness of the lids (Figure 1)
so paningin" 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

Figure 1. Redness and swelling of the eyelid
image. Causes include uncorrected error of refraction, media
abnormalities such as cataract, corneal irregularities and
intraocular lens dislocation.
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" "namumula ang mate; "sore eyes"
Preseptal cellutitis Conjunctivitis (Figure 2)
VS
Orbital cellulitis Iritis (Figure 4)
External hordeolum (Figure 3) 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
a. jaundice
b. 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),
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
Superficial discomfort is usually caused by ocular surface

abnormalities.
Figure 20. Hypotropia, left eye
a. Itching - Often a sign of allergic sensitivity, "makati"

b. Dryness - Burning, gritty, mild foreign body
sensation. Can occur with dry eyes or other types of
mild corneal irritation, "may buhangin: "may puwing",
"maaligasgas"
c. Tearing - may be due to irritation of the ocular
Figure 21. Small right eye
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: d. Ocular Secretions - "nagmumuta: Characterize
discharge as to color, consistency, amount
a. Periocular - may be tenderness of the lid, tear sac,
sinuses or temporal artery i. Watery - allergic (Figure 24)
b. Retrobulbar - may be due to orbital inflammation, ii. Mucoid discharge - allergic , viral conjunctivitis
orbital myositis, optic neuritis (Figure 25)
c. Ocular - may be due to corneal abrasion, iii. Ropy or stringy discharge - allergic (Figure 26)
corneal foreign body, glaucoma, corneal ulcer, iv. Mucopurulent - bacterial/viral conjunctivitis
endophthalmitis v. Purulent and copious- gonococcal conjunctivitis
d. Non-specific - fatigue from ocular accommodation, (Figure 27)
binocular fusion, or referred discomfort from non- vi. Bloody - viral conjunctivitis (Figure 28), Steven-
ocular tension or fatigue Johnson's syndrome
vii. Dried matter-crusts on lashes - blepharitis
Deep seated aching, boring or throbbing pain may be due (Figure 29)
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.
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 Students should pair and role play. One will be the doctor and
cause headache referred to the eyes or brow and comes the other the patient. The doctor should take the history of the
with reading and computer work. Migraine headaches and patient with any of the following chief complaint:
sinusitis are frequent causes of headache. Headaches may not
always come from the eye. High and low blood pressure may 1. "Malabo ang mata"
also give rise to headaches around the eyes. Headache from 2. "may sore eyes"
rise in intracranial pressure is usually severe and associated 3. "mahapdi ang mats"
with nausea and vomiting. Clearly demarcated one-sided 4. "banlag"
headache, originating from the ipsilateral eye, associated with
nausea and vomiting, with or without ciliary injection of the The doctor will write the patient's history and the partner will
eye may be due to angle closure glaucoma. 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 Case 1. You have a 20 year old female patient with chief
order to get sufficient detail to pinpoint the etiology of the complaint of blurring of vision. What questions you will
ocular disorder. 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?
REFERENCE
Answers to Self-test on page 220.
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
li:111,1,)iii,l,,))(1,11111)1111,uovippocumolodndo, 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. perform gross examination of the eye and its adnexae
4. perform pupil examination and interpret its findings
5. evaluate ocular motility
6. determine intraocular pressure
7. perform direct ophthalmoscopy for a systematic fundus examination
8. 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 eye during occlusion as this may affect subsequent
general physical examination. Visual acuity, gross examination visual acuity testing of the occluded eye.
of the eye and its adnexae, extraocular muscle movements,
intraocular pressure determination and fundus examination 3. Ask the patient to read the chart starting at the
using the direct ophthalmoscope constitute the basic eye first line (20/200 or 6/60 line) proceeding until the
examination. smallest line that he/she can distinguish more than
half of the figures.
I. VISUAL ACUITY TESTING 4. Record the acuity using a ratio or fraction which
compares the performance of the patient with an
Measurement of visual acuity (VA) is a fundamental element of
agreed upon standard.
the basic eye examination. It should be performed prior to any
manipulation of the eye to avoid any medico-legal issues that
Visual Acuity (VA) = distance of patient from the chart
may arise. Distance visual acuity testing should be performed distance at which normal eye can
in all patients, including children. Near visual acuity testing on read the given line
the other hand, is routinely performed only for patients over 35
years of age. Otherwise, this is done only if the patients have For example, a patient whose VA = 20/50 indicates that
complaints with their near vision. Occasionally, near vision the patient can see at 20 feet what a person with normal
testing is done in lieu of distance vision testing if the latter is acuity can see at 50 feet.
difficult or not possible as in instances when vision testing has
to be performed at bedside. Table 1 shows the various notations commonly used for
recording distance visual acuity.
Distance Visual Acuity is generally performed using the Snellen
Chart (Figure 1), which may come in the form of letters, 5. Instruct the patient to occlude his/her other eye and
numbers, tumbling E or pictures. repeat steps 3 and 4.
Table 1. Alternative Notations for Recording Distance VA
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A, B,
2a*. •
Figure 1. Snellen Charts used for distance visual acuity testing. (A) Letter chart,
(B) Tumbling E chart, (C) Lea Kindergarten chart k'4111111=111111111111rat
The standard distance of the patient from the chart is 6 meters If the patient's visual acuity is less than 20/20 in either eye,
or 20 feet. 1 he general steps are as follows: 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. Position the patient 20 feet or 6 meters from a well-
illuminated Snellen Chart. In patients consulting
1. With one eye occluded, instruct the patient to place
for the first time, naked visual acuity (without any the pinhole (Figure 2) over the eye being tested
correction) is initially taken. Follow-up patients who and ask him/her to try to read the chart through the
wear corrective lenses should be asked to wear their pinhole.
correction during the test.
2. Record the acuity using a ratio or fraction.
2. Instruct the patient to occlude one eye using his/her Repeat steps 1 and 2 with the opposite eye looking
3.
palm or an opaque occluder when available. Care thru the pinhole if warranted.
should be taken to avoid exerting pressure on the
5. 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.
Figure 2. Patient looking thru pinhole (white arrow) as she reads the
Snellen Chart.
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
(listed in order of decreasing vision): possible to measure visual acuity. When evaluating vision in
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
Step 2. assessed by passing light or brightly colored objects before
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
to a distance of 2 feet, VA is recorded as CF at 2 feet. charts (Figure 3). Near vision charts usually contain numbers
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
(-) HM. reflects both the size and distance of the smallest figures that
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 Table 2 shows commonly used abbreviations used in
fair LPj: able to identify light source in 2-3 out of the four recording visual acuity.
quadrants
poor LPj: able to identify light source in only one quadrant
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.
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
Figure 3. Near VA testing in a patient using the Rosenbaum (Jaeger) inspection of the medial and lateral conjunctival regions. Take
Pocket Vision Chart. note of the presence of redness, discharge, lumps and masses,
or any other abnormality.
Table 2. Abbreviations Used in Recording Visual Acuity 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
VA visual acuity for pigment changes as well the presence of any masses or
OD (oculus dexter) Right eye nodules (Figure 4).
Os (oculus sinister) Left eye
OU (oculus uterique) Both eyes
so without correction
cc with correction
ph pinhole
NV near vision
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 Figure 4. Gross picture of normal eye. Note the outwardly directed
towards the more internal eye structures. lashes and the lids partially covering the superior and inferior limbos
Patient has deer cornea, brown iris and round pupil.
The position of the eyes in relation to other facial structures is

first assessed. Check for the presence of any gross asymmetry Pupil examination is composed of three components. These
between the two eyes. Eye position should be examined from are
the front, above (looking down over the patients brow while
seated) and from the side. These views would highlight any 1. Assessment of pupil size and shape. Darken the room
possible protrusion of the eye ball. and instruct the patient to fixate on a distant target. Shine
just enough light onto both eyes and observe the size of
With the aid of a flashlight, one inspects the lids, the the patient's pupils.The normal pupil size ranges from 2 to
surrounding tissues and palpebral fissure. The exposed 4 mm. Although size of individual pupils of a patient may
portion of the eye between the upper and lower eyelids, fall within this normal range, any asymmetry in pupil size
called the palpebrai fissure should be symmetrical. Take note of more than two millimeters is considered abnormal.
of the presence of redness, masses or abnormal pigmentation/
discoloration on the eyelids or periocular tissue. The eyelashes 2. Assessment of pupil reaction to light (Light Reflex
should not touch the eye and should be directed outward. Test). This test is used to evaluate the integrity of the
The lid margins should be smooth and well opposed against pupillary light reflex pathway. Cranial nerve II (optic nerve) and
cranial nerve III (oculomotor nerve) comprise the afferent as light is moved from one eye to the other. The normal
and efferent arms of the pathway respectively. reaction is for the pupil to constrict slightly and to remain
constricted as light shines on it. If dilation is observed
a. Direct pupillary reaction. This is performed by shining when light is shone on an eye, it means that its direct
a penlight at the patient's eye. Normal response is a light reflex is weaker than its consensual light reflex and
brisk constriction of the pupil. is suggestive of an optic nerve problem in the dilating
eye. This test compares direct and consensual responses
b. Consensual pupillary reaction. To perform this test, of each eye and provides an objective way to rule out a
light is directed at one eye while the opposite eye is unilateral optic nerve lesion or bilateral but asymmetric
observed for a response. Normal response is a brisk optic nerve pathology. The abnormal response is called a
constriction of the pupil of the opposite eye. relative afferent pupillary defect (RAPD). A positive RAPD
signifies that an optic nerve lesion is present on the side
Absence of a direct response to light would indicate a of the dilating pupil. Note that as this is a comparative
problem in the afferent arm of the same eye, while absence of test, hence it is not possible to have bilateral RAPD.
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
III. OCULAR MOTILITY TESTING
problem lies in the efferent arm of the involved eye. In such
Examination of eye movements begins by examining ocular
cases, however, this finding should be associated with ptosis
alignment in the primary position (straight gaze). The simplest
or drooping of the lids of the involved eye as the muscles
method to observe this is by observing the position of the
responsible for lid opening is also innervated by CN Ill or the corneal light reflections. This is performed by instructing the
oculomotor nerve. patient to look straight and fixate at a distant object while
a light is shone towards both eyes. A reflection of light will
3. Assessment of the reactions of the pupils to a appear in the cornea of each eye. If the eyes are properly
swinging light (Swinging Flashlight Test). This test is aligned, the reflection should appear in the center of the pupil
performed by shining a light on one eye, then swinging it in both eyes (Figure 5). The presence of misalignment will be
across to the opposite eye. The process can be repeated observed as appearance of the corneal reflection outside of
several times, allowing for about one second interval for the center of the pupil in the deviating eye. Table 3 lists the
each swing. Change in pupil size of both eyes is noted common abnormalities in the alignment of the eyes.
Table 3. Common Abnormalities in Alignment of the Eyes
'
Esotropia inward light reflection appears It!!
misalignment displaced laterally in the
non-fixating eye
Left Esottopia
Ipotio
-pie outward light reflection appears
misalignment displaced medially in
the non-fixating eye
Left Esotropia
Hypotropia downward light reflection appears

misalignment displaced superiorly in
the non fixating eye
Right Hypotropia
tHypertropia upward light reflection appears

displacement displaced inferiorly in
the non-fixating eye
Right Hypeiti opia
4 EYE EXAMINATION
Figure 6. Motility examination being conducted on a patient.
Figure 5. Normal ocular alignment showing comeal reflexes at center (A) cardinal positions of gaze to be tested following the arrows or the
of pupils. letter "H", (B) Examiner asks patient to follow his finger thru the different
cardinal gaze positions.
Proceed to examine eye movement by instructing the patient
to follow your finger, a penlight or a small target through the Normally, the white of the sclera should disappear completely
six cardinal positions of gaze. Move the target slowly through with sideways movement. On upward movement, only a
the different positions (Figure 6) keeping it roughly 14 small part of the cornea should disappear behind the upper
inches or 35 centimeters from the patient. This will allow for eyelid, while with downward movement, at least half of the
systematic testing of each of the extraocular muscles in their cornea should disappear. In order to allow better visualization
primary fields of action (Figure 7). When extraocular muscle
of downward movement of the eye, the patient's upper eyelids
(EOM) movement is tested with both eyes open, this is referred
may be lifted.
to as version test. When performed one eye at a time, it is
referred to as duction test. Results of EOM testing are recorded diagrammatically as
shown in Figure 8A. The limits of gaze in the various positions
Observe the excursion of each eye as it moves from one are delineated by small lines while the EOM movements are
position of gaze to another and take note of any limitation in represented by lines ending in arrows or circles. For duction
movement. Also observe for parallelism of eye movements tests a separate diagram is used to represent each eye.
between the two eyes and presence of jerky, oscillatory or
Version test results are presented in a similar manner except
rotational movements like nystagmus in any direction of gaze.
that the diagrams for each eye overlap each other. When
While conducting the examination, the patient is also asked if movement in any direction is limited, the lines representing
double vision occurs at any point.
RSR LIO Sup Recii & Inf Obliques RIO LSR
RLR LM R PRIMARY POSITION RMR LLR
RIR LSO Id Recli & Sup Obliques RSO LIR
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 if globe perforation is suspected, as in cases wherein a
gaze. Length of said lines should approximate the extent of history of ocular trauma is elicited from the patient.
imitation in EOM. Figure 8B shows the results for limitation in
movement of the right lateral rectus muscle for both duction 2. Indentation Tonometry provides a quantitative
and version tests. method for determination of 10P by measuring the
amount of pressure required to indent the cornea with
Additional motility examinations are performed in cases when the use of the Schiotz tonometer (Figure 10). While
abnormalities in ocular alignment and EOM movements are this is the preferred method for 10P measurement in
noted when performing the basic eye exam. 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
MOTION VERSION
position.
SR 10
LR 1e sf MR le
IR SO
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
Figure 9. Palpation tonometry is performed by alternately pressing on
the patient's upper lid using the index fingers of both hands while patient
IV. INTRAOCULAR PRESSURE looks down without closing her eyes.
DETERMINATION
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 Figure 10. Indentation Schiotz tonometry gives a quantitative
measurement of the 10P by measuring the amount of pressure required to
methods commonly used for determining 10P levels follow:
indent the cornea
1. Finger Palpation/Tension Tonometry provides a 3. Applanation tonometry using the Goldman

rough estimate of 10P. This is performed by first asking Applanation Tonometer is considered as the gold
the patient to look down without closing his/her eyes. standard for lop determination (Figure 11). Its primary
The examiner then places his two index fingers on the disadvantage Is that it requires special equipment and
patient's upper lid over the globe and alternately exerts can only be used by an ophthalmologist. Intraocular
pressure on the globe (Figure 9). Findings are reported pressure measurements are based on the amount of
as soft (normal), hypotonic or firm. Care is taken that only pressure required to flatten a standard diameter (3.06
pressure sufficient to slightly indent the globe is applied. mm) or area (7.35 mm2) of the cornea. Unlike the Schiotz
Note that this method of 10P determination is avoided tonometer, the instrument requires a smooth cornea and
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
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
Figure 11. Applanation tonometry which uses the Goldman Applanation physician learn and gain confidence in performing fundus
Tonometer, considered the gold standard for 10P determination takes 10P examination using the direct ophthalmoscope as this is
by measuring the amount of pressure required to flatten a specified area
generally used for screening purposes.
of the cornea
can not be used in individuals with corneal abnormalities Prior to performing direct ophthalmoscopy, it is essential to
such as scars. This instrument is more accurate than the gain familiarity with the instrument's basic parts (Figure 12).
Schiotz tonometer in determining the 10P of patients with Ophthalmoscopy is best performed in a darkened room.
altered scleral rigidity. 10P measurements taken with the Sufficient examination of the fundus can be done even in a
applanation tonometer are however affected by corneal non-dilated pupil, provided that there are no media opacities.
thickness and irregular or altered corneal curvatures (e.g. However, a more thorough examination of the peripheral
in post refractive surgery patients and patients with high retina can be performed through a dilated pupil.
corneal astigmatism).
Before beginning the procedure, one should ensure that the
4. The air puff noncontact tonometer is a machine that ophthalmoscope is working properly and that both you and
takes 10P readings by calculating the amount of corneal 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 10. Examine the retinal vessels by moving the beam slowly
aperture. The intensity of light from the ophthalmoscope along the nasal retinal vessels and the temporal retinal
should not be too much as this could lead to excessive vessels.
constriction of the patient's pupil.
11. Inspect the retinal background for the presence of
2. Place your index finger on the lens selection dial and hemorrhages, exudates or any other abnormality.
adjust the lens setting to 0 diopter. The index finger is
placed on the lens selection dial to allow for adjustment 12. Examine the macular area. Take note of the presence of
of the lens power during the conduct of the examination. the foveal reflex.
3. When examining the patient's right eye, hold the 13. Repeat the procedure with the opposite eye.
ophthalmoscope with your right hand and use your right
eye to view the patient's eye. Use the left hand and left There are five structures that should be observed in a systematic
eye to examine the patient's left eye. fundus examination: (1) ocular media, (2) optic disc, (3) retinal
vasculature, (4) retinal background and (5) the macular area.
4. The patient's glasses should be removed. The examiner Figure 13 shows these areas in an actual fundus photograph.
may also opt to remove his glasses while performing
direct ophthalmoscopy. Contact lenses worn by the 1) Ocular Media is observed for presence of the red-orange
patient or examiner may be left in place. reflex (ROR) which is a result of the reflection of light
coming from the ophthalmoscope that bounces off the
5. Instruct the patient to focus on a distant target. The patient's fundus. The status of the ROR is an indication of
patient should also be instructed to maintain that gaze the clarity of the ocular media (cornea, lens, aqueous and
throughout the examination. vitreous humor) and condition of the retina. A normal
ROR (Figure 14) is evenly colored and is not interrupted
6. Begin to look at the patient's eye thru the instrument's by shadows. The presence of any opacity in the lens or
viewing aperture from about a distance of one to two cornea, cells or bleeding in the aqueous/vitreous humor
feet. When you look straight down the patient's line of will generally appear black or create a silhouette against
sight at the pupil, the red-orange reflex should be visible. the red-orange reflex. Retinal detachment will also affect
the bouncing of light as it is reflected from the retina and
7. Slowly come closer to the patient at an angle of about 150 alter the appearance of the ROR.
temporal to the patient's line of sight keeping the pupil
in view at all times. Turn the lens selection dial with your -RETINAL VEIN
- RETINAL ARTERY
index finger to bring the patient's retina into focus.
f---- DISC
8. You may place your free hand on the patient's upper lid FOVEA
r- - - —)
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.
F,ACKGROUND
9. Move the beam until a retinal vessel comes into view. If
MACULA PHYSIOLOGIC CLIP
the image is not clear, turn the lens selection dial up and
TEMPORAL NASAL
down until it becomes clear. Follow the retinal vessel
until it converges to the optic disc, which lies nasal to the Figure 13. Normal Fundus. Photo shows the different parts of the right
center of the retina. Take note of the disc color, its margins 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
The optic disc is examined taking note of its color, shape Approximation of the vertical cup-to-disc ratio (CDR) is
2)
arid margins. In most cases, when viewed through the described in Figure 16. Normal cup-to-disc ratios should
ophthalmoscope, the normal optic disc will appear slightly be less than 0.5. The cup becomes enlarged when the
oval vertically and yellowish-orange to pink in color. Its ganglion cells die as observed in glaucoma (Figure 17).
margins should be sharp or distinct. Also note for the
presence of abnormal structures such as new vessels or The optic disc is often used as a "yardstick"of the ocular fundus.
hemorrhages within the disc (Figure 15). A central pit Lesions seen with the ophthalmoscope are measured and
or depression seen on the surface of the disc is called the described in terms of disc diameters.
"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.
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
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
Figure 15. Examples of presentations of the optic disc. aspect of the disc follow an arching course while those
(A) normal disc showing healthy neuroretinal rim with distinct margins and on the nasal side have a radial course. The arteries
approximate CD ratio of 0.3. (B) tilted optic disc with a scleral crescent often usually appear brighter red in color than the veins with a
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 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 structures within or on the retina such as hemorrhages
arteries in comparison to the veins (normally 2:3 to 4:5); and exudates (Tables 4 and 5).
presence of pressure effects of the arteries on the more
pliant veins at areas of their intersection (indentation 5) The macular area is located approximately 2.5 disc
or displacement of the veins); transparency of the diameters temporal to the optic disc. There are no
vessels; presence of focal narrowing particularly of the blood vessels in the area and it appears darker than the
arterioles; and presence of abnormal structures within or surrounding retina. This is due to the specialized retinal
surrounding the vessels such as atheromatous plaques, pigment epithelial cells of the macula that are taller and
perivascular infiltration (sheathing) or hemorrhages. more heavily pigmented. At the center of the macula is
a central depression called the fovea which may act as
4) The retinal background is generally reddish orange in a convex mirror and produce a light reflection known
color. The retinal pigment epithelium, blood and pigment as the foveal reflex. As with other areas of the retina, it
of the choroid contribute to the appearance of the retinal is important to take note of the presence of abnormal
background. Take note of changes in its color as observed pigmentation as well as other structures such as exudates
in retinal detachment or ischemic conditions. Note for and hemorrhages which may prevent the appearance of
the presence of pigmented lesions or other abnormal the foveal reflex.
Table 4. Yellow-White Lesions on the Retina
Distinctive
Yellow-White Common Associated
Ophthalmoscopic Photo
Lesions Conditions
Features
Hard Exudate Deep yellow with Diabetes, hypertension

sharp margins, often von Hippel Lindau
circinate disease, radiation
Fluffy gray-white; Hypertension, diabetes,

Soft Exudate
usually near optic disc connective tissue
disease, HIV
Drusen Clusters of yellow- Age-related macular

orange spots, usually degeneration
centered around
fovea
Laser Marks Clusters of yellow- Post retinal

white spots, usually photocoagulation
uniform in size and
regularly distributed in
entire retina or around
macular area
4 EYE EXAMINATION
Table 5. Hemorrhages (red lesions) commonly observed in the fundus
Common Associated
Hemorrhages Source Phot0911111.
Conditions
Dot Hemorrhages Bleeding from capillaries Diabetes
Flame Hemorrhages Bleeding from superficial pre- Hypertension. retinal

capillary arterioles, small vein occlusion. blood
veins dyscrasia. trauma
Boat Hemorrhage Bleeding from large Trauma, blood

superficial retinal veins into dyscrasia. sudden
the space between the retina increase in intracranial
and vitreous: sometimes pressure
these bleeds break into the
vitreous cavity
Vitreous Hemorrhage Bleeding from superficial Diabetes. hypertension.

retinal vessels or vessels on trauma
a fibrovascular stalk
extending into the vitreous
Su bmacular/ Bleeding from choroidal Age-related macular

subfoveal vessels under the fovea degeneration
Hemorrhage
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 sharp/distinct blurred/indistinct (papilledema, papillitis)
color yellowish orange to creamy pink pale (optic atrophy)
shape round or oval
cup to disc ratio (CDR) < 0.5 > 0.5 (glaucoma)
Retinal Circulation
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)
Retinal Background
color red orange - gray, pale (retinal detachment)
— pale (central retinal artery occlusion)
pigment changes. absent — pigmentation

hemorrhages and - hemorrhages (diabetes. hypertension)
exudates
- exudates (diabetes, chronic hypertension)
Macula
vessels absent present (neovascularization)
exudates absent macular star (hypertension)
hemorrhages absent present (macular degeneration)
drusen absent present (macular degeneration)
fovea! reflex present absent
The following is an example of an eye exam report of a 54/M

SUMMARY patient with Left Lateral Rectus Palsy.
Acquiring the skills to be able to properly perform the basic Sc PH NV T OD soft

eye examination will allow physicians to recognize potentially VA OD 6112 617.5 J5
OS soft
vision threatening conditions early so that such cases are OS 6115 617.5 J5
referred to the ophthalmologist for appropriate management. 000111111mIeftioi
Summary of the steps in performing the basic eye exam is 1/4,
listed in Table 7.
Table 7. Summary of conduct of basic eye exam
Pupils equal and briskly reactive to light

Intact direct and consensual light reflex
1 Measure the distance and near visual acuity (-) RAPD
(+) L esotropia
2. Inspect the lids. ocular adnexae. Palpate the orbit if
necessary. EOMs
3. Inspect the conjunctiva, sclera. cornea and iris. (+) diplopia on
left gazes with
4. Inspect the pupil and check the pupillary reflexes. It><)1 MX I version: (-)
diplopia with
5. Check the ocular alignment and test the extraocular OD OS duction test
movements.
6. Perform tonometry. (+)ROR, pink disk with distinct borders, CD 0.4, AV 2:3,
OD hemorrhages, exudates. good fovea! reflex
7. Examine the fundus (red orange reflex, disc. vessels, retinal F (+)ROR pink disk with distinct borders, CD 0.4, AV 2:3,
background and macula. OS (-) hemorrhages, exudates. good foveal reflex
4 EYE EXAMINATION
A. replace the Snellen Chart since it is possible that he is
RECOMMENDED FOLLOW-UP just not familiar with its figures
ACTIVITY B. instruct the patient to count your extended fingers at
a distance less than one meter
This self-instructional material should be utilized as a guide C. Shine your penlight on his left eye to check for
to identify specific areas that should be focused on by the presence of pupillary light reflexes
student concerning the Basic Eye Examination. It should D. Repeat visual acuity testing, this time asking patient
be supplemented by the following small group activities to to look thru a pinhole
maximize the learning experience: (1) a demo-return demo
session with a faculty member and (2) examination of patients 3. Shown below is a gross picture of the patient's left eye.
at the General Clinic under the supervision of a faculty member. Based on the picture below, which of listed findings are
Students are further encouraged to practice the examination present in this patient (may have more than one answer
skills during their self-study session. A. round, normal sized pupil
B. Mild redness of the conjunctiva
C. Clear cornea
REFERENCES D. Presence of opacity in pupillary area
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, L.
2011).
5. The Eye Examination. In: Basic Ophthalmology for Medical 4. Shown below is a diagram of patient looking at straight
Students and Primary Care Residents. Berson, FG. (exec ed). gaze.
San Francisco: American Academy of Ophthalmology.
1993. chap 1: 1-26.
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
Based on this diagram, you conclude that the patient has
has been wearing soft contact lenses for both eyes for the past
A. Left esotropia
five years.
B. Left hypertropia
C. Right exotropia
1. After taking his history, the first thing that should be
D. Right hypotropia
done is
A. ask patient to remove his contact lenses 5. On EOM testing, you note that the patient is unable to
B. take the patient's visual acuity without removing his abduct his left eye. Movement was full on all positions
contact lenses of gaze for the right eye. This would imply weakness of
C. palpate the patient's orbital rim for any fractures his left
D. palpate the left globe to rule out globe rupture A. lateral rectus
B. medial rectus
2. On visual acuity testing, the patient was unable to read C. inferior rectus
even the first line of the Snellen chart with his left eye D. superior rectus
despite moving him closer to a distance of 1 meter. You
should
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
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 2. Refraction of Light: In order for light entering the eye to oe
and the lens. Of the two, the cornea, together with the pre focused on the retina, incoming parallel light rays have to be
corneal tear film is responsible for two-thirds of the total refractive bent or refracted. This is made possible by the smooth anterior
power of the eye, thus making it more powerful than the lens. 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
I. MAIN FUNCTIONS OF THE refraction between air, tear film, cornea and aqueous humor.
CORNEA Therefore any disturbance in the shape or curvature of the
cornea and the indices of refraction of the different structures
1. Transmission of Light: The cornea is a highly transparent can cause the failure of the converged light rays to be focused
tissue and this is largely due to its unique anatomy. It on the retina leading to blurry vision.
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 radius of curvature
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
Figure 2. Radius of curvature the cornea
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. II. COMMON CAUSES OF BLURRING
A-
OF VISION DUE TO CORNEAL
PATHOLOGY OR DISEASES
A. Conditions causing Disruption in the

• • • • • • • 0 • • • Transmission of Light
• • • • • • • • • • • •
• • • • • • • • • • • 1. Corneal Scars
• 0411 • • • • • • • •
• .4• • • •ii • •
• i• •
• • )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).
Figure 1. Theory of comeal transparency. Since the oiameter of tne
Scars are usually formed after an inflammatory process when
collagen fibrils (black dots) and the distance between them is homogenous
fibrosis sets in. In fibrosis, new and abnormal collagen fibrils and
(arrows) and measures less than one-half the wavelength of visible light (top),
light is not diffracted and is therefore transmitted through the cornea. other cellular elements are laid down in a "haphazard" manner,
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 b. Corneal trauma: This includes mechanical and
of the collagen fibrils. This prevents proper transmission of light chemical injuries to the cornea and is among the major
and is reflected back instead; thus, making the cornea appear causes of corneal problems in the Philippines. Corneal
opaque. lacerations and perforations are usually caused by sharp
objects (knife, scissors, nails, glass etc), and high velocity
Causes of corneal scar: projectiles (iron nails due to hammering, shattered
glass, darts, bullets etc). Most of these injuries require
a. Microbial keratitis: These are infections of the cornea surgical management in the form of corneal repair
which can be caused by viruses, bacteria, fungi and or suturing with the goal of closing the wound and
protozoans (Figure 4). Invasion of microorganisms restoring the integrity of the globe (Figure 5 A). Similar
into the cornea induces an intense inflammatory to skin lacerations, healing will bring about fibrosis and
response and with the actions of microbial toxins and subsequent corneal scarring along the wound and
enzymes, causes corneal tissue necrosis, melting and suture track (Figure 5 B). Depending on the extent
sometimes rupture of the cornea. During the active of involvement, vision will be variably affected either
infection, corneal opacity is associated with marked by the opacity itself or the distortion of the shape of
eye redness, tearing and photophobia. Once healing the cornea. Acid chemical burns of the cornea cause
ensues, either due to treatment or due to the natural denaturation and precipitation of the collagen and lead
course of the disease, redness and other symptoms to scar formation. In alkali burn, corneal destruction is
will disappear except for blurring of vision (more so generally more severe since it causes corneal necrosis
if lesion is overlying or affecting the pupillary area) and melting due to its ability to penetrate deeply into
which perists, as it is caused by the corneal opacity. 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 2. Corneal Edema
desiccation if left exposed to the environment.
Failure of the lids to close properly (lagophthalmos) The corneal endothelium is the single most important
will lead to a condition called exposure keratopathy structure of the cornea and is responsible for the active
wherein the exposed cornea (usually the inferior pumping of water away from the cornea to the aqueous
half) opacifies due to the drying effect (Figure 6). humor, thereby maintaining corneal clarity. the human
This condition can also lead to severe scarring if corneal endothelial layer does not regenerate when lost or
secondary microbial keratitis occurs. This problem injured and the endothelial cells decrease in number as a
is usually seen in comatose patients, those with person ages. An adequate number of endothelial cells must
CN VII palsies, lid and orbital deformities, acute be present throughout life for the endothelium to function
proptosis, nocturnal exposure etc. Bilateral inferior properly. When the cell density dips below a critical level, the
corneal scars are commonly seen in patients with a direction of the flow of water is reversed and the cornea will
history of severe measles occuring in childhood. The retain water and swell like a sponge (corneal decompensation)
condition usually starts as exposure keratitis in a very resulting in the disruption of the normal arrangement of the
sick child compounded by dehydration, pneumonia, collagen fibrils.The edematous and markedly thickened cornea
malnutrition, immunodeficiency, vitamin A becomes hazy or ground glass in appearance. Affectation may
deficiency and lack of tears. The exposed cornea be diffuse or focal. Patients will usually complain of marked
develops secondary bacterial infection and usually blurring of vision, recurrent eye pain, redness, foreign body
ends in corneal rupture and subsequent scarring. It sensation and tearing.
should be noted that exposure keratopathy can be
prevented. 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
Figure 6. Exposure keratopathy secondary to lagophthalmos due
to CN VII palsy cell density, corneal decompensation may ensue.
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 Figure 7. Congenital hereditary endothelial dystrophy (CHED)
is bilateral in 80% of cases and more than half have
glaucoma.
5 DISTURBANCE IN VISION 1 5.1 Disorders of the Cornea 1111

b. 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.
c. 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. Lipid keratopathy: This is usually seen in vascularized

corneal scars of various etiologies (trauma, infection,
immune-mediated). The invasion of blood vessels
Figure 8. Post cataract extraction corneal edema
into the cornea will lead to leakage and eventual
deposition of glycoproteins, cholesterol and neutral
3. Corneal Deposits
fat into the cornea. The opacities are usually yellow
or cream-colored located at the corneal stromal layer
Aside from acting like a sponge, the cornea is also like a sieve.
typically associated with a branch or several branches
Substances can get trapped within the corneal collagen
of blood vessels at the core (Figure 10)
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. 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 sLruc-ture
a result of a single enzyme defect. Most or these
in patients with high serum calcium and disorders conditions are rare and are autosomal recessive.
in phosphate metabolism. Calcium hydroxyapatite Examples are systemic mucopolysaccharidoses,
particles deposit at the Bowman's layer starting hyper- and hypolipoproteinemias, sphingolipidoses,
at the 3 and 9 o'clock areas. These eventually meet mucolipidoses, and an array of protein and amino
at the center over time to form a white horizontal acid metabolic disorders.
band across the cornea with a Swiss cheese pattern
(Figure 11). 4. Corneal Melt
d. Corneal staining: Hyphema (blood in the anterior Apart from microbial keratitis, corneal melt or necrosis can be
chamber) coupled with high eye pressure will lead brought about by Vitamin A deficiency, chemical burn and
to deposition of heme in the corneal stroma. This autoimmmune diseases (Figure 13). Prompt and appropriate
appears as a central golden brown to yellow discoid therapy may arrest the process and lead to healing and fibrosis,
opacity on the cornea (Figure 12). 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. 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),
Figure 12. Corneal staining secondary to heme deposition corneal ulcers and scars and eventually, diffuse
corneal necrosis (keratomalacia).
e. Metabolic disorders: Systemic metabolic disorders
can cause alterations in corneal clarity due to
b. Alkali chemical burn: Strong alkali raise the pH of
abnormal storage of metabolic substances within tissues and cause saponification of fatty acids in
the epithelium, stroma or endothelium. Abnormal
cell membranes and ultimately cellular disruption.
substances typically accumulate in lysosomes
5 DISTURBANCE IN VISION 1 5.1 Disorders of the Cornea Egi

Alkaline solutions rapidly penetrate the corneal lesion that behaves malignantly. It is a wing-shaped
stroma, destroying the proteoglycan ground or triangular fold of conjunctiva and fibrovascular
substance and collagen fibers. It also destroys the tissue with its apex invading the superficial cornea
limbal stem cells, preventing normal epithelial (Figure 15 C). Strong correlation with UV exposure
healing. Severe scarring and corneal vascularization has been documented. It affects vision in two ways:
are seen in severe cases (Figure 14). (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 Figure 15. Comeal Tumors; (A) Dermoid choristoma, (B) Corneal and
conjunctival neoplasia, (C) Pterygium covering the pupil axis
included here. Pterygium is a benign conjunctival
B. Disturbance in the Refraction of Light components are abnormal, patients will complain
of dry eye symptoms even if there is adequate tear
1. Abnormalities in the Corneal Epithelium and Tear volume. They will also complain of fluctuating vision
Film due to rapid evaporation and break up of the tear
film in between blinking. In some patients, all three
The main refractive surface of the eye is the anterior cornea. components are affected. As in dry eye syndrome, the
An important prerequisite for any refractive surface is that corneal surface epithelium can also be injured. Mucin
it should be smooth. Presence of cracks, smudges and deficiency can be caused by vitamin A deficiency,
the like will cause degradation in the quality of the image. severe dry eye, alkali chemical burn, Stevens-Johnson
The outermost layer of the corneal epithelium per se is not syndrome (Figure 17), and cicatricial pemphigoid.
smooth. When seen under scanning electron microscopy, Lipid deficiency can be caused by blepharitis and
the surface is thrown into dense microvilli. To make the meibomian gland dysfunction.
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.
Causes of abnormalities in corneal epithelium and tear

film:
a. Deficiency in tear volume: Dry eye syndrome is a

Figure 17. Severe dry eye disease with ocular surface damage due to
common disorder with different etiologies wherein Stevens-Johnson syndrome
there is decreased tear production. Most cases are
mild and just cause occasional symptoms. In severe C. Toxic keratitis: This pertains to microtrauma to the
and chronic cases however, it can cause irregularities corneal surface epithelium secondary to contact
on the corneal surface due to microtrauma to with chemicals (such as alcohol-based products like
the epithelium (Figure 16). Patients complains of hair spray) or topical medications (active ingredient,
dryness, foreign body sensation, burning sensation preservatives or both). Presence of these superficial
and blurring of vision. This condition is also known punctate lesions makes the surface irregular and will
as keratoconjunctivitis sicca. thus affect vision.
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
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,
Figure 16. Dry eye disease with ocular surface damage (stained with
Rose Bengal dye)
light rays will converge on different focal planes. This
is known as astigmatism. Myopia, hyperopia and
b. Tear quality abnormalities: The tear film is a complex astigmatism are collectively known as errors of refraction
structure composed of three main components: lipid, and are discussed in another chapter of this SIM. Only
aqueous and mucin. The lipid component prevents corneal diseases and disorders that result in severe errors
rapid tear evaporation and mucin allows molecular of refraction and therefore severe blurring of vision will be
interaction between the tear film and the corneal discussed in this section.
surface (surface tension). If one or both of these
5 DISTURBANCE IN VISION I Disorders of the Cornea 1111
Causes of abnormalities of corneal size, shape or curvature:
III. GUIDE TO DIAGNOSIS
a. Keratoconus: This is a common disorder where the
It was mentioned at the start of this chapter that one needs
central or paracentral cornea undergoes progressive
specialized equipments to arrive at an accurate diagnosis. The
thinning and bulging, so that the cornea takes on the
lack of such equipment should not be a hindrance for a rational
shape of a cone (Figure 18). Hereditary pattern is
differential diagnosis to be formulated as to what corneal
not prominent. Its etiology is unknown and is most
condition is causing the blurring of vision. All one needs are a
likely, multifactorial. Due to the progressive bulging
good history, an appropriate light source, an observant
of the cornea, the cornea becomes abnormally and
eye and a firm foundation of the basic pathophysiology of
irregularly steep resulting in very severe myopia and
corneal diseases as discussed above.
astigmatism. It is almost always bilateral but usually
asymmetrical. The patient complains of rapidly
When blurring of vision due to a corneal pathology
progressive blurring of vision during adolescent
is suspected, the first step is to examine the cornea
years which then stabilizes when the patient attain
with an appropriate light source such as a penlight, an
full growth. The cornea usually appears grossly clear,
ophthalmoscope or a transilluminator. Determine if the
except in severe cases where an apical scar is visible.
cornea is clear/transparent or not. If an opacity is observed,
On profile view, one may see a focal area of bulging
one has to decide if it is due to a corneal scar, edema,
which is best appreciated when examined using the
deposition of substances, corneal melt or tumor growth. If
slit lamp biomicroscope.
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
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
Figure 18. (A) Keratoconus with acute hydrops, (B) Slit lamp view of the differential diagnosis of xerophthalmia with all its ensuing
comeal profile in keratoconus corneal complications. These two conditions usually involve
both eyes.
b. Corneal distortion due to peripheral scars or lesions:
This is to emphasize the fact that you do not need If there is a history of mechanical trauma or of the eye being
to have direct involvement, like a scar, on the center injured by foreign bodies, then consider scars from previous
of the cornea to cause disturbance in vision. This corneal infections like central microbial keratitis or from
concept becomes easy to understand if one imagines corneal lacerations or perforations. Central microbial keratitis
the cornea as a silver mylar balloon. By looking at is also associated with improper use of soft contact lenses.
your reflection at the flat surface of the balloon, Chemical (acid and alkali) burn usually manifests as diffuse
you will notice that the image can be distorted by corneal haze or cloudiness, which may or may not lead to frank
either pulling or pushing the sides of the balloon, melting of the cornea.
because by doing so, you change the curvature of
the center. Always remember that the cornea is one If there is inability of total lid closure, exposure keratopathy
whole integral structure. Flattening of one meridian should be entertained. If you see corneal opacities
causes a corresponding steepening in the meridian accompanied by lid margin irregularity and inward turning
90 degrees away and vice versa. This effect is seen in of lashes, you should think of trichiasis, trachoma, entropion,
pterygium, scars from peripheral corneal perforations, chronic blepharitis and sequelae of Stevens Johnson
effect of sutures after cataract surgery and peripheral Syndrome.
thinning disorders.
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 epithelium may have occurred due to lack of normal tears in
surgery leading to what is known as pseudophakic bullous patients with severe dry eye disease.
keratopathy. If the corneal edema is accompanied by acute rise in
intraocular pressure or chronically high intraocular pressure, then Recent onset of blurring of vision in patients with long-term
the cause is glaucoma. Corneal edema is typically accompanied use of multiple preserved eye drops may have toxic epithelial
by recurrent eye pain, foreign body sensation and tearing due to keratitis. This is especially common in glaucoma patients
bullae formation and sloughing of the corneal epithelium. who are usually on multiple anti-glaucoma medications. This
condition is also seen in patients with a history of inadvertent
Opacities on the cornea that are golden brown to yellow in exposure of the cornea to noxious chemicals or alcohol based
color with a previous history of blunt eye trauma is probably agents.
due to blood staining as a complication of hyphema. Cream
or ivory colored corneal opacities accompanied by blood If a teenager or young adult patient complains of very poor
vessels growing into the cornea are due to lipid keratopathy. vision and has a history of frequent change of glasses due to
This is usually a sequelae of interstitial keratitis due to Herpes rapid and progressive increase in myopia and astigmatism, one
simplex virus, Herpes zoster virus, tuberculosis or syphilis. should consider corneal thinning disorders like keratoconus.
Horizontal dirty-white band-shaped Swiss cheese-like opacity The cornea is clear in early keratoconus and is quite difficult
involving the exposed portion of the cornea is due to calcium to diagnose without sophisticated instruments. However, in
deposition (band keratopathy). This condition is usually seen advanced cases, the paracentral or central conical protrusion
in eyes with a chronic history of inflammation such as uveitis. of the cornea can be seen by examining the profile of the
Symmetrical corneal opacities found in a patient with a family cornea or by eliciting the tenting of the lower lid margin as the
history of the same condition should make one consider the patient looks downwards (Munzon's Sign).
large group of corneal dystrophies. Discrete bread crumb-
like white deposits is typical of granular stromal dystrophy.
Macular stromal dystrophy presents as diffuse central corneal IV. PRINCIPLES OF
haze not accompanied by thickening of the cornea. Lattice MANAGEMENT
stromal dystrophy is difficult to diagnose with just a pen light
but should be suspected if recurrent eye pain is elicited in As a rule, corneal scars are permanent. There is no medical
the history. Bilateral corneal opacities seen in patients with therapy available to turn scar tissue into normal corneal
multiple systemic anomalies are usually related to metabolic tissue. Depending on the location, size and degree of visual
storage diseases like systemic mucopolysaccharidoses, hyper involvement, management is geared towards two goals,
and hypolipoproteinemias, sphingolipidoses, mucolipidoses, either improvement of vision or cosmetic or both. To improve
and an array of protein and amino acid metabolic disorders. vision, management is usually surgical, which may range from
manual excision to laser removal to corneal transplantation.
Tumors or growths on the cornea can easily be seen by the To improve appearance, corneal scars may be covered with
naked eye. If the mass is a triangular fleshy vascular conjunctival cosmetic contact lenses, dyed by tattooing or removed by
mass with the apex growing towards the central area of the corneal transplantation (Figure 19).
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.
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 Figure 19. Clear corneal graft. Post penetrating keratoplasty
fluctuating and fairly constant, desiccation of the surface (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 Disorders that can disrupt the normal transmission of light are
and is also permanent because the cells do not regenerate. corneal scars, corneal edema, corneal deposits, corneal melt
Definitive treatment is corneal transplantation. The role of and corneal tumors. Scars are caused by infection, trauma,
medical therapy is to minimize pain and discomfort and to exposure, vascularization or can be congenital. Corneal edema
prevent secondary infections. If it is due to high eye pressure, can be congenital, due to surgical and non surgical trauma
then the therapy should be directed towards lowering the or due to chronic glaucoma. Deposits in the cornea can be
pressure to appropriate levels. 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
option. light includes dry eye disease, corneal epithelial dysfunction,
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 Management of these disorders involves the restoration of
procedure aimed to restore the integrity of the globe. Corneal the cornea's normal anatomy primarily through corneal tissue
transplantation is usually done. transplantation; excision of abnormal growths or tissues;
control or removal of etiologic and contributing factors;
Corneal masses are usually treated by surgical removal if the surgical interventions to improve corneal shape and curvature
indications for surgery are present. Sometimes corneal grafts and use of optical appliances to enhance the transmission and
are also used to restore corneal clarity. refraction of light into the eye.
Dry eye syndrome is treated by using topical lubricating agents

and/or by preserving existing natural tears by preventing tear
REFERENCES
drainage. With adequate lubrication, the health of the corneal Krachmer JH, Mannis MJ, Holland EJ. (Eds) Cornea . St
epithelium will be restored. Moreover, all other possible risk Louis MO, Mosby ,1997, Vol 1 to 3.
factors that may aggravate tear quality should be removed 2. Smolin G,Thoft RA. (Eds) The Cornea: Scientific Foundations
or minimized. This principle also holds true in treating toxic and Clinical Practice, 3rd Ed, Little, Brown & Company, 1994
keratitis.
There are several treatment options for corneal disorders with SELF-TEST
abnormal shape or curvature in order to improve vision. The
1. Two thirds of the refractive power of the eye is supplied
goal is to correct the refractive errors so that the image will
by the:
be sharply focused on the retina. This is done by employing
A. cornea
optical appliances or by surgically altering the cornea so that
B. lens
the shape will be restored to normal. Depending on the
C. tear film
indications, choices may include glasses and contact lenses,
D. vitreous
incisional or laser refractive procedures, or corneal grafting and
transplantation. A recent treatment option for keratoconus
2. To maintain the transparency of the cornea, the water
is corneal collagen cross-linking wherein topical riboflavin
content should be:
drops are applied on the cornea and exposed to ultraviolet
A. 50%
light which promotes formation of new collagen bonds.
B. 67%
This procedure increases corneal rigidity to stop or delay the
C. 78%
progression of keratoconus.
D. 95%
3. The following affects the normal refraction of light into

SUMMARY
the eye, EXCEPT:
The main function of the cornea is to transmit and refract light. A. color of the iris
If the normal anatomy of the cornea is altered, it will lead to B. index of refraction
C. quality of the corneal surface
blurring of vision.
D. radius of curvature of the cornea
1. The major causes of corneal scarring in the Philippines 9. Steepening of the cornea caused by keratoconus leads
is/are: to what form of refractive error?
A. anterior segment dysgenesis A. hyperopia and astigmatism
B. corneal dystrophy B. monocular diplopia
C. corneal infection and trauma C. myopia and astigmatism
D. surgical complications D. presbyopia
5. Which statement about the corneal endothelium is 10. The following are treatments options on the cornea to
FALSE? improve vision, EXCEPT:
A. The corneal endothelium can be damaged by A. corneal tattoo
intraocular surgery B. corneal transplantation
B. The corneal endothelium is a monolayer of cells C. excimer laser photoablation
lining the posterior surface of the cornea D. hard contact lenses
C. The corneal endothelium is responsible for actively
pumping water out of the corneal stroma 17. You are suspecting that the patient's complaint of
D. The human corneal endothelium retains its mitotic blurring of vision is due to a cornea problem. But
activity throughout life you cannot see any obvious corneal abnormality after
examining with a penlight. What will you do next to
6. What is the main mechanism of corneal scarring in a confirm your suspicion?
patient suffering from measles? A. dilate the pupils
A. deposition of blood in the cornea B. have refraction done
B. direct invasion of the cornea by measles virus C. measure the diameter of the cornea
C. exposure of the cornea due to poor lid closure with D. request for test to measure corneal curvature
secondary bacterial infection
D. misdirection of eye lashes towards the cornea 12. The patient and other family members have bilateral,
symmetrical corneal opacities. Your main differential
7. White horizontal band-like opacity across the cornea diagnosis is
with Swiss-cheese pattern is due to deposition of what A. bullous keratopathy
substance ? B. corneal dystrophy
A. amyloid C. dermoid choristoma
B. calcium D. lipid keratopathy
C. iron
D. lipid Answer to Self Test on page 220.
8. Peripheral corneal lesions can cause blurring of vision
by:
A. blocking the transmission of light
B. decreasing tear production
C. increasing central corneal thickness
D. 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:
Upon history taking, you found out that the patient has
'our friendly neighbor tells you that his 78 year-old
been having gradual and progressive cloudiness of distance
grandfather who lives with him has been complaining of
vision in both eyes (right eye worse than the left) over the
)ad vision lately. Knowing that you are a senior medical past several years. He notes that recently, he seems to be
student, he wants you to drop by his house, take a look at his able to read small prints better. He does not report any
grandfather and give them sound medical advice on what eye pain, discharge, itchiness, redness, or tearing. He has
ò do next. Are you up to the task? 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
WHAT IS A CATARACT? diabetes for the past 6 months, both of which are fairly
(DEFINITION AND ETIOLOGY) controlled. Are his symptoms consistent with cataract
formation?
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
TYPES AND SYMPTOMATOLOGY
but undergoes changes that result in gradual loss of its
Cataracts usually cause a gradual decrease in visual acuity that
transparency over time. On average, a younger person's
worsens with aging. This process of senile cataract progression
lens should be clearer than an older person's. In reality, this
and worsening of vision may take years (or decades) and
"degeneration" varies from individual to individual, with some
can vary from individual to individual. Knowledge of basic
having relatively clear lenses well into their 60's, while others
lens anatomy enhances our understanding of cataract types,
already requiring cataract surgery in their early 40's.
symptomatology, and surgery (Figure 2).
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 ANTERIOR CAPSULE
cataracts that are seen in the pediatric population. The

pathophysiology of cataract formation is not fully understood z
0
but is likely to be multi-factorial in nature. Biochemical n n
U
changes in the lens are characterized by protein aggregates
that alter its optical properties. These changes take the 0
S S
form of discoloration (from yellow to brown in increasing NM.
maturity), the appearance of vacuoles (lens hydration clefts),

POSTERIOR CAPSULE
and aberrant migration and enlargement of epithelial cells.
Other contributing factors include malnutrition, damage from Figure 2. Review of basic lens architecture.
ultraviolet light rays, and other causes of oxidative damage
resulting in free radical formation?
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
Figure 1. Cataract - an opacity of the lens. 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)
Z
Is
NO1 A, I No), Nrs htbs NCA

111
11°1
NOS NC5 N06 NC6
(Pi
C.) Cs
lb 41 P3
Leo T. Chylack. Is.. M_D.

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itirviad Medical School

Boom. MA
3666 K. Wolfe, PA. U. M. CrINIra Leese, M.P.K. Mut A. 11.66.63re., f1 D The I Or% %gamey Crop
suNY it Stony Note. NY L Daley. RD Prone. MA
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Cent! for C116661Calrica tjte. Ilea, of Col dere. Sine, Rem*. SW
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• Maley. CA
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 red-
radiation.' 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.
The Swinging Flashlight Test is a simple and very useful

bedside examination when evaluating cataracts. If the
Figure 4. Posterior subcapsular cataract seen thru slit lamp biomicroscope
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 Figure 5. Leukocoria
cataractous eye.
Funduscopy with the direct ophthalmoscope may be difficult Additional ancillary tests that may be performed by the
in the presence of significant cataract as the media is hazy. ophthalmologist for surgical planning include refraction
With mature cataracts, the patient's pupil might appear and biometry (a procedure that extrapolates the refractive
whitish/opaque, called leukocoria (Figure 5). With less outcome with various IOL powers), corneal topography (to
mature cataracts, this might not be obvious. Grossly, using address astigmatism), and specular microscopy (to assess the
the hyperopic correction of your direct ophthalmoscope health of the corneal endothelium) among others.
(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 SURGERY
round and homogenous red-orange-reflex may be seen with
this maneuver. Despite all the technological advances and innovations in
ophthalmic science, there is still no proven medical treatment
Cataracts are best viewed via a slit lamp biomicroscope. to reverse the progression of cataracts. It would be safe to say
This instrument allows for visualization of the layers of the that anyone who lives long enough will eventually develop
lens and the extent of cataract involvement. In addition, the significant cataracts and require surgery. Surgical removal of the
ophthalmologist uses the slit lamp to look for associated opacified lens to clear the visual axis is the only treatment option
findings that may make the surgery difficult. For example, the for cataracts. Visual rehabilitation after cataract removal is varied
presence of phacodonesis (lens movement), Irldodonesis (iris and depends on the type of procedure performed. The evolution
movement) on slit lamp exam, as well as pseudoexfoliation of cataract removal and visual rehabilitation highlight one of the
(from pseudoexfoliative glaucoma) on the lens capsule may great success stories in medical innovation.
indicate weak zonules and can lead to complications during
surgery. Other factors that may affect the course of surgery z CAPSULOTOMY z
include the presence of uveitis, posterior synechiae, non- 0 0
n n
dilating pupils, shallow anterior chamber, corneal opacity and
1 IOL Optic
low endothelial cell count. e e
S
Dilated fundus examination should be performed in an
attempt to view the fundus pre-operatively. Checking for
IOL Haptic CAPSULAR BAG IOL Haptic
posterior pole pathology (glaucomatous optic neuropathy,
optic atrophy, retinopathy, age-related macular degeneration,
etc.) is very important for prognosticating visual outcome in Figure 6. Post-op appearance in Extracapsular Cataract Extraction (Manual)
cataract surgery. When there is virtually no view of the fundus Phacoemulsification/Small Incision) with IOL secure in the capsular bag.
because of the density of the cataract, an ocular ultrasound is
Cataract surgery had evolved from intracapsular cataract
sometimes performed as part of the pre-operative evaluation.
extraction (ICCE), which leaves a patient aphakic, to extracapsular
A detailed medical history is important in assessing other cataract extraction (ECCE) with intraocular lens (IOL) implantation
(Figure 6). Procedures for ECCE have evolved from manual
factors that may affect surgical outcome. These include the
nucleus expression and irrigation/aspiration of the cortical
patient's cardio-pulmonary status (surgical risk), the presence material with rigid IOL implantation to phacoemulsification with
of diabetes (non-dilating pupil makes the surgery more implantation of foldable 10Ls. Table 1 lists the characteristic
difficult), and even drug history as certain medications may features of the various types of procedures performed for surgical
predispose patients to intra-operative complications. removal of cataracts.
5 DISTURBANCE IN VISION 15.2 Cataract 63

The trend in cataract surgery has gone towards smaller incisions, You were able to convince the patient that his cataracts
usually 2-4mm (to minimize the surgically-induced astigmatism of probably need surgery. Before he sees an ophthalmologist,
larger incisions) and foldable 10Ls (to maintain the small incision he asks for your advice on the risks of cataract surgery. What
during lens implantation). Phacoemulsification, a form of ECCE, will you tell him?
utilizes an ultrasonic probe to break up the cataract into smaller
pieces, which can then be removed by aspiration. Manual Small COMPLICATIONS OF CATARACT SURGERY
Incision Cataract Surgery (MSICS) is another surgical option
that boasts of the advantages of small incision cataract surgery In a well-equipped ophthalmic surgical operating room and
without the need for a phacoemulsification machine. A shelved, under an experienced surgeon's hand, present day cataract
self-sealing incision, usually 5-7mm, is dissected from the sclera surgery should be 99.99% successful. As with any other
and into the anterior chamber. The nucleus is prolapsed out of surgical procedure, however, complications can and do occur.
the bag and out of the eye with the advantages of a suture-less, Complications may range from minor to severe, potentially sight-
closed system like phacoemulsification. threatening ones. Intra-operative complications include posterior
capsule rupture, vitreous loss, retention of lens fragments in the
Cataract extraction surgery has evolved into a 10 to 30-minute, vitreous and thermal or mechanical trauma from the phaco
surgical procedure that is often performed on an out-patient probe. Post-operative complications include inflammation
basis and under topical anesthesia. As a result of these, recovery and/or increased intraocular pressure. unplanned refractive
period has shortened and the faster visual rehabilitation allows outcomes, i.e., biometry was off-target or the wrong IOL power
patients to return to their regular activities even a day after their was inserted , cystoid macular edema and pseudophakic bullous
surgery. Furthermore, advances in intraocular lens technology keratopathy. A severe and the vision-threatening complication
have widened a patient's choice. When formerly only regular of this procedure is intraocular infection or endophthal mitis. The
monofocal lenses (which correct for only one focus - either distance key to prevention of permanent loss of vision that can result
or near vision depending on the patient's choice) were available, from this complication is its early recognition and treatment.
there are now toric 10Ls that can correct a patient's pre-existing Hence, close and regular follow-up of patients following cataract
corneal astigmatism (which cannot be corrected by a monofocal extraction surgery should always be performed in order to
lens), as well as multi-focall0Ls that allow vision for both distance immediately address any post-operative complication that may
and near without the aid of spectacles. arise.
Table 1. Types of cataract surgeries
Extracapsular Cataract Extraction (ECCE)

n racapsular Manual Phacoemulsification Manual Small
Cataract Extraction Incision
(ICCE)
Anesthesia* retrobulbar retrobulbar
peribulbar peribulbar retrobulbar retrobulbar
peribulbar peribulbar
Incision 180.. limbal 160°, limbal 2-4 mm. corneal 5-7 mm. scleral
Part of lens that Entire lens Anterior capsule. nucleus Anterior capsule nucleus Anterior capsule.
is removed and cortex (nucleus and cortex (nucleus nucleus and cortex
delivered without fragmented using (nucleus fragmented
fragmentation) phacoemulsification manually)
machine)
IOL used No IOL Rigid Intraocular lens (IOL) Foldable IOL Foldable
(Visual rehabilitation thru Rigid IOL
aphakic spectacles or
contact lenses)
*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.
2. Type of cataract that gives the worst visual symptoms
SUMMARY
outdoors (in bright sunlight)
Definition and Etiology A. Nuclear
Types of Cataracts B. Cortical
Nuclear C. Posterior subcapsular
Cortical D. All of the above
Posterior Subcapular
3. The following symptoms are typical for isolated
Symptomatology cataract EXCEPT:
Evaluation A. decreased visual acuity and color perception

Funduscopy B. glare
Slit lamp Examination C. haloes
Medical and Drug history D. ocular pain
Ancillary Procedures E. monocular diplopia
• Refraction
• Biometry 4. Bedside examination most useful for evaluating and
• Corneal Topography prognosticating cataracts
•Specular Microscopy A. Direct ophthalmoscopy
B. Slit lamp examination
Cataract Surgery C. Ocular ultrasound
Types off Cataract Surgeries D. Swinging flashlight test
• Intracapsular Cataract Extraction (ICCE)
• Extracapsular Cataract Extraction (ECCE) 5. The following slit lamp findings may warn the surgeon
• Phacoemulsification with IOL implementation of potential difficulties during surgery EXCEPT:
A. Posterior synechiae
Complications B. Corneal Opacity
• Intra-operative complications:
C. Phacodonesis
• Post-operative Complications
D. Pseudoexfoliative material on the lens
E. Well-dilated pupil
REFERENCES
6. In the setting of a very dense/mature cataract with
1. Cubillan LDP, Olivar-Santos EO. Third national survey on media opacity and poor vision, the following exams
blindness. Philipp J Opthalmol. 2005:30(3);100-114. may be useful for prognosticating visual outcome
2. Riordan-Eva P, Whitcher JP. eds.Vaughan's and Asbury's EXCEPT:
General Ophthalmology. 16th ed. New York: McGraw Hill A. Color discrimination
Com pan ies;2004. B. Fluorescein angiography
3. Kahn HA, Leibowitz HM, Ganley JP, et al., The Framingham
C. Ocular ultrasonography
eye study. II. Association of ophthalmic pathology with D. Swinging flashlight test
single variables previously measured in the Framingham
heart studyAm J of Epidemio. 1977:106 (1);33-41.
7. Which type of cataract surgery will routinely require
4. Stanga PE, Boyd SR, Hamilton AMP.Ocular manifestations
aphakic lenses for visual correction post-operatively?
of diabetes mellitus.CurrOpin Ophthalmology.1999:10(6);
A. ECCE
483-489.
B. ICCE
5. Chylack LT Jr., Wolfe JK, Singer DM, et al.The Lens opacities
C. phacoemulsification
classification system III. The longitudinal study of cataract
D. A and B
study groupArch Ophthalmol. 1993;111(6):831-836.
6. Awwad S. Cataract surgery. http://www.eyeweb.org/ Which type of IOL is best suited for patients who do not
8.
cataract_surgery.htm. Accessed April 28, 2011.
wish to wear spectacles for both distance and near after
cataract surgery?
SELF-TEST A. Monofocal IOL
B. Multifocal IOL
1. The following factors are associated with cataract
C. Phakic IOL
formation:
D. Toric IOL
A. diabetes
B. trauma
C. damage from UV rays
D. toxins
E. All of the above
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.
Photographs representative of various vitreo-retinal and choroidal pro:_ ems wil, vsented, with typ c cases discussed at
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. Ophthalmologic examination
3. Ancillary examinations
4. 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, RETINA, CHOROID vitreous during syneresis
A. THE VITREOUS
Subhyaloid space: between

The globe is filled with a gel called the vitreous. This gel is 99% posterior hyaloid and retina
water and only 1% solid. The solid portion consists of collagen
fibrils that make up the meshwork, hyaluronic acid molecules, Figure 1. Diagram of vitreous in relation to lens, retina and optic disc.
and the very few cells called hyalocites. The vitreous has a Adopted from Yanoff P.'
peripheral or outer layer called the cortex, and a central part,
the gel. The outermost limit of the cortex is the hyaloid face, and posterior vitreous detachment (PVD) may also occur
both anterior and posterior. The anterior hyaloid is just behind after vitreous hemorrhage, inflammation, trauma, and after
intraocular surgery. When liquefaction and PVD have set in,
the lens.The posterior hyaloid is adjacent to the retina's internal
patients usually start seeing "floaters" and occasionally "flashes"
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 B. THE RETINA
vitreous is firmly attached to the optic nerve, the macula, along
blood vessels and also at the so called vitreous base (where 1. The 3 Neuron Relay System: The human retina is a tall
the retina ends peripherally and anteriorly). Many disorders in structure that has ten layers. In the ten layers are three main
vision originate from problems with the vitreoretinal interface. cell types that relay photochemical information through the
For example, vitreous liquefaction and anterior displacement retina , from outside inwards, and to the optic nerve, and finally
(towards the lens) can cause undue traction on the vitreous into the occipital cortex. These are, from scleral (outer side),
base and may cause the formation of a retinal tear or dialysis, towards the vitreous (inner side) : photoreceptor cells, the
possibly leading to retinal detachment. Another example is bipolar cells and the ganglion cells. The axons from these cells
undue traction of the vitreous gel and posterior hyaloid of the form the nerve fiber layer, and course towards the optic disc,
vitreous, on the macula, causing the formation of a macular and into the optic nerve (Figure 2, 3). There are supporting
hole, or the formation of an epiretinal membrane. cells that keep the tall ten layered retina "together These
are the Muller cells which are structural cells, and horizontal
Vitreous syneresis is degeneration of the vitreous gel and amacrine cells which allow multiple photoreceptors to
(liquefaction of the gel) with eventual detachment of the "plug into" a smaller number of bipolar and ganglion cells.
vitreous from the retina. This event is a normal physiologic Any breakdown in the neurons, the supporting cells and the
occurrence starting at age 45-50 years and is present in around relay system itself can manifest as visual disorders. The ten-
70% of 70-year old individuals . Liquefaction of the vitreous layer system is supplied by two different vascular systems. The
RPE •""10"
Rods & Cones

1\10•
Horizontal Cells
Bipolar Cells
Arnacrine Cells
1 1
1,
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
t ' NERVE FIBER LAYER
" " ' ••••• bes'''tl‘t ta ": GANGLION CELL LAYER
• INNER PLEXIFORM LAYER

•
o•
••.• • 4— INNER NUCLEAR LAYER
. cl
• OUTER PLEXIFORM LAYER
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, to which it is adjacent. An additional
of the choroid. The inner layers, from the inner nuclear layer feature is the presence of a physiologic "pump" that
inwards, are supplied by the retinal vasculature. Certain retinal keeps fluid contained outside the retina.
diseases can be traced to problems of perfusion. Knowledge
of the blood supply of the inner and outer retina will help the C.THE CHOROID
clinician predict the severity and depth of retinal involvement.
The choroid is the middle coat of the wall of the globe. It is a
2. The Retinal Pigment Epithelium: The retinal pigment vascular layer that comes from the long and short posterior
epithelium (RPE) is the first of the ten layers, and is the ciliary arteries, mostly from the short, that in turn emanate
outermost layer, adjacent to the choriocapillaris of the choroid, from the ophthalmic artery. The choroid is arranged in
separated only by Bruch's membrane. It takes care of most lobules , giving rise to some peculiarities in choroidal disease
metabolic processes of the outer retinal layers, keeps the retina presentations. More importantly is its role in 'maintaining" the
"dry" with its "outer blood-retina barrier", participates in the health of the outer retina and providing the vascular supply
recycling of retinol and disposes of metabolic wastes of the especially to the macular area. The dense barrier between the
other cells. A breakdown of the"outer blood-retina barrier"can RPE of the retina and the choriocapillaris (the layer of choroid
lead to accumulation of fluid in the subretinal space and the made of finer vessels and closest to the retina) is called Bruch's
sub RPE space. This can lead to retinal edema. A physiologic membrane. It is impermeable to fluids, and diseases involving
"pump" also exists in the human RPE layer and this pumps Bruch's membrane can lead to subretinal accumulation of fluid
fluid away from the retina and back into the choriocapillaris, and blood.
keeping the retina" dry".
3. The Blood -Retina Barriers: There are two so called blood- II. DIAGNOSIS OF A RETINAL,
retina barriers that keep the retina "dry": VITREOUS AND CHOROIDAL
a. The Inner Blood-Retina Barrier: This is attributed DISORDER
to the tight endothelial cell junctions of the retinal
capillaries. Any disturbance in the integrity of these There are four elements needed for making a working
tight attachments leads to oozing of fluid and/or diagnosis that involves the retina, vitreous and/or choroid.
blood, as well as lipids and proteins from the retinal
vascular tree. This manifests as retinal edema, hard 1. History: Good history taking is a must, especially
exudates, and/or hemorrhages. in patients where loss of vision or changes in vision
are the chief complaints. Many vitreo-retinal and
b. The Outer Blood-Retina Barrier: This is found in the choroidal diseases have peculiar affectations of vision
RPE.The tight intercellular attachments between RPE which immediately suggest the type of problem.
cells, called "zonula occludens" keep the RPE layer
leak proof from the highly vascular choriocapillaris
1111MI ,nritr,r,nni tonrcrinil I F, Ili. ,F1

2. Ophthalmologic Examination: A basic eye Floaters (muscae volitantes) are black to gray spots and/or
examination should be done for all patients:
fibers that move about in the field of vision of the patient.
They seem to float freely and may vary In number. They are
1. Visual Acuity
commonly observed after the age of 45 to 50 when vitreous
2. Gross Eye Examination
liquefaction and vitreous collapse and/or detachment have
3. Pupils
begun as part of the ageing process. The onset of this process
4. Intraocular Pressure Determination occurs earlier in individuals who are myopic. Floaters may also
5. Extraocular Muscle Movements be caused by particles suspended in the pre-corneal tear film.
6. Funduscopy
Flashes (photopsias) caused by retinal problems are described
3. Ancillary Examinations: Special ophthalmologic as arcuate lightning like streaks of bright light in the periphery,
and laboratory examinations are done to help the noted with or without eye and/or head movements. Patients
ophthalmologist confirm his working impression describe them as" gumuguhit sa gilid "parang kidlat sa gilid".
and establish an etiologic diagnosis for patients Photopsias, however, may be of optic nerve origin. Care must
suspected to have disorders of the retina, vitreous be taken not to confuse these lightning like flashes with the
and choroid. visual aura of migraine headaches.
4. Systemic Examination: A thorough physical Sometimes patients do not know that they have color vision
examination of all systems is done in cases where problems, and only discover it at work (seamen's pre- boarding
the eye problem is suspected to be part of a systemic tests, fabric factory mishaps in color choices), or unusual
condition or distant trauma (away from the eye). personal choices in colors of their clothes and similar activities
When a systemic disease is suspected, a referral to an requiring precise color recognition.
internist is recommended.
2. Did the visual disturbance come gradually or
HISTORY TAKING IN CASES SUSPECTED suddenly?
OF POSTERIOR SEGMENT DISORDERS 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
The importance of history taking cannot be over emphasized.
progressive and where the blurring started, from the center or
The information gathered, either volunteered by the patient or
from the periphery. One must take pains to extract this from
extracted by the clinician helps in the formulation of a working
the patient who may not volunteer the information, thinking
diagnosis, that guides the clinician to request for ancillary that it is not important or relevant.
examinations, to help confirm it. The information also gives
the clinician an idea as to possible etiology, present state of
3. What other eye problems accompanied the visual
severity, treatment response and prognosis.
disturbance?
Pain is rarely present in retinal, vitreous and choroidal disorders.
The following are important questions to ask patients
The pain in diabetic retinopathy with neovascular glaucoma,
suspected of having a vitreo-retinal, or choroidal problem:
for example, is due to the severely elevated intraocular
pressure. Ocular discomfort and/ or redness may accompany
1. What is your patient's chief complaint?
intraocular inflammatory conditions with retinal involvement.
These patients usually complain of some type of visual
disturbance.
4. How long has this been going on?
This may come in the form of:
The duration of the problem is a significant information. It
• persistent blurry vision
is also important to know how long the problem has been
• transient blurry vision
present, if this is the first episode, or if it is recurrent. If the
• change in shape or distortion (metamorphopsia)
problem is recurrent, be sure to ask about the timing and
• change in image size (usually smaller : micropsia; if
sequence of events, duration, interval, and treatment as well
bigger-macropsia)
as treatment responses.
• color vision problems : difficulty in identifying colors
(dyschromatopsia), 5. Which eye is involved?
change in shade, contrast, brightness Laterality is as important as knowing if the same or similar
visual field loss : (scotoma) central, peripheral, other problems have occurred in the fellow eye, Do not forget to
patterns ask when the problem started. If bilateral, ask which eye was
difficulty in the dark (nyctalopia or night blindness) affected first, followed by questions regarding the sequence of
difficulty in bright light (hemeralopia) signs and/or symptoms.
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? be deliberately withholding information. The clinician must
What medications have been used? What medications be observant of patient responses, reactions, attitude and
are being used? Did the patient have any eye operation demeanor. For example, history taking of AIDS patients and
or interventions like laser treatment, injections into the drug addicts is particularly challenging.
eye, for this or other problems?
These information has bearing on the present state of the eye, OPHTHALMOLOGIC EXAMINATION
if you are seeing a patient who was or is under treatment by
OF THE PATIENT
someone eke.
The basic tools needed for an examination of a patient
7. Other aspects of the patient's history that should be
suspected of posterior segment disease are:
considered include:
1. Visual acuity charts : both for distance and near vision
Family History : Is there a history of similar eye problems
2. Penlight : for nross examination of the eye , adnexae and
in the family? Is there a history of any hereditary illness? It is pupils
also very important to ask about hypertension and diabetes
3. Tonometer: .,ed to determine intraocular pressure. For
mellitus. medical students, the technique of finger palpation is
performed to estimate intraocular pressures.
Social History: Does the patient smoke? Does he drink and 4. Ophthalmoscope: used to examine the fundus ( retina
how much alcohol does he consume? Does he have pets and and optic disc)
what kinds of pets (particularly interested in dogs and cats)? 5. Slit lamp: a biomicroscope that allows for a highly
Does he eat raw food? Does he engage in contact sports or magnified view of the eye and assessment of the ocular
other unusual sports like deep sea diving, sky diving, bungee media, optic nerve and retina with the help of special
jumping, competitive weight lifting, boxing, contact sports, lenses.
etc, and has he been injured in the head and/or eyes? Does
6. Amster grid: a black and white card with a fine grid and
he take prohibited drugs or has he ever taken any? What is a fixation point, used to detect and quantify central visual
his occupation? Is there exposure to chemicals or toxic fumes? changes.
Does he travel often and has he been to places like Africa, the
Middle East, China? Gross Eye Examination: In the absence of any systemic
illness or trauma, the ocular adnexae are usually not affected in
Medical History: Does he have cardiac disease, hypertension, retinal disease. Except in some retinal disorders of inflammatory
diabetes mellitus, asthma, hematologic disease, cancer ,
origin, there will be no ciliary flush or redness.The pupils must
pulmonary tuberculosis and other diseases? Has he ever had
be examined for direct and consensual light reactions. Severe
accidents that required surgery and/or hospitalization? Has he
retinal damage as well as some optic nerve diseases can cause
been operated on and for what? Does he have symptoms like
abnormal pupillary responses . A'white pupil" in a small child
angina, pedal edema, joint pains, oral ulcers, intractable fever,
is always an alarming and significant finding. The absence of,
to name a few. Has he ever had a blood transfusion and when?
or a faint 'red orange reflex' or 'ROW may indicate vitreous
Has he ever had cobalt therapy? Is he on any medications for
opacities like hemorrhage or inflammatory material. One must
other illnesses? What are these medications? How long has
remember however, that an absent ROR can also be caused by
he been taking these? A perfect example of knowing about
a dense cataract or a dense corneal opacity or dense material
systemic medications is that of ethambutol toxicity and its
in the anterior chamber.
effect on the optic nerve. Sudden usually bilateral painless
significant visual loss ( for example, sudden deterioration
Visual Acuity: Vision is usually affected in some way in most
in visual acuity from 20/20 to 20/400) in a patient who has
vitreo-retina and choroidal posterior segment disorders.Typica l
been on ethambutol for pulmonary tuberculosis for several
affectations in vision are seen in specific diseases. For example
months, should raise suspicion about a possible ethambutol
retinal edema at the macula can cause decreased vision and
optic neuropathy. In ethambutol toxicity, all other ocular
metamorphopsia. In retinal detachments, many patients
findings including posterior segment findings, are normal.
report seeing floaters and light flashes before the onset of
"wavy vision", actual blurring, visual field "cuts". Macular disease
Sexual History: The presence of a history of any sexually
causes blurry central vision while extramacular retinal diseases
transmitted disease should likewise be elicited from the
will cause peripheral visual loss. Vitreous opacities also cause
patient. What is his sexuality?
blurry vision and/ or floaters. Many retinal disorders come
with vitreous abnormalities. A few affect all three structures:
During history taking keep your mind open to the possibility retina, vitreous and choroid.
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

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 Figure 5. Indirect ophthalmoscopy. Examiner views fundus using an
Diseases. Long standing retinal disease with retinal scarring indirect ophthalmoscope on his head while holding an aspheric lens.
rnd poor vision may result in outward deviation of that poorly Patient is examined lying down.
ieeing eye. Inward or outward deviation of the eye can be a
presenting sign of retinoblastoma, a tumor most commonly
3een in infancy.
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
Slit Lamp Biomicroscopy with Special Lenses: A third method non-contact fundus lens.
of fundus examination is with the slit lamp and a fundus lens Amster Grid Examination: This is a simple examination
(Figure 6).This examination allows the examiner to see details performed in a clinic on patients complaining of central
of the vitreous, retina and optic disc in high magnification. visual problems. The patient can also perform this at home
Findings of slit lamp examination depend on the disorder and to monitor changes in central vision. He observes changes in
will be discussed in a separate section. Problems in the vitreous the grid presented to him on a black and white chart (black
and the anatomic-pathologic vitreoretinal relationships can be card with white grid or vice versa) , relative to a central fixation
determined with this examination. 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

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Figure 7. Amsler grid :on lower part, note 3 examples of problems with
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 Figure 8. Fundus fluorescein angiography. (A) Sodium fluorescein
is carried with the circulation and outlines the retinal and dye is injected into the antecubital vein and pictures of the retina are
taken and recorded with a fundus camera, (B) Color picture showing
choroidal vascular system. This is then picked up by a special
hard exudates (clusters of punctuate yellowish dots, examples indicated
fundus camera. Retinal and choroidal diseases have typical by black arrows), microaneurysms (small punctuate reddish dots, red
fluorescence qualities and patterns, thereby allowing the arrows), small retinal hemorrhage (white arrow) in diabetic retinopathy,
observer to confirm certain clinical observations. The optic (C) Fundus angiography of B showing microaneurysms (small punctuate
white dots, red arrows), small retinal hemorrhage, in the angiogram seen
nerve head also has typical angiographic fluorescence . Any as a small dark area that corresponds with the hemorrhage in the color
changes seen on FA may thus, be pathologic and can then be picture (white arrow)
correlated with clinical findings (Figure 8).
Idocyanine Green Angiography (ICGA):
This is similar (blood sugar, cholesterol, triglycerides, BUN, creatinine, etc.)
) FA but uses indocyanine green dye instead of sodium
and x-rays form an important part of "systemic examination"
Jorescein.The choroidal circulation is better highlighted with
and must be done when a patient is suspected of having a
:GA. It is helpful in studying problems of the choroid not seen
certain disease. Patients can present with pedal edema, skin
FA.
discoloration of the lower extremities, non healing ulcers and
wounds in the lower extremities in diabetes mellitus.
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).
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),
Figure 9. Ocular B scan ultrasound showing retinal detachment
branch retinal vein occlusion (BRVO), branch retinal artery
(yellow arrow), optic nerve shadow (white arrow).
occlusion (BRAO), retinopathy of prematurity (ROP), Von
Hippel Lindau disease
)ptical Coherence Tomography (OCT): Optical Coherence
Maculopathies: age related macular degeneration
tomography is a "scan" of the retina, made possible by light
(ARMD), central serous chorioretinopathy (CSCR), macular
Naves , creating images of the ten layers of the retina at the hole, cystoid macular edema ((ME.), macular pucker
nacular area, Bruch's membrane , the choriocapillaris and Heredodegenerative diseases of the retina: retinitis
•
arger choroidal channels, and defects in these layers. It can
pigmentosa (RP), color blindness, Stargardts disease,
ilso be used to image the optic disc and cup (Figure 10). juvenile foveal retinoschisis, Best's vitelliform macular
degeneration
Electroretinography (ERG) and Electro-oculography Tumors: metastatic tumors, melanomas,
;EOG): These examinations assess retinal function, by retinoblastoma, intraocular lymphomas, choroldal
measuring electrical activity of the retinal layers. In essence, capillary hemangiomas
:hese are similar to an electrocardiogram( ECG). Retinal Detachments, retinoschisis
Vitreous opacities and degeneration : vitreous
scintillans,
SYSTEMIC EXAMINATION hemorrhage, asteroides hyalosis, sync hisis
vitritis, amyloidosis
Viany retinal diseases are part of systemic problems like diabetes • Retinochoroiditis : toxoplasmosis, toxocariasis,
mellitus, hypertension, systemic lupus erythematosus and serpiginous choroiditis
Dther collagen diseases, pulmonary tuberculosis, malignant Uveal Effusion : Vogt-Koyanogi-Harada syndrome
disease or hematologic disorders . Some of these like diabetic Infectious Retinopathies : HIV retinopathy
-etinopathy, hypertensive retinopathy, collagen disease, may
present with typical funduscopic findings. Blood chemistry
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 it
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 A
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.
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 Figure 11. Retinal findings in diabetic retinopathy. (A) NPDR with
hard exudates (black arrows), microaneurysms (red arrows), dot and blot
PDR characteristics are present. Macular focal and grid laser hemorrhages (yellow arrows), soft exudates (white arrow), (B) PDR High
treatment can be done at any stage if maculopathy causes Risk with Pre-retinal hemorrhages (white arrow), NVDs (black arrow),
significant visual loss. Intraocular injections with anti-vascular NVEs (yellow arrow), (C) PDR with retinal hemorrhages and extensive
fibrovascular membranes (white arrows) with vitreoretinal traction.
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 Diabetic retinopathy causes varying degrees of visual loss
clearing vitreous hemorrhage, premacular hemorrhage, depending on the fundus and vitreous changes. It is, however,
vitreoretinal traction, traction and bullous retinal detachment. possible to have a patient with fairly good vision despite the
resence of PDR if the macula is minimally affected. Diagnosis Treatment of ischpmir CRVO is retinal
made with a thorough history and good clinical assessment (scalier laser treatment similar Lo FliF' of diabetic retinopathy)
f the fundus. To confirm the working impression and identify when certain criteria are met, as recommended by the Central
Ither possible retinal changes, a fluorescein angiogram (FA) Vein Occlusion Study. Usually the non-ischemic type needs
nd optical coherence tomography (OCT) are performed. An no definitive ocular treatment but the primary cause must be
icular B scan ultrasound may be requested if there are media identified and addressed.
goblems such as vitreous hemorrhage and/ or a cataract
)recluding adequate visualization of the fundus. CENTRAL RETINAL ARTERY OCCLUSION
:ENTRAL RETINAL VEIN OCCLUSION Central retinal artery occlusion or CRAO , is one of only
two "true" emergencies in ophthalmology. It does not
ventral retinal vein occlusion or CRVO manifests in two types: occur as frequently as CRVO.
schemic and non ischemic (also called stasis retinopathy) .
rhe ischemic type is more severe. The fundus is covered with It manifests as sudden painless loss of vision.Visual loss is severe,
multiple splinter and blot hemorrhages . One typically finds and residual vision just after the episode is usually in the area
;oft exudates (cottonwool spots) indicating retinal ischemia. of light perception to count fingers . The retina is very pale so
Retinal veins are tortuous and dilated. The optic nerve may that the usually darker macula becomes more prominent and
lave blurry borders covered with splinter retinal hemorrhages is described as a "cherry red spot". "Box tarring" of blood flow in
-adiating from the disc and which appear to be following the the arterioles is oftentimes observed. Occasionally a glistening
disposition of the nerve fiber layer. Vision is very poor in this thrombus called a Hollenhorst plaque is seen blocking an
situation due to macular edema, and/or macular ischemia. arteriole (Figure 13).
Retinal hemorrhages covering the fovea also cause poor
vision (Figure 12). With examination of the pupils one may
find afferent pupillary defects (APD).
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
In contrast,the non-ischemic type of CRVO, shows fewer retinal the actual CRAO. This "wipeout" is very brief and lasts for a
hemorrhages and usually no soft exudates. The disc borders few seconds. At this time the patient's vision appears white
are not markedly obscured by splinter hemorrhages. However, or gray with all details gone temporarily. When vision returns,
there is definite retinal venous tortuosity and dilation. Vision everything is normal. Even the retina appears normal except
and prognosis are much better than in the ischemic type. perhaps for vascular changes indicative of hypertension and
arteriosclerosis.
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 A

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).
Figure 14. Age related macular degeneration (A) Non-neovascular
type, showing round patch of atrophy of the retinal pigment epithelium at
Age is a definite risk factor in ARMD. Other risk factors the macula (black arrowheads), (B) Neovascular type, showing subretinal
implicated, but with no established causal relationship are: hemorrhage and choroidal neovascular membrane (black arrows) at the
smoking, cardiovascular disease, ethnicity, undue exposure to macula and perirnacula
UV light, lack of vitamin C and other factors related to oxidative
stress. Recent studies show that there is association of smoking types must be advised regarding managing the modifiable
to ARMD. risk factors such as smoking, diet, excessive UV light exposure,
dyslipidemia and hypertension.
The non-neovascular type causes gradual painless
deterioration of central vision while the neovascular type RETINITIS PIGMENTOSA
causes sudden onset of central visual problems such as blurry
vision, metamorphopsia and scotomas (blind spots). Retinitis pigmentosa (RP) is a retinal disorder belonging to
the family of heredo-degenerative diseases and" ta petoreti na I
A good clinical examination of the fundus, an FA and an diseases. It is characterized by progressive degeneration of the
OCT are necessary for the confirmation of the type of ARMD, rods and cones, and in most cases is associated with migration
and for monitoring response to treatment especially in the of pigment epithelial cells into the retina. There are several
neovascular type. Occasionally, an ICGA is needed. patterns of inheritance: autosomal recessive, X-linked recessive
and autosomal dominant .The first two have the earliest onset
Management of the neovascular type is thermal laser and worst prognosis. Patients with the autosomal dominant
treatment to the abnormal vascular complex, if extrafoveal form may be symptom free until middle age. Genetic analysis
(outside the foveal center). The subfoveal (under the foveal has shown that the defect in most affected individuals is in the
center) types are treated using intravitreal injections of anti- gene that encodes for rhodopsin.There are 2 types of RP: type
vascular endothelial growth factor (anti-VEGF) medications. I in which the rods are affected earlier than the cones, and type
Photodynamic therapy (PDT), a "cold laser", is also a treatment II in which the cones are affected earlier than the rods.
option for neovascular ARMD. There is no current treatment
for the non-neovascular type. Monitoring must be done, as Symptoms include night blindness or nyctalopia for most cases
a few convert to the neovascular type. Patients with both of type I , progressive contraction of peripheral visual fields,
Splf-InctrurtionAl WtpriAlc in Onhthalmoloav I 2nd Edition

)Iurring of vision in some cases (with macular involvement), tumors, accelerated hypertension as in eclampsia or other
ind development of cataracts . Absence of night blindness is vascular diseases like diabetes mellitus. Causes of traction
)ossible especially in type II RP.
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 arrows indicate areas of retinal traction from the fibrovascular membranes
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.
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. Figure. 19. Fundus partially obscured by dark red patches of vitreous
hemorrhage; optic disc is hardly seen (black arrow)
Management of rhegmatogenous retinal detachment is
surgical. The basic principles of retinal reattachment surgery ocular B scan ultrasonography must be done to determine if
are: 1) to find the break, 2) to close the break 3) to seal the retinal detachment, tumors or other abnormalities are present
retinal breaks with a chorioretinal scar 4) neutralize vitreoretinal behind the blood.
traction. Management of traction detachment is surgical as
well. The management of exudative detachment is primarily The general rule is, if no retinal detachment or tumor is
medical, addressing the primary cause. detected, the hemorrhage may be observed for 4-6 months
and allowed to resorb by itself. In the presence of retinal
VITREOUS HEMORRHAGE detachment, tumor or other diseases requiring immediate
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
eye doctor. When a vitreous hemorrhage is seen, one must detachment and/or retinal neovascularization, surgical
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
retinochoroiditis. There are two types of ocular toxoplasmosis:
Symptoms are sudden onset of blurry vision, frequently with congenital and acquired. The congenital type is acquired by
floaters in the form of "many dust like particles" which are the pregnant immune-incompetent mother, and passed on
dispersed RBC, or "streaming dark lines". Massive vitreous to the unborn child. The later in pregnancy the infection is
hemorrhage can cause significant loss of vision without the acquired by the mother, the more serious the ocular problem.
floaters. Lighter hemorrhages may manifest as large clumps of The acquired type is by ingestion of the organism in uncooked
floaters. Occasionally there are reports of light flashes in the food or infected fomites. The infection is easily quelled by the
peripheral field of vision (Figure 19). patient but the organism finds its way into the eye and causes
an inflammatory reaction in the vitreous, retina and choroid
Management is directed at finding the cause and clearing hence, a retinochoroiditis.
the blood. In most cases where the bleeding is mild, retinal
examination will permit adequate assessment of the situation Scarring of the retina and choroid are prominent in the
and identification of cause.When vitreous hemorrhage is dense quiescent phase. Recurrences of activity are possible and can
>e found at the edges of scars from previous attacks. Visual The patient usually complains of sudden onset of blurry vision,
iffectation is dependent on the part of the retina affected. photophobia, perhaps floaters, sometimes with headache,
lacular involvement will certainly lead to poor vision
neck stiffness an/or tinnitus. The disease presents with
Figures 20, 21).
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
Figure 21. Composite fundus picture of two scars (red arrows, - a•

toxoplasmosis, and an active lesion with indistinct borders (yellow arrow ; CHOROIDAL CAPILLARY HEMANGIOMA
with hemorrhage at its upper and nasal borders
:_horoidal capillary hemangiomas are benign, isolated, round ,
Diagnosis is best made clinically although immunolog.:
examinations are helpful. Treatment is in the form of oral well circumscribed reddish orange tumors under the retina, of
antibiotics that interfere with the organism's pathway for varying sizes, usually discovered as an incidental finding during
protein transcription, such as sulfadiazine, clindamycin, a routine eye examination. On occasion the patient complains
pyrimethamine. Intraocular injection of antibiotics has also of gradual onset of blurry vision due to induced hyperopia
been shown to be an effective route of treatment. The use of or to serous exudation from the tumor. These rarely grow in
steroids whether oral, topical, peri-bulbar or intra-ocular is not size. Large ones can cause exudative retinal detachments and
without hazard. eventually have pigmentary retinal changes overlying the
choroidal mass. These tumors have distinct angioigraphic and
VOGT-KOYANAGI-HARADA SYNDROME ultrasound features (Figure 23).
Vogt-Koyanagi-Harada syndrome (VKH) is a rare and unusual Management options are laser treatment, cryopexy,
form of diffuse granulomatous uveitis. This is found more in photodynamic therapy, external beam irradiation and
transpupillary thermotherapy if vision is threatened by retinal
pigmented individuals and is a bilateral disease.
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.
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
Figure.23. Choroidal capillary hemangioma with classic red orange
course of the systemic HIV infection.These localized ischemic
color (white arrow) areas are located at the posterior pole and may be related to
circulating immune complexes. In most cases cotton wool
METASTATIC CHOROIDAL TUMOR spots are asymptomatic and blurry vision occurs only if the
lesion is at or close to the macula. Diagnosis must exclude
Metastatic tumors to the uveal tract are the most common other causes of cotton wool spots (diabetic retinopathy,
intraocular malignancies. Most are found in the choroid more collagen vascular disease, retinal vaso-occlusive disease).The
often than in the iris or ciliary body. Metastasis to the retina other ocular manifestations of disease depend on the type of
and optic disc are rare. Spread from the primary cancer is opportunistic infection.
by the hematogenous route. The primaries are, in men, lung
carcinomas, and in women, breast carcinomas. They may The eye disease is managed together with the systemic
appear as bumpy elevations under the retina, with or without treatment of AIDS. Intravitreal implantation of gancyclovir
surrounding exudation, or an almost flat mottled lesion under and foscarnet is an option . Vitreoretinal surgery is indicated
the retina, also with or without exudation (Figure 24). They when there is vitreoretinal traction, non-clearing vitreous
may be solitary or multiple, big or small. hemorrhage and/or retinal detachments.
Visual symptoms occur if the tumors or exudative detachments

are at or close to the macula. Extramacular or peripheral SUMMARY
detachments may cause photopsias and visual field problems.
Small tumors that do not cause visual symptoms frequently It is the primary objective of this material to guide the medical
go undetected. 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
Figure 24. Choroidal metastasis from lung adenocarcinoma with can alert the ophthalmologist regarding the presence of a
leopard skin-like mottling (black arrow) of the elevated mass, and
surrounding shallow exudative retinal detachment (red arrows)
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 Based on the data given above:
1. What is your working diagnosis of the case ?
1. American Academy of Ophthalmology . Basic and Clinical
2. Why ?
Science Course, Retina and Vitreous. San Francisco USA.
LEO. 2008
3. Is there anything else that you would want to ask the
2. Diabetes Control and Complications Trial Research (DCCT)
patient?
Group. The Effect of Intensive Treatment of Diabetes
on the Development and Progression of Long-term
4. What ancillary procedures would you ask for?
Complications in Insulin-dependent Diabetes Mellitus.
N Engl J Med 1993; 329:997
Case 2.
3. Kanski. Clinical Ophthalmology : A Systematic Approacn.
London. Elservier. 6th ed. 2007.
A // yr old female consults you for blurring of central vision in
4. Yanoff, Podos. Textbook of Ophthalmology, Retina and the left eye, since 3 weeks ago. Right eye is "somewhat blurred"
Vitreous. London. Mosby. 1st ed. 1994. Vol 9 but is better than the left eye. She had cataract surgery in both
5. Riordan-Eva, Witcher, Vaughn & Asbury's General eyes 10 years ago and has intraocular implants. She is not
Ophthalmology. Lange Medical Books/McGraw-Hill. 16th diabetic, is a hypertensive with good control with medications,
ed. 1999 has no heart disease, but is on lipid lowering medications.
6. Ryan S. ed. Retina. The Mosby Company. 4th ed. 2006
7. Tasman, Jaeger. Duane's Ophthalmology. Lippincott, Your findings are:
William & Wilkins. 2009 Best corrected vision OD: 20/30 J2 OS: 20/100 J16
8. United Kingdom Prospective Diabetes Study
10P OU: 16 mm Hg
(UKPDS) Group: Intensive Blood Glucose Control with
Sulphonylureas or Insulin Compared With Conventional
EOMs are normal in both eyes
Treatment and Risk of Complications in Patients with
Type 2 Diabetes ( UKPDS 33), Lancet 352: 837-853, 1998 Slit lamp findings of anterior segment OU: clear cornea, +arcus
9. United Kingdom Prospective Diabetes Study (UKPDS) senilis,. deep AC, + 10Ls in place, no AC cells and flare
Group: Tight Blood Pressure Control and Risk of
Macrovascular and Microvascular Complications in Type
Fundus findings: OD: Normal optic disc with CD 0.3, +
2 Diabetes ( UKPDS 38), BMJ 317: 7160-7176, 1998
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
Case 1.
attenuation; there is a small subretinal hemorrhage at macula,
covering fovea, around 2 disc diameter size. Peripheral retina
A 50 year old female comes to you with a complaint of sudden
is normal.
onset of blurry vision of the right eye since a week prior to
consult. She reports that she has had diabetes mellitus for
Based on the data given above
the past 15 years and is on insulin, with poor control of blood
1. What is your working diagnosis of the case?
sugar.
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;

Answers to Self- Test on page 221.
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
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 2. Aqueous is produced by the chary body in the posterior

Figure 1. Glaucomatous optic nerve
chamber, circulates around the lens, passes through the pupil, and flows
into the anterior chamber. Eighty percent of the outflow goes through the
Glaucoma is a leading cause of irreversible blindness and trabecular meshwork and drains into the episcleral venous system; the
remaining 20% passes through the uveoscleral pathway via the interstitial
is second only to cataracts as the most common cause of spaces between the iris root and ciliary muscle. Adopted from Adatia FA,
blindness overall. Worldwide, glaucoma affects more than 70 Damji KR.,
million people, of whom about 10% are estimated to be blind.
In the Philippines, this condition ranks among the top 3 causes microcirculation, ischemia, deprivation of neuronal growth
of blindness. The economic and social impact of this disease is factors, neurotoxic agents like glutamate and nitric oxide have
enormous but is very difficult to quantify. been shown to affect retinal ganglion cell viability (Figure 3).
The elucidation of cellular and molecular events that occur
The understanding of the glaucomatous disease process during the glaucomatous disease process will most certainly
entails a thorough comprehension of the complex physiologic evolve over the next decade and will provide a more definitive
relationship that exists between aqueous humor dynamics, biologic basis for the disease.
intraocular pressure and their effects on the optic nerve.
Mechanical
Tissue Damage
Aqueous humor is an intraocular fluid that is vital to the
health and function of the eye. It is produced in the anterior Decreased
Elevated —4. Axoplasmic
portion of the pars plicata along the tips or crests of the ciliary 10P Flow
processes.The circulating aqueous humor enters the posterior
chamber and flows around the lens and through the pupil Retinal Ganglion
into the anterior chamber. It leaves the eye at the anterior Cell Death
chamber angle through the outflow system consisting of Vascular ..„,,,„,„,,,,,Ischemia
trabecular meshwork, Schlemm's canal, intrascleral channels, Dysregulation
and episcleral and conjunctival veins. This is referred to as
the conventional or trabecular outflow (Figure 2). In the 1
Free Radicals Neurotoxic
unconventional or uveoscleral outflow, aqueous humor exits Agents
by passing through the root of the iris, between the ciliary
muscle bundles, then through the suprachoroidal-scleral Figure 3. Concept of glaucoma pathogenesis . Adopted from the
tissues. European Glaucoma Society.
Intraocular pressure is a function of the rate at which aqueous There are several approaches by which the glaucomas may be
humor enters the eye (inflow) and the rate at which it leaves classified.
the eye (outflow). An impediment in outflow would therefore
result in elevation of intraocular pressure leading to pathologic Based on etiology, they can either be "primary" or "secondary'l
alteration and loss of the nerve fibers of the optic nerve. In the "primary" form, there are no identifiable ocular or
systemic conditions that contribute to the condition. These
Although elevated intraocular pressure (10P) is the most typically affect both eyes and probably have a genetic basis.
frequent causative risk factor for the development of glaucoma, In contrast, glaucomas are classified as"secondary"when there
there are other factors that are also known to play a role. Thus, is a partial understanding of underlying or predisposing ocular
attempts to define glaucoma solely on the basis of IOP alone or systemic events. These may be unilateral or bilateral, some
may not always be appropriate. Other pathophysiologic may have genetic basis, while others are acquired conditions.
However, as our knowledge about the mechanisms of the
mechanisms, either working separately or in combination with
glaucomatous disease process continues to expand, we realize
10P, may contribute to retinal ganglion cell death. Impaired
5 DISTURBANCE IN VISION 15.4 Glaucoma 83
that the "primary and secondary" classification approach has diagnosis and proper management of glaucoma.
become increasingly inadequate.
When meeting a patient for the first time, it is helpful to observe the
A classification system based on the mechanism and site ofaqueous patient as he or she walks into the examination room. Can the patient
outflow obstruction may be a more appropriate approach. walk unassisted? Does the patient walk confidently or does he or she
shuffle into the room wary of the surroundings? Is the patient able
In open angle mechanisms, there is no obstruction to aqueous to locate the examination chair accurately? All these clues give the
outflow by iris tissue (Figure 4). Elevation of I013 results from examiner an idea of the degree of visual deficiency that the patient
obstruction within the trabecular meshwork and beyond. may have.
Many patients with open angle glaucoma are asymtopmatic.
They may have blurring of vision, which they usually attribute It is important that the examiner ask the patient the reason for his
to an error of refraction or the development of cataracts. Focal or her visit. In particular, detailed inquiries about visual problems,
loss of vision, unless severe, is rarely noticed by the patient. accompanying ocular signs and symptoms, family history of eye
disease, previous eye surgery, trauma, other systemic or medical
In angle closure mechanisms, the peripheral iris is in apposition conditions, and medications being taken systemically or topically are
to the peripheral cornea blocking egress of aqueous humor essential. A comprehensive history may eliminate, or rule out, some
through the conventional anterior chamber angle outflow of the diagnostic possibilities or corroborate a suspected diagnosis.
tract resulting in the elevation of 10P.
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 In patients found to have impaired vision, it is important to try and
YH.s 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
Occlusion of the anterior chamber angle can occur thru the crystalline lens to the retina? Are the retina and optic nerve
intermittently and is characterized by the development of normal? Is there pathology invoMng the brain? It must be remembered
peripheral anterior synechiae. Elevation of I013 is gradual in that although glaucoma alone can cause visual disturbance, it may
these cases. These patients may be asymptomatic or may also co-exist with any of the conditions previously cited.
have recurrent short episodes of unilateral pain, redness and
blurring of vision associated with haloes around lights. These The slit lamp biomicroscope is an ophthalmological instrument
attacks may resolve spontaneously. that allows stereoscopic examination of ocular tissue under good
magnification and illumination (Figure 5). It is used to visualize
An acute angle closure attack occurs when there is sudden and evaluate the various tissues and layers of the eye. Its use in
complete obstruction of the outflow tract by peripheral iris. glaucoma evaluation is invaluable.
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.
DIAGNOSING GLAUCOMA
A. Patient History
Careful history-taking, followed by a comprehensive physical

Figure 5. Slit lamp biomicroscope examination
examination, will most likely provide enough information for
Tonometry of 10P elevation in a particular case of glaucoma. In patients,
it allows for determination whether patient's glaucoma has an
The clinical measurement of the 10P is called tonometry open or closed angle mechanism.
(Figure 6).
(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. Gonioscope Mirror
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
Ocular Lubricant Cornea
clinicians however agree that there is no sharp demarcation Iridocorneal Angle
line between what is "normal"and "abnormarlOP. A statistically Iris
abnormal 10P is not synonymous with present or impending
Figure 7. Principle of gonioscopy
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.
Figure 8. Structures in the anterior chamber angle (as viewed thru a

gonioscopic lens)
The chamber angle is considered closed when none of the

Figure 6. Applanation tonometry
angle structures are seen on gonioscopy. It is considered open
Gonioscopy when the structures anterior to the scleral spur are visible.
The examination of the anterior chamber angle is called An accurate gonioscopic assessment is essential in planning for
gonioscopy. This is accomplished by using a variety of special appropriate therapy since the therapeutic approach to angle
lenses that need to be coupled to the eye. Under normal closure glaucoma differs from that of open angle glaucoma.
conditions, the anterior chamber angle cannot be visualized
through the intact cornea because light coming from the Optic Nerve Head Evaluation
angle undergoes total internal reflection at the cornea-air
interface. These special lenses eliminate this interface allowing The assessment of the morphologic features of the optic disc or
visualization of the angle and the structures that lie within it optic nerve head is important in glaucoma evaluation.
(Figure 7).
This structure can be examined clinically with a direct
The anterior chamber angle is where the main outflow system ophthalmoscope, an indirect ophthalmoscope, or a posterior
for aqueous humour is located.This area is comprised of a series fundus lens. The direct ophthalmoscope, although providing
of structures lying between the iris root and the peripheral high magnification, does not provide sufficient stereoscopic
cornea. These include, from posterior to anterior, the ciliary detail. On the other hand, while the indirect ophthalmoscope
body band (CBB), scleral spur (SS), trabecular meshwork (TM) provides for stereoscopic view, its main disadvantage is the small
and Schwalbe's line (SL) (Figure 8). Examination of each of image size one can view with it.The best method to examine the
these structures and their relationship to one another provides optic nerve head is with a posterior fundus lens at the slit lamp.
valuable information regarding the etiology and mechanism 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 Generalized enlargement of the cup may be the earliest
contains a central cup. The tissue between the cup and the change detected in glaucoma (Figure 10). It is also useful to
disc margin is referred to as the neuroretinal rim. In normal compare the optic cups of both eyes as asymmetry is unusual
patients, this rim has a relatively uniform width and a color that in most individuals.
ranges from orange to pink (Figure 9).
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
Figure 11. Notching at the inferior rim (arrow)
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)
If this occurs at either, or both, the superior or inferior pole of In the normal eye, the nerve fiber layer can be best visualized
the disc, the cup becomes vertically oval. In more advanced with red free illumination, and appears as a pattern of striations
glaucoma, the tissue destruction extends behind the cribriform that radiate toward the optic disc. With the development of
plate and the lamina bows backward. The optic nerve head glaucoma, the nerve fiber layer thins and becomes less visible.
then takes on an excavated and undermined appearance that Diffuse loss of the nerve fiber layer may be a very important
has been likened to a "beanpot" (Figure 12). 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.
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
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 using the more sophisticated instruments used in perimetry
(beanpot appearance) testing. The detection of small field defects in early glaucoma
may be missed using this technique.
Splinter hemorrhage usually appears as a linear red streak on or
near the disc surface (Figure 13). The hemorrhage clears over Kinetic visual field testing is performed, as the name implies,
several weeks but is often followed by localized notching and with a moving test object.The object, usually a light of variable
pallor of the neuroretinal rim with subsequent visual field loss. 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
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
Figure 13. Splinter hemorrhage at inferior border of optic disc
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 Glaucomatous damage at the optic nerve head produces
to fixation. Visual sensitivity is greatest in the center, the fovea, visual field defects in the region subserved by the affected
and decreases toward the periphery. By convention, the visual nerve fibers. The location, distribution, size and shape of the
field of each eye is plotted as the patient sees it (Figure 14). resulting visual field defect, called a scotoma, are therefore
determined by the location and extent of the anatomic
60° defect. Typical glaucomatous visual field defects include
Bllndspot
Fixation localized paracentral scotomas, arcuate defects, nasal steps,
Superior
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
60 100° 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 30

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
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 Glaucoma is a progressive neurodegenerative disease affecting
involves the lowering of KW and the adoption of therapeutic the eye that may result in visual field disturbance or blindness.
strategies to protect the optic nerve from further damage In this condition, there is death of retinal ganglion cells
(Table 2) resulting in a characteristic optic neuropathy with cupping, or
excavation, of the optic nerve head. Although elevated 10P is
Table 2: Treatment of Elevated 10P
the most frequent causative risk factor for the development
Medical Treatment of this condition, there are other factors that are also known
to play a role. The key to successful glaucoma management
A. Suppression of aqueous production
is early detection, appropriate and adequate treatment, and
1. Beta adrenergic blocking agents - betaxolol, levobunolol regular monitoring of the disease.
Timolol
2. Alpha adrenergic agonists - apraclonidine. brimonidine REFERENCES
3. Carbonic anhydrase inhibitors - brinzolamide,
Dorzolamide. oral acetazolamide Allingham, R. Rand (ed.). Shield's Textbook Of Glaucoma.
B. Facilitation of aqueous flow Philadelphia, PA: Lippincott Williams and Wilkins. 5th
Edition, 2005
1. Parasympathomimetic agents - pilocarpine
2. American Academy of Ophthalmology. Basic and Clinical
2. Prostaglandin analogs - bimnatoprost. latanoprost, Science Course Section 10: Glaucoma. San Francisco, CA.
travapost 2008.
C. Reduction of vitreous volume 3. Epstein, David L. (ed.). Chandler and Grant's Glaucoma.
1. Hyperosmotic agents - oral glycerol. intravenous Baltimore, MA. Williams and Wilkins. 1997.
mannitol 4. Higginbotham, Eve J. and Lee, David A. (ed.). Clinical Guide
To Glaucoma Management. Woburn, MA. Butterworth
Surgical and Laser Treatment
Heinemann. 2004.
A. Peripheral iridotomy or iridectomy 5. Kwon, Young H. (ed.). A Patient's Guide To Glaucoma.
B. Laser 1- abeculoplasty Coralville, IA. F.E.P. International, Inc. 2008.
6. South East Asia Glaucoma Interest Group. Asia Pacific
C. Glaucoma Drainage Surgery
Glaucoma Guidelines. Sydney, Australia. 2nd Edition. 2008.
1. Trabeculectomy Weinreb, Robert N., et al (eds.). Glaucoma In The 21st
7.
2. Glaucoma shunts and filtration devices Century. London, UK. Mosby International. 2000.
D. Cyclodestructive Procedures 8. Weinreb, Robert N., et al. (eds.). World Glaucoma Association:
Consensus Series. Amsterdam, The Netherlands. Kugler
I reatment should be appropriate to the type and severity of Publications. 2010.
the glaucoma that is present in a patient. 9. Adatia FA, Damji KF. Chronic open angle glaucoma.
http://www2.cfpc.ca/cfp/2005/Sep/vo151-sep-cme-3.asp
One or a combination of topical medications is given to lower accessed October 24, 2011
intraocular pressure. Laser therapy is used, when appropriate,
to improve fluid drainage within the eye.
SELF-TEST
In instances when there is progression or worsening of
the glaucomatous condition, despite maximum use of 1. Visual disturbance in glaucoma is the direct result of:
medications and laser, glaucoma surgery is done. This would A. elevation of lop
involve the surgical creation of new drainage systems in the B. death of retinal ganglion cells
eye to relieve pressure buildup. Intolerance to medications C. obstruction of flow at the trabecular meshwork
and inability to sustain medical treatment are also indications D. presence of cataract
for surgery. 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. scleral spur A. conventional outflow
B. trahecular meshwork B. extraocular outflow
C. ciliary body band C. infrachoroidal outflow
D. Schwalbe's line D. suprachoroidal outflow
E. lamina cribrosa
8. Impediment in aqueous humour outflow would result
3. Morphologic finding in the optic nerve head is NOT be in:
suspicious for glaucoma: A. IOP elevation
A. notching B. optic disc edema
B. splinter hemorrhages C. pupillary block
C. drusen D. retinal detachment
D. enlarged cup-disc ratio E. swelling of the crystalline lens
E. thinning of the nerve fiber layer
9. Which of the following eye medication lowers IOP thru
4. Which of the following does NOT affect the character the facilitation of aqueous humour outflow:
and dimension of the visual field of an eye: A. orinzp,a
A. lateral rectus muscle paralysis B. dorzolar
B. miotic pupil C mannitol
C. glaucomatous optic neuropathy D. pilocarpine
D. ptosis E. timolol
E. high bridge of nose
10. In kinetic visual field testing, the boundary of "seeing"
5. Which of the following statements is true? and "non-seeing" is called:
A. Automated perimeters employ kinetic visual field rs. olinaspot
testing strategies. B. fixation
B. Blindness in glaucoma is reversible. C. isopter
C. Genetics does not play a role in the causation of D. nasal step
glaucoma. E. scotoma
D. Peripheral anterior synechiae are found in open
angle glaucoma. Answers to Self-Test on page 221.
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
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, Discuss the basic anatomy of the optic nerve
2. Discuss the signs and symptoms of optic nerve disorders
3. Discuss various tests used in evaluating optic nerve function
4. Recognize disorders of the optic nerve
5. Identify field defects along the visual pathway
CONTENT
I. Anatomy of the optic nerve
II. Evaluation of patients with optic nerve disorders

1. History taking
2. Ocular examination
A. Visual acuity
B. Pupillary testing
C. Ophthalmoscopy
3. 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
The optic nerve is approximately 50 mm long and consists of requirement in assessing visual disturbances. Corrected visual
about 1.2 million axons originating from the retinal ganglion acuity should be 6/6 (20/20) or better in individuals with
cells. The optic nerve is composed of an anterior (intraocular) normal vision.
and posterior (retrobulbar) portions.
IL Pupils
The intraocular portion (-1mm long) can be visualized using Patients with optic nerve problems may have abnormal
an ophthalmoscope. The retrobulbar portion starts behind pupaary responses. Clinicians should be able to differentiate
the eyeball and can further be divided into the intraorbital normal from abnormal pupils. See Chapter 4 for pupillary
(-30 mm long), intracanalicular (-6 mm long), and intracranial tests. One should suspect optic nerve problems in patients
(-10 mm long) segments. Normally, myelin covers the entire with unequal or unreactive pupil or pupils with relative afferent
retrobulbar portion and myelination ends just behind the pupillary defects (RAPD) (Figures 1 and 2).
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 RIGHT EYE LEFT EYE
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.
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.
Figure 1. Normal response to swinging flashlight test. Pupils

The common complaint among patients with optic nerve remain constricted as light is transferred from eye to eye.
disease is blurring of vision.
1111 Solf-Inonirtinnal lubtarialc in nnhtrulmolonv I lnd Edition

RIGHT EYE LEFT EYE
Short
ciliary -
nerve
Ciliary .---
ganglion
Ill nerve "
Edinger-
Westphal
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.
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).
Figure 2. Relative afferent pupillary defect (RAPID; ;n :._tested
with the swinging flashlight test. Note dilation of pupils wne- i;-.1 Table 1. Conditions that can cause optic disc edema
transferred to the affected left eye.
Papilledema Raised ICP

ANISOCORIA
Inflammatory Optic neuritis, uveitis
Pupillary control is basically an interplay between the Vascular Ischemic optic neuropathy, CRVO,
parasympathetic (constriction) and the sympathetic system hypertension
(dilation). The parasympathetic constriction pathway which Toxic Ethambutol, methanol, lead
originates in the midbrain pretectal area (Edinger-Westphal Infiltrative Leukemia. lymphoma. metastasis
nucleus) sends impulses to the eye via the ciliary ganglion Traumatic Traumatic optic neuropathy
to connect to the cranial nerve Ill. The sympathetic dilation Meningioma orbital tumors
Compressive
pathway which originates in the hypothalamus sends impulses
N Vitamin B deficiency
down to the C-8 to T-2 spinal cord level (ciliospinal center of
Budge) then to the superior cervical ganglion via the ciliary InfeCtiOUS Herpes, cavernous sinus thrombosis.
nerves to connect to the dilator muscles (Figure 3). AIDS
Hereditary Leber's hereditary optic neuropathy,
Unequal pupils or anisocoria may be a sign of a neurologic drusen, myelination, crowded disc
disease. A dilated pupil may be caused by cranial nerve (small CID ratio)
III paralysis, head trauma, brain herniation or Adie's pupil Medications Sildefanil, amiodarone, omeprazole,
(ciliary ganglion damage). A constricted pupil can be seen in interferon
Horner's syndrome, neurosyphilis (Argyll-Robertson pupil) or
parasympathomimetic drug intake.
5 DISTURBANCE IN VISION I S S Disorders of the Optic Nerve 93

Table 2. Common terms used to describe visual field defects
015iammatic
A7rtt , Definition Representation
Scotoma 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
Figure 4. Normal optic disc
3. ANCILLARY TESTS Arcuate arc-shaped defect

ansing in an area near
the blind spot
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
Attitudinal involves the inferior or
of field testing is the confrontation test (Figure 5) This supenor area
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 mianopia
examined separately. It is important that the patient maintains Homonymous loss of the right or left
half of the visual field in
fixation on the examiner's nose. A test target or usually finger both eyes
counting is used. Automated perimetry is requested to confirm
and document visual field defects.
Bitemporal loss of the nght half of
the visual field of the
Table 2 lists the various visual field defects, their definitions right eye and left half of
and their diagrammatic representations. the visual field in the left
eye
Quadrantanopia loss of one fourtn of tne
VISUAL FIELD DEFECTS
visual field
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
•• Right optic nerve — central scotoma/generalized
Ae• depression of the right eye
Optic chiasm- bitemporal hemianopia
BCE) Left optic tract- Right Homonymous Hemianopia
Left optic radiation (temporal lobe)- Right Superior
c44 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
Ef4 14 (Temporal Lobe) Homonymous Hemianopia
F
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 Figure 7. Papilledema
of papilledema include brain tumors, intracranial trauma,
meningitis, hydrocephalus, subarachnoidal hemorrhage and 2. OPTIC NEURITIS
conditions that obstruct the flow of cerebrospinal fluid.
Inflammatory edema of the optic nerve is known as optic
True papilledema is almost always bilateral. Symptoms include neuritis. Any portion of the optic nerve can be affected.
headache, nausea and vomiting. The severity of papilledema Therefore, the inflammation may be localized anteriorly
is proportional to the increase in intracranial pressure. Visual to the optic disc (papillitis), posteriorly behind the eyeball
acuity in the initial stages may be normal. Enlargement of the (retrobulbar neuritis) or may even extend to the adjacent
physiologic blind spot is an early visual field defect. retina (neuroretinits).
Ophthalmoscopy findings include optic disc edema which The foremost symptom is severe loss of vision. This is
causes the disc margins to become blurred and indistinct. The accompanied by eye pain that is aggravated by movement of
swollen disc obliterates the physiologic cup and displaces the the eye. A diffuse central visual field loss is a common finding.
central vessels forward. There is dilation and tortuosity of the Optic neuritis is usually unilateral and RAPD can easily be
retinal veins. Papilledema when fully developed will show a detected.
severely hyperemic disc with hemorrhages, nerve fiber layer
infarcts (cotton-wool spots) and exudates (Figure 7). Absence
Ophthalmoscopy will show a swollen hyperemic optic
of spontaneous venous pulsation may be noted. disc with blurred margins (Figure 8). It may be difficult
to differentiate papillitis from papilledema based on the
Once the diagnosis of papilledema is considered, neuro-
ophthalmoscopic appearance alone. In retrobulbar neuritis,
imaging studies should be done. Treatment is directed to the
there may be no visible ophthalmoscopic changes of the optic
underlying cause. Untreated papilledema will eventually lead disc. Neuroretinitis would frequently present with disc edema
to optic atrophy and permanent visual loss. 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 Figure 9. Opoc Atroohv

sudden painless, non-progressive blurring of vision in patients
over 50 years of age. 6. DEVELOPMENTAL ANOMALIES
Occlusion of the posterior ciliary arteries typically results in Developmental optic disc anomalies when they occur
optic disc edema and an altitudinal field defect. bilaterally may mimic true papilledema. These congenital
disc disorders are called pseudopapilledema or structural
AION has two types: non-arteritic (NAION) and arteritic congestion of the optic disc. On the basis of ophthalmoscopy
(AAION). The NAION occurs more frequently and is commonly alone, they may be mistaken for papilledema. The common
seen in patients with hypertension, diabetes mellitus, causes of pseudopapilledema are severe hyperopia, optic disc
dyslipidemia and coronary artery disease. Less common is the 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 Disc margins can appear blurred in certain conditions despite
predisposing medical problem. Administration of steroids is absence of disc edema. Severe hyperopic (far-sighted) eyes
necessary in patients with AAION. have significantly smaller eyeballs than normal. This results
in crowding of the optic disc structures resulting in blurring
4. TOXIC OPTIC NEUROPATHY of the disc margins. Optic disc drusen (deposition of hyaline
crystals) frequently cause the disc borders to be indistinct.
Ethambutol has been known to be harmful to the optic 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 Other optic disc anomalies include optic disc hypoplasia
vision is characteristic of toxic optic neuropathies. Impaired (small disc), optic malformation (colobomas) and a tilted optic
color vision may be detected early and the typical visual field disc (seen in myopia). These abnormalities can be associated
defects are central or cecocentral scotomas. If ethambutol with developmental disorders of the central nervous system.
is not immediately discontinued, vision may not recover and
prognosis becomes poor when optic atrophy occurs.
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?
Figure 10. Myelinated nerve fibers
A. 1 foot
B. 3 ft
C. 10 ft
REFERENCES D. 20 ft
1. Martin Ti Corbett ii. Optic nerve disorders. In: Neuro- 7. Optic disc edema can be a result of
ophthalmology the requisites in ophthalmology. Stiouis. A. Cortical blindness
Missouri: Mosby. 2000. 57-94. B. Complicated neck surgery
2. Kline LB. Optic nerve disorders ophthalmology monographs. C. Orbital meningioma
San Francisco: American Academy of Ophthalmolgy. D. Serous retinopathy
1996
3. Maas EF, Tomsak RL. Diseases of the optic nerve. In: The 8. The color of the optic disc in optic atrophy is
basics of neuro-ophthalmology. St. Louis. Missouri: Mosby. A. pale yellow
1991. 241-275. B. light brown
4. Fajardo RV, Noche RR. Neuro-ophthalmology. Fajardo RR, C. pastel pink
Espiritu, RB Naval CIN. In: Textbook of ophthalmology. D. soft red
Quezon City: JMC Press. 1980. 115- 123.
9. On ophthalmoscopy, signs of papilledema include
A. hemorrhage, macular star
SELF-TEST B. tortuous vessels, crowded disc
C. exudates, hyperemic disc
1. What is the shortest portion of the optic nerve? D. cotton wool spots, cupping
A. Intraocular
B. intraorbital 10. The pupillary parasympathetic pathway passes
C. I ntraca nalicular through the
D. Intracranial A. Edinger Westphal nucleus
B. Hypothalamus
2. What artery supplies the intraorbital portion of the C. Cervical ganglion
optic nerve? D. Center of Budge
A. Ciliary
B. Optic Answers to Self-Test on page 221.
C. Carotid
D. Ophthalmic
3. 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 of refraction
II. Diagnosis of error of refraction

1. rtistor) tacr
2. Eyeexamirw.
3. Anallary exa— Dns
III. Classification of errors of refraction
IV. Management of errors of refraction

Vision 20/20, a proposal for the elimination of avoidable II. DIAGNOSIS OF ERRORS OF
blindness in the Philippines cited a 1995 University of
the Philippines and Department of Health survey that REFRACTION
showed that there were at least 7.3 million Filipinos with
one or more kinds of error of refraction (EOR) and with a 1. HISTORY TAKING IN A PATIENT WITH ERROR
visual acuity of worse than 20/40 in the better eye. The OF REFRACTION
same source said that about 30,000 were blind from EOR.
Glasses are sufficient to improve the vision of these people. As in any disorder, the patient's history guides the clinician in
In 2002, the Philippine National Survey of Blindness found arriving at a complete diagnosis, particularly as to the possible
that of the main causes of low vision, 53% were due to EOR,
type of error of refraction. Furthermore, the history can provide
0.15% of children had visual impairment due to EOR, and the clinician with an idea as to the visual needs of the patient
that from 1995 to 2002 EOR increased from 1.06% to 2.06%. and the appropriate treatment modality. The clinician should
The same study showed that EOR is the main cause of visual ask each and every patient suspected to have an error of
impairment of children accounting for 33.9%. Amblyopia,
refraction the following questions.
usually a unilateral decrease in best-corrected vision
without any apparent structural abnormality of the eye or its
A. What is the chief complaint?
nervous pathway, can be caused by significant differences
in refractive errors between the two eyes. High refractive
The most common presenting complaints of patients with
errors on both eyes can result in bilateral amblyopia though
errors of refraction are blurring of vision for distance, for near, or
the condition is not as common. In children suspected of
both.Clearnearvision but blurred distance vision indicates near
having amblyopia accurate cyclopegic refraction is critical
sightedness or myopia. Hyperopes (far-sighted individuals)
for diagnosis and treatment.
may complain of early visual fatigue when performing visual
tasks (especially at near). Headache, especially after prolonged
There may be differences in the prevalence of errors
of refraction among races. In a study in Singapore. they eye use, is common with hyperopes and astigmatics but is non-
found that myopia is 1.5 to 2.5 times more prevalent in specific and will have to be differentiated from other causes.
adult Chinese residing in Singapore than in similarly aged As a person loses accommodation (the ability to focus at near)
European - derived populations in the United States and progressively as one ages, he or she will complain of blurring
Australia. 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?

I.WHAT IS AMETROPIA OR ERROR
OF REFRACTION? The duration of the problem should be extracted from the
patient. Errors of refraction usually present with a prolonged
I his is a condition where the refractive elements of an historyoftheir complaints. Whether it is recurrent or progressive
eye at rest are unable to focus light rays from 6 meters or should also be noted. As mentioned above, one should be
aware of a condition of middle age called presbyopia where
more onto the retina. It may be caused by abnormalities in
the lens of the eye gradually loses its ability to focus at near
length of the eyeball or of the refract veelements of the eye
(mainly the cornea and crystalline lens) or both. objects. Sudden blurring of vision seldom results from an
error of refraction except in cases of spasm of accommodation
Errors of refraction fall into several categories,. Myopia or after prolonged near work or due to exposure to an anti-
near-sightedness is a condition where parallel light rays cholinesterase like some insecticides.
(those from a source more than 6 meters or 20 feet away
C. Which eye is involved?
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 far- Does the problem involve one eye or both eyes? Significant
difference of refraction between the two eyes may be the
sightedness, parallel light rays are focused beyond the
cause of amblyopia or a lazy eye.
retina and can only focus on the retina when the person
accommodates or when convergent lens is placed in
D. Are there other associated eye problems?
front of the eye. Astigmatism is a condition where
the refractive power of the eye differs in one meridian
Elicit from the patient whether or not there is any history of
compared to another.
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 where the eyeball is elongated, the fundus and optic nerve
correction of his/her error of refraction to help determine the head may exhibit some changes.
course of the condition. Frequent increases in the power of a
myopic patient's spectacles may mean a progressive form of 3. ANCILLARY EXAMINATIONS
myopia.
The more commonly requested ancillary procedures include:
F. Other aspects of the patient's history that should be
considered include:
A. Retinoscopy is an objective method of measuring errors
of refraction by examining the characteristic of light coming
Family History. Is there a history of similar illness in the family?
from the instrument and reflected by the retina. It will reveal
Genetic factor strongly determine refractive errors of the eye.
the type and amount of refractive error.
Is there any history of any hereditary illness like diabetes?
Changing blood sugar levels may affect a person's refraction B. The common use of automatic refractors in both table-
and cause frequent changes in spectacle correction. top and portable models has made the measurement of errors
of refraction less time-consuming and more convenient.
Social History. What is the patient's occupation? What are the
patient's usual visual tasks? Prolonged near work may lead to C. Keratometry. The keratometer is an instrument that can
spasm of accommodation causing blurred vision for far. measure central anterior corneal curvature. It can be used
to check the type and amount of astigmatism. It is also used
Medical History. Has the patient suffered any form of in fitting contact lenses, a form of correction for errors of
illness in the past, particularly diabetes? Is she under any refraction.
form of medication for any illness? These may affect vision.
Sulfonamides and related compounds for example. may cause D. Corneal topography is a sophisticated instrument that
the ciliary processes to swell and cause forward movement of produces a color-coded topographic map of the cornea that
the lens blurring vision for far. shows the pattern of the corneal curvature. It usually functions
as a keratometer as well, measuring corneal curvatures. It
2. OPHTHALMOLOGIC EXAMINATION demonstrates irregularities of curvature like keratoconus.
OF THE PATIENT
E. Biometry or A scan ultrasonography is a test that
COMMON OCULAR FINDINGS IN AMETROPIA 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:
III. CLASSIFICATION OF
A. Visual Acuity. Most patients with an error of refraction will AMETROPIAS
present with reduction in vision either for far, near, or both.
Snellen charts are commonly used for distance vision testing
DIAGRAMMATIC CLASSIFICATION
and Jaeger or Snellen equivalent cards for near vision. If the
vision improves when the patient looks through the pinhole, OF AMETROPIAS
the patient most probably has an error of refraction that can
be corrected with lenses. The emmetropic eye (Figure 1) focuses light rays from infinity
on the retina even at rest or without accommodating.
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
Figure 1. Emmetropic eye
esotropia is associated with hyperopia.
he myopic eye (Figure 2) focuses light rays from infinity in In regular astigmatism, the refractive power changes
ont of the retina. An object at a finite distance focuses on successively from one meridian to the next and each meridian
s retina. has a uniform type of curve.
With the rule and against the rule astigmatism
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
,figure 2. Myopic eye
plus cylinder is located at or near axis 90°. In "against the rule"
astigmatism, a correcting plus cylinder is located at or near
-he hyperopic eye (Figure 3) theoretically focuses light rays 180° and the horizontal meridian is steepest.
rom infinity behind the retina. It can only focus convergent
ight rays on the retina.
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,
Figure 3. Hyperopic eye or refractive corneal surgery. Other refractive surgical procedures
include the placement of an intraocular lens (I0L) implant, either
ASTIGMATISM in front of the crystalline lens (phakic 10L) or in place of the
crystalline lens (refractive lens exchange)
In astigmatism, the refracting surface (usually the cornea)
The most common means of managing errors of refraction is either
is toroidal (like the surface of an American football) rather
than spherical, and therefore the refracting power of the by spectacles or contact lenses. There maybe some situations in
surface is not the same for all meridians. If retinoscopy which contact lenses are preferred, e.g. anisometropia, monocular
aphakia, or high refractive errors.
has achieved neutrality in one meridian but is still
or 'against' in another, this indicates different refracting Table 1. Advantages and Disadvantages of using spectacles and
powers in the two meridians. This is a sign of astigmatism. tic e-SeS
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 Spectacles • Safe For high errors of
may not be the same in the two meridians (Figure 4).The • Easily adjusted refraction or
anisometropia
cornea may thus be astigmatic. • Inexpensive
• Restricted visual field
t Direction of scan
• marked aniseikonia
• distortion of image
and prismatic effect
410110 • heavy weight
Direction e scar debilitating visually,
cosmetically and
with psychologically
180° • Relay safe • patient-parent
Easily adjusted compliance
• suitable for unilateral • psychological trauma
Figure 4. Astigmatic reflex as seen thru retinoscope
aphakia frequency of lens loss;:
Jim
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 RECOMMENDED FOLLOW-UP
ERRORS OF REFRACTION (FAQ)
It is recommended that the students be given demonstration
FAQ 1: If a child wears glasses early, will it contribute to the sessions on how to properly conduct history taking and
progression of the error of refraction? ophthalmologic examination of patients. Following this
exercise, the students should be provided with clinical sessions
Answer 1: No. Major components of an eye's refractive state to allow them to see actual cases of patients with errors of
are the cornea, the lens, and the length of the eye and their refraction.
size, shape and the power are determined genetically.*
FAQ 2: If I use glasses for my astigmatism 0, REFERENCES

astigmatism go away?
1. Results of the Workshop On Vision 2020 conducted by
ANSWER 2: Depending on the age of the patient. errors of the Department of Health on July 26 to 28, 2000 at the
refraction may change. In young individuals with eyes that SEAMEO-INNOTECH, http://www.yision2020australia.
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 National%20PIan.pdf
even "go away". In animals, research has shown that there may 2_ University of the Philippines Manila, Philippine National
be a mechanism that influences the development of the eyes Surveyof Blindness, published by UP Manila, Manila, 2004
towards normal or emmetropia.6 3_ Arnblyoaia, Preferred Practice Pattern, Prepared by
the American Academy of Ophthalmology Pediatric
FAQ 3: If I wear contact lenses, will the progression of my Ophthalmology/Strabismus Panel 2008
myopia decrease compared to wearing glasses? 4 TienYin Wong, Foster 1'J, Hee J, Invest. Ophthalrnol. Vis. Sci.
August 2000 vol. 41 no. 9 2486-2494 http://www.iovs.
ANSWER 3: Rigid or hard contact lenses have been shown to cogicontent/41 /9/2486.s hort accessed 12 April 2011
retard or even decrease myopia through the fitting of special 5. IlAd_eod SD, Chuck RS, Hamilton R, et al Preferred Practice
lenses that reshape the cornea that is usually steep in myopes. fbuerrr Refractive Errors and Refractive Surgery, one.aao.
os9yassetaxd?id=0faa6a59-ef36-42fc-8d80-79b22c...
FAQ 4: Will I see better after a laser procedure (like LASIK) accessed 12 April 2011
than with spectacles? Young11.Metapally R, Shay AE. Complex trait genetics of
adman* errors. Arch Ophthalmol, 2007 ; 125 (1), 38-'18
ANSWER 4: Although a laser procedure such as LASIK ww Opiel. Refraction and Contract Lenses. Basic and Clinical
improve vision in a large majority of patients, there may be Sdence Course, Section 2. California: American Academy
trade-offs compared to the use of contact lenses or spectacles. atOphthalmology, 1990.
These include some glare especially at night and some loss of 8 Exam— ROphthalmologic Optics. Manila: Department of
contrast sensitivity. Opfinhairnology &Visual Sciences, 2001.
Head Funk W Ophthalmology, Principles and Concepts,
-1.1osby and Co., 1986
CONCLUSION
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
refractive error between the two eyes) or severe ametropia is C usually iirtvorêe vision
present.
Intraocular pressure in isolated errors of refraction is 11. In astigmatism due to the cornea
usually The curvature is not the same in all meridians
A. normal B. The curvature is flatter than normal
B. high C. The index of refraction of the corneal surface is not
C. low the same in all meridians
D. The curves of the surface are convex
Errors of refraction
A. show no hereditary pattern since it is caused solel 12. A patient can work on a computer without difficulty but
by the type of visual work a person performs has difficulty reading street signs. What is his refractive
B. cannot occur in children since the eye is still state?
developing A. I le is probably normal.
C. if significantly different between the two eyes can B. He may be myopic.
lead to progressive loss of vision C. l le may be hyperopic.
D. He may have compound hyperopic astigmatism.
Retinoscopy is
A. the same as funduscopy 13. On visual acuity testing, a 20 year old patient had 6/6
B. an objective means of measuring errors of refraction vision but difficulty with reading Jaeger 1 print. What is
C. a means to take retinal photographs to determine the patient's refractive state?
retinal changes due to errors of refraction A. presbyopia
B. hyperopia.
i. If the poor vision of a patient does not improve when C. myopia.
viewing the test chart through a pinhole D. no error of refraction
A. the blurring may not improve with corr...
B. there may be error of refraction 14. If the horizontal meridian of the cornea is steeper than
C. it is a sure sign of amblyopia the vertical meridian, what type of astigmatism does
the patient have?
7. Measurement of refractive errors A. "with the rule"
A. can not be done for infants and young children B. "against the rule"
B. is usually very subjective C. "natural"
C. can be performed using automatic refractors
Case 1.
9. In middle age, one may
A. gradually lose the ability to focus for near or develop A 7 year old pupil's teacher informs her mother that her child
presbyopia seems unable to copy words from the white-board and squints
B. suddenly lose the ability to read due to ably spasm her eyes when she looks at the board from her seat. She keeps
C. usually develop hyperopia and thus lose darity of far books near her face when she reads.
vision
V OU: 20/200 or 6/60 improved to 6/7.5 with pinhole.
9. Normal or emmetropic eyes looking at an object Intraocular pressure: soft OU
6 meters or 20 or more feet away EOMs: full
A. need to accommodate to c-A:us Fight on the retina FOU: normal
B. need to squint to focus light on the retina
C. should be able to focus light on the retina with the 1. With the given information would it be safe to say
eye at rest that the patient has an error of refraction?
2. What type would it be, hyperopia or myopia?
10. When the image of an object at infinity falls behind the 3. What examination can measure the error and lead to
retina, the patient is the prescribed correction?
A. hyperopic
B. myopic
C. toric
D. phthisic
Casa 2.
1. With the given information would you say the patient
A 42 year old employee complains of frequent afternoon may have an error of refraction?
headaches and blurring of vision after prolonged near work. 2. What information in the history and ophthalmic
She has experienced the symptoms for the last ti months. She examination tells you that this might be part of the
has had clear vision for both far and near before this and has a process?
never been prescribed glasses.
V OU: 20/20 or 6/6, Jaeger 1 with difficulty at about 50 cm. Answers to Self-Test on page 221.
Intraocular pressure: soft, OU
EOMs: Full
F OU: Normal
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
discharge, photophobia and itchiness
complication
2. 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 This clinical algorithm is presented to aid the medical student
as well as the primary care physician in the diagnosis of the
RED EYE more common causes of eye disease presenting as a red
eye. The common symptoms of eye pain, eye discharge,
Red eye is a common eye symptom Or pal Is with eye photophobia and itchiness are used for this algorithm.
disease. Red eye is seen as a result of dilation of conjunctival
or scleral blood vessels in response to an inflammatory or A. EYE PAIN
infectious process. Another common cause of red eye is
subconjunctival hemorrhage which results from trauma or
The first step in the algorithm is to determine whether the
injury to the small conjunctival vessels.
patient presenting with a red eye has eye pain or not (Figure 1)
Eye pain may be described as a sharp localized pain, pain
The following are the differential diagnoses of a red eye:
when exposed to bright light or a severe eye pain radiating
1. Conjunctivitis
to the head. The symptom of eye pain divides the common
a. Infectious
i. Bacterial dilksential diagnoses of eye pain into two groups: eye pain
ii. Viral "cup and no eye pain group.
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
Awe 1. Red Eye Algorithm: Eye Pain
4. Acute Glaucoma
5. Keratitis
a. Infectious 1. EYE PAIN WITH EYE DISCHARGE
i. Bacterial
ii. Viral For patients with red eye and eye pain, the next question will
iii. Fungal be the presence or absence of eye discharge. If there is eye
iv. Acanthamoeba discharge, microbial keratitis or infection of the cornea may be
b. Non-Infectious considered (Figure 2). The presence of abundant nerve fiber
i. Recurrent Epithelial Erosion endings in the cornea (CN V) is responsible for the pain when
ii. Foreign Body infection is present
6. Eyelid Abnormalities
a. Entropion /Trichiasis yes MICROBIAL
b. Lagophthalmos DISCHARGE? KERATITIS
7. Orbital Disorders
a. Preseptal and orbital cellulitis
b. Idiopathic orbital inflammation
Figure 2 EyeAlgCritttrn: Eye Pain with Eye Discharge
II. CLINICAL ALGORITHM FOR THE

2. EYE PAIN, NO DISCHARGE,
DIAGNOSIS OF THE RED EYE WITH OR WITHOUT PHOTOPHOBIA
Ophthalmologists are the experts in the diagnosis and If there is no eye discharge in a patient with eye pain, the
treatment of eye diseases. In the Philippines, however, access next step will be to establish the presence or absence of
to an ophthalmologist may not be easy. The primary care photophobia (Figure 3). Photophobia is usually described as
physician may still be the first line medical worker in the a dull eye pain when exposed to bright lights. This pain due
identification and initial treatment of eye disease. to the pupillary spasm of an inflamed iris. If photophobia is
present, uveitis or eye inflammation, may be considered. In the 2. NO EYE PAIN, WATERY DISCHARGE,
absence of photophobia, acute glaucoma may be entertained. WITH OR WITHOUT ITCHINESS
The eye pain in glaucoma is moderate to severe often with
radiation to the head. Patients presenting with watery discharge can be suffering
from either allergic conjunctivitis or viral conjunctivitis. To
differentiate between the two, the presence or absence
_.111111H MICROBIAL of itchiness may be asked. Eye itchiness is very prominent
CFSC,,ARGE? KERATITIS
symptom in allergic conjunctivitis (Figure 6). It is also
PAIN?
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.
I-7
M ACt
inS ACUTE
GLAUCOMA
DRY EYE
Figure 3. Red Eye Agc-thr-. Eye Pain. No Eye as: - - 7 or

without Photophobia TYPE OF
DISCHARGE?
B. NO EYE PAIN, NO EYE DISCHARGE ALLERGIC MUCOPURULENT

CONJUNCTIVITIS
ITCHY? BACTERIAL
The second group of differential diagnoses are the red eyes CONJUNCTIVITIS
without eye pain. The presence or absence of discharge is the VIRAL
next question to ask. Dry eye syndrome may be considered in CONJUNCTIVITIS
patients without eye discharge (Figure 4). Figure 6. Red Eye Algorithm: No Eye Pain. Watery Discharge. with or
without Itchiness
INE! DRY EYE

III. DIFFERENTIAL DIAGNOSES OF
F RED EYE
DISC1-.ARGE ,
A. VIRAL CONJUNCTIVITIS
Figure 4. Red Eye Algorithm. No Be Pair tea Er Di.:
CLINICAL CLUES
1. NO EYE PAIN WITH MUCOPURULENT DISCHARGE Viral conjunctivitis or"sore eyes" is the most common cause of
acute onset eye redness (Figure 7). The main feature of this
Red eye patients with no eye pain but with discharge comprise disease is the presence of watery discharge in the early part
the conjunctivitis subgroup. The type and character of the of its course. The most important information in the history
discharge will help one differentiate the possible etiology. that points to this disease is the history of exposure to other
In patients with an initial presentation of mucopurulent individuals with "sore eyes" or similar clinical manifestation.
discharge, bacterial conjunctivitis should be the primary
consideration (Figure 5).
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 In majority of the patients, the disease resolves without sequelae.
common type of the viral conjunctivitis is caused by adenovirus In a few cases, subepithelial opacities (Figure 9) may develop in
types 8, 19, 29 and 37 (Figure 8). Spread is through a direct thecornea that, in turn, lead to blurring of vision.The subepithelial
contact with eye discharge. The virus may not be neutralized obes may persist for weeks or months and in some cases may
by alcohol. Proper hand washing is the best way to prevent - dithout scars.
the disease.
F e. - the cornea.
B. ALLERGIC CONJUNCTIVITIS
Figure 8. Structure of adenovirus CLINICAL C ES
SIGNS AND SYMPTOMS Allerg&c sa cnronic or recurrent eye disease

characterized by eye redness, itchiness and watery or stringy
Onset of symptoms is acute. Duration varies from few days discharge Pipe 10). Eye itchiness is the most prominent
to 2-4 weeks. It usually starts on one eye and may become feature
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.
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 ETIOLOGY / PIIIHOGENESIS
is the best way to prevent the spread of viral conjunctivitis.
There is no treatment needed. However, antibiotic eye drops The etiology of this disease is immunologic in nature. Often,
may be given in patients with secondary bacterial infection or it is difficult to identify the specific allergen. The hay fever
as a prophylaxis for bacterial infection. Mild steroid drops and type of allergic conjunctivitis is mainly a type I hypersensitivity
reaction to airborne allergens. In atopic keratoconjunctivitis,
cold compress may be given to help reduce inflammation.
-' k I
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
Figure 12. Cataract resulting from chronic steroid use.
The diagnosis of allergic conjunctivitis is arrived at from an

adequate history and thorough clinical examination. However, C. DRY EYE
the presence of eosinophils in cytologic studies of conjunctival
scrapings confirms the diagnosis (Figure 11). Often this is CLINICAL CLUES
done only in academic institutions.
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- . Patients usually complain of a sandy and gritty sensation
associated with slight eye redness and eye fatigue. The
TREATMENT symptoms are worse with wind and dry climates.
Treatment involves the identification and removal of DIAGNOSTIC WORK-UP

environmental triggers. Cold compress and mast cell
stabilizers / antihistamine eye drops may help control the Schirmers test with or without anesthesia is done to confirm
symptoms. In moderate to severe cases, short-term topical dry eye. Standardized strips of filter papers are used to absorb
steroids are needed. Oral antihistamines may also be tears. Consistent measurements of less than 5 mm of wetting
prescribed to control the symptoms. 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
COMPLICATION surface of the tear film is observed for areas of disruption.
Rose bengal stain can also be instilled to identify areas with
Vernal type of allergic conjunctivitis often occurs in young devitalized epithelial cells which can be seen in dry eyes
children which lasts for several years. In these cases, when (Figure 13). Normal tear break-up time is generally greater
steroid drops are over used, cataract may develop as a than 10 seconds.
complication of the steroids use (Figure 12). In some patients,
steroid-induced glaucoma may occur.
6 RED EYE, TEARING AND DISCHARGE I 1 The Red Eye 109

Figure 13. Rose Bengal stain on devitalized epit2
gure 15. Blepharoconjunctivits from Moraxella organism.
TREATMENT
SIGNS AND SYMPTOMS
Treatment is mainly topical instillation of aqueous
replacement or artificial tears. For patients requiring tear- Most often, bacterial conjunctivitis is unilateral and is acute
substitute eye drops more than 4x a day, non-preserved in onset. There is a mucoid to muco-purulent discharge
topical eye drop preparation is recommended to prevent associated with a red eye but no blurring of vision.
hypersensitivity to the eye drop's preservative. In severe cases,
punctual occlusion may be done using a silicone plug to
increase tear retention.
DIAGNOSTIC WORK-UP
Conjunarva~~scrapings from children with bacterial

D. BACTERIAL CONJUNCTIVITIS
conjunctivkisandURTImight reveal gram negative coccobaci I I i
(charactsistic of Hernophilus organism) (Figure 16). Bacteria
CLINICAL CLUES
from con#anctivai scraping may also be cultured on a blood
agar plate to further identify the causative organism.
Conjunctivitis caused by bacteria presents with mucoid to
muco-purulent discharge. In children, it may be associated
with upper respiratory tract infection (URT1).
In children with URTI, the most common etiology is Hemophilus

influenza. Among newborns, Chlamydia or gonococcus
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
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
Figure 17. White lesion in the cornea in a patient with microbial Walls needed to save the eye (Figure 19).
ETIOLOGY / PATHOGENESIS 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
Figure 19. After penetrating keratoplasty (corneal transplantation) in a
Corneal scraping is done to determine the etiologic agent patient with ruptured microbial keratitis.
(Figure 18) 3ram stain is used to initially identify the bacteria
but definitive diagnosis is achieved with culture studies F. ACUTE GLAUCOMA
in blood agar-plate and brain heart infusion (BHI) media.
Sensitivity studies are done to determine the most appropriate CLINICAL CLUES
antibiotic agent.
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).
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 irido-
corneal 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 Figure 22. leaume rrt gut nerve cupping in chronic glaucoma.
Acetazolamide or hyperosmotic oral solutions may be used

to facilitate immediate lowering of the eye pressure. Topical
G. UVEITIS
ocular hypotensive agents are also used. Laser iridotomy is
the definitive management. Surgical iridectomy may be done
CLINICAL CLUES
in the absence of a laser machine. AVF and OCT are used to
monitor response to treatment as well as progression and
Uveitis is an ocular inflammation characterized by eye redness
control of the disease. around the cornea (ciliary injection) associated with sensitivity
to bright lights (photophobia).
COMPLICATION
When glaucoma becomes chronic or is left untreated, there
is damage to the optic nerve causing initial blurring of vision Almost haif of the uveitis cases are idiopathic. In some cases,
of the peripheral fields which eventually leads to blindness the condition is associated with systemic disease such as
(Figures 21and 22). 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
Figure 23. Keratic precipitates in uveitis.
disease will help in the prognostication and treatment of the
disease.
TREATMENT
4. ENTROPION /TRICHIASIS
Steroid is the mainstay of treatment in patients with uveitis.
Topical steroid drops are used for uveitis located in the anterior Entropion and trichiasis are seen among the elderly presents
part of the eye. Periocular steroid injection is recommended with eye redness due to misdirected lashes that irritate the
for patients with uveitis in the posterior pole. In patients cornea. Removal of the misdirected lashes is done as an initial
with bilateral disease or when there is systemic evidence of treatment. Permanent treatment may require cautery of the
root of the eye lashes or surgery of the eyelids.
inflammation, oral steroids are used. Immunosuppresive
agents are also given in moderate to severe cases.
COMPLICATION
SUMMARY
A red eye is one of the more common ocular problems that a
Moderate to severe uveitis is a brining disease. Common
primary care physician will encounter. While most cases may
complications include cataract and secondary glaucoma.
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
H. OTHERS a diagnosis that was presented in this chapter. Basic principles
for managing the various red eye conditions have also been
1. EPISCLERITIS / SCLERITIS presented.
Scleritis and episcleritis present with a red eye and eye pain. The importance of extracting a comprehensive history as well
Some are associated with collagen vascular diseases. Topical as performing a meticulous examination of the eye can not
steroids and oral NS bilDs are 7r"...'" ',7".F. ..'7,ibed for this condition. be overemphasized. Recognizing the pattern of eye redness
that a patient presents has also been shown to be helpful in
2. CONTACT LENS-RELATED EYE REDNESS arriving at a logical diagnosis. Table 1 lists non-trauma red
eye conditions that are potentially threatening to vision.
Eye redness may be seen among contact lens wearers. This Recognition of these conditions is essential so that urgent
results from overwear of the contact lenses, which causes
referral to an ophthalmologist can be done.
decrease in oxygen supply to the cornea. This condition
resolves with rest from contact lens wear. Antibiotic eye drops
An overview of the more common red eye conditions has
may be given as a prophylaxis for eye infection.
been discussed in this chapter. Subsequent chapters shall
3. CORNEAL ABRASION / FOREIGN BODY 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
NO YES
MICROBIAL TYPE OF
PHOIOPHOBIA? DRY EYE DISCHARGE?
K E RAMIS
YES MUCOPURULENT
BACTERIAL
ACUTE UVEITIS CONJUNCTIVITIS
GLAUCOMA
YES
VIRAL ALLERGIC
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
11.1111111.11.1
1111
).„,.,.,.
Condit
Redness Vision Pain up! 10P
Daiisa! most Moderate to Moderate to severe. Mid-dilated;

- on-reactive to
Glaucoma prominent around severely reduced; often with headache
the limbus iridescent vision and vomiting ght
Anterior LIveitis Diffuse: most Mild to moderately Mildto moderate; Moho; irregular normal to
prominent around reduced photophobia shaped: poorly hypotonic
the limbus reactive to light
Keratitis Diffuse; more Moderate to Moderate to se iere yes r May be affected generally
prominent around severely reduced adidlorts associated not affected
the limbus =LSE with uveitis
Scleritis Focal or diffuse with Normal to mildly Moderate b serer Not affected Not affectedi
purple-tinged color reduced usually bonder
Endophthalmilis Diffuse Moderately to Moderate to wow-. •• - 3 -.•7- elevated

severely reduced
4. A 45 year old executive, complained of severe headache
REFERENCES AND
and right eye pain associated with blurring of vision
RECOMMENDED READING after watching a movie. Vision of the right eye was
20/200, not improved with pinhole. Upon examination,
1. Vaughan DG, Asbury and Riordan-Eva P. General she had a hazy cornea with eye redness. No discharge
Ophthalomology. 14th ed. Appleton & Lange: Stamford, was seen. What is the most likely diagnosis?
CT. 1995. A. Acute Glaucoma
2. Chern K and Zeagans M. eds. Ophthalmology Review B. Allergic Conjunctivitis
Manual. Lippincott Williams and Wilkins: Philadelphia. PA. C. Dry Eye
2000. D. Microbial Keratitis
3. Tasman W and Jaeger EA. eds. Duane's Ophthalmology- E. Uveitis
Lippincott Williams and Wilkins: Philadelphia, PA_ 2011.
4. Santos E0 and Cubillan LDP. National Survey of Blindness, 5. Ten nurses in the operating room have eye redness
Philippines 2002. University of Philippines Manila: Mania. associated with watery eye discharge suggestive of
Philippines. 2004. 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?
SELF-TEST A. 1,000 mg of ascorbic acid
B. Daily intake of multivitamins
1. A 35 year old male consulted for eye redness. A group C. Frequent hand washing
of medical students were assigned to get the history D. Topical antibiotic as prophylaxis
of medical illness. Student A asked if the patient E. Use of alcohol-based hand sanitizers
experienced eye pain. The patient answered yes: to
the first question. Student B was not able to elicit any 6. Two of the ten nurses who had adenoviral conjunctivitis
history of eye discharge. The patient told Student C consulted the ophthalmology clinic 2 weeks later for
that she experienced photophobia. What eye condition blurring of vision. What might be the cause of their
would you consider as your initial impression? blurring of vision?
A. Acute Glaucoma A. Corneal opacities
B. Allergic Conjunctivitis B. Dry Eye
C. Dry Eye C. Error of refraction
D. Microbial keratitis
D. Microbial Keratitis
E. Toxic keratitis
E. Uveitis
7. A 5-year-old boy consulted your clinic for muco-
2. A 15-year-old male consulted for recurrent eye redness purulent discharge associated with cough. He had no
associated with watery eye discharge and itchiness. eye pain. What eye condition would most likely explain
What eye condition would you consider as your initial
these symptoms?
impression based on the history?
A. Acute Glaucoma
A. Allergic Conjunctivitis B. Allergic Conjunctivitis
B. Bacterial Conjunctivitis C. Bacterial Conjunctivitis
C. Dry Eye D. Dry Eye
E. Viral Conjunctivitis
E. Viral Conjuncitivitis
8. An 80-year old grandmother has been treated for
3. A second year medical student consulted for eye
glaucoma over the last 10 years. Eye pressure control
discharge and blurring of vision 3 days prior to consult.
She is a contact lens wearer for several years. She also was not very successful. What kind of visual disturbance
complained of eye pain. On gross examination, a white would this patient have?
opacity was seen at the center of the cornea. What is A. Blurring of the central vision
your initial impression? B. Blurring of the peripheral vision
A. Acute Glaucoma C. Central scotoma
B. Allergic Conjunctivitis D. Enlargement of the blindspot
C. Dry Eye E. No visual disturbance is expected
E. Uveitis
6 RED EYE, TEARING AND DISCHARGE I ^ 1 The Red Eye OE

9. A muco-purulent discharge was observed in a newborn 10. A 60 year old woman came in for a chronic eye redness
baby. What is the most common etiologic agent of both eyes. Student A asked if she has eye pain.
responsible for this disease? The patient said that she did not experience any eye
A. Chiamytha pain but she felt some foreign-body sensation. Upon
B. Hemophilus examination, no discharge was observed. Using the
C. Pneumococcus algorithm, what would be your initial impression?
D. Pseudomonas A. Acute Glaucoma
E. Staphylococcus B. Allergic Conjunctivitis
C. Dry Eye
E Uveitis
Seeanswers to Self-test on page 221.

6.2 Uveitis and Scleritis
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
primarily on providing the medical student with knc 7.'1- :fa how to go about recognizing and assessing patients with uveitis
and scleritis. Students are however encouraged to . • -owledge that they will acquire from this material to , a al,a
simulated clinical cases that they will encounter durina -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. Identify the various elements in a patients history and ophthalmologic examination that leads to the
formula n of
diagnosis of uveitis and scleritis_
3. Formulate a diagnosis of infiammaTcry conditions involving the sclera and the uvea according to their location and
course.
4. Discuss the therapeutic goals of w' uveitis and scleritis.
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. Episcleritis
B. Scleritis
C. Uveitis
I. UVEITIS The onset of these changes should likewise be noted, that is
whether or not they occurred suddenly or progressively over a
Eye redness is a common complaint among patients seeking prolonged period of time.
ophthalmologic consult. While not all patients with intraocular
inflammation will present with eye redness, the differential (2) How long has this problem been going on?
diagnosis for the red eye should include inflammatory eye
conditions involving the uveal tract and the sclera. The duration of the problem should be extracted from the
patient Furthermore, it should also be determined whether
DIAGNOSING UVEITIS or not a similar problem has occurred in the past.
Uveitis is a nonspecific term used to denote intraocular (3) Which eye is involved?
inflammation involving the uveal tract, that is, the iris, ciliary
body and the choroid. Uveitis can involve one eye or both eyes. Does the problem involve one or both eyes? If both eyes
Inflammation may not be limited to the uveal structures alone are involved, cki the patient experience his or her symptoms
and may also involve any part of the eye, including the sclera in both eyes simultaneously or did involvement in one eye
(sclerouveitis), cornea (keratouveitis), vitreous body (vitritis), precede the involvement in the other eye? If the onset of
retina (retinitis) and even the optic nerve (optic neuritis). symptoms difered between the two eyes, also inquire as to
the interval in the onset of symptoms between the two eyes.
In order to formulate a diagnosis of uveitis, it is important
(4) Are there otherassociated eye problems?
that a thorough, comprehensive history is extracted from
the patient and an accurate eye examination be performed.
Elicit for the presence of ocular symptoms aside from the chief
Information from both history and exam provides the basis
complaint of the patient_ Aside from the symptoms previously
for the generation of differential diagnosis and appropriate
mentioned (redness. floaters, vision changes, photophobia),
selection of ancillary examinations for the patient. General
patients with melds may also present with history of ocular
systemic examination is done when intraocular inflammation
pain, eye trauma or ocular surgery. Each symptom should
is suspected to be a component of a systemic condition.
be further c+a-actierized, particularly in terms of the temporal
There are four basic elements which should be considered in
relation of 7- onset to the patient's chief complaint and
the formulation of a diagnosis of uveitis. 12
presence c' = . -ssion (improvement or worsening) of the
symptoms.
HISTORY-TAKING IN THE UVEITIS PATIENT
(5) Has the patient consulted previously? If so, were

Extracting a comprehensive history from a uveitis patient
medications prescribed and used by the patient?
can not be overemphasized. The patient's history guides the
clinician in arriving at a complete diagnosis, particularly as
Inquire as -.= -7 consultations made by the patient
to the possible etiology of the condition. Furthermore, the
and treatme-: :a Des given to the patient. Gather data
history can provide the clinician with an idea as to the patient's
on how the pa: -1- -: responded to previous treatment as this
possible response to treatment. The following are important
questions regarding the patient's current illness that the will provide valuate information for purposes of determining
clinician should ask each and every patient suspected to have prognosis.
uveitis.
(6) Other aspects of the patient's history that should be
(1) What is the chief complaint? considered include:
Family history. is -_-T a nistory of any similar illness in the

The two most common presenting complaints of patients
family? Is there any - story of any hereditary illness?
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 Social History Does the patient have any exposure to pets?
distortion of vision. In addition to blurring of vision, patients Inquire also as to the patient's diet (ingestion of raw foods), any
may also complain of photophobia, defined as sensitivity to history of alcohol intake, smoking, drug intake or travel.
light or eye pain in high illumination.'
Medical History. Has the patient suffered any form of illness in
Floaters on the other hand refer to black or white floating the past? Inquiry as to the presence of any systemic symptoms
"objects" that the patients appreciate in their field of vision.' such as joint pains, oral and skin ulcers, hearing problems,
These are often described by patients as "flies" or "insects" gastrointestinal or genitourinary problems to name a few,
which move about in their field of vision. should also be made.
Sexual History. The presence of a history of any sexually Corneal Abnormalities. The cornea may lose its normal
transmitted disease should likewise be elicited from the luster and clarity in anterior segment inflammation.
patient. Patients typically present with deposits of
inflammatory cells on the corneal endothelium
EYE EXAMINATION OF THE UVEITIS PATIENT called keratic precipitates (Figure 2). Keratic
precipitates are characterized according to their size,
The basic eye examination is performed after extracting the distribution and pigmentation as these provide clues
history of the patient. Common ocular findings in uveitis as to the particular type of uveitis the patient has.
patients are listed below. Although more often confined in the inferior portion
of the cornea, they may also be diffusely distributed
(1) Visual Acuity. Vision is frequently compromised in in certain forms of uveitis. Large keratic precipitates
patients with active inflammation.' Reduction in vision would point to a granulomatous type of uveitis while
can also occur as result of complications of chronic small to medium-sized keratic precipitates are more
inflammation. As with most eye conditions, accurate commonly associated with the non-granulomatous
recording of vision is important as this may serve as an type. The presence of pigmentation, on the other
indicator of improvement or deterioration of the patient's hand, would generally indicate that the condition
condition. is chronic while non-pigmented keratic precipitates
would indicate a more acute inflammation.' 3
(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
Figure 2. Medium sized to large keratic precipitates which are
redness results from congestion tithe deeper ciliary
commonly seen in granulomatous type of uveitis (A) front view, (B) as
blood vessels and therefore does not blanch with viewed thru slit lamp
pressure or diminish with the use ofvasoconstrictors.4
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
because of the presence of posterior synechia which
Figure 1. ciliary iniection. Note that redness or congestion is
accentuated in the limbal area, hence called perilimbal flush as well. This are adhesions between the iris and the anterior
type of redness is more commonly seen in uveitis and glaucoma capsule of the lens (Figure 4).L23 In some instances,
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 Flume S. Eye roil small pupil and an overlying pupillary membrane.
Waft peierce or oiary injection and diffusely distributed large non-
an inflammatory membrane may also cover the foiAcn-faU keratic precipitates. There is also a localized area
al irisMap" (ghee arrow)
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). note the presence of inflammatory cells in the anterior
chamber as a result of the inflammation. If the number
Anterior Chamber abnormalities. Protein leakage of inflammatory cells within the anterior chamber
from iris blood vessels that become affected by the becomes large, the cells accumulate and settle
inflammation would affect the clarity of the anterior inferiody, assuming a level referred to as hypopyon
chamber. This is referred to as flare. One may also (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

varying fundus -tgs depending on the anatomic area
of the uveal tract that is involved in the inflammatory Figure 8. (A) Vitreous snowballs. (B) Snowbanking in peripheral
process. retina. Both findings consist of aggregates of inflammatory cells. These
are findings commonly seen in patients with intermediate uveitis
If the inflammation is confined to the anterior segment,

ANCILLARY OPHTHALMIC DIAGNOSTIC
patients would have nomial funduscopic findings. Patients
EXAMINATIONS
with intermediate or peripheral uveitis may present with
vitritis or haziness of the vitreous. Fundus examination
Additional examinations may be requested to aid in the
may further reveal the presence of cellular aggregates
diagnosis of some conditions. The more commonly requested
in the vitreous ("snowballs') or in the periphery of the
retina referred to as "snowbanking" (Figure 8). In cases ancillary procedures include:
wherein the posterior segment of the eye is involved,
more frequently encountered findings in patients are (1) Ultrasound of the Eye. In most cases of uveitis, a view of
listed below: (Figure 9): the posterior portion of the eye is compromised due to the
presence of anterior segment pathology (cataracts, pupil
• Cystoid Macular Edema - seen as dullness or absence membranes, etc) or vitreous pathology. Ultrasonography
of the foveal reflex on direct ophthalmoscopy gives the clinician a picture of the posterior segment and
• Vasculitis - often comes in the form of perivascular 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
pr000e.s 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.
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.
In 1987, the International Uveitis Study Group (I USG) developed

criteria based on the anatomical location of the inflammation.
Figure 9. Posterior segment findings in uveitis (A) Vitreous haze with
In 2004, the Standardization of Uveitis Nomenclature (SUN)
macular edema in a patient with Behcet's Disease, (B) Vasculitis as classification for onset
evidenced by perivascular sheathing (white arrows), (C) Posterior pole working group added criteria for
granuloma obscuring clear view of the optic disc, (D) Retinal pigment duration and course of the disease.9
changes in a patient with serpiginous choroidopathy
Based on the primary anatomical structure involved, uveitis is process primarily involves the choroid and/or retina. Specific
classified as anterior, intermediate, posterior or diffuse/panuveitis terminology such as "choroiditis" and "retinitis may be used if the
(Table 1, Figure 10) As implied by the term, anterior uveitis, this choroid or retina is inflamed respectively. If both structures are
type of inflammation primarily affects the anterior segment of involved in the inflammatory process, this may be referred to
the eye. It can also be called iritis when inflammation primarily as "chorioretinitis" or letinochoroiditis", depending on whether
involves the iris. Usually, both the iris and ciliary body becomes it is the choroid or retina that is the primary location of the
inflamed and this is called iridocyclitis. Intermediate uveitis refers inflammation. Aleuroretinitis refers to posterior uveitis wherein the
to inflammation involving the ciliary body, anterior vitreous, optic nerve is also involved in the inflammatory process. When
peripheral retina and the pars plana (middle portion of the ail weal structures (iris. ciliary body, choroid) becomes inflamed,
globe). Posterior uveitis is the term used when the inflammatory this is caled ponuveitis or diffuse uveitis. Most cases of anterior and
totermedhate uveitis are idiopathic in nature while most posterior
Table 1. Anatomical Classification of Uveitis aid diffuse uveitis have an identified etiology or constitute a
presentation of a systemic condition.
Classificati°n'41111
Mother method by which uveitic conditions are classified
Anterior Uveitis anterior segment is based on the course of the condition (Table 2). As can
iritis iris be seen from the table, acute cases are differentiated from
cyclitis ciliary body recurrent or chronic type by their generally sudden onset
iridocyclitis both iris and and limited duration (often less than 3 months). When the
irdlammatory process persists beyond three months, these
Intermediate Uveitis pars • '
an me labeled as recurrent or chronic depending on presence of
periods of reactivity between periods of exacerbation. Cases
Posterior Uveitis posterior secrnerr_ c. with periods of inactivity are labeled as recurrent while those
retinitis retina without are labeled as chronic cases?
choroiditis
retinochoroiditis 7-0—Je •221tr
. —cr-1.1 Table 2. Climikaim of Live& based on Course of the Disease
chorioretinitis -;
• Sudden onset and limited duration
Diffuse Jorix1 7BC* • acute anterior uveitis presents with many
UveitislPanuveitis 3t: cells and severe flare
• cells generally smaller in size and flare is
conspicuous
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 non-
granulomatous. 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
Lastly, the various uveitides can be classified based on the
Diffuse/Panuveitis etiology of the inflammation as presented in Table 4. Etiology
is often arrived at after conducting laboratory investigation.
Figure 10. 5E--s `_v or veitis is based on localization of With the aid of careful and thorough medical examination,
the infiamma::- (A) Anterior Uveitis :nmary site is the anterior
segment, (B) Intermediate uveitis - solves the anterior vitreous, one can request for the appropriate laboratory examinations
peripheral retina and pars plena. (C) Posterior uveitis. involves that can confirm the etiology of uveitis.
the retina andlor choro: When all three areas are involved.
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 A complete diagnosis of uveitis should generally include all
these (anatomic involvement, duration and course, etiology)
Features Granulomatous Non-
as well as the level of activity of the inflammatory process. For
granulomatou
purposes of this manual, however, the latter classification shall
Structures usuail entire uveal usually anterior not be discussed.
involved tract segment only
Onset insidious sudden TREATMENT OF UVEITIS
Course often chronic acute with
exacerbations and As with any oisease condition, therapeutic intervention should
remissions be based on a thorough clinical evaluation of the patient and
Characteristic Features sound therapeutic guidelines. Therapeutic goals in the uveitis
patients indude (1)control of inflammation; (2) prevention and
keratic large greasy (mutton fine or small
treatment of vision-threatening complications; (3) alleviation
precipitates fat)
and relief of the patient's symptoms; and (4) treatment of the
posterior forms during acute less likelihood of underlying cause
synechia inflammation. often synechia formation
at location of
Inflammatory coneoltakes into consideration both immediate
nodules
and long-term caned since adequate inflammatory control
iris nodules frequently present generally absent is also the key it minimizing the development of unwanted
posterior with granuloma frequently spared complications of the inflammatory process. Drug classes that
segment are well suited fur immediate control may not be appropriate
for long-term usedue to the side effects that accompany their
prolonged use.
Table 4.
Group
Bacterial
Etiology of welt s
• Tubercul:,
Etiology Aim. 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
~~ Syphilis
underlying infection has been adequately addressed. While
Viral • Herpes simplex ideal for iminnediaseinflarnmatory control, the long-term use
• Herpes zoster of this class of dogs is not encouraged due the unwanted
• Cytomegalovirus systemic andeaslartdeeffects that accompany them when
Fungal • Histoplasmosis taken for prolonged periods- Steroid-sparing therapies in
• Coccidiomycosis the form of non-soesoidal anti-inflammatory drugs (NSAIDs)
and immunoinodulalosy drugs should be considered if it
Parasitic • Toxoplasmosis
becomes apparent that therapy will be required for more
• Toxocariasis
than three months. Table 5 lists some of the various drugs
• Onchocerciasis
currently in use for the control of inflammation in uveitis
Immunologic • Lens induced iridocyclitis patients. The choice of which specific agent to be used is
• Sympathetic ophthalmia based largely on its efficacy and tolerability in a particular
Systemic • Reiter's Disease patient situation.
• Sarcoidosis
• Collagen Disease Cycloplegic agents are used to prevent adhesion of the iris to
• Rheumatoid arthritis the anterior lens capsule (posterior synechia formation), which
• Multiple sclerosis =gm can lead to pupillary block and elevated intraocular pressure.
They are also used to break recently formed posterior synechia
• Vascular Disease
and to stabilize the blood aqueous barrier and therefore
Neoplastic Reticulum sarcoma prevent further protein leakage (flare). The shorter acting
Lymphoma agents (tropicamide and cyclopentolate) play a role in
Miscellaneous • Heterochromic iridocyclitis preventing new posterior synechia formation as their shorter
• Pigmentary syndromes 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
Both conditions may result from either the inflammation
Selection of 10P lowering
itself or prolonged steroid use.
agents would depend on the mechanism of glaucoma. When
Table 5. List of Commonly Used Anti-Inflammatory Agents used for Uveitis Cases
I.Corticosteroids • Inhibition of cyclo-oxygenase and Topical • elevation of 10P

lipooxygenase pathways • cataract
• Decrease complement levels • exacerbation of infection
• Decrease migration of lymphocvies • corneal or scleral thinning/
• Decreased production of vasoactise amines perforation
and interleukins Periocular • Same as topical
Decreased circulating monocOes • Ptosis
Decreased macrophage act* • Scarring of Tenon's capsule
• Scleral perforation
• Hemorrhage
• Abscess
Systemic • 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
II. Immunosuppresive -7-77'e--e.S. NZ' Z.P.A. sratess a-c x4.. a, All bone marrow suppression
Medications ■ terratogenicity
• increased risk of infection
A. Antimetabolites
Methotrexate !rj-Dloiate reductase • Hepatotoxicity

• Gastrointestinal upset
• Pneumonitis
• Stomatitis
Azathiopnne ;ter!. • Gastrointestinal upset

• Hepatitis
Mycophendez rtrubis .rre sprrne&s • Diarrhea/

• Nausea
L. Alkylating Age
Cyclophosphanide • Lymphotoxicity. cross-links DNA

• Hemorrhagic cystitis
• Sterility
• Increased risk of malignancy
B.T-cell Inhibitors
■ Renal toxicity
• Hypertension
■ Hirsutism
■ Tremor
■ Renal toxicity
• Hypertension
• Neurotoxicity
• Hepatitis
• Diabetes
6 RED EYE, TEARING AND DISCHARGE 1 6.2 Uveitis and Scleritis

medical intervention fails, patients are advised to undergo Table 6. 7 =e-e-t 2', c- between Scleritis and Episcleritis
surgery. Cataract surgery is likewise advised for patients when
the degree of visual disturbance warrants it. Episcleritis Scleritis
redness severe, radiating eye

Specific therapy is also directed towards the relief of eye pain
pain
and photophobia which are common symptoms of acute ZZ:g
anterior uveitis. Topical instillation of mydriatic/cycloplegic bright red bluish red
111111hkess
agents relieve pain by immobilizing the iris. Longer acting Tenderness rare present
agents such as atropine and homatropine are ideal for this
4" to 5th decade zIth to 61h decade
purpose.
Gender frequently females frequently females
In cases where the underlying cause for the inflammatory of cases 50% of cases
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.
EPISCUMITIS
The choice of specific treatment also takes into consideration
the degree/severity and location of the inflammatory process. Episcleritis is a benign inflammatory disease characterized
Administration via the topical route is useful primarily in by edema and celkilar infiltration of the tissue between the
patients who have anterior uveitis, as topically applied drugs conjunctiva and sclera, the episcleral tissue. It is a self-limiting
poorly penetrate the posterior segment. The periocular condition usualy lasting for one to three weeks. Episcleritis
route is effective for administering anti-inflammatory agents usually occurs in the fourth to fifth decade, with females
to patients who have intermediate uveitis, posterior uveitis, being more affected by males. Eye redness in this condition
or cystoid macular edema, particularly if the condition is is commonly confined to the interpalpebral area and would
unilateral. It may also be beneficial in patients who have blanch on pessuie or topical instillation of vasocontrictors like
severe anterior uveitis found to be unresponsive to topical phenylephrinE Patients often complain of mild discomfort,
therapy. Periocular injections may be given via various routes: described as sWit adze, feeling of heat or irritation in the
subconjunctival, subtenons or retrobulbar. The selection involved eye_ Male commonly unilateral, the condition is may
of the location for the injection would depend on the site be bilateral in one thiud of cases.1°
where higher concentration of the anti-inflammatory agent
is desired. Periocular injections of corticosteroids should Episcleritis is trite- &wit:led into two clinical types: simple
be avoided in cases of infectious uveitis (e.g.toxoplasmosis) diffuse and nodiaiar Rpm 11). Table 7 summarizes the
and should be used with caution in patients who have a various lean/ES Cif tl'ese Nrio types.
history of corticosteroid-induced 10P elevation. Intravitreal
injections may also be given in cases where the primary site of
inflammation is the posterior segment.
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 Nodular Episcleritis
Frequency more common
Course often self-limiting (2-19 days . :a(es longer to resolve (4-6 weeks)
Characteristic Features
- injection of invoier; a-ea - , _ with movable non-tender nodule
- often without disccr7‘art - :: :3 , -:re painful
- may be recurrert teccrres - -3 associated with systemic
frequent in 3 to 4 yea's
Since majority of episcleritis resolve spontaneously, these Tne primary sign of scleritis is redness which is gradual in
patients frequently do not seek consultation. However, onset and has a characteristic bluish-red tinge that may be
since it is an inflammatory condition, patients who come in best observed under natural light (Figure 12). Such redness
for discomfort may benefit from a regimen of topical anti- fails to blanch with local instillation of vasoconstrictors.
inflammatory agents and lubricants. 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
Systemic associations are found in about one thild of patients
with episcleritis. This is however not correlated to the type. described as severe and penetrating with radiation to the
laterality or chronicity of the disease. Systemic conditions forehead, brow, jaw or sinuses. It can be severe enough to
associated with episcleritis include connective tissue ciseases keep patients awake at night and may be exacerbated by
(rheumatoid arthritis, SLE, relapsing polychonckitisk 827- touch. Analgesics provide only temporary relief of the pain.
associated conditions (spondyloarthropathits, inflammatory Aside from these, patients may also present with tearing,
photophobia and at times decreased vision which results
bowel disease); vasculitic diseases (polyarteritis noclosa.
Behcet's disease, Wegener's granulornatosis, giant cell arteritis, from extension of scleritis to adjacent ocular structures
Cogan's syndrome); infections (herpes, bacterial, fungal, leading to keratitis, uveitis and sometimes even glaucoma,
parasitic) and some miscellaneous conditions ( atom. rosacea. cataract and fundus abnormalities.1°
gout). 10,11.12
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
Figure 12. Typical redness seen in patients with scleritis showing
degree. The condition has been reported to occur bilaterally characteristic bluish-red tinge (best seen under natural light).
and is recurrent in about one third of cases. 1"
Scleritis is commonly assnriated with systemic autoimmune Classification of Scleritis. Based on the location of the
disorders, induding rheumatoid arthritis, systemic lupus inflammation, scleritis is classified into anterior and posterior
erythematosis, spondyloarthropathies, Wegener granulomatosis, type." Figure 13 shows representative photographs of
polyarteritis nodosa and giant cell arteritis. Scleritis may even various types of scleritis. Rarely, a patient may present with
precede other symptoms associated with these systemic illness. both anterior and posterior scleritis.
Diagnosing scleritis. As with uveitis, a thorough and 1. Anterior Scleritis. Anterior scleritis can be diffuse,
complete history is essential in making a diagnosis of scleritis. nodular, necrotizing with inflammation (necrotizing),
Aside from the patient's major complaint and history of present and necrotizing without inflammation (scleromalacia
and past illness, investigate as to any history of infection, injury perforans). The most common clinical forms are
or surgery. A thorough review of systems will also assist in diffuse scleritis and nodular scleritis. Necrotizing
determining if the ocular disease is related to any systemic scleritis with or without inflammation is much less
condition.
6 RED EYE, TEARING AND DISCHARGE 1 6.2 Uveitis and Scleritis
frequent, more ominous, and frequently associated
with systemic autoimmune disorders.
a. 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
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 yellow-
gray 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. 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.
Figure 13. Four types of anterior scleritis: (A) Diffuse Sdentis, (B) Frequently, patients are older than 50 years and
Nodular Scleritis, (C) Necrotizing scieritis, (D) Scleromalacia perforans
showing choroid 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
,rif Fe-111-1,r1
may reveal disc swelling, choroidal folds, serous systemic corticosteroids, nonsteroidal anti-inflammatory
retinal detachment, uveal effusions and macular drugs or immunomodulatory drugs. In cases where scleritis
edema. B-scan ultrasonography, the key to making a is suspected to have infectious association, anti-inflammatory
diagnosis of posterior scleritis, may show flattening of therapy should never be started without accompanying or
the posterior aspect of the globe, variable degrees of prior treatment with antimicrobial therapy. 10,11,12
thickening of the posterior coats of the eye (chc-
and sclera), associated with edema of the retrot
space. Accumulation of fluid in the tenons s: CONCLUSION
manifests as the characteristic "T" sign (Figure 14)
seen on B-scan ultrasound:3 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
Figure 14. Accumulation of lkid in lie lims woe Essissis as toe
permanent visual impairment may be avoided.
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
RECOMMENDED
these conditions As with theitt. selection of diagnostic./laboratory FOLLOW-UP ACTIVITY
examinations is aimed at confirrring or rejecting suspected systemic
association and, should therefore be guided by information It is recommended that the students be given demonstration
gathered from the patient's history and physical eamination. sessions on how to properly conduct history-taking
and ophthalmologic examination of patients with
Treatment. In majority of cases, topical anti-inflammatory
ocular inflammation. Following this exercise, it is further
therapy is inadequate and would require systemic therapy.
recommended that the students be provided clinical sessions
Treatment should be incbvidualized based on the severity
to allow them to see actual cases of patients with uveitis and
of the disease, prior response to treatment and presence of
scleritis.
associated disease. Non-infectious scleritis is treated with
Table 8. Systemic Diseases Associated with Sderitis
rheumatoid arthritis (RA) viral (herpes zoster, simplex, mumps)

systemic lupus erythematosus bacterial (tuberculosis, syphilis.
B27 spondyloarthropathies Pseudomones, Hemophilus, Borellia)
inflammatory bowel disease fungal
relapsing polychondritis (RP) parasitic
Wegener's granulomatosis
rosacea
polyarteritis nodosa gout
Behcet's disease chemical injury
giant cell arteritis Psoriatic arthropathy
Cogan's syndrome Psoriatic rash
6 RED EYE, TEARING AND DISCHARGE 16.2 Uveitis and scleritis 129
2. Shown are representative pictures of eye redness.
REFERENCES Which of these pictures best corresponds to that found
in patients with uveitis?
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
ed. 1996.
4. 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): 389-
96. 3. The most frequent complaint of patients with uveitis is
13. Biswas J et.al. Posterior scleritis: Clinical profile and A. disturbance in .
imaging characteristics. Indian J Ophthalmol 1998; 46:195- B. eye pair
202. C. eye rec
D. itchiness
4. Signs that would lead to a working impression of uveitis

SELF - TEST would be
A. ciliary injection, irregularly-shaped reactive pupil,
1. Inflammation involving any portion of the uveal tract normal OOP with enlarged cup to disc ratio
(iris, ciliary body, choroid) is collectively referred to as B. ciliary injection, mid-dilated unreactive pupil, corneal
A. conjunctivitis edema, high 10P and pale optic disc
B. keratitis C. ciliary injection, small constricted irregularly shaped
C. neuritis poorly reactive pupil, low lOP with normal fundus
D. uveitis findings
D. diffuse eye redness, central corneal opacity, high lOP
with limitation of EOMs
5. 8-scan ultrasound findings that support presence of See answers to Self-Test on page 222
posterior uveitis
A. calcific deposits in the vitreous
B. choroidal detachment PRACTICE CASES
C. choroidal thickening
D. funnel-shaped retinal detachment Case 1. 50 year old female presents with a history of three-
E. vitreous hemorrhage month duration of blurring of vision and redness in the left
.e. She denies any other associated symptoms but claims to
6. Inflammatory cells can present as any of the following, - and off eye redness in the past year. Ophthalmologic
EXCEPT 2 - 3n revealed the following findings:
A. "snowballs"
Best Corrected %%ion- 00 = 6/21 OS = 3/60
B. flare
Intraoake = s a OD = soft OS = hypotonic
C. Keratic precipitates Ws OU: full
D. Koeppe nodules _rduscapy: 00 - essentialy normal funduscopic findings
E. Posterior pole granuloma - no ROR noted due b a very hazy media
7. Characteristics of granulomatous uveitis Right Eye Left Eye

A. acute onset
_ : 1-.Jt 6/21 6/30
B. diffusely distributed fine keratic pre( .:.,-= Soft Soft
C. often involves both eyes EOM'S Full Full
D. often involves the entire uveal tract
E. tend to present with hypopyon c-retscopi (+)ROR, slightly
(+)ROR- sightly hazy
merle, distinct disc hazy media,
8. Uveitis may be associated with bocteriai ilections. borders, CD 0.3, AV distinct disc
Common bacterial infection that may ~rifest it the 2:3, no hemorrhages, borders, CD
no exudates, slightly 0.3, AV 2:3, no
eye as uveitis
dull fovea reflex hemorrhages, no
A. histoplasmosis exudates, slightly
B. toxopolasmosis dull foveal reflex
C. tuberculosis Sit Late Clear cornea, formed Clear cornea,
D. typhoid Findings anterior chamber, (+) large non-
(+) medium to large pigmented KP's, (+)
9. A patient presenting with localized eye reckless of four non-pigmented KP's, cells, (+)flare, (+)
(++)cells,(++) flare (+) Koeppe nodules,
days duration associated with eye pain is shown in the
Bussaca nodules moth eaten iris
photo. Upon instillation of topic . f!' ctors, yo u
did not note any blanching of the .esse s patient is
Slit Lamp Findings:
most likely to have
A. conjunctivitis OD - dear cornea, no cells or flare, no keratic precipitates, normal appearance
B. episcieritis of the iris, (+) lens opacity
C. scleritis
OS - clear cornea (+) peri-limbal flush, (+) cells/(+) flare. (+)fine. pigmented and
D. uveitis 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?
10. Systemic condition more frequently associated with

3. What ancillary procedure may be useful in
scleritis
A. hypertension
determining the presence or absence of posterior
B. allergy 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 Right Eye Left Eye
bilateral blurring of vision. History reveals that the patient first
experienced eye redness in the left eye about one year prior 6/6 6/7.5
Visual Amity
to consultation that was associated with photophobia and
Gym Elam Rosacea facies; normal pupillary reflexes; normal eyelids
blurring of vision. Consult was done at that time and symptoms
allegedly resolved with unrecalled topical medication. About 15mm Hg 12 mm Hg
10P
1 month prior to consultation, the patient noted recurrence of
Full Full
symptoms in the left eye and a week later, experienced similar BOBIS
symptoms in his right eye. He also noted the presence of oral normal normal
ROIIIIIIIIN
ulcers. The rest of the history was unremarkable.
essentially normal localized redness
clamp
Ophthalmologic examination at time of consultation revealed findings temporally (pls. refer to
Fib
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
1. iE
,
'--,, pa-Jent's history and eye findings, what are
also had a hysterectomy about 2 years ago. Her family history
L mmentud diagnoses?
was positive for glaucoma (grandfather), diabetes mellitus
2. oil you differentiate one condition from
and tuberculosis (grandmother). The rest of her history was
unremarkable. _itilier?
Answers tr, liactice Gases on page 222.

Ophtha Exam revealed the following findings:
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

1. Define the symptom of tearino oelveen laairnation and epiphora).
2. Enumerate the common conditions -.not aaealssing
3. 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
10-15mm
either due to increased production (lacrimation) or from
impaired drainage (epiphora).
The tear film has unique characteristics (Table 1). It is

composed of three layers: an outer oily layer (oily secretions - 12mm
from Meibomian and Zeis glands), a middle aqueous layer
R. antrum
produced by the lacrimal gland and glands of Krause and 5mm
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
.;:41
layer is important for proper wetting of the cornea The pH of fl... - 1_ Lacrimal drainage system (1=valve of Rosenmuller, 2=valve of Hasner
tears averages 7.4 'polars at inferior meatus underneath the inferior turbinate)
Table 1. Characte- os of the Tear Film toseign bodies, misdirected lashes, corneal ulcers, etc. Tearing
in these situations is the body's attempt to wash out the eye
Thickness of thefrritanr
Number of Layers 3
Thickness of the Aqueous Layer Note that patients with dry eye can also manifest with tearing
6 5 Li-
-ems wing). Generally, patients with mild to moderate
Tear Volume 6 - 8 pi MA
ry eye may complain of tearing which is mostly a reflex
Tear Production 1.2 ;es mechanism to compensate for the 'lack of tears Slit lamp
examination show an abnormal tear meniscus. Decreased
The lacrimal drainage system begins at the punctum leading production af ters may be confirmed
by doing the Schirmers
to the canaliculus to the lacrimal sac down to the nasolacrimal *estllmeed Doty).
duct. The duct opens at the inferior meatus under the inferior
turbinate (Figure 1).
HISTORY TAKING IN PATIENTS
WITH LACRIMATION
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 irriporiara questions to oe asked in a patient's history include
the following
of tears in the eye, while increased evaporation (decreased
humidity, prolonged reading, eyelid retraction, etc) will lead to
History of trauma is asked to rule out conjunctival or corneal
a relative lack of tears.
foreign bodies. corneal abrasions. Individuals engaged in
certain occupations (Le. carpenters, construction workers,
Therefore, when seeing a patient complaining of tearing,
etc) are more peecksposed to foreign bodies in the cornea or
the doctor, through history taking and ocular examination, conjunctiva. Lacerations may involve the lacrimal gland or
determines if there are potential causes of increased tear any part of the drainage system which can affect the amount
production (foreign body, conjunctivitis, eyelid malposition). of tears present in the tear lake. Canalicular lacerations should
Once this is ruled out, he may consider the tearing to be due to be suspected when there is a lid margin laceration within 5
impaired drainage (nasolacrimal duct obstruction, canalicular mm of the medial angle of the palpebral fissure. Associated
obstruction, etc). 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
I. INCREASED TEAR form of viral conjunctivitis, while allergies are often associated
PRODUCTION (LACRIMATION) with itchiness.
Tearing is more commonly caused by increased production. It is Previous consults with a doctor, medications used, and history of
important to get a thorough history and physical examination ocular surgery should also be asked. This may suggest a chronic
in order to determine the cause of tearing. Ask for: history process or that tearing may be a result of prior intervention or
surgery. It is important to establish a timeline of consultations,
of trauma, eye redness, use of medication, photophobia,
surgeries, and medications used in order to figure out when the
and blurred vision. Patients who complain of foreign body
symptoms started and how they responded to therapy.
sensation can have conditions such as corneal or conjunctival
Onset and duration of tearing is asked. Tearing that worsens Basal Secretion Test: Schirmers Test may be performed
during prolonged reading or exposure to low humidity with topical anesthetic (such as proparacaine). This test
conditions may indicate a "dry eye While reading or working measures the amount of tear production without the reflex
with the computer, we tend to blink less often which results component (basal secretion).
in increased tear evaporation that, in turn, signals the lacrir- -
gland to produce more tears. These situations uncover t- - MANAGEMENT OF LACRIMATION
presence of dryness or tear instability. Dry eyes are mc - ,
common in the elderly. Both dry eyes and nasolacrimal duct Management of lacrimation is generally directed to
obstruction are more common in women. address the underlying cause of tearing. Management will
range from antibiotic eyedrops for patients with bacterial
History of medical problems particularly allergies and/or sinus infections, removal of foreign bodies for patients with
disease should also be asked. conjunctival or corneal foreign bodies to eyelid surgery for
patients with misdirected lashes, entropion or ectropion.
EYE EXAMINATION IN PATIENTS WITH Correction of these conditions will result in the resolution
LACRIMATION of the patient's tearing.
A thorough ocular examination (visual acute gross

examination, EOM's, tonometry and funduscopi) is necessary
II. DECREASED TEAR DRAINAGE
to determine the cause of a patient's tearingTheeiamination (EPIPHORA)
of patients with lacrimation should foas on the anterior
segment. Any injury or inflammation invoking the lashes. Tearing due to blocked tear drainage can be a very
cornea, conjunctiva, anterior chamber and iris nil res.* in bothersome symptom. Patients frequently carry along
some form of tearing. Ectropion (outward turning of the ids) boxes of tissue paper in order to constantly wipe off
and entropion (inward turning of the ids) may cause ocular overflowing tears. Chronic epiphora can sometimes be
irritation that also leads to tearing. caused by or lead to infections of the lids and lacrimal sac.
DIAGNOSTIC TESTS FOR PATIENTS WITH Any point of the lacrimal drainage system can be blocked:
LACRIMATION from the punctum to the canaliculus, lacrimal sac, and
the nasolacrimal duct. Punctal stenosis can be visualized
Schirmers Test I Tnis directly or with the use of a slit lamp. Canalicular stenosis
reflex tearing. A specially designed Whamonfilierpaper called can be confirmed with probing while a lacrimal apparatus
a Schirmers strip is placed at the junction &the lateral and irrigation is often necessary in orderto diagnose nasolacrimal
middle third of the lower eyelid viithout anesthetic The patient duct obstruction. Blockage may be due to scarring from
can keep the eyes either dosed or open. The strips are then inflammation or topical medication, from injury (canalicular
gently removed after free minutes. The demarcation between transections), or from dacryoliths or lacrimal sac tumors.
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 Punctal ectropion associated with lid laxity can
of 5 mm or less in 5 minutes would support a diagnosis of dry contribute to decreased outflow of tears. Conditions
eye (Figure 2). such as Bells palsy or weakness of the CN VII may also
cause physiologic pump failure of the lacrimal drainage
11111111111111r 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

Dye Disappearance Test (DDT): This assesses the presence or
HISTORY TAKING IN PATIENTS WITH
ce of adequate lacrimal drainage. Fluorescein is instilled
EPIPHORA on the cul de sac of both eyes. Asymmetric clearance of the dye
within 5 minutes indicates relative block in the side with dye
Nasolacrimal duct obstruction (NLDO) should be suspected retention. Retention of dye beyond five minutes in one eye is
in patients with tearing who have normal anterior segment
also indicative of blockage (Figure 4). DDT does not distinguish
examination (i.e. no abnormal finding that can explain the between mechanical blockage and functional blockage.
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.
Infants with history of tearing shortly after birth should be

suspected of having congenital nasolacimal duct obstruction_
-is L. Cloyantill nasolacrimal duct obstruction with dye retention in

DIAGNOSTIC TESTS FOR PATIENTS WITH - Isanoearance test
EPIPHORA
MANAGEMENT OF EPIPHORA
Probing : a fine blunt probe can be inserted through the
punctum and canaliculus in order to determine the patency of
Management d nasolacrimal duct obstruction is surgical. A
the upper lacrimal drainage system. Probing may also confirm
daarcynollinostomy (DCR) is performed for adult patients
the presence of canalicular transections in patients with
with sysnoingsk and complete nasolacrimal obstruction.
history of trauma (Figure 3).
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
Figure 3. A gauge 25 lacrimal irrigating cannula is inserted through the
bicanarratar titubation with silicone tubes or by performing a
punctum (exits at the distal cut end of the canaliculus), confining presence of dacryocystorhinostorny.
canalicular laceration
Epiphora in patients with CN VII nerve weakness or eyelid laxity
Lacrimal Apparatus Irrigation: This involves the irrigation of is managed by correcting the underlying lid laxity through a
normal saline solution through the punctum and canaliculus. lid tighteniv procedure.
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.
19. Stimulation of some cortical areas - thalamus,
APPENDIX hypothalamus, cervical sympathetic ganglia, or
the lacrimal nucleus
I. HYPERSECRETION OF TEARS
a. encephalitis
b. diencephalic epilepsy syndrome (Penfield
A. Primary (disturbance of the lacrimal gland)
syndrome)
c. Giant cell arteritis (temporal arteritis)
B. Central
d Hypothalamic tumors
1. Central nervous system lesions
e Meningitis
2. Corticomeningeal lesions
f. Page syndrome
3. Emotional states
g Pseudobulbar palsy for Parkinson syndrome
4. Hysteria
• Sluder syndrome
5. Physical pain i Tic douloureux
6. Voluntary lacrimation, such as when acting ji various senile dementias
C. Neurogenic Gradenigo syndrome (temporal syndrome)

1. Ametropia, tropia, phoria and eyestrain and 21. Raeder syndrome (paratrigemial paralysis, cluster
fatigue headaches)
2. Caloric, lacrimal and reflex tearing - biatecal 22 Retroparotid space syndrome (Villaret syndrome)
lacrimation when syringing the ear with warm 23. Rhabdomyosarcoma
or cold water and during Tension testing 24. Rothmund syndrome (telangiectasia-
3. Crocodile or alligator tears - unilateral profuse pigmentation-cataract)
tearing when eating 25. Thermal burns
a. Congenital, often associated with ipsiaieral
paresis of lateral rectus muscle D. Symptomatic
b. Acquired with onset in way gage of
1. Bee sting of cornea
facial palsy Welts paby) or sequefia riots 2. Tabes
parasympathetic fibers to the aic gangicin 3. Thyrotoxicosis (Basedow syndrome)
growing back into superficial primal nem
c. Duane retractio- INADEQUACY OF LACRIMAL DRAINAGE SYSTEM
4. Bells palsy
5. Marin-Amat Syndrome .dram ea A. Congenital anomalies of the lacrimal apparatus
Jaw winking phenomenon) 1. Absence or atresia of lacrimal drainage apparatus
6. Mel kersson-Rosenthai syrwhorne OMeacersson 2. Amn iotocele
idiopathic fits° edema) 3. Fistulas of lacrimal sac and nasolacrimal duct
7. Drugs: atenoidt, ciprallokacin. dexamelhasone. 4. Waardenburg syndrome (lateral displacement of
diazepam, ketarnine, heflaran. inorPhine, the medial canthi with lateral displacement of
n ifed i pi ne. naloomme =-7
puncta and lengthening of the canaliculi
8. Exposure to
5. Obstruction of nasolacrimal drainage system
9. Glaucoma
10. Horner sync:troy -
B. Complications from diseases such as pemphigus,
11. Inflammation o _
Stevens-Johnson syndrome and lupus
uvea, cornea, orbit.
12. Lesions aliectirig *E
C. Dacryocystitis
a. ptosis
b. entropion/ ectropion
D. Distended canaliculi with obstruction, such as in
c. facial paralysis
Actinomyces israelii , papilloma or dacryolith
d. trichiasis
13. Morquio-Bradsford syndrome (MPS W)
E. Drugs such as: acyclovir, silver nitrate,
14. Myasthenia Gravis - afternoon ectropion
triflourothymidine, neostigmine,
(Erb-Goldflam syndrome)
fluorouracil, etc
15. Ophthalmorhinostomatohygrosis syndrome
16. Parkinson's disease
F. Punctal eversion
17. Reflex, such as vomiting and laughing
18. Sjogren syndrome
G. Goltz syndrome
6 RED EYE, TEARING AND DISCHARGE I 6.3 Tearing EN

6. Probing is most useful in tearing patients to:
H. Inadequacy of physiologic lacrimal pump
A. determine the level of obstruction in patients witt -
I. Traumaticlesions of the lacrimal drainage system canalicular stenosis
J. Tumor obstruction B. differentiate an upper from lower nasolacrimal du:-
system obstruction
K. Nasal disease C. dilate a stenotic canalicular system
1. Sinusitis D. dilate a stenotic punctum
2. Hypertrophic rhinitis remove foreign bodies in the canaliculus
7. Most common location of blockage in acquired NLDO is at:

REFERENCES canaliculus
3. intraosseus portion of NLD
1. Roy, F. Ocular Differential Diagnosis, 8th Edition, Fep C. punctum
International, 2009 D. valve of Hassner
2. Adler FH, Hart WM (Ed), Adlers Physiology of theEye. valve of Rosenmuller
Mosby 1992
3. Nesi FA, Levine MR, Lisman RD , Smith's Op- - 8. Definitive management of patients with NLDO:
Plasctic and Reconstructive Surgery, Mosby, I A. atropine eye drops
8 botulinum toxin injection
C. probing and irrigation
SELF-TEST a stewed antibiotic eyedrops
E. surgery
For questions 1-5 . What is the mechanism of tearing in the
following conditions? 77_ 'f Test on page 222.
Possible answers are
A: increased production
B:decreased drainage
1. canalicular transaction
2. facial nerve palsy
3. after cataract surgery
4. uveitis
5. trichiasis
7.1 Strabismus
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 innenabon. and actions_
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
complete ocular examination. irrickams basic moollity examination (extraocular muscle movement, corneal light reflex
test and cover tests)
- 'estations and principles of management.
4. Discuss the most common
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
1. 3n of strabismus
2. Types of strabismus:
3. Examination of the patient
4. Common types of strabismus
5. Systemic illness associated with strabismus
6. Psychosocial impact of strabismus
7. Principles of management of a strabismic patient
movement
only 15° to 20° -from primary position before head
I. ANATOMY AND PHYSIOLOGY
Occurs.
OF EXTRAOCULAR MUSCLES
Walk 1 summarizes the origin, insertion, actions and
The extraocular muscle is a specialized form of skeletal muscle
innervation of the extraocular muscles.
with several fiber types. At one extreme is a slow tonic type
resistant to fatigue and active in holding gaze straight ahead. MOTOR PHYSIOLOGY
At the other extreme is a muscle type adapted for participation
in extreme gaze. The high ratio of nerve fibers to eye mus = A. AXES OF FICK, CENTER OF ROTATION, LISTING'S
fibers (1:3 to 1:5) allows for more accurate control of muss PLANE AND MEDIAN PLANE
movement compared to other skeletal muscles. The ratio ir
other skeletal muscles ranges from 1:50 to 1:125. 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
ORIGIN, INSERTION, INNERVATION AND civatior;volutary vertica I rotations of the eye occur at this axis.
ACTION OF EXTRAOCULAR MUSCLES Z axis is a vertical axis; voluntary horizontal movements
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 Insertion Drre=,- ction from

Wow
Medial rectus Annulus of Zinn 5.5 mm from medial limbus
any Position
Innervation
Cranial Nerve
(MR)
Lateral rectus Annulus of Zinn 6.9 mm from lateral limbus Atilictan
(LR)
Superior rectus Annulus of Zinn 7.7 mm from superior
(SR) limbus
:1
Inferior rectus (IR) Annulus of Zinn 6.5 mm from inferior limbus Depression
Extorsion
Adduction
Superior oblique Orbit apex above Posterior equator at 51Z
Torsion
(SO) Annulus of Zinn superotemporal quadrant Depression
(functional origin at
Abduction
trochlea)
Inferior oblique Behind lacrimal Posterior to the equator in 51* E rc III
(10) fossa infero-temporal quadrant aton
Lbduction
The median plane is a sagittal plane passing antero-posteriorly the agonist. Table 3 shows the agonists with their respective
through the body, bissecting the head into symmetric parts. synergists and antagonists.
B. POSITIONS OF GAZES Table 3. Agonists with Their Respective Synergists and Antagonists
1. Primary position - straight ahead

Medial Rectus Superior rectus Lateral rectus
2. Secondary positions - straight up, straight down,
Inferior rectus Superior oblique
right gaze, left gaze
Inferior oblique
3. Tertiary positions - four oblique positions of gazes: up
and right, up and left, down and right, down and left for obriclue Medial rectus
4. Cardinal positions - Right and left plus the tertiary tenor oblique Superior rectus
positions (up and right, up and left, down and right, Inferior rectus
down and left) Inferior rectus
'Abla Superior oblique
C. PRIMARY, SECONDARY AND TERTIARY ACTIONS
gliOr oblique Superior rectus
Mer:.a rectus Inferior oblique
When the eye is in primary position, the horizontal
'ectus Inferior oblique
purely horizontal movers along the Z axis and have only a
primary action. The vertical recti have a direction of pull that rectus Superior rectus
is primarily vertical. However, the angle of pull from nie-or Superior rectus Superior oblique
to insertion is 23° inclined to the visual axis, giving f- Lateral rectus Inferior rectus
torsion and adduction. The obliques are incli-ed
visual axis, giving rise to torsion as their prima- . - Sherrington's law of reciprocal innervation states that an
some vertical and horizontal rotations as we Table 2 - - _ - and contraction of a given extraocular
actions of the extraocular muscles. musde accor-- aniedbya reciprocal decrease in innervation
— action of its antagonist. For example, as the right eye
Table 2. Action of Extraocular lAusoles From The Primary Pawky
—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 . of their respective eyes in a given direction of

gaze For example, as the eyes move to the left gaze, the right
Inferior rectus Depression Euclidean:10r
medial rectus and the left lateral rectus are simultaneously
Superior Oblique cc :- innervated and contracted.
Inferior Oblique Excycioductkn Eresancr
Each extraocular muscle in one eye has a yoke muscle in the
D. EYE MOVEMENTS 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 L
R
(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
corneal meridian.
An agonist is the primary muscle that is moving the eye in Figure 2. Cardinal Positions of Gaze and Yoke Muscles
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
eye as the agonist that acts in the direction opposite to that of
7 DEVIATION AND DISPLACEMENT OF THE EYE I

RSR LIO Sup Recti & Inf Obliques RIO LSR
RLR LMR PRIMARY POSITION RMR LLR
RIR LSO I nf Rect & Sup Obliques RSO 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
III. AMBLYOPIA
desired direction of gaze. Ordinarily, a patient with a weak
Andijapia is a condition in which there is a unilateral or
muscle in one eye will use the contralateral eye to fixate.
bilateral decrease in visual acuity that is not fully attributable
If he will be forced to fixate using the eye with the weak
to organic claim abnormalities. Table 4 shows the diagnostic
muscle, the increased innervation needed to maintain that
criteria for amblyopia.' It is usually caused by opacities in
eye at the center will be transmitted to the yoke muscle,
the media. high refractive errors, anisometropia (difference
causing increased amount of deviation in the normal non-
in refractive errors of the 2 eyes) or ocular misalignment or
fixating eye. 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
II. BINOCULAR VISION development of amblyopia.
The eyes are spaced 50 to 65 mm apart. The slightly different is diagnosed and properly treated,
The earlier an
image originating from each eye is fused in the brain as a
the better the chance of visual acuity recovery. However, all
stereoscopic image. Each eye must be directed simultaneously
children should be considered for treatment regardless of age.'
to the same object. Amblyopia usually results in lifelong visual loss if it is untreated
or insufficiently treated in early childhood.
The visual axis is an imaginary line that connects an object in
space with the fovea. In a person with normal ocular, sensory
The prognosis for attaining and maintaining essentially normal
and motor systems, the visual line in each eye intersects at the
vision in an amblyopic eye depends on many factors, including
object in space and there is binocular fixation. If visual lines
the age of the patient at diagnosis, the cause and severity of
are not directed at the same fixation point, fixation is by one
amblyopia, the history of previous treatment, the duration of
eye only.
amblyopia, and compliance with treatment.
Normal development of stereoscopic vision requires binocular,

There are two principles in treating amblyopia. The first is
simultaneous use of each fovea during the critical time that
to present a dear retinal image to the amblyopic eye by
occurs early in life.
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.'
Table 4. Diagnostic Criteria For Amblyopia' TYPES OF STRABISMUS:
11•111111111111r"' FindieMPOW
-
A. According to direction of deviation:
Unilateral Amblyopia . Horizontal - esodeviation, exooe\
Fixation preference Unequal fixation behavior 2. Vertical - hyperdeviation, hypodeviation
4
3. Torsional - excyclodeviation, incyclodeviation
Preferential looking 2-octave difference*
Best corrected visual 2-line interocular difference B.According to age of onset:
acuity U
Congenital, infantile - documented prior to age 6
Bilateral Amblyopia months
Best corrected visual Vision less than 20/40 ear" eye 2. Acquired
acuity
*2-octave difference is a 4-card difference in the set of Tee 4:41r." C According to fusion status (whether the deviation
Cards, which is equivalent to multiplying or dividing the visual arse can be controlled by fusion mechanism)
by 4
Phoria - latent deviation, controlled by fusion
mechanism so that under binocular condition, the
Table 5. Causes of Amblyopia
eyes remain aligned.
minvompepr- triple
Refractive
MEI 2. Intermittent phoria or tropia - fusion control present
part of the time
Myopia 2.00 D - 2.50 C - 3 Tropia - manifest deviation in which fusion control is
difference. dece- : not present.
Hyperopia 1.50 D - 2.50 C
difference. deQemci-r:. D. According to variation of deviation with gaze position
Astigmatism 2.00D-2 50 D or fixating eye
differerce _>:e-6n; 7 NA
1. Comitant - deviation does not vary with direction of
Visual Deprivation Ptos is c fmacro
gaze or fixating eye.
catarac4. eTiturp.kie
2. I ncom itant - deviation varies with direction of gaze or
Strabismus Es::-:_cc-xra *Nice-me
fixating eye. Most incomitant strabismus is paralytic.
Bilateral Amblyopia Exam* AMMON
Refractive E. According to fixation
Myopia 3 X 2 - X 2 3...e.1.11-ig :r 33e 1. Alternating - There is spontaneous alternation of
Hyperopia SS_:- 733e fixation from one eye to the other and there is no
Astigmatism 2:c2-312 3erie-bric r aoe. preference for one eye for fixation.
2. Monocular - There is preference for fixation with one
Visual Deprivation
eye.
Bilateral ptosis Sewell! Diet
Bilateral corneal 7trartarternit =153 2rir1:C.
opacities EXAMINATION OF THE PATIENT
MESSES 111101207C sr A. Historytaking: information should be obtained about

Bilateral cataract Scaadc. aulasorral dominant. the following
era -a.-iassve
- 1. Chief complaint
2. Age of onset - document onset with photographs
Bilateral
hemorrhage 3. Direction of deviation
4. Constant or intermittent
5. Alternating fixation or monocular fixation
IV. STRABISMUS 6. Magnitude of deviation
7. Associated eye complaints - diplopia, blurring of vision
DEFINITION OF STRABISMUS 8. Antecedent or concurring illness - seizures , diabetes,
hypertension, thyroid disease
Strabismus means ocular misalignment of whatever cause. 9. Trauma
When the eyes are not aligned or are "dissociated': strabismus 10. Previous consultation, treatment - patching, glasses,
is present. surgery
11. Maternal and birth history - maternal infection,
Orthophoria refers to the ideal condition of ocular balance, so
eyes are aligned in all directions of gazes at all distances even
prematurity
12. Developmental history
after occluding one eye.
13. Family history
7 DEVIATION AND DISPLACEMENT OF THE EYE 1 7.1 Strabismus 103

B. Ocular examination 3. Tests for ocular alignment
1. Visual acuity A. Corneal light reflex test (Hirschberg method)
Children often pose a difficult assessment problem. (Figure 4)
Various tests are available for visual acuity determination a. Ask the patient to sit facing you with head
(Table 6). The method of evaluating visual acuity varies straight and eyes directed in primary gaze.
according to the child's age and level of cooperation. For b. Hold a penlight in front of the patient's eyes
verbal and cooperative children, charts using tumbling at a distance of about 2 ft, directing the light
E or pictures can be used. The child's fixation pattern between the patient's two eyes. Instruct the
will give a clue as to the comparative vision of the two patient to look directly at the light.
eyes. For example, a strabismic child who can alternate c. Compare the position of the light reflex and
fixation in his two eyes will probably have equal visual record the estimated degrees of deviation.
acuity. Another strabismic child who prefers one eye to
fixate probably has a better vision in that eye compared
to the fellow eye. lit3ORTHOPHORIA
Table 6. Visual acuity testing in children
150 ESOTROPIA
Pre-verbal children Clinical methods ability to follow moving

(less than 24 target. presence or absence of fixation
months) preference. presence or absence of
nystagmus 300 ESOTROPIA
CSM I central. steady and maintained

Preferential looking techniques (Teller
acuity cards)
450 ESOTROPIA
Verbal children HOTV chart (four-letter shapes), tumbling
( 3-5 years) E chart
Lea symbols (shapes) from 36 months of Figure 4 :7-'63 Light Reflex (Hirschberg method)
age.
Literate children Snelier, chaos (letters or numbers) 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
2. Ocular motility examinations
in uncooperative patients.
The following clinical protocol may be used to assess
ocular movements:
a Ask the patient to fixate on a light.
b. Place increasing amount of prism on the straight
a. Sit facing the patient. Hold your finger or a
eye until the corneal reflex on the deviating eye
small fixation target 10-14 inches in front of the
is centered.
patient, with the patient in primary position
c. In patients with incomitant or paralytic
(straight ahead).
deviations, it is preferred to place the prism in
b. Ask the patient to follow target as you move it
front of the deviating eye.
into the six cardinal positions. When examining
down gaze, elevate upper eyelid with a finger of
C Cover tests
your free hand. The validity of a cover test depends upon the
c. Note whether the amplitude of eye movements patient's ability to maintain constant fixation on
is normal or abnormal in both eyes. Rate
an accommodative target. Each eye must be able
amplitude for all fields of gaze by considering
to move adequately when fixating. The cover-
normal amplitudes as 100%, and rate lesser uncover test is done to establish the presence of
amplitudes accordingly. To record relative over either a manifest deviation (heterotropia) or a latent
or underaction, designate normal as 0, that deviation (heterophoria). The alternate tests are then
is, no over or underactions are present. Use 4 performed to measure the deviation.
to designate maximum over or underaction.
Underactions are rated -1 to -4 while overactions C. 1. Cover-uncover test
are rated +1 to +4. a. Ask the p =nt to look at a distance fixation. The
d. Note any nystagmus and if present record its examiner should be seated slightly to the side of
direction and amplitude in specific field of gaze. 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
- a- Cycloplegia, 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. Esotropia or Infantile Esotropia

Figure 5. Krimsky Prism Test nwaro aeviation of the eye usually
-c or up to 6 months of age. The
b. Cover the fixating eye wit— 3- 3=44.0e, ,5oceAation is t z constant (Figure 6). Cross fixation
your hand and observe the =ler ar'!I :irfart. 1.5es rioht eye to look at left visual field and left eye
movement. Note its direction_ : may be present. There may be over
c. Uncover the eye and allow al a.>: 3 sec, tr a_-:..c.-- . 7ueS (Figure 7), causing elevation
both eyes to be uncove-ed =If 2 =IE.-action is usually appropriate for the
d. Cover the other eye =c-senie its tilos 4:Ir 3-- -E-ss than +2.0 D). Non-alternating esotropia can
any movement _ -3- ::: 3, Aside from the esodeviation, the patient is
e. After about one second, xii..„..re• 7.-te arc se normal. The child is best treated with surgery
observe it for any mmemere.. 5.3 months.
Repeat the test fix near using a neer '783.-.or
point. 2. Refractive Accommodative Esotropia
Repeat the -ear cat_ents accommodative esotropia usually starts at age
g.
eyeglasses. if apcic.-ac.ie 2 ;ears. The child has a significant hyperopia (+3.00 to
+10.00 diopters). In order to see clearly, he accommodates.
C. 2. Alternate cover test ,prism and cover test) Accommodation is however accompanied by convergence
a. With the at a of the eyes. Esodeviation is moderate in magnitude
distance" .Y - 7-3 approximately 30 prisms diopters. Convex or plus lenses are
from one e,e 7 2: prescribed to correct the hyperopia (Figure 8). Constant non-
allowing any periodd - t.- alternating accommodative esotropia can cause amblyopia
should be seated siright 7: 7- 7 ".." 7 and should be treated. Patient should have regular cycloplegic
facing the patient and at ar a -- 3 refraction and spectacle lenses should be changed if needed.
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 Figure 6. Congenital Esotropia, left eye
power unt ^ o me :ted in either eye
(neutraliza:
d. 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 Figure 9. (A) Left eye fixating, (B) Right eye
following: attempt to correct the cause of the poor vision, full
cycloplegic refraction, muscle surgery to correct the deviation.
5. Sensory Exotropia
4. Intermittent Exotropia
An e E.- seewell for any reason may turn outward.
Exotropia is an outward deviation of the eye. It usually starts
_-nent
Princip e. - ei-.- of sensory exotropia are the same as
out as intermittent and becomes manifest when patient is
'
that of sensory esouopia.
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
B. INCOMITANT STRABISMUS.
ophthalmoplegia are some of the dinical findings. Limitation
of elevation because of inferior rectus restriction is the most
1. Paralytic Strabismus
common motility finding. Patients complain of diplopia that is most
There is limitation of action of the involved muscle. The deviation serge r upgaze The thymid disease should be treated. Prisms
is bigger when the involved eye is fixating and in the direction of mote prescribed to aleviate If strabismus persists, surgery
action of involved muscle. Lateral rectus is the most frec _ may be done during the otiescent phase of the disease.
involved muscle as a result of abducens nerve palsy. The
should have a neurologic and systemic evaluation to Diabetes meatus
any underlying cause. Patients may have diabetes me metaboric ease involving small vessels
or hypertension. and causina widespread damage to tissues, including the eyes.
Patents — E. - 77- -77 777_7e onset diplopia due to infarction of a
2. Strabismic Syndromes aanial nerd a-c S C*1an extraocular muscle.
Motility disorders may demonstrate typical feature of a paroailar The attducens 'ectus are most often
syndrome. Examples are Duane syndrome, Brown syndicate, Aimed ithe =Jammu nerve . c ved, the pupil is usually
Mobius syndrome and congenital fibrosis syndrome vend Recovery of oaten - ;unction usually happens
sdiiiirs6rnanthr. Patching of one eye or use of prisms can relieve
Duane syndrome (Figure 10) is a congenital mcf.Tity disadec the dolma& Muscle surgery may be necessary if the deviation
usually unilateral, characterized by limited abduc-. ar Imaged oersigH s beyond six tar Rtn.
adduction or both. The globe may retract and e
may narrow on adduction. There may also be .:1- C- Illyasdieria
' gravis
downshooting of the eye. There may be a face 7_-7- -17 -- littiastrene grans a cnaracterized by abnormal fatigability of
patient to use both eyes together. Muscle - miliedumusides which improves after rest. Presenting complaints
correct significant face turn or a significa — ands and diplopia from involvement of one or more
gaze. _ should be evaluated and treated by
Brown syndrome is caused by restriction of 7"

tendon sheath, limiting elevation in acc_.7. -7...- D. Pieurcriogic conditions
in abduction. It may be congenital or acquinillieviiiessiciltas Cereolowasaaar disoroers arc INS space occupying lesions may
trauma or systemic inflammatory comic,: - - nusas one °fele c nical presentations.
Mobius syndrome is caused by a combir PSYCHOSOCIAL IMPACT OF STRABISMUS

nerve palsies, producing mask-lice 66E'
sometimes accompanied by adduction is may result in a negative impact on a child's self- image.
• can cause embarrassment in children especially when they are
- eased by their peers. Strabismus
was associated with significantly
Congenital fibrosis syndrome is a demo,
e- orse general health-related quality of life in preschool children.'
one or more extraocular musdes williasixamaapice7 w
muscle fibers with fibrous tissue
Studies on the impact of strabismus have been conducted in
both children and adults. By means of simulation photographs,
SYSTEMIC ILLNESS ASSOCIATED
strabismus was found to play a significant role in the selection of
WITH STRABISMUS playmates by children', influencing decisions on inviting children
to a party and in partner selection by adults.'
A. Thyroid disease
Grave's ophthaimpa .- 'ectng
Adults with strabismus may also suffer from discrimination
the extraocular muse: - Js and
in seeking employment A study among Swiss headhunters
orbital connective tiss.. — os and
orbital
Right Gaze Primary Gaze Left Gaze

Figure 10 T._ 3n in both eyes. There is
7 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 SUMMARY
myopia and under correct hyperopia).
Under normal binocular viewing conditions, the eyes
3.Prisms. Incorporation of prisms in spectacles may be useful in are aligned and the image of the object of regard falls
patients with acute onset of strabismus and diplopia and those simultaneously on the fovea of the two eyes. One of the eyes
with small deviations. may be misaligned (strabismus), so that only one eye at a time
viewsthe object of regard. Constant strabismus at an early age
4. Surgery. Muscles are chosen depending on the type and can Result amblyopia. In addition, any condition which can
amount of deviation in the various directions of gaze. Recession resuk rl pooreision can lead to strabismus. It is important that
is a muscle weakening procedure whereby a muscle is detached a physician is able to detect strabismus at an early age so that
from the eye, freed from its fascial attachments and then sutured early teatimes can be instituted. Early treatment improves
to the eye at a measured distance from the original insertion a patient% domes for good vision, binocularity and good
(Figure 11). A muscle is strengthened by resection, a shortening alignment.. Iliimoveledge of anatomy and physiology and skills
procedure. A measured amount is cut from the muscle which is in exam maps! cif the extraocular muscles as well as skill in
then sutured back to its original insertion site (Figure 12). 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/
PPP-
2. 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
Figure 11. Muscle recession
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
agents about strabismic subjects' ability to find a partner. directions of gaze the strabismus is
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.
Ophthalmology. Lange Medical Books : New York, x After removing the cover in one eye, the recently
10. Wilson, F.F. ed. Practical Ophthalmology. 1996. Maar- = = Empowered eye moved outward. The patient is
__
: American Academy of Ophthalmology. : : -
SELF -TEST
1. The agonist in elevating the left eyes & Accommodative esotropia is best treated
A. left lateral rectus
B. left superior rectus
C. left superior oblique
D. right inferior oblique
2. The superior division of the oc... es 9_ When doing the corneal light reflex test, and the light
the superior rectus and falls at the center of the pupil, the eye is
A. superior oblique - -
B. inferior oblique B.. -.E.-
C. orbicularis oculi C h„ zotropic
a hypertropic
D. levator palpebrae
E aligned
3. This test will disting u is , • .:

A. cover uncover tei: 1 0. Choose the correct statement about exotropia.
B. alternate cover test -,termittent exotropia resolve spontaneously as the
C. prism cover test child grows older.
D. modified Krimsky test B. Exotropia is best treated with spectacle correction.
C. Intermittent exotropes close one eye on exposure to
4. Example of incomitont sqi.int is bright sunlight.

A. congenital es :-• D. Intermittent exotropes usually have amblyopia.
B. intermittent =.-. -
C. accomm:::?.- Answers to Self-Test on page 222.
D. lateral recs pa
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. recognize a bulging eye
4. differentiate between a true proptosis and pseudoproptosis
5. evaluate the bulging eye in terms of measurement, direction. and dynamics
6. discuss the various clinical examinations that are utilized in the evaluation of proptosis
7. enumerate the common orbital disorders among adult patients
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

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
ADULT ORBIT position of the globe. Anterior displacement of the globe,
either axial or off-axis is the most common result of lesions
A knowledge of the anatomy of the bony orbit and its in the orbit It is possible, though quite infrequent, for orbital
contents is essential in order to gain a firm understanding lesions to retract the position of the globe.
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).
The forward displacement of the globe is also termed

Figure 1.Asche-3: --- - --- J, exophthalmos. Most physicians use these two terms
Stewart B and Goi::erg RA.' interchangeably, but some prefer to reserve the term
exophthalmos for the description of prominent eyes
The orbital cavity is tightly sunounded by bony walls on four secondary to endocrine disorders, such as thyroid-related eye
sides. The medial walls are parallel to one another and are disease (Figure 3B).
separated by the ethmoid sinuses~~(a width of 25 cm). The
lateral walls, which have the same length as the medial walls Proptosis may be real or apparent. On the initial encounter
(around 4.0 — 45 cm), are directed laterally and outwards, with a patient with a bulging eye, the first concern of the
subtending an angle of 45° (Figure 1, aqua arrow) from the
clinician is to determine whether the prominence of the globe
medial walls or the median sagittal plane (green arrow).
is a true proptosis or a pseudoproptosis.
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
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 Secondly. a huge globe may be misinterpreted as a
pseudoproptosis (Figure 4). One may be able to eliminate the proptosedetc_Itisfrequently observed among high myopes
possibilities through the help of an accurate history and ocular (near-sighted persons) and among pediatric patients with
examination, documentation of a previous ocular trauma or congenital 9auoorna_ Awareness of the spectacle history
inflammation, explicit information regarding past medical and/or perfooming refraction may detect the presence of
histories and treatments, as well as imaging studies. mr: --clatter displays a huge globe or a longer axial
Pseudoproptoses
Lid fissure Globe size Coreraimal

asymmetry asymmetry enophittairms Shallow orbit
alINSIMIIIIIMMII=C I
• Unilateral lid Enlarged globe Phlhisisbulbi
Craniosynostosis
retraction • High myopes • Old blow-out
• Contralateral • Congenital fracture
Homer's glaucoma Scirrhous
syndrome Small globe adeno CA of the
• Unilateral breast, kings rx
microphthalmos stomach
Figure 4. Differential diagnosis of pseudoproptosis. Adapted from Laws ER Jr.'

diameter with an axial diameter > 24.0 mm. An elevated Table 2. Classification of orbital tumors
intraocular pressure in an "expandable" pediatric eyeball, as
Primary Cystic
in congenital glaucoma, may likewise lead to an enlarged
Vascatar (tumors/anomalies)
globe. On the other hand, the presence of an abnormally
Mesenchymal (adipose/ fibrous/ osseous/
small globe (microphthalmos) in one side may give the
cartilaginous/ myxomatous)
impression of a prominent contralateral eye.
Ez al (lacrimal gland)
Thirdly, a normal-sized but retracted globe (enophthalmos)
adjacent ocular structures
may put on the appearance of a prominent contral&e -a.
These conditions are caused by an old blow-out fraz:_ -e : - intraocular
a metastatic tumor to the orbit from a primary scirrho_ Extraocular (lids)
From adjacent non-ocular structures
adenocarcinoma of the breast, lungs or stomach respective.
Nasopharynx/ paranasal sinuses/
cranium
Lastly, a shallow orbit causes a normal-sized globe to
Metastatic
This is exhibited in a craniosynostosis syndrome _
Crouzon's disease (Figure 5B).The characteristic'_ diseases wal orbital manifestations
as well as imaging studies are able to identify the air,:— Hematopoietic
Histiocytosis
TRUE PROPTOSIS Phacomatosis
The causes of true proptosis may be simply cavegtiviaed iltb

inflammatory and non-inflammatory diseases of die obi. The various entities that affect the orbit may appear
(Table 1) The inflammatory causes are furthersabdabledirao Ovisivdselmig but a systematic evaluation procedure which
infectious (e.g. orbital cellulitis) and non-ifeamitasa Non- includes an orbital as well as an ocular examination may
infectious inflammation, thyroid eye &seam is (Mika as nawow down the possibilities further. The following orbital
specific because there is an etiology apipendedseisbdeajair. evakiation is initiated to determine the etiology of the
namely a disturbance of the immune soon le Me Ovoid pep osier It describes the direction, measurement as well as
and the extraocular muscles. The abler disease
die dynamics and clinical behavior of the proptosis.
is idiopathic and non-specific because & to
any causal agent. s
DIRECTION
Table 1. Classification of orbital cleseasei
kiwag of me time a discussion on proptosis is readily presumed
to be an axial displacement of the globe in the anterior
Infectious Orbital cellidis direction. This is not always the case. Because orbital lesions
Non-infectious Soesic 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

Congenital
knowledge of the four surgical spaces within the orbit (Figure 6).
Tumors
Trauma
0 - Central space
The orbital tumors are further cassias rep primary, secondary • - Tenon's space
and systemic diseases with (Aid mankstatiOns (Table 2). 6 • - Peripheral space
O - Subperiosteal space
Primary tumors may original* from am tissue noun,* found
within the orbit (blood vessel nerve% connedive liSSUeS
Tenon's capsule
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
Lateral rectus
detected elsewhere unless they are totally eradicated on initial
treatment.
Figure 6. Surgical spaces of the orbit

7 DEVIATION AND DISPLACEMENT OF THE EYE 1 7.2 Proatcs s Egg
1. central surgical space or muscle cone — space within
the four recti muscles 1. A WYROwiri
2. peripheral surgical space — bound by the four recti

111111111
muscles and the periorbita
by the
3. Tenon's space — a potential space bound
Tenon's capsule and the outer coat of the eye Figure 8. Luedde Exophthalmometer
subperiosteal space- a potential space bound by
the
4.
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 Figure 9. Hertel Exopthalmometer
that the orbital mass is a lacrimal gland fossa lesion, most fielly two eyes.The Luedde and Hertel exophtalometers both utilize
a tumor derived from the lacrimal gland. Other examples of as the bases of measurement the most anterior part of the
orbital pathology in relation to direction of globe displacement cornea and the lateral orbital margin. The examiner stands in
are presented in Table 3.' 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 Lacrimal gland fossa tumor
.--,,,s,..rement of proptosis using the Hertel exopthalmometer
Mass in central surgical space Mucocoele from sinuses
Optic nerve tumor Subperiosteal abscess
A novel instrument that measures not only the anterior
Sphenoid wing tumor
(meningioma) 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
MEASUREMENT rims rather than the lateral orbital rim. It is useful for patients
with irregular or absent lateral orbital rims resulting from
An exophthalmometer is used to quantify the amount of maxillofacial trauma. 8
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.
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 RESILIENCY
without the benefit of an exophthalmometer, the examiner
stands behind a seated patient and looks over the head of the It is normal to be able to retrodisplace the globe by applying
patient. From this position behind the patient the examiner your thumb over the eyeball (Figure 13). In the absence
lifts both upper lids. The examiner observes and compares of any orbital pathology, one can easily push the eyeball
from above the head of the patient the degree of protrusion posteriorly because of the compressibility of the orbital tissues
of either cornea (Figure 12). 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. - Form 13. tr ae r. 7 . r ?obe

measured and compared with Caucasians (Table r -
is the asymmetry between the left and right orbtstliuttii Mare
important than the actual measurement A dikeremue et nue
than 2 mm between the two sides is considered Want ireenninent proptosis refers to varying degrees of eye
probusicxi as a function of change in the immediate
Table 4. Normal exophthalmometry values
eriviionment ofthe patient A stimulus may be internal such as
Aver. No a systemic infection; or external, like a change in head posture
Measurement or positionlhe proptosis is noted to increase in size followed
bya spontaneous resolution after the stimulus is removed.
Filipinos 13.5
Caucasians 16.0 a The proptosis in a child with capillary hemangioma may
increase noticeably fast when he is crying but resolves soon
DYNAMICS OF PROPTOSIS after (Figure 14). Another instance is an adult patient with a
mix or abnormally expansile venous channels. The proptosis
In evaluating the dynamics ofproci-:-._. "K":21-5 esacerbates when he bends forward into a prone position or
are considered: strains during a Valsatva maneuver.
1. resiliency
2. intermittency
3. clinical behavior / pulsating por-c,...1..,
4. duration
5. clinical course
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 DURATION

a sudden exaggerated eye protrusion in the presence of an
upper respiratory tract infection. This expansion is caused Duration of the orbital disorder is important in the clinician's
by increased vascularity in the tumor followed by bleeding formulation of differential diagnoses. It may be described as
within the lymph channels of the tumor, leading to the acute, chronic or subacute. An acute onset is accompanied
formation of "chocolate cysts". The lymphangioma is expected by a short history prior to consultation. It implies a rapidly-
to resolve spontaneously within a few months of conservative evolving disease entity like a malignancy or an inflammatory
management (Figure 15). 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 On the other hand, there are tumors which may spontaneously
regress. A capillary hemangioma grows rapidly during the first
The clinical course describes the growth characteristics of the year of life, then stops and continues regressing until the early
tumor. It also provides information on the rate and direction teens (Figure 20)_
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
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
The patient with a true proptosis undergoes a thorough

Figure18. 56-year old male viih a imortima -erwripoinait dm* um dnical evaluation. Utilizing the same routine eye examination
noted 17 years prior b ileac ccnsulatria. appied to any eye patient, certain special considerations are
emphasized For instance, in the gross examination, there is
Most malignant tumors, like thabCtr-teCsar--Irea 3- 104
particular attention focused on lid and conjunctival changes.
cystic carcinoma of the lacrimal gland yes hawri; a short
Lid retraction and/or lid lag are almost pathognomonic of
duration of history of less than a "east. rapid progiession.
thyrOid-related eye disease (Figure 21). Pupillary reaction
A faster and more explosive course of 'Flat a steel& 6 seen
is also doubly appraised because of optic nerve dysfunction
in orbital cellulitis. Occasionally. the berms clinical course
secondary to compression by a tumor or enlarged extraocular
of thyroid eye disease may proceed ttu IGNOC r1101:40515 after
muscles.
radioactive iodine therapy or surgital thponeCtorny. in as
these conditions, the sudden resultant mouse can damage
the integrity of the cornea Mime 11It
Figure 19. 19 year old female ctiagnosedw i alluse toxic goiter Her Figure 21. Bilateral lid retraction in thyroid eye disease
rapid proptosis of less than one month duration has resumed n severe
bilateral lagophthalmos and intunous exposure Manges b the cornea
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
sk. achieve proper timing of intervention.
Figure 22. Auscultation of the orbit
1. Ocular ultrasonography
A novel maneuver such as auscultation over the periorbital
2. Visual field examination — for optic nerve evaluation
areas of a proptosed eye may reveal conditions such as
arteriovenous fistulas. In such cases, bruits may be heard by in thyroid eye disease, arteriovenous fistula, and optic
the examiner (Figure 22). In addition, delicate palpation of nerve tumors
the same area may actually reveal rhythmic pulsation 3. Electrophysiology — for optic nerve evaluation
4. Laboratory exams — thyroid function tests
CLINICAL METHODS OF ORBITAL DIAGNOSIS 5_ Tissue biopsy
1. Gross Examination iio and conjunctival

III. INCIDENCE OF ORBITAL
abnormalities
2. Palpation pulsation, resiliency, DISORDERS
anteriorly-located mass
3. Auscultation After a thorough clinical evaluation using the present and
4. Routine Eye Exam Vision, extraocular past history, an orbital and ocular examination, and relevant
muscles, intraocular radiographic and laboratory examinations, there is still room
pressure, for epidemiological data in order to narrow further the
ophthalmoscopy
diagnosis of the orbital disorder.
5. Color vision
6. Cranial nerve function - pupil, corneal reflexes
Depending on which institution conducts the survey, certain
7. Systemic examination
orbital diseases stand out. Local efforts by different authors
spanning four decades have revealed the predominance
RADIOGRAPHIC METHODS OF ORBITAL EXAMINATION
of certain tumors like dermoid cysts, lacrimal gland tumors
and angiomatous new growths. The frequency of tumors is
1. Venography
explained by the fact that these studies were conducted on
2. Arteriography
histologically-proven specimens. 11,12
3. Plain film
5. Computerized tomography (CT scan) A more recent survey compiled all the available clinical records
Magnetic resonance imaging (MRI)
in the Orbit Section of the Department of Ophthalmology
and Visual Sciences in the Philippine General Hospital. The
Radiography is an essential tool among orbital patients. There usefulness of the following epidemiologic data is depicted
is an absolute need to visualize the concealed structures in the occurrence of orbital disorders in certain ages. The
of the orbital cavity. The usefulness of radiography was not differential diagnoses of pediatric and adult patients do not
evident with the first available machines for plain X-ray film
share many diseases in common. (Table 5) shows that the
because only the bony walls were readily seen. The advent overall most common orbital diseases are inflammatory in
of computerized tomography revolutionized the diagnosis
nature, specifically thyroid eye disease. 13 In children less than
and treatment of orbital diseases because it was able to 12 years old, vascular tumors, such as capillary hemangioma,
view and distinguish the soft tissues within the orbit. Further are more commonly encountered 14
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.
Table 5. Incidence of Orbital Disorders by Age Group" 3. Zuckerman J. Diagnostic Examination of the Eye.
(arranged in decreasing order)
Philadelphia: JB Lippincott. 2nd edition 1964 p73.
1111 11111.1b7dren (<12 years 4. Laws, ER Jr. (ed). The Diagnosis and Management of Orbital
Tumors. New York: Futura Publishing Co.1988, pp153-
• Thyroid eye disease • Vascular tumors (capillary
155_
• Orbital inflammatory disease hemangioma)
5_ Jones IS and Jakobiec, FA (eds). Diseases of the Orbit.
• Secondary tumors (from the • Cystic tumors (dermoid cysts
Maryland: Harper & Row, 1979. Chap 12.
paranasal sinuses • Orbital infections (orbital
cellulitis) 6. Hogan MJ, Zimmerman LE (eds). Ophthalmic Pathology
• Vascular tumors (cavernous
hemangioma) an Atlas and Textbook. Philadelphia: WB Saunders Co 2nd
• Systemic disease with orbital
• Lacrimal gland tumors manifestations (leukemia) edition 1962. pp739-40.
• Trauma 7_ Nerad JA, Krachmer JH (eds). Ocuplastic Surgery The
• Neural tumors (meningioma)
• Rhabdomyosarcoma Requisites in Ophthalmology. St. Louis Missouri: Mosby.
• Systemic disease with
orbital manifestations • Neural tumors (opt< new 2001, p 355.
(orbital lymphoma) glioma) Karcioglu ZA (ed). Orbital Tumors Diagnosis and Treatment.
• Cystic tumors • Orbital inflammatory Jsease New York: Springer Science + Business Media Inc, 2005,
pp 51-60.
3_ Fajardo RV, Aquino MV. Exophthalmometric
SUMMARY measurements among Filipinos, Philipp.lofSurg
Specialties 22:1967.
Proptosis is an ocular complaint and manifestation Kt Wilson ME, Parker PL, Chavis RM. Conservative
occurs rather infrequently in comparison with ot*-ie, correrion managementof childhood orbital lymphangiomas.
complaints such as headache, redness and biaTirg of Ophthalmology ,1989; 96:484-90.
IL Lim GD. Symposium: unilateral exophthalmos
vision. Despite its relative rarity, the complaint mint be
ophthalmologic aspects. Trans Phil Acad Ophthalmol
evaluated because it is peculiarly an orbital commicAant. Ike
Otolaryngol 3:0P-5, 1973.
most important value of learning the flange and behavior of
12 Vergara M. I ntraorbital tumors. MD Journal, 10:811, 1961
proptosis is the knowledge that this manifestation cormanaes
13_ Tuano PC, Remulla HD. A survey of orbital diseases
its own share of problems to the well-being of theeye
in the UP-PGH Department of Ophthalmology 1991
(unpublished).
There is difficulty in identifying the lesion because it ernes
14. Sy RT, Remulla HD, Tuano PC. A review of 75 cases of
behind the eyeball where it is InratisiditetD mane eye
orbital tumors in children at the orbit clinic, Philippine
examination. As such, the clinician needs 1D COndila not anily
General Hospital from 1980-1991. Transactions
the routine eye examination but also cdrer recominended
Department of Ophthalmology UP College of Medicine 2:1
steps in a systematic evaluation of the tedlgingepe
December 1994 pp 66-74.
It is important to determine if the peopiosis is red ix not The

differential diagnoses of pseudopiopsomis include unilateral
SELF-TEST
myopia, lid fissure asymmetry and oontodaterafenopluhaimos,
1. The bony orbit is directed forwards and

True proptosis, should undergo further dried evaluation,
A. laterally and upwards
namely, measurement, direction and dynamics ' or clinical
B. laterally and downwards
behavior. In general, the clinical considerations indude lesions
C. medially and upwards
that are inflammatory or non-fir_
D. medially and downwards
Clinical examination is folosved bg the use of ancillary

2. The volume of the orbit is:
procedures such as CT scan or MN of the skull and orbit_
A. 30 cc
Other laboratory eluminatinns indude visual field tests,
B. 35 cc
biopsy procedures on accessible tumors. ultrasonography.
C 40 cc
e I ectrophysiology and selective carotid cinigiugaphy. D. 50cc
3. In which bone does the lacrimal gland fossa lie?

REFERENCES
A. trontal
1. Rootman J, Stewart B, Goldberg RA. Orbital Surgery a B. lacrimal
Conceptual Approach. Philadelphia: Lippincott — Raven. C. maxillary
1995 p79. D. zygomatic
2. American Academy of Ophthalmology. Basic and Clinical
Science Course Sec 7 Orbit, Eyelids and Laaimal System, 2003.
7 DEVIATION AND DISPLACEMENT OF THE EYE I 2 Proptosis 159
4. The normal range of exophthalmometry measurements 9. A globe with negative resiliency and positive
among Filipinos is: intermittency may indicate the presence in the orbit of:
A. 9.0 - 14.5 mm A. lymphangioma
B. 10.0 - 19.5 rnm B. orbital floor fracture
C. the same as Caucasians C. inflammatory pseudotumor
D. still unknown / unreported D. cavernous hemangioma
5. One of the landmarks in measuring proptosis using the 10. One suspects a lacrimal gland tumor if the globe is
Hertels exophthalmometer is the proptosed forward,
A. bridge of the nose A. powrivvaras and medially
B. lateral orbital rim B. upwards and medially
C. pupil C. downwards and laterally
D. lateral canthus D. upwards and laterally
6. Pseudoproptosis is evident in the following situation: 11. A vascular orbital tumor which spontaneously stops
A. ipsilateral Horner's syndrome growing and even regresses is exemplified by a:
B. pseudotumor A. cavernous hemangioma
C. axial myopia B. capillary hemangioma
D. elevated intracranial pressure C. lymphangioma
D. varix
7. Acute proptosis (rapidly-progressive proptosis) of the
globe is noted in the following, EXCEPT: 12. CT scan of the orbit is most needed in a:
A. cavernous hemangioma A. proptosis with positive resiliency
B. thyroid-related eye disease B. proptosis with unexplained ophthalmoplegia
C. inflammatory pseudotumor C. proptosis accompanied by palpable lid masses
D. rhabdomyosarcoma D. exophthalmometry difference of 2.0 mm
8. A proptosis which increases after a Valsalva maneuver Answers to Self-Test on page 222.
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

8.1 Retinobla oma
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 In a child suspected to have retinoblastoma it is important
of childhood. Its incidence is approximately 1:18000 live births'; to ask about the birth and maternal history. Factors such
however some series have reported an increased incidence as preterm birth, birth weight, family history of metabolic
in the last few decades. There is no known sexual or racial disorders, childhood blindness and early death are important.
predilection. In non-Caucasian populations wherein uveal Occasionally, a complete history is enough to rule in or rule
melanomas are rare, retinoblastoma is the most common out retinoblastoma.
primary intraocular malignancy in all age groups.
The most common presenting symptom of retinoblastoma is
In our country with a very high birth rate, it is logical to expect leukocoria (white pupil) also called cat's eye reflex or"matang
many new cases annually. Local tumor registries in Manila pusa", in Filipino. This is seen in two thirds of retinoblastoma
and Rizal show an incidence of 7.7-8.9 (1983-1995) per million patients with intraocular tumors (Figure 1).
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 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 development of retinoblastoma can be traced to
the leukocoria may be constant. However, if it is located in the
mutations on chromosome 13. The retinoblastoma gene (RB
periphery, the cat's eye reflex might be seen only on certain
gene) is one of the best-studied genes in the human genome.
directions of gaze.
It is a tumor suppressor gene whose presence (even of a single
allele) protects against the development of the tumor.
Retinoblastoma may occasionally present as strabismus,
inflammation or mimic infection. Sometimes tumor cells
Most cases of retinoblastoma are sporadic mutations. This
seed into the anterior chamber and settle inferiorly giving the
means that one single retina cell suffers a mutation on one
appearance of pus (hypopion) .When the tumor grows it may
allele of the RB gene, then after some time suffers another
cause glaucoma and, later, buphthalmos or enlargement of the
mutation on the remaining allele. The loss of the tumor
eye. Advanced tumors that grow beyond the confines of the
suppression from both alleles then allows that particular cell
globe (extraocular extension) may present with exophthalmos
to multiply uncontrollably (Knudson's Two Hit Hypothesis).'
and an orbital mass6 (Figure 2). At this stage, intracranial
extension via the optic nerve and hematogenous metastasis
In around 30% of cases, the condition is heritable. In this
become more likely.
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) IV. PHYSICAL EXAMINATION
have one mutation at birth. Retinal cells are very metabolically
active and are constantly exposed to light energy and in most A complete ocular and physical exam on a child suspected to
instances these children will develop a second mutation in have retinoblastoma is imperative. Unilateral visual loss usually
one or more retina cells producing retinoblastoma. goes unnoticed and must be tested in a child.
Although the average age for the diagnosis of retinoblastoma Gross examination will usually show a white pupil. Great care
is 18 months, patients with sporadic mutations develop must be taken to ascertain the cause of the leukocoria, as this
tumors later (mean age at diagnosis 24 months5) because two may be caused by opacities in the cornea, lens or vitreous
hits are needed on a single cell. Sporadic cases are unilateral. other than a tumor.
Children with the heritable variety are diagnosed earlier at a
mean age of 12 months, because only a second hit is needed A dilated ocular funduscopy will show a yellow, white or pink
after birth and all retinal cells are at risk. These cases are usually mass. Indirect ophthalmoscopy gives more panoramic and
bilateral with multiple tumors on both eyes. Clinically, heritable three dimensional views (Figure 3) compared with a hand
retinoblastoma behaves as an autosomal dominant trait with held direct ophthalmoscope examination.
marked penetrance. Retinoblastoma is very rarely seen after
the age of six.
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 :..e:e -act presenting with leukocoria.
ôllogies 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
Figure 2. Re: extraocurir earscr : • --- = 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
A firm eye and one that is larger than the fellicvi erealesgsof
point the an in the right direction.8
an enlarging tumor. An extraocular tumor. andle the gas
appearance of exophthalmos might also vest* in emmocular Persistent hyperplastic primary vitreous (PHPV) is another
muscle restriction and extraocular movement &soden. In condition which mimics retinoblastoma. The leukocoria
these cases a systemic and neurologic evahmtiOn &the diikl s : -went at birth and the affected eye is usually smaller
should be done to detect signs of metastase. -:halmia). There is a fibrous plaque behind the lens
cc- through a stalk to the optic disc. This is an anomaly
off e ogenesis which is otherwise benign.
Coats 7: ease manifests as telangiectatic changes in the

-E- of c- ::ren_ The blood vessels leak and cause subretinal
..aation, retinal detachment and scarring. Although patients
7.h Coats' Disease can present with leukocoria, particularly if
7 - affected portion of the retina is large enough, a distinct
e
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

It should be noted that even with a thorough expert
VI. ANCILLARY TESTS examination and after performing diagnostic procedures
in many cases making a definitive clinical diagnosis of
Although a complete ophthalmologic exam including retinoblastoma may still be difficult. Foreign studies show
indirect ophthalmoscopy leads to an accurate diagnosis of that 10-20% of eyes enucleated for suspected retinoblastoma
retinoblastoma in the great majority of patients, ancillary
turn out to be pseudoretinoblastomas. In the local setting,
tests might be useful in the few equivocal cases. An ocular a review done at the UP-NIH Institute of Ophthalmology
ultrasound (B scan) is readily available in most eye centers
revealed that 8% of submitted eyeballs with a clinical diagnosis
and can easily demonstrate the presence of a distinct mass
of retinoblastoma turned out to be other benign lesions.'
(Figure 5) in cases where there is doubt especially if there is
These were blind, leukocoric eyes in young children with a
an opacity in the cornea or lens occluding the view.
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.
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
Figure 5. Ultrasound photo showing a solid mass at the center. impact the condition might have on a growing child.
By far, the most useful ancillary procedure in the diagnosis of The management of retinoblastoma is performed by a team
retinoblastoma is a CT scan.9 One particular characteristic of primarily consisting of an ophthalmologist, a pediatrician and a
retinoblastoma is that calcification is seen in more than 90% of radiologist. Small and medium sized tumors (Figure 7) may be
tumors and the CT scan easily demonstrates this (Figure 6). On successfully treated using conservative eye sparing methods.
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.
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 3_ RB, De Jesus AA, Valera EC, Mercado, GV,
hope for vision are enucleated. It is imperative for enucler_ez: - piiidemiological pattern of retinoblastoma at the
eyes to undergo histopathologic examination to look for sigrs Philippine General Hospital. Philipp J Ophthalmol , 2004;
of extraocular spread. Tumors with extraocular extensicr 29:136-139.
have higher rates of metastasis and result in worse pica-cs Mclean IW. Retinoblastomas, Retinocytomas, and
-
Extraocular extension is an indication for chemothe---__D. Pseudoretinoblastomas. In: Ophthalmic Pathology an Atlas
operatively. are Textbook. Spencer WH, editor. Philadelphia, PA: WB
Saunders. 4th edition. 333-1336.
In recent years there has been a focus on the uses -et:- Our , Devron . Clinical Ocular Oncology. New York, NY:
adjuvant chemotherapy to prevent recurrence in - Churchill Livingstone Inc. 1989.
enucleation patients with intraocular retinoblastoma strwing lac Lean IW, Burnier MN, Zimmerman LE, Jakobiec FA.
high risk histopathologic characteristics. These factor_ rtzu3e AVM of the Eye and Ocular Adnexa. Washington, DC:
invasion of the scleral coat, post laminar optic nerve r"..-cr Mned Forces Institute of Pathology. 1993. 103-105.
and massive choroidal involvement.12 Chua CT, Lim MC, Seah LL, et al. Pseudoretinoblastoma in
enudeated eyes of Asian patients. Singapore Med J 2006;
Patients with large tumors involving the orbit have rite sicrg 47:617-620.
prognosis. They are treated with chemotherapy anc —foe Kama P, Muttineni J, Angell L, Karmaus W. Retinopathy of
extensive surgery.The newer chemotherapeutic chrLr_.5 s-c".as pematurity and risk factors: a prospective cohort study.
the platinum compounds are increasing the survika -ems of &ICPediarr 2005; 5: 18.
these patients. Medical therapy may be done in ccr-oraelor, 9. thosh 5, Mukhopdhyay S, Chattopahyay D, Biswas K.
with radiation treatment. Diagnostic accuracy in retinoblastoma. J Indian Med Assoc
2010; 108: 509, 512-513.
Retinoblastoma patients must be closely follow,: sgins 110 Valenzuela RM, Domingo RED, Ranche, JM, Manganip LE.
of recurrence or development of new turno-s -lentabe cases A review of retinoblastoma cases at a tertiary hospital.
are especially at risk and have been reportec 3E'setIC drier Philipp J Opthalmol 2010; 35. http://www.paojournal.
malignancies in later life.'3 Genetic courseirc b adkaed oorn/vol35no1/toc.php . Access date: July 24, 2011.
families planning to have more children is as;. -mewl 11_ Lumbroso-Le Rouic L, Aerts I, et al. Conservative treatments
of intraocular retinoblastoma. Ophthalmology 2008; 115:
1405-1410.
SUMMARY 12. Uusitalo MS, Van Quill KR, et al. Evaluation of
chemoprophylaxis in patients with unilateral
Retinoblastoma is a life threatening eye dose r ditties retinoblastoma with high-risk features on histopathologic
that usually presents as leukocoria_ It is imper-arc e-leran examination. Arch Ophthalmol 2001; 119: 41-48.
a high index of suspicion and differentiae t flaw tub 13_ Draper GJ, Sanders BM, Kingston JE. Second primary
conditions at the first consult. A =wine lislay and neoplasms in patients with retinoblastoma. Br J Cancer
physical examination combined vitt the digit legs ad lead 1986; 53: 661-671.
to an accurate diagnosis necessary 1c
treatment. Delay in diagnosis and
only loss of vision but, more irrtn7-
SELF-TEST
1. The presence of the retinoblastoma gene:
ACKNOWLEDGEMENT A. Causes the development of retinoblastoma.
B. Increases the risk of development of secondary
0140839111001s tumors in later life.
Dr. Allan Joseph L Larona cor
C Protects a child from retinoblastoma.
D. Is a heritable defect that is passed on to future
REFERENCES generations.
1. Yanoff M and Fre BS_ Oadar Padriagy: A Color 2. Unless proven otherwise, a child less than five years
Atlas. Singapore: Gower Medical Publishing rd edition. old presenting with leukocoria, should be considered
1992. 18.5 - 18.11. a case of:
2. Ngelangel CA and Wang EHM, Cancer and the Philippine Retinopathy of prematurity
Cancer Control Program. Jpn J Gin Oncol 2002; 32 B. Retinoblastoma
(supplement 1): S52-561. C Persistent hyperplastic primary vitreous
D. Congenital cataract
SPECIAL TOPICS 1 8.1 Retinoblastoma 165

3. In a child presenting with leukocoria which 8. Orbital recurrence and metastasis after enucleation is
accompanying sign is the least associated with most likely if the histopathologic report shows:
retinoblastoma: A. Poorly differentiated retinoblastoma cells.
A. Congestion B. Tumor seeding in the anterior chamber with
B. Exopthalmos glaucoma.
C. Exotropia C. Massive invasion of the choroid.
D. Hypotonia D. Invasion of the optic nerve beyond the margin of
resection.
4. A child born at 26 weeks age of gestation with a birth
weight of 1.4 kg presents with bilateral leukocoria since 9. A six month old child underwent enucleation of the
3 months of age. The most probable diagnosis is: right eye for intraocular retinoblastoma. The other
A. Heritable retinoblastoma eye was normal on examination under anesthesia. On
B. Persistent Hyperplastic Primary Vitreous (PHPV) discharge you would advice the parents to:
C. Retinopathy of Prematurity A. Not worry since the tumor was completely remove
E. Coats'disease and no further follow up is needed.
B. Bring the patient back for consultation if they nu -
5. A one year old child is brought to you for leukocoria recurrence at the post-enucleation socket.
What other finding would lead you to PHPV as a primary C. Bring the patient back every few months to check for
consideration: tumors developing on the remaining eye.
A. Bilaterality D. Consult the pediatric oncologist for post op
B. Microphthalmia chemotherapy.
C. Preterm birth
D. Gestational infection 10. A man who survived bilateral retinoblastoma marries
and the couple decides to have children. Your advise to
6. A 3 year old child with leukocoria is presented to you. On them would be:
examination the cornea is hazy and the lens is opaque. A. Not to worry because the chance of having children
What examination would be most helpful in definitive with retinoblastoma is very small.
diagnosis of this patient? B. Bring their children to the doctor once they see
leukocoria or other signs of retinoblastoma.
A. CBC and peripheral blood smear
B. Ultrasound C. Do routine CT scans on their children every six
months.
C. CT scan
D. X-ray of skull and orbits D. Take their future children to be seen by an
ophthalmologist the soonest time possible after
A four year old child with left sided leukocoria and birth.
7.
exotropia is diagnosed with retinoblastoma, the most
likely treatment modality is: Answers to Self-Test on page 222.
A. Laser treatment
B. Chemotherapy
C. Enucleation
D. External beam radiation
166 Se-Instructional Materials in Ophthalmology I 2nd Edition

8.2 Ocular Manifestations
of Systemic Diseases
Romulo N. Aguilar, MD, PhD
INTRODUCTION
This self-instructional material is designed to he.: earn key concepts regarding eye manifestations of common
systemic diseases. It aims to emphasize the 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
presence of serious underlying systemic disc - t.. dira gathered from an eye examination can provide the clinic'
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
Upon completion of this unit of cr 5-c4.40.7. De able

the following
1. To recognize charac-:ef,s,-c ccaarlyeai sys,emic diseases, specifically those associated with
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,
The eye can provide clues to the diagnosis of many systemic
vitamin A deficiency, drug or heavy metal toxicity,
diseases because significant effects of these various conditions
immune-mediated diseases, metabolic diseases
may manifest in the eye. The initial diagnosis of a number of
systemic diseases may therefore be made in the course of
Lens: metabolic conditions (diabetes), steroid toxicity,
performing a comprehensive ophthalmic examination.
Apert syndrome, juvenile rheumatoid arthritis, Wilson
Evaluation of the ocular fundus is particularly important in disease, homocystinuria
the evaluation of systemic disease since it is the only region
Posterior segment: diabetes mellitus, systemic
in the body where one can directly visualize manifestations
of macro and microvascular pathology. Nevertheless. various hypertension, infectious diseases (e.g., acquired
components of the comprehensive eye examination may help immunodeficiency syndrome, tuberculosis,
identify existing systemic disease.' For example toxoplasmosis), primary or metastatic tumors,
drug toxicity (ex., hydroxychloroquine, tamoxifen),
• External examination: orbital tumor, thyroid eye cerebrovascular disease, hematologic disorders, brain
disease, acquired immune deficiency syndrome. tumors
tuberculosis
An outline of some of the more significant diseases, along with
Pupillary function, ocular alignment and motility: their ocular presentation, is summarized in Table 1. A review
neurological disorders (e.g., myasthenia gravis, of the important ocular pathology seen in some systemic
central nervous system defects, multiple sclerosis, diseases will subsequently be discussed.
optic nerve disorders, brain tumors), thyroid eye
disease
Visual fields by confrontation: tumors affecting the

optic pathways
Table 1. Overview of Ocular Manifestations of Common Systemic I>
F System/Category Disease Ocular Manifestation
Endocrine Diabetes mellitus Diabetic retinopathy

Thyroid eye disease Thyroid orbitopathy
Pituitary lesions Field loss
Cardiovascular Hypertension Hypertensive Retinopathy
Retinal Emboli Retinal Vessel Occlusion
Hyperlipoproteinemia Corneal Arcus/ Xanthelasma
Marian Syndrome Lens Dislocation
Endocarditis Roth Spots
Rheumatology Rheumatoid Arthritis Scleritis
Sjogrens Syndrome Keratitis sicca
Seronegative Spondeloarthropathes Uveitis
Collagen Vascular Disease Keratitis sicca
Juvenile Rheumatoid Artnntis Anterior Uveitis
Infections Herpes zoster Uveitis. glaucoma
HIV, CMV Retinitis
Candidiasis Endophthalmitis
Syphilis !ribs, Optic Neuritis, Ophthalmoplegia
Malignancy Lymphoma Infiltrate, uveitis
Leukemia Infiltrative retinitis
Metastases C"oroidal mass
Neurological Multiple sclerosis Optic neuritis. uveitis
Giant cell arteritis Ischemic optic neuropathy
Myasthenia gravis Diplopia ptosis
Dermatological Acne rosacea
Atopy ler::: !is oa!aract
ITS3 rnif I rs 1 _1
.:cose is thought to damage retinal (and renal)
I. DIABETES MELLITUS AND -,ne following ways:
DIABETIC RETINOPATHY
1. ca: . basement membrane thickening,
Diabetes Mellitus (DM) is associated with a 3f ''ary pericytes and,
complications. These include cataracts, extra-ocular muscle 3. brea.....:L...^; of the blood-retinal barrier.
palsies (Cranial Nerves Ill, IV, VI), diabetic optic neuropathy.
neurotrophic keratitis and diabetic retinopathy Among these. As a result of these processes (Figure 1), the blood vessels
diabetic retinopathy is the most common and may lead to weaken and form saccular dilatations called microaneurysms
permanent loss of vision if not properly attended ta rigor. 2), which can leak, resulting in hemorrhages
(Figure 3) and exudates (Figures 4 and 5) in the retina.
Based on the 2002 Third National Survey of Phippine Vascular remodeling takes place resulting in capillary
Blindness', the overall prevalence of visual irnpairment was telangiectasie :3:led intraretinal microvascular abnormalities
4.62%, which roughly translates to 3,673.070 Ripinos The ORIAAs a- 7 • beading (Figures 6 and 7). Because
crude prevalence of bilateral blindness a—oing Filipinos was of struct-L.- L- age, vessels eventually close and cause
0.58% or, about 461,121 Filipinos. Re: - Whet inducted ischemia of retina, usually manifested as cotton-wool
diabetic retinopathy, was the 4th lea: - of tandness. spots or patches (Figure 4). These ischemic areas are thought
following cataract, error of refraction 3 = 2: aUCOMel tr ',sad a to produce a special growth chemical (vascular endothelial
prevalence of 0.11%, affecting about iipines. growth factor or VEGF) which is known to be responsible
*x new blood vessel growth (Figure 8). When this occurs,
Also in 2002, the World Health Organization (10101egrnated Proliferative diabetic retinopathy develops.
that there were 37 million cases of blindness due to raying
eye diseases.' Diabetic retinopathy was the 5' leading cause *COW .41'Permeability
Oodala
of blindness after cataract. glaucoma. age-relmed macular was
degeneration and corneal opacities and accourred for 4.8% tam=

avacee-matane
lAcmussaiar
erdotelopolls
Capillary
occlusal Retnopathy
or, roughlyl.8 million persons. The pooperion at blindness Necuasadanzatoo —

due to diabetic retinopathy rangedtfoom newly Air 1 4=C--
*•
swam
Africa, to 3-7% in much of South-East Asia whicii recce
Philippines, and the Western Paw. to 5-17%c it* 8amassica lylc,ns7..iar Mammal
',soma= or-ogo —> Rehoopothy
affluent regions of the Americas, Europe and the
Pacific.' Figure 1. ,:it'-k.Ayerriesiz, of , ,:c Retinopathy
Studies have shown that at any one erne ---

diabetic population will have diabetic rear p~ . _ _ :-
time, 90% of diabetics will eventually &Nem tr€
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 Figure 2. Microaneurysms are the earliest clinically visible changes
of diabetic retinopathy. They are localized capillary dilatations which are

30+ yrs
1111111111111111Mml usually saccular (round). They usually appear as small red dots in clusters
although they may also be isolated (arrows).
Although the likelihooc apathy varies
between Type I and Typ= = 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
Figure 6. Venous beading (arrow heads) is a sign of changes in the
hemorrhages appear dot or blot shaped.
hemodynamic characteristics of blood flow among diabetics. (Image
source: http://www.glostruphospital.dk/menu/Afdelinger/Oejenafdelingen/
Oculus/EURODIAB.htm)
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 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 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 8. or new vessel lorostor ar74.. 1 re 're ,ear-es -ore Wthemic. New blood vessels may arise
from (A) the so or, (B) else/bee it Pe mrire-. 3 re "mrri, --ese ..seks are fragile and bleed easily. hence the
importance of '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
Figure 9. 'A r `c,r -oiirferative Dooetrc Reonopathy with microaneurysms.
Severe Ira--rers-rs ../..ince-
Intra-scra et A., da,=.
- t.-J.2-
Sava: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 Figure 10. Moderate Non-proliferative Diabetic Retincoany with typical
of diabetic retinopathy =, trims of multiple cotbn wool spot. had exudates and intra-relinai
11)1-
condition. Patients wit- - deper
(IDDM ,Type 1 diabetes r- 7-s be
ophthalmologic COIISLP.. 7-* is of five yea• likewise be referred to an eye specialist for proper monitoring
already. All patients Cis. csed tc nave non =c :ent of her ocular status for the duration of her pregnancy.°
diabetes mellitus Type 2 diabetes -re 7_: :.` be
referred to an ophthalmologist at the time of 7 :7-, a• OSiS. Foremost in the management of patients with any stage
Diabetic patients who complain of any vis..s of diabetic retinopathy is strict blood sugar control."i°
should be referred immediately to an eye spec s =r ;:' proper Management of the eye condition will depend on the stage of
evaluation. Pregnant women with history of c-ac-F.es should 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 Figure 14. Grid Laser Treatment
microaneurysms, soft exudates and diffuse intraretinal hemorrhages.
sok
Figure 12. Proliferative Diabetic Retinopathy with new vessels (arrows) Figure 15. Focal Laser Treatment
at the disc and retinal periphery.
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
I
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
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 Figure 19. Subhyaloid hemorrhage (arrows) refers to accumulation of
*eels blood in areas of locaized detachment. Blood accumulates between
of serum cholesterol was associated with increased severity
the retina and the vi re= and is often described as boat-shaped.
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."
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:_ - . as
a consequence of bleeding from tr'e -e... -
traction on the retina, consequent ret,a Arteriosclerosis occurs as a result of intimal layer hyalinization,
loss of vision. medal layer hypertrophy and endothelial hyperplasia.
- this presents as focal narrowing and straightening of
II. HYPERTENSION AND ine retinal arterial walls. Arteriovenous (AV) crossing changes
occurs as the condition progresses.'s
HYPERTENSIVE RETINOPATHY
Gracing systems for hypertensive retinopathy have beer
Systemic arterial hypertension is one of the most common preserved by various authors. The Keith Wagener Barke
diseases worldwide. More than half of the population over 60 (KWB) aassification26 was published in 1939 which classifies
years has hypertension's. Based on the 2004 International Data the condition into four stages (Table 4).
base of the US Census Bureau'', there were an estimated 15.9
million people affected by hypertension in the Philippines (in Table 4. I i Wag en e r Barker Classification of Hypertensive Retinopathy
a population of approximately 86 million). In addition, there
may be another 4.8 million undiagnosed cases of hypertension CHARACTERISTICS
in the Philippines.19
Slight or modest narrowing of retinal arterioles,
The changes leading to primary systemic arterial hypertension ..thAVratio>_ 1:2
is multifactorial.'s In the elderly, an increase in basal smooth Modest to severe narrowing of retinal arterioles
muscle tone occurs as a result of sympathetic activity, (focal or generalized), with AV ratio < 1:2 or AV
renin-angiotensin overactivity, cell membrane changes and nicking
progressive architectural alterations in the vessel walls. Other Above changes plus bilateral soft exudates or
Ill
factors which contribute to this are salt sensitivity, volume ame-shaped hemorrhages
depletion and orthostasis.27.1s
ly Above changes plus bilateral optic disc edema
Both prevalence and incidence of retinal microvascular
changes in hypertension varies widely from 2-15%.20-24 The
Scheie, in 1953, proposed a different grading system which
ocular picture is directly related to status of retinal arteries and
incorporated changes due to arteriolar sclerosis." This is
the rate of rise and degree of systemic blood pressure. Arterial
shown in Table 5 and Figures 22 to 24.
sclerosis occurs in the normal aging population (involutional
sclerosis) as well as in long standing hypertension.'s
Vision threatening complications of hypertension include the
following (Figure 25):
Retinal manifestations of hypertension include vascular
constriction, leakage and arteriosclerosis.25'738
1. Central retinal vein occlusion (CRVO)
2. Branch retinal vein occlusion (BRVO)
Vasoconstriction manifests as generalized or focal arteriolar
3. Central / branch retinal artery occlusion (CRAO / BRAO)
narrowing.2,18,25 Leakage occurs due to abnormal vascular
4. Anterior ischemic optic neuropathy (AION)
permeability and manifests as a variety of clinical signs: flame-
shaped hemorrhages, retinal edema, hard exudates and
Recent studies have demonstrated an association between
optic disc edema (in cases of malignant hypertension) 2'7 '8
hypertensive retinopathy and cardiovascular morbidity and
The presence of hard exudates in Henle's layer of the fovea mortality.28 This is shown in Table 6.
presents in a star-like configuration referred to as the"macular
star"5.25 (Figure 21).
Table 5. Scheie Classification for Grading of Hypertehs'.e Rs •-
GRADE Arteriolar Reflex Changes Blood Vessel Changes
I broadening of the arter -• AV aossing changes
II obvious broadening of the airclar Igrc changes
III copper-wire artenc es —_= - . - _ _ -anges
IV silver-wire artero es '''ierfr. =SS-Ng changes
Figure 22 Scree Classification based on Hyperte-s - (A ) (B) Grade II: (C) Grade III; (D) Grade IV showing swollen optic nerve, retinal
artenotar narrowing. nerve fiber layer infarcts and blot Herr•,;--âge
8 SPECIAL TOPICS 18.2 Ocular Manifestations of Systemic Diseases GE

(C) 'silver wire"
Figure 23. Arteriolar Reflex Changes: (A) normal: (B) broad light reflex or 'copper wiring;"
A 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 Description Systemic Associations

Mild One or more of the following signs: Weak associations with stroke, coronary
(KWB Grade I — II) Generalized arteriolar narrowing, focal arteriolar heart disease and cardiovascular mortality
narrowing. AV nicking, arteriolar wall opacity
(silver wiring)
Moderate Mild retinopathy with one or more of the Strong association with stroke, congestive
(KWB Grade III) following signs: heart failure. renal dysfunction and
Retinal hemorrhages (dot/blot. flame-shaped). cardiovascular mortality
microaneurysms, cottonwool spots, hard
exudates
Accelerated Moderate retinopathy signs plus optic disc Associated with mortality and renal failure
(KWB Grade IV) swellingi maybe associated with visual loss
onal Materials in Ophthalmology 12nd Edition

No
Hypertensive Rooms Care
Retinopathy
Medical
history,
titer
fileimpolig
HI • Routine Care
• Closer monitoring of vascular risk
examination, • Exdude diabetes

• Closer monitoring of vascular risk
appropriate Retinal
Patient with •loireesige • Posible indication for treatment of
Hypertension laboratory Examinato" zeircestor hypertension and other risk factors
investigation
and
management
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 - Homosexuals and bisexuals

associated with: - Health workers
1. Diabetic retinopathy - hoiVerVirsOn tortmed Prevalence of HIV infection in the Philippines remains low at
progression of DR less than 0.1% of the adult population.3° Data gathered in 2009
2. Age-related macular oeoere•atccr - .14wrierision estimated 8,700 people living with HIV/AIDS. As of 2010, the
increases the risk for Al0C--: Seaver err ,E-se, Study' Department of Health has reported 315 AIDS-related deaths.
3. Glaucoma - Hypertensor r"..w Arcliesset~e, risk and While the Philippines is perceived as a low-HIV prevalence
development of glaucoma-I` country, incidence had increased by 25% from 2001 to 2009.
From 2007, the number of reported cases has doubled every
The primary management of OC.1.7( 1550Cialled two years, suggesting that two new cases of HIV/AIDS are
with hypertension is adequate brood pais..re. control reported daily (DOH, 2009)."
Figure 26 shows the summed .nanage.7-e
—rti:r ryzeetensive
retinopathy. Ocular manifestations of HIV/AIDS include the following:
For complications such as vascular occiLsors, Dose follow-up • dry eye

by an ophthalmologist is reconvneno= - .user treatment is • retinal microangiopathy often manifested as cotton-
performed whenever indicat-?,-.! wool spots
opportunistic infections commonly presenting as
Cytomegalovirus (CMV) retinitis
III. ACQUIRED IMMUNE tumors like Kaposi's sarcoma of the lids or conjunctiva
DEFICIENCY SYNDROME neuro-ophthalmologic lesions
Infection with the numan drirnonooeuciency virus ( HIV) causes Cotton wool spots (Figure 27) are the most common finding
immune system suppression of patient which subsequently in these patients. It is found in 100% of HIV infected patients.
allows opportunistic infections and neoplastic conditions to Cotton wool spots may be associated with retinal hemorrhages
affect the eye. Individuals at risk of acquiring this infection and microaneurysms. Patients are usually asymptomatic and
include the following these lesions may disappear spontaneously. It is proposed
that this occurs as a result of immune complex deposition
• People receiving transfusions and/or HIV infection of retinal vascular endothelium.
• IV drug users
• Healthy sex partners of infected patients Cytomegalovirus (CMV) retinitis (Figure 28) affects 40% of
• Babies born of infected mothers patients with AIDS. Its presence signifies severe systemic
• Hemophiliacs
• Prostitutes, sex workers
S SPECIAL TOPICS 1 82 Ocular Manifestations of Systemic Diseases El

Figure 29. Kaposi's Sarcoma of the conjunctiva
Figure 27. Cotton wool spots (arrows) in a patient with HIV infection. (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
• 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
Figure 28. CMV retinitis in a patient with HIV infection
dysfunction."
Among patients with thyroid disease, thyroid eye disease

involvement. This condition may however occur in other occurs in 37.5% (25% — 50%). Severe eye disease develops in
immunodeficiency states. 3-5%. Women are affected five times more often than men.
Smoking is a significant risk factor in the development of
Kaposi's sarcoma (KS) is a tumor caused by human herpes thyroid eye disease.34 Ocular involvement may be unilateral or
virus 8 (HHV8), also known as Kaposi's sarcoma-associated bilateral. Symptoms may include excessive redness, tearing,
herpes virus (KSHV). It was first described in 1872 by Moritz itching, pressure, puffiness and pain.
Kaposi (KA-po-she), a Hungarian dermatologist .31 AIDS-
associated Kaposi sarcoma or KS-AIDS presents with skin The pathophysiology of the eye findings of Grave's disease
lesions that typically start as one to several red to purple-red remains obscure although it is widely accepted to be an
macules, rapidly progressing to papules, nodules, and plaques. autoimmune disorder. For still unknown reasons, the body's
Unlike the classic form of Kaposi sarcoma, KS-AIDS is often host inflammatory cells attack tissues around the eye,
seen on the head, back, neck, muscular palate and the area of specifically, the orbital fat, the directional eye muscles, and the
the gingiva" (Figure 29). muscles in the eyelid."
Since ocular manifestations often imply severe systemic Unilateral or bilateral lid retraction (Dalrymple's sign) is the
involvement, management should be closely coordinated most common sign ofTED.2,5" As a result of lid retraction, the
with an infectious disease expert. 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.'
IV. THYROID EYE DISEASE
TED is the most common cause of unilateral or bilateral
It was Robert Graves, in 1835, who described signs of thyroid proptosis in adults.2-5 Proptosis is due to inflammation of the
disease, including exophthalmos. His name has since extraocular rnueidesand orbital fat, causing anterior protrusion
become an eponym for an eye condition associated with 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.
proptosis.' Proptosis or exophthalmos can be measur, 3-
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

._ §
often referred to as the "Thyroid Stare' (Koc'Ner s7
Other common signs of TED are lid lag Figure 31. Soft tissue involvement = Class 2
Graefe's sign), injection over the recti
esotropia and hypotropia.25"5 In sc-
extraocular muscles may enlarge resuiti-
to 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
Disease activity is assessed using the Clinical Assessment

Score (CAS) of Mouritsr (Table 8). For every criterion met,
2 Solt tissue eibillorat torizeitelf one point is assigned. A CAS of 3 or less responds poorly to
involvement call Web= immunosuppressive therapy, indicating that these patients
Otsti tteetisia• have passed the stage of active inflammation. A CAS of 4 or
more responds well to corticosteroid therapy.38
3 Proptosis PIWCW
Table 8. Clinical Assessment Score for Thyroid Eye Disease
some
4 EXtra0CuiF Pain • Pain at rest on or behind the eye over the

involveTe-: past 4 weeks
5 Corneal invotverervt Stanng vlMtt fluoresce n Pain on attempted movement over the last 4
Ulceration. infiltrate. weeks
certration
Redness • Redness of one or both eyelids
6 -
nerve imiaved : iecease Diffuse conjunctival congestion involving at
• :ss least 1/4 of eyeball
7e valor
Swelling • Swelling of one or both eyelids
Swollen caruncle
• Chemosis
Proptosis increasing .? 2 mm over past 1-3
months
Loss of • Reduced eye movements 5° in any

Function direction over 1-3 months)
• Decreased pinhole visual acuity by 1 line
on Snellen's chart over 1-3 months
8 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). According to the World Health Organization (WHO) report
201039, one-third of the current world population is infected
Less serious complications of TED are tearing, foreign body
with the tubercle bacillus. Five to ten percent of these
sensation, lid and conjunctival edema / chemosis. More
eventually get sick. In 2008, the largest number of new TB
serious complications include exposure keratitis, diplopia,
cases was found in the Southeast Asian region, accounting for
ophthalmoplegia and loss of vision.57
35% of all new cases."
Loss of vision usually results from compression of the optic
In the Philippines, the incidence ofTB was reported to be 284.8
nerve by swollen tissues surrounding the eye. Urgent
treatment is required otherwise visual loss can be permanent. per 100,000 population in 2008.4°
Other complications include glaucoma and exposure of the
Ocular involvement in tuberculosis can be caused by either
anterior surface of the eye resulting from the inability to
direct invasion of organism, or as a result of hypersensitivity
completely close the eyelids5•'
reaction to tuberculoprotein.18 Ocular involvement is more
common in patients with miliary tuberculosis, although, it
There is no single laboratory examination that will confirm the may also be seen in patients with no evidence of pulmonary
presence of thyroid eye disease. As was mentioned earlier, disease.
the condition is not related to thyroid hormone levels and
T
Figure 37. Other Manifestations of Ocular TB: (A) choroidal tubercle

(B) phlyctenulosis (C) retinal periphlebitis
Figure 36. (A) •cera::

(B) Busacca -cc.. (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
REFERENCES
Other manifestations (Figure 37) are:
American Academy of Ophthalmology Preferred
Practice Patterns Committee. Preferred Practice
• Phlyctenulosis — conjunctival condition featuring a
Pattern® Guidelines. Comprehensive Adult Medical Eye
phlyctenule, which is a small pinkish white nodule
Evaluation. San Francisco, CA: American Academy of
near the limbus, believed to be a non-specific delayed
Ophthalmology, 2010.
hypersensitivity reaction
2. Ka nski JJ. Clinical Ophthalmology:A SystematicApproach,
ed 3. Oxford: Butterworth-Heinemann, 1994.
Vitritis — inflammation of the vitreous
3. Cubillan LDP, Olivar-Santos EO. Third National Survey
Retinal periphlebitis — inflammation of the retina~~ on Blindness. Phil J Ophthal 2005; 30 (3): 100-114.
venules 4. http://vision2020.org/main.cfm?type=WIBDIEBETIC.
May 18, 2011
Choroidal tubercles — choroidal masses believed to 5. Tang RA, Coleman AL, Wilkins JK, Brown J, Newman
contain tubercle bacilli. Histopathologically, they SA, Skootsky S, Whitcup SM: Ocular Manifestations of
represent caseating granulomas' Systemic Disease: A Slide-Script Program. San Francisco:
American Academy of Ophthalmology, 1996.
• Panuveitis — inflammation of the entire weal tract 6. American Academy of Ophthalmology Retina
choroid, ciliary body and iris Panel. Preferred Practice Patterns Guidelines. Diabetic
Retinopathy. San Francisco, CA: American Academy of
The ocular inflammatory condition associated with TB is Ophthalmology; 2008
usually treated with topical and/or systemic corticosteroids. 7. Federman JL, Gouras P, Schubert H, Madison Slusher M,
It is however, imperative that patients be treated with the Vrabec TR. Retina and Vitreous, in Podos SM, Yanoff M
appropriate anti-TB medication prior to institution of the (eds): Textbook of Ophthalmology, Vol 9. London: Mosby,
anti-inflammatory regimen to avoid exacerbation of the 1994.
systemic infection. 8_ Diabetes Control and Complications Trial Research
Group. The relationship of glycemic exposure (HbA1c)
to the risk of development and progression of
SUMMARY retinopathy in the Diabetes Control and Complications
Trial. Diabetes 1995;44:968-83
The importance of being able to recognize ocular signs, 9. Diabetes Control and Complications Trial Research
symptoms and complications of many systemic diseases is a Group. The effect of intensive treatment of diabetes
vital part of good medical practice. It is therefore necessary on the development and progression of long-term
for the primary care physician to be able to perform a complications in insulin-dependent diabetes mellitus.
thorough eye examination, particularly that of the fundus. N Engl J Med 1993;329:977-86.
Early diagnosis of the conditions earlier discussed, in 10. Diabetes Control and Complications Trial Research
particular diabetic retinopathy is crucial in the ultimate Group. The effect of intensive diabetes treatment on
outcome of treatment. the progression of diabetic retinopathy in insulin-
dependent diabetes mellitus. The Diabetes Control and
This instructional material is by no means complete. Only Complications Trial. Arch Ophthalmol 1995;113:36-51.
conditions that are more commonly encountered in local 11. Early Treatment Diabetic Retinopathy Study Research
practice have been emphasized. Additional reading is Group. Photocoagulation for diabetic macular edema.
recommended to supplement the information provided. Early Treatment Diabetic Retinopathy Study report
number 1. Arch Ophthalmol 1985;103:1796-806.
12. Early Treatment Diabetic Retinopathy Study Research
RECOMMENDED READING Group. Treatment techniques and clinical guidelines
for photocoagulation of diabetic macular edema.
Other systemic diseases with ocular manifestations: Early Treatment Diabetic Retinopathy Study report
• Sickle-cell Retinopathy number 2. Ophthalmology 1987;94:761-74.
• Collagen-vascular diseases:
13. Diabetic Retinopathy Study Research Group.
Rheumatoid Arthritis (RA), Systemic Lupus Indications for photocoagulation treatment of diabetic
Erythematosus (SLE), Polyarteritis Nodosa (PAN), etc.
retinopathy: Diabetic Retinopathy Study report number
• Blood dyscracias
14. Int Ophthalmol Clin 1987;27:239-53.
Leukemia, anemia, hyperviscosity states
14. Diabetic RetinopathyVitrectomy Study Research Group.
Others:
Early vitrectorny for severe vitreous hemorrhage in
Sarcoidosis, Herpes Zoster, Leprosy diabetic retinoperhy_ Four-year results of a randomized
trial: Diabetic Retinopathy Vitrectomy Study report 5. sarcoma May 22, 2011
Arch Ophthalmol 1990;108:958-64. 33. httpi/www.thyroid.org.aunhySociThySocTED.html May
15. UK Prospective Diabetes Study Group. Tight blood 21,2011
pressure control and risk of macrovascular and 34_ Cawood T, Moriarty P, O'Shea D. Recent developments in
microvascular complications in type 2 diabetes: UKPDS thyroid eye disease. BMJ 2004; 329:385-90
35. htflx//eirmitipeciaorg/wikinhyroid_eye_d i sea se May
38. BMJ 1998;317:703-13.
Klein R, Klein BE, Moss SE, et al. The Wisconsin 21,2011
16.
Epidemiologic Study of Diabetic Retinopathy. IX. Four- 36. Werner SC. Modification of the classification of the eye
year incidence and progression of diabetic retincipathy
changes of Graves' disease: recommendations of the Ad
when age at diagnosis is less than 30 years. Arch Hoc Committee of the American Thyroid Association. J
Ophthalmol 1989;107:237-43. Qrr Endocinol Metob 1977;44:203-4.
Klein R, Klein BE, Moss SE, et a I.The Wisconsin Epcierniaiolic
37_ Mounts MR Koornneef L, Wiersinga WM, Prummel
17.
Study of Diabetic Retinopathy. X. Four-year incidence and Berghout A. van der Gaag R. Clinical criteria
progression of diabetic retinopathy when age at diagnosis for the assessment of disease activity in Graves'
is 30 years or more. Arch Ophthalmol 19619007:244-9. ophthalmopathy: a novel approach. Br. J. Ophthalmol.
18. Schachat AR Murphy RP (eds). Medical Rank in Ryan. Si 1989; 73,639-644
(ed): Retina, ed 2. St Louis: Mosby, 199k 38 Mounts MR Prummel MF, Wiersinga WM, et al. Clinical
19. http://www.cureresearch.com/h/hyper ats- activity score as a guide in the ma nagement of patients
country.htm. May 22, 2011 with Graves' ophthalmopathy. Clin Endocrinol (Oxf)
20. Klein R, Klein BEK, Moss SE. The relation of systemic 1997;47:9-14.
hypertension to changes in the veinal mouse 39_ httpJ/www.who.int/med iacentre/factsheets/fs104/
the Beaver Dam Eye Study. Trans Ass Sac en/ May 21, 2011
1997;95:329-48. 40. http://www.tradingeconomics.com/philippines/
21. Wang JJ, Mitchell P, Leung H. et atitvenissitesetinall nal incidence-of-tuberculosis-per-100-000-people-wb-
signs in a general older population the ire Mountains datahtml May 21, 2011
Eye Study. Hypertension 20014Z53,11-41 41. Helm CJ, Holland GN. Ocular tuberculosis. Sury
22. Wong TY, Hubbard LD, Klein 111„ et allleand alba. 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,:
SELF-TEST
abnormalities related It) allhandlerosis? _a: of func....s pictures.
Atherosclerosis Risk in Commingles SIN* Anelosder
Thromb Vosc Biol 20002a1644-50 Picture 1. Identify the encircled lesions. Give a
24. Couper DJ, Klein Ft, Hubbard L. et at Illelabilty of retinal diagnosis.
photography in the assessment of retinal miamescular
characteristics. The Atherosclerosis Illsk M Communities.
Study. Am J Ophthalmol 200Z13:178-416
25. Yanuzzi LA, Guyer, DR, Green.ViR AreMinaAtkli
St Louis:
Mosby, 1995.
26. Keith NM, WagenerHP,BarkerMACSomediferent types of
essential hypertension: their course and prognosis ' . Am J
Med Sci 1939; 197: 332-43_
27. Scheie HG. Evaluation of ophthalmoscopic changes of
hypertension and arteriosderosisArdr Ophthalmo/ 1953;
v\70 -612,1iAcontosh R Hypertensive
risk retinopathy signs as
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 1. In order to prevent diabetic retinopathy from becoming
of hypertensive retinopathy the world's leading cause of blindness, the following
should be done:
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. Fasting Blood Sugar and HbA1 C
B. Chest X-ray and PPD
C. HIV test
D. T3 and T4 determination
3. A 45-year-old male consulted a doctor for a bulging left

eye. He was advised to undergo an MRI. Because of the
Picture 3. In what disease condition is this fundus expense involved, he decided to seek a second opinion
picture associated? What are the abnormal findings? from you. You will:
& orcer a CT scan instead
B. go on with the MRI
C. order a T3 &T4 determination
D. order an HIV test
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
• Concomitant diabetic retinopathy
C. A strong association with stroke and cardiovascular
mortality
D. Renal failure
Picture 4. In what disease condition is this fundus S. In the management of diabetic retinopathy, the
picture associated? What are the abnormal findings? folrowing will apply:
aaloetics of > 2 years duration should be
referred to an ophthalmologist
B. 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
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 9. In the progression of Grave's ophthalmopathy the
28 year old guest relations officer (GRO) was found following may be encountered:
to have a small, solitary whitish lesion with binned A. "thyroid stare" resulting from the combination of lid
margins on the left fundus. You will order for: lag and lid retraction
A. T3 &T4 determination B. a "frozen" eyeball
B. fasting blood sugar C. sudden, painless loss of vision
C. serum cholesterol D. consistently abnormal thyroid hormone levels
D. HIV test
10. Mild nonproliferative diabetic retinopathy is best
8. A 50-yr old female who has had Type 2 diabetes farthe managed with:
last 10 years consults for blurred vision. Yon nought A. panretinal photocoagulation and strict blood sugar
A. look for vitreous hemorrhage control
B. order ultrasound examination tc a ierrai B. vitreoretinal surgery and endolaser treatment
detachment :17 control of risk factors and regular fundus fluorescein
C. examine for corneal defects wrtr a ocrlicr:.- xre angiography
D. do a thorough retinal examination D. 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. Define and recognize the four basic lid malpositions: Ectropion, Enbopion, Ptosis and Lid Retraction.
2. Discuss the pathophysiology of the different types of Ectropion. E—tropion, Ptosis and Lid retraction.
3. Classify the different types of Ectropion, Entropion, Ptosis and •e.--action
4. Discuss the diagnostic maneuvers performed to evaluate the feu- malpositions
5. 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 reflex closure while the periorbital portion is responsible for
.•oluntary closure_
The eyelids are important accessory structures that give

support and complement the proper functioning of the eye
-evator Palpebrae Superior's
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.
".'r•Jr.m Sulam
To understand the malpositions of the eyelids, a short 'edam' =ni-wieuratc

of the anatomy and physiology of the eyelid retractors and
protractors and other pertinent eyelid structures (Forms 1. Accra-mos Muller s Muscle
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. 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 wr-
the superior rectus muscle almost throstpout e-grr., t
Merlon tarsal muscle
held up and supported by the Whitnallt liga-rert. arc
the eyelid its muscle fibers terminalleillo a broad ieriircts biension of retractors to
iideriog fornix
sheet, the levator aponeurosis, which ir-sers ruc Lockwood's Inferior rectus
portion of the anterior surface of the 1:35.5 Ber- ^ê e, - ligament muscle
and superior rectus muscles are inne-ia.L-t1 Capsulopalpebral
branch of the 3-3 cranial nerve. and its fr-rincr- s r ape'' head
Swan
eyelid.
Orticeilirts oaf Inferior oblique
wmescie muscle
Closely associated with ti-e
This is a lid retractor - i'.^-oattielic nerves. f
function is eyelid open:- a as v 7h5 angirialEs from
the underside of the belly of the reeler mi..sdie and inserts on
the superior tarsal border_ tt ies between Me *valor muscle Figure 2. Anatomy of the Eyelid Schematic cross section of lower eyelid
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
II. BASIC EYELID MALPOSITIONS
on top of it, along the superior tarsal Nyder.
-here are four basic eyelid malpositions: ectropion, entropion,
blepharoptosis or ptosis, and eyelid retraction.
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 A. ECTROPION
beneath the skin of the eyelids ad originates from the rn..:
canthal tendon_ It has three portions the pretarsall preseptal Ectropion is the outward turning of the upper and/ or lower
and periorbital portions The pietarsal portion forms the eyelid margin. It can be easily recognized in patients due to
innermost circle, and overlies the tarsus of the upper and lower the everted position of the lid margin, which creates a space
lids. The preseptal portion forms the middle circle and overlies or gap between the palpebral conjunctiva and the globe.
the septum. The outermost circle is formed by the periorbital In severe cases, this eversion leads to visualization of the
portion, which overlies the orbital rim and bone The orbizulais palpebral conjunctiva. If the ectropion is carried medially, one
muscle is innervated by the facial nerve (N VII).The anal and may even visualize the punctum, which is normally not visible,
preseptal portions are responsible for involuntary c F.. - 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 3). Figure 5. Eyelid distraction test
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.
Sende involutional ectropion is best treated by a horizontal

Figure 3. Senile involutional ectropion of the right lower eyelid eyelid tightening procedure. Examples are lateral tarsal strip
operation and id shortening procedures such as a wedge
Eyelid laxity can be tested with the snap back test resection tithe tarsus. Figure 6 shows a patient with senile
(Figure 4). This is done by pulling the eyelids downward involutional ectwopion before and after surgical correctior
toward the orbital rim, then letting them go. Normally, the with a tarsal strip procedure.
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.
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 of earopion is done by checking on the
ughtness of the ulterior lamella, checking while the patient is
When the orbicularis oculi becomes paralyzed in affectations in upgaze or with the mouth open.
of the facial nerve (CN VII), there is loss of eyelid tone. This
is reversible in temporary cases such as Relitlolley_ Set huger ent invokies lengthening of the existing anterior
prolonged cases, such as a stroke, or CN VII palsy or paresis, lamella. Depereing on the severity of the condition,
lengliening d the anterior lamella may be done by scar
atrophy of the muscle can occur resulting in more per— =
endtkiliand zunlasty or skin grafts (Figure 8).
laxity of the eyelid (Figure 7).
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 77--4"r7-
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.
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
Figure 7. •7-a:e--: eirr ,;:ezra.fsc kaki lower Id (A)_ Nose

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 B. ENTROPION

lamella and the posterior lamella_ If there is shortening of
the anterior lamella (skin and orbicularis muscle), cicatiical Entropion is the inward turning of the eyelid margin (Figure 9). This
ectropion can occur. Some conditions that can cause this are inward rotation of the eyelid margin results in loss of visualization
scarring of the eyelid skin due to trauma, healed lacerations. of the lid margin. The lashes are also turned in and rub against
thermal and chemical burns, healed infections or abscesses, the globe. There is frequent irritation, redness and possibly
and longstanding chronic infections of the lid 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:
1. Cicatricial entropion
2. Senile involutional entropion
3. Congenital entropion
4. Spastic entropion
Figure 9. Entropion of the lower lid
the cornea. In severe cases, corneal abrasion and scarring CICATRICIAL ENTROPION
may occur, subsequently causing decrease in visual acuity.
Entropion can also result to infections of the cornea or corneal Cicatricial entropion is caused by scarring of the posterior
ulceration, which if left untreated can lead to rupture of the lamella of the eyelid, the conjunctiva and tarsus. This scarring
eye. causes a deformity of the tarsus, causing it to rotate inwards
permanently. Frequent causes of scarring are chronic infection
One should also examine the lid margin under slit lamp for of the eyelids, trauma, chronic irritation from artificial eye
conjunctivalization of the lid margin. Its presence signifies use in the anophthalmic socket, inflammatory conditions of
chronicity of the condition. One may even detect the mildest the conjunctiva such as pemphigus, pemphigoid or Stevens
of entropions with this technique. Johnson Syndrome and systemic diseases such as leprosy.
The normal mucocutaneous junction along the lid margin lies Cicatricial entropion, being caused by a permanent deformity
posterior to the meibomian glands. If the mucocutaneous of the tarsus, is best managed by surgical correction.
junction looks like it has advanced to the level of the meibomian Depending on the severity of the entropion, management
glands, or even more anteriorly, to the gray line, or the lash line, may be a wedge resection of the eyelid, a lid margin rotation
this implies that the posterior portion of the lid margin is in procedure such as a tarsotomy or a grafting procedure to
apposition with the globe, making the posterior portion of the replace the severely deformed tarsus.
lid margin conjunctivalized. One should also examine the lid
margin under slit lamp to check for its conjunctivalization. This SENILE INVOLUTIONAL ENTROPION
is a telltale sign of chronic entropion.
Senile involutional entropion is caused by aging and laxity of
Entropion must also be differentiated from trichiasis (Figure 10) tissues. There are four factors that come into play causing the
which is the inward turning of lashes and from distichiasis inward turning of the eyelid margin:
which is the presence of extra row of lashes, usually from the area
of the meibomian gland orifices. 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
~~cicatricial from senile involutional

• ng test: Press on the lower lid to return
pfl entropic position. If upon releasing it, the
Figure 10. Trichiasis (red arrow heads) _ 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 - C. PTOSIS (BLEPHAROPTOSIS)
then the patient has senile involutional entropion_
E laroptosis is drooping of the eyelids below the normal
There are several surgical procedures used to correct position. This is commonly referred to as just ptosis (drooping).
involutional entropion. Tarsal strip with retractor reinsertion is The normal position of the upper eyelid is two mm below the
the preferred procedure for this condition as it adcliessesthree superior limbus. If the upper eyelid position is any lower than
factors causing the entropion, namely lid laxity. lid serracsor this, ptosis is present (Figure 12).
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 Eye conditions may simulate ptosis and they are called
to resolve spontaneously. As the dulds toe ssassier es~~the pseudoptosis. When an eye is deviated downward
nasal bridge grows higher, and the medal eyelid sib macts (hypotropia), the eyelid may follow the eye mimicking a ptosis.
leading to resolution of the entropion. Dermatochalasis, a condition where there is overhanging skin
from the upper eyelid, may simulate a ptosis. Enophthalmos
I n moderate to severe cases, or in instances shaesponsarreous may also simulate a ptosis.
resolution does not occur, surgical couectirtse womanted
This involves removal of the cress skin ad hypersophic A complete eye examination for ptosis should start with the
muscle with concomitant use of everting eyelkl susses. basic eye examination. In addition to this, one should also
check the following:
1. Test for degree of ptosis

A. palpebral fissure height
B. Marginal Reflex Distance (MRD)
2. 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
In bilateral ptosis cases, comparing the two eyelids is not
This type of entropion may occur due to the constant practical. In these cases, one can judge the level of ptosis by
squeezing of the eyelids and spasm of the orbicularis. The observing the level of the eyelid. Since the normal position of
presence of irritative conditions oldie eye in association with 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
constant foreign body sensation causes the patient to squeeze
his eyelids frequently. This is also observed in conditions limbus; a 3 mm ptosis would mean that the upper lid margin is
located 5 mm below the limbus and so on.
such as blepharospasm. Relief of the spasm by relieving the
irritative condition will usually resolve this type of entropion.
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
Marginal reflex distance method (MRD) The MRD technique may be subject to misinterpretation in
cases of hypertropia or hypotropia, and extra caution should
The marginal reflex distance (MRD) is defined as the distance be exerted in interpretation of these cases.
between the lid margin and the central corneal reflex. This is
taken by shining a light onto both corneas, and measuring Measuring levator function
the distance between the lid margin and the corneal light
reflex. MRD1 is the margin to reflex distance of the upper lid, Levator function is measurement in millimeters of the
while the MRD 2 is the margin to reflex distance of the lower lid amount of excursion of the upper eyelid from extreme
(Figure 14). For MRD1, the measurement is expressed in + mm downgaze to extreme upgaze while immobilizing the
if the upper eyelid margin is above the reflex or — mm if the lid frontalis muscle. This is done by laying one hand on the
margin is below the light reflex. For MRD2, the measurement is patient's forehead and using the thumb to prevent the
expressed in + mm if the lower eyelid margin is below the reflex motion of the eyebrow. The patient is then instructed to
or — mm if the lid margin is above the light reflex. look down or up as far as he can without moving his head.
The difference in the palpebral fissure height on upgaze
2 and downgaze is measured and recorded (Figure 15). The
test is repeated on the other eye.
- 5 mm
0 1
cm
6 mm
0
A B cm
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) 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— , - -
morning but may begin to droopasthetilaypeopessm
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. -_
_ -: _ Figure 17. Congenital ptosis
may be good or normal Majority& ac4—re -
under thrs type.
5. Traumatic ptos is s caused by trauma to the *valor 2. Acquired ptosis refers to ptosis that is acquired
l• after birth. This type of ptosis is more commonly
associated with a strong levator muscle whose
Mechanical ptosis _ ...sed by the Asighing down of the aponeurosis has detached from its tarsal attachment.
6.
unoer lid by a mass or wow& This is commonly manifested by a comparatively
higher lid crease in the affected eye compared to
B. ACCORDING TO TIME OF ONSET the opposite eye. This difference is best seen when
the patient is asked to look down. Upon asking the
1. Congenital ptosis ptosis :-.. -esent at birth. This patient to look downwards, the ptotic eyelid will
-_ 2 2 ---ore commonly associated with a weak be lower than the opposite side, due to the levator
levator e and absence of the lid crease. As the detachment from the tarsus (Figure 18).
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)
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 Figure 19. Bell's phenomenon
(unaffected) upper lid may be used as the basis for normal lid
position. 2. Orbicularis tone - Orbicularis tone has to be evaluated in a
patient whose eyelids will be raised, to check if the patient has
Table 1. Severity of ptosis based on MRD1 and Palpebral Height Drop
enough muscle tone to cause adequate closure of the eyelids.
Se of Ptosis 11011.1D 4111111111111.1111
This is done by asking the patient to squeeze his eyelids
Mild > 1 mm 2 mm ptosis
forcibly. Now using the thumb and forefinger, try to forcibly
Moderate 1 mm 3 mm ptosis open the patient's eyes. One should feel the forceful closure of
Severe 0 or less 4 mm ptosis the eyelid against the fingers, and one can gauge the strength
of the orbicularis muscle.
D. ACCORDING TO STRENGTH OF LEVATOR
FUNCTION 3. Tear production - In a procedure that will raise the eyelids,
e.e acequate tear production to ensure proper
Ptosis may also be classified based on the strength of the lubrication df the corneal surface. One would not want to
levator muscle.Table 2 shows classification for levator function expose a patient with dry eye to a ptosis operation which
strength. would cause further exposure and drying of the cornea.
Table 2. Classification of Levator Function
This can be done by performing the Schirmer's test (Figure 20).
Classification Levator Function Put the folded end of the Schirmer's strip in each lower eyelid,
Measurement (mm) with the strip hanging out, and observe for 5 minutes.The strip
Poor 0-4 with the corner cut off is traditionally placed in the right eye.
Fair 5-7 * It may remain open, or closed, whichever
The eyes of the patter
Good 8-10 is more comfortable. After 5 minutes, one must measure the
amount of tears absorbed by the Schirmer's strip using a
Very Good 11 - 12
13- 15
millimeter rule( Dry er is suspected if the result is less than 2
Excellent
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
Figure 20. Schirmer's test mode map cause hither lid retraction. In the chronic
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.
light. One may see if there is any superfv.-:a1 n. F.3-04* lliewarilkt. A Mend flare may frequently accompany the lid retraction of
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 ID-
exaggerated 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,- Figure 21. Lid retraction in thyroid opthalmopathy
1. To elevate the eyelid above -.- _ the p era 2. Anterior Lamellar shortening - This may be caused by
to see cicatricial changes of the skin, such as in trauma or burns, or
2. To elevate the eyelid high sat" it to dose excessive removal of skin during blepharoplasty.
properly and cover the corn€.
3. To maintain proper cosmetic- e eyelid 3. After muscle surgery - Patients who undergo recession
of the rectus muscles may occasionally develop lid retraction.
Surgical repair for perisis bickides itarsomullerectomy and
levator resection for good Immix function ptosis or fascia lata
4. Idiopathic- In some cases, no known cause can be identified
sling procedure fix poor legator function ptosis.
TREATMENT OF LID RETRACTION

D. LID RETRACTION
All cases of iia retraction must be worked up for their etiology.
Lid retraction is the abnormal displacement of the eyelid Thyroid ophthalmopathy must be ruled out by requesting
toward the orbital rim, resulting in exposure of the sclera for the pertinent laboratory examinations: serum T3, T4 and
above or below the limbos (Rgure21). thyroid stimulating hormone (TSH) levels. Axial and coronal
views of an orbital CT scan will also help to determine the
Upper lid retraction may result in retraction of the eyelid presence of thyroid induced hypertrophy of muscles. To
above the superior limbus, while lower lid retraction results in minimize effect of exposure of the globe, topical lubricants
retraction of the eyelid below the inferior limbus. Sclera which 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.
3. Entropion may cause significant decrease in vision by:
Examples of surgery performed are tarsorrhaphy, recession of A. increased tearing
levator-Muller's muscle complex in upper lid retraction and B. corneal abrasions from the lashes
use of spacer grafts. C. corneal scarring from keratitis
D. none of the above
SUMMARY 4. Senile involutional ectropion is commonly caused by:

A. canthal tendon laxity
The four basic eyelid malpositions — ectropion, entropion, B. eyelid inflammation
ptosis and lid retraction - their definition, classification, C. mass on the eyelid
pathophysiology, recognition, diagnostic maneuvers, and D. tarsal shortening
management were discussed. It is important to recognize that
these conditions, if uncorrected wil adversely affect the eye 5. Entropion can be easily recognized by:
and may ultimately affect the patien*vision. Early recognition A. inward turning of the eyelid margin
and management can save the eye and sight of the patient. B. inward turning of eyelashes, rubbing on the cornea
C. superficial punctate keratitis on the cornea
due to lashes
ACKNOWLEDGEMENT D. all of the above
Dr. Catherine Vigo-Matic provided some of the pictures.

6. The following can cause ptosis EXCEPT
A. Cranial nerve III paralysis
B. Horizontal upper lid laceration 20 mm above the lid
REFERENCES margin
C. Hypotropia
1. Kersten RC (editor) et al. Basic and Clinical Science Course
D. Myasthenia gravis
2003-2004 Section 7 Orbit Eyelids and Lacrimal System,
American Academy of Ophthalmology, San Francisco,
7. The following will predispose a patient undergoing
USA, 2003. ptosis surgery to post-operative complications EXCEPT
2. Beard C. Ptosis, 3rd edition, CV Mosby, St. Louis, 1981 A. absence of Bells phenomenon
3. Hatt M. Ophthalmic Plastic and Reconstructive Surgery, B. corneal anesthesia
Georg Thieme Verlag, Stutttgart, 1986.
C. epiphora
4. Collin, JRO. A Manual of Systematic Eyelid Surgery, D. spasm of the orbicularis oculi
Churchiull Livingstone, 1983.
5. McCord Jr. CD. Chapter 5 Surgery of the Eyelids, Duane's 8. Identify the picture with lid retraction:
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.
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: Answers to S64---e 223.

A. acute blepharoconjunctivitis
B. scarring of the anterior lamella
C. scarring of the lid margin
D. scarring of the posterior lamella
8.4 Ocular Trauma
and Emergencies
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
If the globe is undamaged, the lids, palpebral conjunctiva and
I. OCULAR AND fomices can be more thoroughly examined.
ORBITAL TRAUMA
INJURIES TO THE LIDS AND ADNEXA
Any patient who comes to the emergency room 1. ECCHYMOSIS OF THE EYELIDS
possible eye injury or condition should be evaluated k -
possible life-threatening conditions. If the patient is sta.= -a, Orbital contusions due to blunt trauma may cause localized
an initial assessment of the eye should be ma.-Je tissue damage like lid eccymosis (Figure 1) with minimal
any of the two true eye emergencies: chemical bum disability. Blunt trauma, however, can also cause orbital fracture
and central retinal artery occlusion. In - and globe injury like hyphema, angle recession, iridodialysis,
appropriate management should be initiated retinal edema and retinal breaks.
and concurrently with history taking and ocular e •
Immediate referral to an ophthalmologist is manca:ory_ Treatment of lid ecchymosis consists of cold compress in the
first 24 hours followed by warm compress and analgesics as
EVALUATION OF THE EYE TRAUMA PATIENT 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 A:lac& Figure 2) can be caused by sharp objects,
eye. An eye shield should be taped to the orbital rim in cis arias al blows from a blunt object. Injury to the
of lid laceration, foreign bodies or suspected globe rupture. globe should be first ruled out before repairing the laceration.
Physical examination should begin with measurement of Lacerations ineolving the lid margin and the medial aspect of
visual acuity. If visual loss is severe, check for light projection, the ids should be referred to an ophthalmologist. Cosmetic
pupillary reaction including relative afferent pupillary defect and functional success of lid margin laceration repair
Test for eye movement, palpate the orbital rim and test depends on precise approximation of lid margin, tarsus and
for periorbital sensation. If a slit lamp is not available in the skin_ Lac ations near the medial canthus may involve the
emergency room, a penlight or a direct ophthalmoscope on
+10 D can be used to inspect the anterior segment of the eye.
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. Serail conjunctival laceration does not need to be repaired.
Antibiotics, analgesics and tetanus prophylaxis are aisc _aceraitions bigger than 5 mm should be sutured. Surgical
to the patient. 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

Figure 4. Subconjunctival hemorrhage
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 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 Figure 6. Semi Isceraion
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).
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.
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
Figure 9. Foreign body on palpebral conjunctiva. From Lightman S and patch or bandage contact lens.
McCluskey
•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
ai—oef) (Figure 13). V. 3-terior chamber is totally
e.d with blood (Figure 14) and increase in intraocular
ng may result. The treatment
- .assure is present. cornea
hypherna is yea:: = 7 n controversial. Among the
suggested treats-1-, .
- alization, bed rest, sedation,
anti-glaucoma medications, anti-
eye patch, cycle:
fibrinolytic agents :al evacuation.
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
by injury to trie ins, tens arra retina. Sts ' war deperxis on
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 Penetrating corneal injury can result to rupture of the lens
Atlas of
capsule and cataract. Blunt trauma resulting to cataract
and/or lens subluxation is often associated with posterior
3. INJURIES TO THE IRIS
segment sequelae. Complete rupture of the zonules results
in a free-floating lens in the anterior chamber (Figure 15) or
Blunt eye trauma can cause injury to the iris sphincter muscle, in the vitreous (luxated or dislocated lens). Partial severance
causing traumatic nos (constriction) followed by traumatic
of the zonules result in a subluxated lens (Figure 16).
mydriasis (dilation). Associated ciliary spasm or paralysis Management of subluxated lens depends on the severity,
may cause blurred vision especially for near tasks. Signs of iris presence of cataract and of glaucoma.
injury are constricted or dilated pupils, iris sphincter tears, and
inflammatory or pigment cells in the anterior chamber.
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
One should suspect intraocular foreign bodies (Figure

Figure 16. Lens subluxed superiorly (edge of lens indicated by 18) when a patient complains of eye pain and/or blurred
white arrows)
vision with a history of striking metal, explosion or projectile
Cataract which occurs together with a corneal laceration is injury. The anterior portion of the eye should be inspected
usually removed during the primary corneal repair. Cataract for possible site of entry. If possible, direct visualization by
resulting from blunt trauma may have varying severity. If visual funduscopy should be done. Localization of the foreign body
acuity is not decreased and inflammation and glaucoma are can be made by orbital x-ray, ultrasound or CT scan. MRI is
absent, observation is the preferred management. absolutely contraindicated for metallic foreign bodies because
the foreign body may move and cause further injury.
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.
Whenever possible, intraocular foreign bodies shoukf be Complications of chemical burns include corneal scars,
surgically removed. Iron and copper foreign bodies c case glaucoma, symblepharon (adhesions between bulbar and
inflammation and toxicity to the retina and other sr_ .7...,615 in palpebral conjunctiva) and entropion.
the eye while organic foreign bodies can cause infer — —mon
and infection. Inorganic foreign bodies like glass
inert.
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 ac inoude car
battery fluid, bleach. Figure 19 acid burns or' z eyes
of varying severity. The paies conitanct~. arly the
area around the limbus, the more , _ = Lal burn.
Figure 19. Acid burns of both eyes. OD has very cloudy cornea and
Figure 20 shows add bum resuiting ..:3:ion of the pale chemotic conjunctiva. OS has very hazy cornea and moderate
corneal epithelium chemosis
Figure 20. (A) Aad bums ::.)— ea 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

Measures to decrease intraocular pressure should be
II. NON-TRAUMATIC OCULAR initiated. These include topical anti-glaucoma medications,
EMERGENCIES acetazolamide, intravenous mannitol and glycerine. Patient
should also be given analgesics. Definitive management is
laser iridotomy or surgical peripheral iridectomy. Fellow eye of
CENTRAL RETINAL ARTERY OCCLUSION 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
Lt fee, \tit i
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 Endophthalmitis is an intraocular infection which manifests as eye
with acute eye pain and/or headache, associated with pain that worsens on eye movement, blurred vision, eye redness
blurring of vision and red eye. Some patients may have and sweing. It can occur after an intraocular surgery, tra uma, from
vomiting. Ocular examination will show red eye, hazy or a leaking glaucoma filtering bleb or from endogenous source like
cloudy cornea, mid-dilated pupil, shallow anterior chamber an intravenousine_ Prompt referral to an ophthalmologist should
be made Management will include vitreous culture, vitrectomy
and firm eyeball on palpation (Figure 22). Tonometry will
show increased intraocular pressure. and intravitreal systemic and topical antibiotics.
ORBITAL CELLULITIS Appendix 10.3 illustrates a step-by-step diagnosis of ocular
erne gencies which can serve as a guide to primary care
Orbital cellulitis is the most common cause of proc - --.L.Th-F:fa.ns in the emerce^7% 'oom
in children. It can also occur in the elderly and in imr-
compromised patients. It can be preceded by trauma o'
be associated with infection in the paranasal sinuses. ACKNOWLEDGEMENT
Patient will present with pain, lid swelling and Carrnvia Quito anti Dr. Jonn Alfred Lim provided some of
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 REFERENCES
eye movement and blurring of vision points to a
cellulitis. Extension of the infection to the cavern., 4loiclan-Eva P, Whitcher, J.P.. Vaughn and Ashbury's
can cause bilateral CN II—VI palsy and high levet C: .;eneal Ophthaknology , 16th Edition, New York: Lange
corn plications are meningitis and brain abce, Medical Books/ McGraw Hill, 2004, pp 371-379
Nelson LB. 01rtsicy SE Harley's Pediatric Ophthalmology, 5th
5Ation. Philadelphia : Lippincott Williams & Wilkins, 2005 ,
As soon as nasal, conjunctival and blood GAEL
pp 508-525
the patient should be started on intravenous
Piefenrd practice Pattern for Acute Angle Closure
antibiotics. CT scan or MRI are helpful in dIF -
20/0031710. American Academy of Ophthalmology.
septal from orbital cellulitis, for localizing an
2005. www.aao.org
foreign body and identifying sinusitis.
4_ Lightrnan 5, McCluskey P, Handbook for Medical Students
leaning Ophthalmology, International Council of
SUMMARY Ophthalmology, 2009
5_ Webb LA Manual of Eye Emergencies, Diagnosis and
Doctors working in the emergency Koos oboold be farnirar
Management. Edinburg: Butterworth and Heinman, 2004
with the clinical presentation and 111111111111111111 dose injuied
6_ Selected pictures from the files of External Disease
eye and its adnexae. He should be compolloot iii powiding
Service ,Retina Service and Glaucoma Service of the
immediate treatment while widening kodoaribjuties so the
Department of Ophthalmology and Visual Sciences,
patient. He should likewise be ''salt Illion-ilaumatic
University of the Philippines Manila, College of Medicine
emergencies like central retinal army 00:6111011 and &axe
angle closure glaucoma. He should lotogrdie the conditions and Philippine General Hospital.
that require referral to the ophthalmologist 101 defirlitiVe 7. http://www.sarawakeyecare.com/
treatment Table 1 classifies ocubr emegenoles to true Atlasofophthalmology/anteriorsegment/
emergency, urgent condition a-7 F.e—f-lageit concitirxi_ anteriorsegmentpicture7cornealaceration.htm
accessed October 24, 2011
Table 1. Classiicalon of OctibrEmer-L.
8. Ocular Urgencies and Emergencies, downloaded
from www.opt.uab.edu , accessed last August 2011.
Therapy should be • Cherrica
instituted witrtin menuaes . cerra
SELF-TEST
Therapy should be •
1. A true ophthalmologic emergency:
instituted with,' one to •
several hours A. Central retinal vein occlusion
B. Chemical burns
C. ntra-ocular foreign body
D. Retinoblastoma
• a: ' -
• oceiar - - E-. 2. A patient has a conjunctival laceration. What will make
• --a-rnatC
you suspect an underlying scleral laceration?
- J unctival laceration is more man 10 mm long.
Therapy should be • Mule exophta6nT,s B. Conjunctival laceration is located
3 mm from the
days • Attila ribs limbus.
(whe- e .
• Acute rer. C. There is bullous subconjunctival hemorrhage around
• Bkrii-:• 7_ the conjunctival laceration.
D. Vision is 20/25.
• Optc ne-'
Adap:ec a- . -
gexaes a:4 Emergencies. from wvivr.optuab.edu
8 SPECIAL TOPICS 13.4 ,,,,4
3. This condition can cause severe eye pain: 8. One should expect visual recovery from this type of
A. Central retinal artery occlusion injury EXCEPT
B. Conjunctival laceration A. Conjunctival laceration
C. Corneal abrasion B. Corneal abrasion
D. Subconjunctival hemorrhage C. Optic nerve avulsion
D. Subconjunctival hemorrhage
4. The most important management of chemical burns is
A. Analgesic 9. The patient felt foreign body sensation while walking in
B. Anti-glaucoma medication the sidewalk on a windy day. Upon reaching home, he
C. Copious irrigation of saline solution to the injured got a basin of water, submerged his face with his eyes
eye. open. Because of the persistent eye pain which was
D. Topical anesthetic worse when he blinks, he went to the emergency room
for consult. The resident on duty saw linear abrasions

5. A machinist comes to the ER because of eye pain and on his cornea. The foreign body is most likely located in
foreign body sensation he felt after working on metal. the
You suspect a corneal foreign body. What must you do A. Bulbar conjunctiva
first before instilling topical anesthetic? B. Cornea
A. Measure visual acuity C. Limbus
B. Measure intraocular pressure D. Palpebral conjunctiva
C. Do funduscopy
D. Examine extraocular eye movement. 10. The following eyelid laceration needs to be repaired by
an ophthalmologist
6. The definitive management of acute angle closure A. Horizontai laceration, 10 mm in length, located 10
glaucoma is mm inferior to the lower lid margin
A. Laser iridotomy B. Horizontal laceration, 20 mm in length, located 1C
B. Intravenous mannitol mm inferior to the lower lid margin
C. Topical anti-glaucoma medications C. Vertical laceration, 10 mm in length, located 5 mm
D. Acetazolamide below lid margin
D. Vertical laceration, 5 mm in length, located 5 mm
7. The following clinical finding is suggestive of central from the medial canthus, involving lower lid margin
retinal artery occlusion
A. intraocular pressure of 30 mm ng Answers to Self-Test on page 223.
B. Pale and grayish retina on funduscopy
C. Pale optic disc
D. Visual acuity of 20/40
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. education and simple reassurance may be sufficient for mild conditions
or asymptomatic patients. Patient compliance 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 c- must discuss
with patients the cost, dosage, side effects. anC 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. Discuss the diagnostic and theraoeuticsiiesdaphtharndogic medkations.
3. Discuss the effects of syste— adn i+iseeddingsaoaaularfl%Xlion.
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. Anti-inflammatory drugs
8_ Anti-allergy drugs and decongestants
9. Drugs for dry eye and ocular surface disease
total volume of the conjunctival cul-de-sac of 30 microliters.
I. PHARMACODYNAMICS The excess is either drained by the lacrimal drainage system
or is blinked out of the eye by the eyelid. Increasing the drop
Pharmacodynamics or mechanism of action refers to the size, therefore, does not increase drug absorption through
biological and therapeutic effect of the drug. A drug is the cornea; rather, there is an increase in systemic absorption
an agonist or antagonist if it binds at the receptor level resulting from increased volume drained through the punctum
(e.g.neurotransmitters); and is an activator or inhibitor if it of the lacrimal drainage system into the mucosa of the nasal
binds at the enzyme level (e.g. hormone receptors). cavity and later swallowed.
The normal rate of unstimulated or "basal tear flow" is 0.5 to

II. PHARMACOKINETICS 2.2 microliters per minute. Tear flow is decreased with age
and is increased by ocular irritation caused by many ocular
The effect of drugs on the eye is dependent on specific medications. The available drug in tears for ocular absorption
pharmacokinetic properties, namely: is inversely proportional to tear flow rate.
1.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
computed. is likewise vascular. Together, the conjunctiva and sclera
constitute less than one-fifth of drug absorption to the iris and
OCULAR STRUCTURES AND ciliary body.The conjunctiva may function as a major depot for
subconjunctival injections, allowing the active drug to dissolve
PHARMACOKINETICS
slowly and be gradually released to the tears.
TEARS
MIS
The iris has sphincter and dilator muscles for pupillary
The tear film over the cornea is composed of 3 layers:
constriction and dilation, respectively. The iris functions to
regulate the amount of light reaching the retina, and contains
1. Oily layer - An outermost lipid monolayer is produced
pigment to absorb light. The pigment granules of the iris
mainly by the meibomian glands in the eyelid. It
also absorb lipophilic drugs and act as a depot or reservoir of
functions to stabilize the underlying aqueous layer
some drugs, concentrating then re-releasing drugs for longer
and retard evaporation.
periods. Drug response may vary depending on amount of iris
2. Aqueous layer - More than 95% of tears is aqueous pigmentation_
secreted by the lacrimal glands. The layer is
approximately 7 microns thick over the cornea and CILIARY BODY AND AQUEOUS HUMOR
conjunctiva, and is inherently unstable, thinning Tne recn cecr or capillaries of the ciliary body constantly
centrally at the end of each blink. generates aqueous humor, which occupies the anterior and
3. Mucinous layer -The inner thin hydrophobic coating, posterior chambers. In the anterior chamber, aqueous exits
composed of glycoproteins secreted by the goblet thee)edvough the trabecular meshwork at the angle formed
cells, functions to cleanse the tears of particulate by the cornea and iris, enters the Schlemm's canal, goes to
debris. 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
the aqueous and vitreous humor. degradation. A change in the normal pH of 7.4, however, can
causeoadar irritation and increased lacrimation. This results in
VITREOUS lammed tear flow, decreasing available drug concentration
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,
through the lens zonules, into the aqueous. and through arid increasing bioavailability of the drug.
aqueous outflow pathway.
RETINA AND OPTIC NERVE

III. OPHTHALMIC DRUG
The blood-retinal barrier resembles the blood-boin bowie DELIVERY
in form and function, with both the retina ad bait beinc
derivatives of the neural tube. Most hydooptdrc dugs an: TOPICAL ADMINISTRATION
metabolites and toxins of high molecular wieiglitull not erne-
the inner blood-retina barrier formed by theendothellal cells
of retinal capillaries. On the other hand Ilpoplac drugs cross Most ophthalmic drugs are applied topically because it is
the barrier easily in either direction. Some S)clismic drugs can simple, convenient, non-invasive, and can be self-administered
be toxic to the retina a^-_' = 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
FACTORS AFFECTING DRUG PENETRATION
posterior segment.
INTO OCULAR TISSUE
1. SOLUTIONS AND SUSPENSIONS
DRUG CONCENTRATION AND SOLUBILITY Eyearop soiutions and suspensions are the most commonly
The rate of C.7 used form of topical administration. Eye drops, however are
Law, is linearly dependent On the ccr _ fference an inconsistent and imprecise method of drug delivery.
between the compartments on either side c- -- e barrier. A Compared to ointments, eye drops are easier to instill and
higher drug concenuation improves drug penetration. 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,
VISCOSITY
one drop is SO microliters, which exceeds the volume of the
Molectha: is a function of molecular weight and
conjunctival cul-de-sac of 30 microliters.
concentration_ Addition of an "ophthalmic vehicle' to the
active ingredient and preservative complements drug action Standard colors for drug labeling help lessen confusion: red
by providing proper tonicity, buffering, and viscosity to the for mydriatics and cycloplegics, green for miotics, pink for
formulation_ Vehicles such as methylcellulose and polyvinyl steroids, brown or tan for anti-microbia Is, teal for prostaglandin
alcohol are water-soluble viscosity enhancers with both analogues, yellow or blue for beta blockers, and orange for
hydrophilic and lipophilic sites. carbonic anhydrase inhibitors.
SPECIAL TOPICS I 8.5 Ocular Pharmacology 209
Instillation of eye drops may be done with the patient looking 5. SOLID DELIVERY DEVICES
down and retraction of the upper eyelid, or with the patient Solid delivery devices allow for a more regulated release
looking up with head inclined backwards and retraction of drugs, instead of the pulsed administration of solutions,
of the lower lid. The drop is applied to the exposed bulbar characterized by an initial period of over dosage followed by
conjunctiva, avoiding the cornea to minimize a blink reflex. relative under dosage.
The dropper is kept away from the globe to prevent contact
a. Soft contact lenses
contamination and possible injury. The eyelids are gently
Contact lenses with high water content, when placed in
closed without squeezing to retard nasolacrimal drainage and
soaking solutions, absorb more water-soluble drugs for
minimize potential side effects associated with systemic drug
later release into the pre-corneal tear film. However, rapid
absorption. Nasolacrimal occlusion for 2 to 3 minutes; done by
loss of drug from the contact lens lessens the significance
applying finger tip pressure over the punctum and canaliculi,
of this advantage over topical administration of solutions
may enhance intraocular drug absorption.
and ointments.
2. OINTMENTS b. Collagen shields
Ointments have the advantage of prolonged ocular contact
Collagen shields are thin membranes of porcine or bovine
time compared to solutions, allowing for less frequent dosing
sclera collagen, and are similar to contact lenses in shape
of the medication. When ointments are applied during the
and application. They are packaged in a dehydrated state
day patients frequently complain of blurred vision and "oily"
and are rehydrated with a drug solution before placing on
skin around the eye. Hypersensitivity to the preservatives and
the cornea. The drug is released as the shield dissolves.
certain sensitizing agents in the ointment may occur due to
Topical anesthesia is placed into the eye to minimize
prolonged contact time.
discomfort caused by application of the shield.
Administration of ointments is done while asking the patient
c. Filter paper strips
to look up with head inclined backwards. While retracting
the lower lid, a 1 centimeter strip of ointment is placed in the Drug-impregnated filter paper strips allow for easy
inferior conjunctival cul-de-sac. When applied to the cul-de- administration of drugs in amounts adequate for
sac, ointments melt immediately and spread to the eyelid their intended clinical purpose. The use of filter paper
margin, lashes, and skin. Ointment in the eyelid margin acts strips prevents administration of excessive amounts
as a reservoir and increases drug contact time. An alternative and eliminates the risk of solution contamination
method of applying ointments is by placing it on a cotton- with Pseudomonas aeroginosa. Three staining agents,
tipped applicator and applying it to the upper eyelid margin sodium fluorescein, lissamine green, and rose bengal,
and lashes. This method minimizes blurred vision and drug are commercially available in filter paper strips. The
irritation.
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 The drug-impregnated filter paper strip is moistened with
shampoo, by lid scrub is helpful in the treatment of seborrheic a drop of normal saline prior to touching the exposed
bulbar conjunctiva and conjunctival cul-de-
or infective blepharitis. This aids in the removal of oil, debris, sac of an eye
and desquamated skin from the inflamed eyelid. Lid scrubs are with retracted lower eyelid. Separate strips can be used
also used for hygienic eyelid cleaning. for each eye to avoid cross-contamination between eyes.
d. Cotton pledgets
Lid scrub involves placing a strip of ointment or several drops A pledget is a small elongated tuft of cotton constructed
of solution or detergent on a cotton-tipped applicator and by teasing the cotton tip of an applicator. The cotton
applying it to the lid margin with eyes open or closed. pledget is saturated with 1 or 2 drops of solution, usually
mydriatics like phenylephrine, and placed into the inferior
4. GELS conjunctival cul-de-sac (fornix).
Gelling agents transform from gel to liquid upon contact
with the eye, rendering the drug hydrophilic and minimizing PERIOCULAR ADMINISTRATION
complaints of blurred vision.

Compare° w topecai administration, local injections into
periocuiar tissues bypass the conjunctiva and corneal
Gel-forming agents are applied as eye drops and are converted epithelurn. and delver higher concentrations of drugs with
by temperature changes into a gel-like viscosity that prolongs IOW lipid sdubdity such as corticosteroids and antibiotics.
vision or
contact time with the eye without causing blurred There are four main routes for periocular injections. Selection
ocular discomfort. of the injection SINP depends primarily on the location of the
target aneet-
1. 5 UBCONJUNCTIVAL INJECTION
INTRAVITREAL ADMINSTRATION
Subconjunctivai injections between the conjunctiva arc,
Tenon's capsule allow for higher local drug concert-atcrs
Because of the blood- retinal barrier, there is decreased
with the use of smaller drug quantities.This eliminates.use
penetration into the eye of systemic antibiotics. Intraocular
systemic effects of the drug, avoids the need for oca or infections like endophthalmitis can be successfully treated
systemic drug administration, and minimizes probes we" with intravitreal rather than systemic administration.
patient compliance.
SYSTEMIC ADMINISTRATION
2. SUBTENON'S INJECTION
1. Oral
Compared to subconjunctival injection, subtenon's ripEction
2. Intravenous
between the Tenon's capsule and sclera offers ktIlle advantage Intramuscular
3.
and may even deliver lower quantities of drug into the
eye, as well as increase the risk of globe perforaton For PHOTODYNAMIC THERAPY
certain inflammatory diseases, like severe weird. cystoid Photodynamic therapy involves systemic administration of
macular edema, and diabetic macular edema. injection of
a photosensitive drug followed by the application of non-
corticosteroids may penetrate the underlying sclera. and so thermal laser to produce a "dynamic' reaction which causes
the drug must be placed immediately adjacent ID die site of
necrosis of the lesion. This method is used to treat choroidal
inflammation.
neovascularization associated with age-related macular
degeneration. Non-thermal light converts the drug and
3. RETROBULBAR INJECTION
produces cell death of abnormal tissues. Unlike conventional
Drugs injected into the intraconal space for inside the
laser procedures, photodynamic therapy produces minimal
muscle cone posterior to the globe) En da& aneghetics.
damage to normal retinal and choroidal tissues.
corticosteroids, phenols, and alcohot. Fletrobulbar ilection of
anesthetics results in rapid onset of anesthesia and akinesia
(or skeletal muscle paralysis) for anterior segment arc IV. OCULAR
vitreoretinal surgery. The retrobuIbar technique however. is a
blind procedure where a needle is placed ediemely dos-7 -
PHARMACOTHERAPEUTICS
the globe while aiming for the roust* cone. vitich c----
vital structures like the optic nerve. Potential risks LOCAL ANESTHETICS
inadvertent globe penetration. ietrobufbar hemorrhage
direct injury to the optic nerve Local anesthetics act on cell membranes to produce
completely reversible conduction blockage of nerve impulses,
4. PERIBULBAR INJECTION resulting in sensory anesthesia and skeletal muscle paralysis
The peribulbar technique invokes one or more injections (or akinesia), without structural damage to nerve fibers and
around the globe, without directly aiming forthe muscle cone loss of consciousness. Duration of the anesthetic effect is
Anesthetic injected around the globe eyeing,* infiltrates proportional to the length of time the drug is bound to nerve
the muscle cone. Although also a bind procedure, the proteins, which depends on the chemical structure of the
peribulbar technique is safer than the retrobubar technique. drug, the drug concentration, the amount of administered
Compared to the retrobutpar technique. penbulbar injection drug, and the rate of drug removal by diffusion and circulation.
Of anesthetics provides a simian anesthesia and akinesia, but Local anesthesia containing amide is metabolized primarily by
with less rapid onset. the liver.
LINJECTABLE ANESTHETICS
INTRACAMERAL ADMINISTRATION
a. Lidocaine
Intracamerai acknirisnation involves directly plating a drug
Lidocaine is the M05: frequently used injectable
into the anterior chamber. During anterior segment surgeries.
anesthetic. One percent lidocaine without preservatives
such as cataract extraction and glaucoma filtering surgery,
substances can be placed in the anterior chamber, like can be injected into the anterior chamber during cataract
viscoelastics to prevent damage to the comeal endothelium, surgery to supplement topical anesthesia. Addition
sustained-release pelets to provide high intraocular drug of local vasoconstrictors like epinephrine to lidocaine
levels for a longer duration. and unpreserved 1% lidocaine decreases the rate of absorption into the systemic
to anesthesize the iris and diary body and decrease patient circulation, resulting in longer duration of action, less local
discomfort. bleeding, and lower risk of systemic anesthetic toxicity.
8 SPECIAL TOPICS 1 85 Ocular Pharmacology MI

b. B upivacaine b. Non-salicylate non-steroidal anti-inflammatory
c. Procaine drugs (NSAIDs)
d. Etidocaine
e. Mepivacaine The analgesic effect of NSAIDs is produced by inhibiting
cyclooxygenase. The drug is metabolized in the liver and
2. TOPICAL ANESTHETICS excreted by the kidneys. Like salicylates, NSAIDs can cause
Topical ocular anesthetics suppress corneal sensitivity. GI discomfort and GI bleeding. NSAIDs also interfere with
However, it can cause eye irritation and, if used frequently, platelet aggregation, resulting in prolonged bleeding
localized or diffuse corneal desquamation.The onset of action time.
is 10 to 20 seconds and the duration is 10 to 20 minutes.
Moderate stinging or a mild burning sensation immediately i. Propionic Acids
follows instillation, and corneal anesthesia lasts for 20 to 30 1. Ibuprofen
seconds. Combining two or more topical anesthetics has no 2. Naproxen
additive effect and can increase the risk or side effects. 3. Fenoprofen
4. Ketoprofen
Although rare, side effects include allergic hypersensitivity, 5. Oxaprozin
epithelial keratitis, corneal edema and corneal desquamation
resulting in tear film dysfunction. ii. Cox-2 Inhibitors
1. Celecoxib
a. Proparacaine
Proparacaine is available as a topical 0.5% solution. c. Acetaminophen
b. Tetracaine The analgesic action of acetaminophen is unclear. It is a
c. Benoxinate weak inhibitor of cyclooxygenase. Unlike aspirin, it has
d. Cocaine no anti-inflammatory properties. Therefore, aspirin is
superior to acetaminophen in treating pain associated
ANALGESICS FOR TREATMENT with inflammation. Acetominophen, however, does not
cause gastrointestinal irritation or prolonged bleeding
OF ACUTE OCULAR PAIN
time from inhibition of platelet aggregation. It can be
used safely during pregnancy and breastfeeding. When
Patients may experience substantial pain from ocular
used in patients with chronic alcoholism and pre-existing
conditions like corneal or conjunctival foreign bodies (even
liver impairment, acetaminophen can lead to serious liver
after their removal), corneal abrasion, and ocular trauma.
toxicity and ultimately death.
Nociceptors in specialized pain endings of peripheral
nerves, activated in response to trauma, can be found
d. Non-narcotic combinations
in the subcutaneous tissues and periosteum of the eye
and orbit. Pain signals are conveyed to the brain through
2. OPIOID (NARCOTIC) ANALGESICS
the trigeminal nerve; in turn, the trigeminal nucleus
Opioids are natural or synthetic compounds that possess
sends pain signals to the somatosensory cortical areas in
morphine-like analgesic effects. They are the first drug of
the brain. Analgesics act as: (1) Peripheral acting agents,
choice for treatment of severe acute pain affecting both
like nonsteroidal anti-inflammatory drugs (NSAIDs), block
noxious stimulation (pain) and the emotional component
the formation of inflammatory and pain mediators at the
of subjective distress (suffering). Analgesia is produced by
cyclooxygenase pathway; (2) Anesthetic agents, which block
binding to various opioid receptors in the brain, brainstem,
nociceptive signals from the peripheral source to the brain or
and spinal cord, thus mimicking the effect of endorphins.
spinal cord; and (3) Centrally acting agents, like opioids, that
The amount of analgesia produced is directly proportional
react with specific receptors in the central nervous system.
to dose. with no ceiling effect, thus the potential for abuse
and ackfiction_ It produces a high degree of sedation and GI
1. NON-OPIOID (NON-NARCOTIC) ANALGESICS
Non-opioid analgesics like NSAIDs are the most effective and
safest for short-term use.
a. Codeine
b. Oxycodone
a. Salicylates c. Hydrocodone
Acetylsalicylic acid, or salicylate aspirin, has analgesic, d. Propoxyphene
anti-inflammatory, and antipyretic properties. Aspirin e. Hydromorphone
inactivates the cyclooxygenase pathway. The most f. Tramadol
common side effect is gastrointestinal disturbance,
particularly increased gastric acid secretion.
MYDRIATICS AND MYDRIOLYTICS :-. a - . 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
billydniatic-cycicc agents can increase the intraocular
(norepinephrine) and adrenaline (epinephr and affect
pressure it with open angle glaucoma and can
various ocular functions like pupil size, pa 1pebra ssuie. bksod
precipitate a- attack of acute angle closure glaucoma in
vessel diameter, aqueous flow, and accommoca - 7r_ These
J,"" -?—,W0Cfl.':,1?tde angles.
are two main groups of receptors: a (alpha) and F -- --
several subtypes. Adrenergic nerve terminals air ___
1. ATROPINE SULFATE
in the ciliary smooth muscle, iris dilator muscle. aid wOrillees
,s a .ective muscarinic antagonist. It is
muscle.
:st potent mydriatic and cycloplegic agent, with
ass starting at 12 minutes and lasting up to 10 days,
Adrenergicagonistsorsympathomimetics causeasympathetic
and cyc = 7. a 7. a starting at 12 minutes and lasting 7 to 12
response (flight-or-fight response), like increase in heart rate
-- paralyzes accommodation up to 8 days. It is
and pupillary dilation. Mydriatics are used to dianeihe Dam
.:_.• ng cycloplegic refraction of young, actively
Adrenergic receptor antagonist, anti-ackenergi:3. or
adrenergic-blocking agents block the - g children with suspected latent hyperopia
Midriolytics are a-receptor blocking agent -.- a - La - and acz: - -odative esotropia. In school-aged children and
constriction (miosis). adults~~hov.E. er, the prolonged paralysis of accommodation
7 — ear vision, thus a short-acting cycloplegic is
, c. -E• to prevent this inconvenience. The
1. MYDRIATICS
. caused by atropine has been used in
arra:: . . as a form of 'penalization" of the eye with
a. Phenylephrine
nor-; Per combined with optical over-
Phenylephrine is a selective a-receplotagortist It 6 nxistty
or a - a :ernative to direct occlusion of the
used clinically for dilating the pupi ugh _-
better e.-s - a-:: a :-.erapy. In inflammatory conditions,
dilation at 45 to 60 minutes and cloaricr _-_- 77 77 - = . lbs. atropine relieves pain by relaxing ciliary
as
It contracts the iris dilator muscle arc : --
_ide spasm, prevents formation of posterior synechiae by
of the conjunctival arterioles. cau9ing that prevents iris-corneal touch, and reduces
7--.7- :7
and blanching of the conjuncLikra corn wasp.: 7 -
Other effects include widening of the a=_==_a :e a and flare by decreasing excessive permeability
a -led vessels.
from sympathetic stimulation tithe Mid& s
decreased intraocular press se bom 5,4ueous
production by the ciliary body_ Because a' - a^ry local Adverse systemic reactions appear to be dose dependent.
and systemic side effects of plienylephrim_ ong term Topically applied atropine is absorbed systemically through
clinical use is unsatisfactory the conjunctival vessels and the nasal mucosa. Children
and elderly are more susceptible to anti-cholinergic toxicity,
b. Hydroxyamphetarnine including depressed salivation, fever, hallucinations,
convulsions, and death. The treatment of atropine overdose
c. Cocaine is supportive: preventing hyperpyrexia and dehydration.
Physostigmine, in repeated doses, is reserved for severe and
2. MYDRIOLYTICS life-threatening side-effects.
Dapip-azole 2. HOMATROPINE HYDROBROMIDE

e is an a-receptor blocking agent in the
iris dilator muscle, re:. 7 - in miosis and decreased 3. SCOPOLAMINE HYDROBROMIDE
intrao_ 'a c -essure_ is concentratior
dep, :an "E 4. CYCLOPENTOLATE HYDROCHLORIDE
Cyclopentolate is the cycloplegic agent of choice for
CYCLOPLEGICS cycloplegic refraction in all age groups due to its relatively
fast onset of about 20 to 30 minutes and short duration of 24
Cycloplegic agents are a E-7 - an; - :- hours. Recovery of accommodation to permit reading is about
muscarinics, and cr.: 6 to 12 hours.
:• j ace--3 —
the action of acetylchc e on 7- s inre- .
autonomic nerve fibers, and on srr: :71 Compared to atropine, cyclopentolate has more CNS side
e cells that la
cholinergic autonomic innervation. Cholinergic innervation effects, such as cerebellar dysfunction, visual and tactile
hallucinations.
in the eye is seen in the ciliary body, iris sphincter muscle,
8 SPECIAL TOPICS 18.5 Ocular Pharmacology MI

3. ADRENERGIC AGONISTS
5. TROPICAMIDE
Tropicamide is a non-selective muscarinic antagonist. Like In the 1920s, epinephrine, an adrenergic agonist, was
cyclopentolate, the onset is fast (20 to 40 minutes) and the documented to decrease 10P after topical application to the
duration of action is short (6 hours). The mydriatic effect is eye. Alpha 2-receptor agonists in presynaptic adrenergic nerve
greater than the cycloplegic effect, so it is not the drug of terminals of the ciliary body decrease production of aqueous
choice for cycloplegic refraction. Unlike atropine, scopolamine, humor and enhance uveoscleral outflow. When administered
and cyclopentolate, topical tropicamide absorbed systemically thrice daily, it is an effective short term therapy for patients
has little affinity to systemic muscarinic receptors, thus adverse on maximal medical therapy who still require additional 10P
systemic effects are rare. reduction. It is effective in preventing 10P spikes after laser
procedures like argon trabeculoplasty, YAG capsulotomy, and
OCULAR HYPOTENSIVE DRUGS YAG peripheral iridotomy.
a. Apraclonidine
The group of diseases collectively known as "glaucoma" is
Common ocular side effects include conjunctival
managed pharmacologically or surgically by lowering the
blanching, lid retraction, and mydriasis.
existing intraocular pressure (10P). Ocular hypotensive agents
each have their unique mechanisms of action, so drugs can be
b. Brimonidine
used alone or in combination.
Unlike apraclonidine that causes mydriasis, brimonidine
causes miosis. Dry mouth is the most common systemic
1. PROSTAGLANDIN ANALOGS
side effect. Other side effects include headache,
Prostaglandin analogs are the "first-line" treatment for most
drowsiness, and fatigue.
patients with open angle glaucoma and ocular hypertension
because of their convenience (once daily dosage) and good
4. CARBONIC ANHYDRASE INHIBITORS (CAI)
safety profile. The most common side effect is conjunctival
Inhibition of carbonic anhydrase activity in the ciliary
hyperemia. Other side effects include reversible increased
processes by CAI decreases aqueous production because
pigmentation to the eyelid skin and iris color, hypertrichosis,
carbonic anyhydrase catalyzes the cellular production in the
allergy, anterior uveitis, cystoid macular edema, and punctate
corneal erosion. There is no drug tolerance with prolonged ciliary epithelium of bicarbonate, an essential component of
use. the aqueous humor. Systemic CAls, such as acetazolamide
(250 mg capsule every 6 hours), lowers 10P by inhibiting the
Latanoprost, the first commercially successful prostaglandin activity of carbonic anhydrase throughout the body. CAls are
analogue available, decreases l01) by decreasing uveoscleral excreted unchanged by the kidneys. Impaired renal function
outflow. It is most effective when used in combination with may require substantially lower doses of CAls. Oral CAls can
Timolol. cause hypokalemia; thus, necessitating potassium monitoring
and replacement.
a. Latanoprost
b. Travoprost Topical CAls, as a twice or thrice daily dose, have an onset of
c. Bimatoprost action at 2 hours and duration of 8 hours. Topical and oral CAls
do not produce an additive effect, and their combined use is
2.11-ADRENERGIC ANTAGONISTS (j3-BLOCKERS) not indicated in glaucoma treatment.
The ocular hypotensive effect of (3-blockers is from antagonism
of the (32 adrenoceptors,in the ciliary body. With twice daily a. Acetazolamide (available locally in tablets of 250 mg)
dose, 13-blockers decrease the production of aqueous humor, b. Methazolamide
and have an insignificant effect on outflow. Drug tolerance c. Dorzolamide ,available locally as a topical eye drop)
has been described with chronic use of (3-blockers, making d. Brinzolamide (available locally as a topical eye drop)
prostaglandin analogues better in terms of long-term efficacy
and compliance. Systemic side effects include bradycardia, 5. CHOLINERGIC AGONISTS (MIOTIC)
Cholinergic agonists, also known as parasympathomimetics
systemic hypotension, heart block and failure, bronchospasm,
or cholinomimetics, are biologically similar to acetylcholine.
diarrhea, and amnesia.
They are divided according to their mechanisms of action,
into direct and indirect acting (cholinesterase inhibitor). Direct
a. Timolol
acting agents. like pilocarpine, act directly at the neuroeffector
b. Betaxolol
junctions of the iris sphincter muscle and ciliary body, resulting
c. Levobunolol
in pupilary constriction, spasm of accommodation, and
d. Metipranolol
reduction d 10P. Indirect acting agents inhibit cholinesterase,
e. Carteolol
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: . :in
four times a day, pilocarpine is indicated in acute angle- col
closure glaucoma. It is also useful in stre-.:"jng ti' iris
prior to laser iridotomy. Ocular side effects common. d. Inhibiting folk acid synthesis. is seen in:
making pilocarpine intolerable to mans -.:..a-Lencs. Side - _ amides
effects include blurring of vision due to acconignonatiwe it Pyrimethamine
spasm in the young, miosis in the elderly with tracts. Trirneth C'irT1
pupillary block with secondary angle-closure glaucoma.
and retinal detachment. Systemic side effec-_--1, assoomed e. Inhibition of enzymes DNA gyrase and
with the cholinergic activity of pilocarpine are topoisomerase IV, which are specific for bacteria.
b. Carbachol quinolones (fluoroquinolones) like

7, norficcocin, dprofloxacin, ofloxacin,
c. Echothiophate ic •- a :in, gemifloxacin, levofloxacin, and
ANTI-INFECTIVE DRUGS
-±-e-af,-; starts with obtaining a history
".-e patient. A tentative diagnosis
Anti-Infective drugs exhibit selec-u.e towicity.The dilemmas
of the causative .--.icroc - :anism is made, which becomes
between the cells of humans and of miC100111111111191115 allow
the basis kw empiric trey- — ent using one or a combination
drugs to kill microorganisms while causing eniirlirnall or no
adverse reactions to the host. "Spectfurn of activity' velars to
a agents. usually a .7-spectrum agent that is the least
wick. The route of ad— - stration (topical application, oral
whether a drug is "narrow- or broad-spec:rise', diepencing on
administration. ar injection, intravitreal injection,
the number of species the drug is active against.
intravenous kijection. or a combination of routes) and the
dose are determined. For ocular surface infections, topical
1. ANTI-BACTERIAL DRUGS
appicaion is preferred. Laboratory culture of tissues or body
Bacteria can oe divided into C:i;an Star !maim cell shape and
kids is used to confirm the clinician's initial diagnosis and
cell arrangement. Common 7 ?..sing - = -- pm
to determine the sensitivity and resistance of the isolated
are Staphylococcus aureus _ 43 ix
microorganism to the agents started.
Gram-positive, and Neisseria _ Estnerthia co&
Serratia marcescens, Proteus ;sada/Toms aerughosa
for Gram-negative bacteria. Reasons for antimicrobial failure include: wrong diagnosis,
drug resistance, inadequate dosage, patient non-compliance
Anti-bacterial drugs act against bactertathroucfrvthefollowing and inadequate immune response. Bacteria can mutate to
mechanisms: cause drug resistance by: producing enzymes that inactivate
the ar--.Thiotic, blocking the binding of the antibiotic to the
recec -.: - site, and preventing antibiotic entry into the bacterial
a. Inhibiting cell wall synthesis of peptidoglycans,
cell.
which is necessary for structural integrity of the
bacteria. :
2. ANTI-VIRAL DRUGS
i. Pe-
- ;ge --.erfere with viral replication and
ii. CephatiSpOriln
on by in - siting thymidine kinase needed for
iii. Ba:
nucleic acid synthesis.
N. Ite'
Herpes simplex virus (HSV1) is the most frequent cause
b. Selectively disrupting bacterial cell membranes.
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,

a. Tr ifl u rid ine
which differ from that of humans in size and
b. Acyclovir
composition, thereby inhibiting bacterial protein
c. Valacyclovir
synthesis. - s see- :
d. Famcyclovir
Armnogrycosides like neomycin, gentamicir
tobrarnycin, and amikacin e. Gancyclovir
8 SPECIAL TOPICS 1 8.5 Ocular Pharmacology arif

release in type I (Ig-E mediated) hypersensitivity immune
Admovirusos (serotypes 2, 7, g,19, and 37) cause conjunctivitis
response; and (4) the inflammatory prostaglandin pathway
and epidemic keratoconjunctivitis. Currently, no antivirals are
by blocking phospholipase A2, which prevents biosynthesis
approved for ocular adenoviral infections.
of arachidonic acid, and production of prostacycline,
Cytomegalovirus (CMV) retinitis is the most common thromboxane A, prostaglandins, and leukotrienes. Steroids
opportunistic ocular infection in patients with AIDS and decrease capillary permeability and fibroblast proliferation.
immune-compromised transplant patients. They affect the quality of collagen deposition, thereby
influencing tissue regeneration and repair.
3. ANTI-FUNGAL DRUGS
Fungi can infect any eye structure, including the cornea, Corneal penetration of topical steroids is affected by the
conjunctiva, lens, ciliary body, vitreous, retina and the entire steroid base of the drug. Acetate and alcohol derivatives make
uveal tract. The most common ocular fungal pathogens are the steroid molecule more liphophilic. Salts, such as sodium
the yeast Candida and the molds Aspergillus, Fusarium, and phosphate and sodium hydrochloride, make the steroid
Curvularia. molecule more hydrophilic. Acetate derivatives produce the
highest corneal concentration. The route of administration is
There are four classes of anti-fungals based on mechanism of determined by the location of inflammation. The dosage and
action: frequency of administration are determined by the clinical
a. Polyenes increase cell permeability by binding experience of the physician, but should be high enough to
ergosterol in the cell membrane. They are fungistatic suppress inflammation. Short-term, low dose topical steroid
at low concentration and fungicidal at higher treatment generally does not produce side effects. Long-
concentration. Resistance is relatively rare. term, high dose treatment must be gradually tapered and not
i. Amphotericin B discontinued abruptly.
ii. Natamycin
Corticosteroids can be classified as short acting
b. Pyrimidines inhibit DNA synthesis by blocking (hydrocortisone, cortisone, prednisolone), intermediate
thymidine kinase. It is fungistatic and drug resistance acting (trimcinolone, fluprednisolone), and long acting
can occur. An example is Flucytosine (dexamethasone, betamethasone).
c. Azoles inhibit fungal growth by increasing cell Ocular hypertension and cataracts are the most common
permeability through binding ergosterol in the cell ocular side effects of steroid treatment to the eye by any route.
membrane. They are fungistatic. Drug resistance can Steroids can also retard corneal healing and can increase
occur with their use. Examples are: susceptibility to viral, fungal, and bacterial infection. Other side
i. Ketoconazole effects include paradoxical anterior uveitis, mydriasis, and ptosis.
ii. Miconazole Systemic side effects include adrenal suppression, peptic ulcer,
iii. Itraconazole
hypertension, increased blood sugar, osteoporosis, mental
iv. Fluconazole
changes, and activation of tuberculosis and other infections.
v. Voriconazole
2. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
d. Echinocandins weaken the cell wall by inhibiting (NSAIDS)
glycan synthesis. Like steroids, NSAIDs reduce inflammation but without
i. Caspofungin the side effects of steroids. Topical NSAIDs, however, are
Micafungin less effective than topical steroids in controlling anterior
iii. Anidulafungin chamber inflammation. It blocks the cyclooxygenase arm
of the inflammatory prostaglandin pathway. Ketorolac and
diclofenac reduce pain and discomfort after corneal refractive
ANTI-INFLAMMATORY DRUGS
surgery.
1. CORTICOSTEROIDS NSAIDs can prolong clotting time from decreased platelet

Corticosteroids, particularly prednisolone, are the most
aggregation.
common agents for ocular inflammation. They affect every
tissue in the body and every aspect of the immune system by
3. CYCLOSPORINE A
inhibiting: (1) neutrophil migration into the extracellular space
Cyclosporine A is used to treat keratoconjunctivitis sicca (dry
and adherence to vascular endothelium at the site of tissue
eye). It is safe and well-tolerated.
injury; (2) B-cell and T-cell lymphocytic activity by preventing
mnii 1 - /ALLLKGY DRUGS AND
antihistamines, such as pheniramine maleate and antazoline
DECONGESTANTS phosphate, are commercially available in combination with
naphazoline, an adrenergic agonist decongestant. Second
generation antihistamines, such asazelastine, ketotifen, and
The eye, particularly the conjunctiva, eyelids, and cornea, is a
olopatadine, also 6?...e ? ?. stabilizing effect.
common sitefor allergic reactions.The immunesystemprovides
a defense mechanism against antigens, such as pollen
3. MAST CELL STABILIZERS
dander. A normal immune response removes ar _ _
as cromolyn sodium, lodoxamide,
with an inflammatory reaction that results in minimum tissue
nedocromi, and pemirolast, inhibit type I immune response
damage. Hypersensitivity or allergic reactions are exaggerated
and release of mediators of allergic disease by preventing
immune responses that result in tissue damage. -Twes I and
mast cell degranulation and calcium influx across mast cell
IV hypersensitivity responses play a significant to,. = -_- -
—embr
eye disease. Type I or humoral hypersenolioir
mediated mainly by histamine, involves immette-
4. NONSTEROIDAL ANTI-INFLAMMATORY
of B lymphocytes and production of Immo-
DRUGS ,NSAIDS)
(IgE) that binds to mast cells and basophils
•etoiciac uoinewomine is the only topical NSAID approved
cyclooxygenase arm of the inflammatory p
for beatinent of seasonal allergic conjunctivitis. It inhibits
pathway. Histamine release can result in a vice range of
cydoonygenase, an enzyme needed for the conversion
clinical manifestations, from life-threatening a-azrglapc
of asachidonic acid to prostaglandins, an itch-producing
shock to the relatively benign presentations at ad—T
substance in the conjunctiva.
tearing, and conjunctival hyperemia. Histamine aso
hypotension, tachycardia, and decreased atricneiasitular rode
S. 00111TKOSTEROIDS
conduction time. Type IV or cell-mediated immune resPorse
SterOidS are effective in treating seasonal allergic conjunctivitis
is a delayed hypersensitivity reaction involving TIlriphocyles.
by deaeasing histamine release, preventing degranulation of
mast cells, and preventing formation of various mediators.
Avoidance of environmental allergen= "P,
management. Treatment of ocular allerry.
PREPARATIONS FOR DRY EYE
and characteristics of symptoms.
AND OCULAR SURFACE DISEASE (OSD)
1. DECONGESTANTS
•ftmphainine.
Ocular decong:__ .ants, such as pherigl pilline. Dry eye syndrome is described as a deficiency in the quantity or
oxymetazoline, and tetrahydrozoine are sysligicatbenergic quality of the tears or tear film due to inadequate aqueous tear
agonists that cause conjunctival Va500311INICNOn iD lessen production (referred to as keratoconjunctivitis sicca or KCS) or
hyperemia and edema. to excessive tear evaporation. Dry eye causes ocular surface
disease and is associated with symptoms of ocular discomfort
2. ANTI-HISTAMINES and varying degrees of ocular surface inflammation.
Anti-histamines inhioit tne action of histamine_ They prevent
further release of histamine but usualllydoesnot reverse &mica' Treatment of OSD involves relieving ocular symptoms, healing
manifestations already present ilia nasal and conjunctival the ocular surface, and preventing serious complications.
itching, sneezing. congestion., and maser, aid red eyes. Oral Treatment of dry eye can be categorized into: (1) tear
antihistamines may be sedating (first generation antihistamines supplementation (seen in artificial tears and lacriserts), (2)
like diphenhydramine and prOmediazine) or non-sedating tear conservation (seen in ointment and punctal occlusion),
(second generation andigarnines like felarenackne, and (3) tear stimulation (seen in secretagogues and anti-
loratadine, desloratacine. and catkin?), depencing on their inflammatories or immunomodulators).

ability to penetrate the bbod brain bailer, which is affected
by factors like kpophillecity and low molecular weight. Non- 1. ARTIFICIAL TEARS
sedating second generation antibistamines bind less to 3e5 arz.t.c.a. tears snould reproduce the metabolic, optical,
cholinergic and a-adrenergic receptors. resulting in less adverse and physical characteristics of natural tears, should have a
effects associated with first generation anti-histamines, such long ocular residence time, and should contain therapeutic
as CNS depression, dry mouth, blurred vision, and tachycardia. additives to treat primary and secondary damage to the eye.
Oral antihistamines. compared to topical anti-histamines. have Water-based artificial tears with added polymer are commonly
a deeper penetration of ocular tissues, and are therefore more used to treat dry eye. Polymers, such as methylcellulose (MC),
effective in moderate to severe eyelid edema and chemosis. polyvinyl alcohol (PVA), povidone or polyvinylpyrrolidone
Topical administration, with more frequent dosing, provides a (PVP), dextran, and propylene glycol, enhance viscosity,
more direct and rapid route of relief. First generation topical lubrication, and retention time, to promote tear film stability.
8 SPECIAL TOPICS I 8.5 Ocular Pharmacology Ells

2. OINTMENTS
SELF-TEST
Non-medicated ointments containing esters of fatty acids with
long-chain alcohol, such as petrolatum, mineral oil, lanolin,
7. Which of the following INCREASES ocular drug
and lanolin alcohols serve as lubricants and create a lipid layer
absorption?
that retard evaporation. Ointments are indicated for moderate
A. Increase in age of the patient
to severedry eye, especially with lagophthalmos, exposure B. Increase in hydrophobicity of the drug
keratopathy, or severe corneal epithelial compromise. C Increase in rate of tear flow
D. Increase in size of released drop from the container or
3. SECRETAGOGUES
bottle
Secretagogues or lacrimomimetics stimulate lacrimal gland
2. Which of the following DECREASES ocular drug
function to enhance tear production. It includes cholinerg
penetration?
agents (carbachol, bethanecol, pilocarpine) and mucolytics , ncrease in drug concentration betweer
(bromhexine and ambroxol). compartments of the eye
B. Increase in lipid solubility through the epithelial cel
4. ANTI-INFLAMMATORIES/IMMUNOMODULATORS membrane
Hormonal (like androgens), anti-inflammat: C. Increase in pH of the drug formulation
corticosteroids), or immunomodulatory agents (like D. Increase in tonicity relative to tears
cyclosporine) can suppress cytokine and receptor-mediated
inflammatory process of the lacrimal gland that leads to Which is TRUE about eye drops?
3.
decreased tear production and chronic dry eye.
A. Eye drops are easy to instill but causes blurring of
vision.
B. Nasolacrimal occlusion decreases intraocular drug
SUMMARY absorption
Successful diagnosis and treatment of ophthalmic C. The bottle of the eye drop precisely delivers 50
disease require proper drug selection and administration. microliters with every drop
Inappropriate, inadequate, or contraindicated drug regimen D. The volume of a drop from the bottle is more than
may lead to potentially adverse consequences_ Pharmacists the volume of the conjunctival cul-de-sac
or other qualified drug experts must be consulted when
necessary. 4. Which of the following statements is TRUE regarding
topical eye drug preparations?
A. Eye drops have a high absorption rate into the
REFERENCES vitreous.
B. Gels are hydrophobic and this leads to complaints of
1.Bartlett JD and Jaanus SD. Clinical Ocular Pharmacology, bluffing of vision.
5th edition. St. Louis, MO: Butterworth-Heinemann, C. Ointments are most commonly used due to ease of
Elsevier, 2008.
application and minimal subjective complaints from
2. Flach AJ and Fraunfelder FW. Chapter 3: Ophthalmic patient use.
Therapeutics, in Vaughan & Ashbury's General D. Ointments have prolonged contact time, allowing for
Ophthalmology 16th edition. New York, NY: McGraw Hill less frequent dosing of medication.
Companies, 2004.
3. Weitzman S and Caprioli J. Chapter 61, Ocular
5. Addition of local vasoconstrictor epinephrine to
Pharmacology of Antibacterial Agents, in Duane's Clinical lidocaine results in which of the following?
Ophthalmology, 2006 edition. Philadelphia, PA: Lippincott A. Decrease in duration of action
Williams & Wilkins, 2006. B. Decrease in local bleeding
C. Increase in risk for systemic toxicity
4. Sutphin JE and Wells JM. Chapter S6: Medical Treatment
of Glaucoma, in Duane's Clinical Ophthalmology, 2006 D. Increase in rate of absorption into the circulation
edition. Philadelphia, PA: Lippincott Williams & Wilkins,
2. OINTMENTS SELF-TEST
Non-medicated ointments containing esters of fatty acids with
long-chain alcohol, such as petrolatum, mineral oil, lanolin, 1. Which of the following INCREASES ocular drug
and lanolin alcohols serve as lubricants and create a lipid layer absorption?
that retard evaporation. Ointments are indicated for moderate
A. Increase in age of the patient
to severe dry eye, especially with lagophthalmos, exposure B. Increase in hydrophobicity of the drug
keratopathy, or severe corneal epithelial compromise.
C. Increase in rate of tear flow
D. Increase in size of released drop from the container or
3. SECRETAGOGUES bottle
Secretagogues or lacrimomimetics stimulate lacrimal gland
2. Which of the following DECREASES ocular drug
function to enhance tear production. It includes cholinergic
penetration?
agents (carbachol, bethanecol, pilocarpine) and mucolytics
A. Increase in drug concentration between
(bromhexine and ambroxol).
compartments of the eye
B. Increase in lipid solubility through the epithelial cell
4. ANTI-INFLAMMATORIES/IMMUNOMODULATORS
membrane
Hormonal (like androgens), anti-inflammatory (like
C. Increase in pH of the drug formulation
corticosteroids), or immunomodulatory agents (like
D. Increase in tonicity relative to tears
cyclosporine) can suppress cytokine and receptor-mediated
inflammatory process of the lacrimal gland that leads to
3. Which is TRUE about eye drops?
decreased tear production and chronic dry eye.
A. Eye drops are easy to instill but causes blurring of
vision.
SUMMARY B. Nasolacrimal occlusion decreases intraocular drug
absorption
Successful diagnosis and treatment of ophthalmic C. The bottle of the eye drop precisely delivers 50
disease require proper drug selection and administration. microliters with every drop
Inappropriate, inadequate, or contraindicated drug regimen D. The volume of a drop from the bottle is more than
may lead to potentially adverse consequences. Pharmacists the volume of the conjunctival cul-de-sac
or other qualified drug experts must be consulted when
necessary. 4. Which of the following statements is TRUE regarding
topical eye drug preparations?
A. Eye drops have a high absorption rate into the
REFERENCES vitreous.
B. Gels are hydrophobic and this leads to complaints of
1. Bartlett JD and Jaanus SD. Clinical Ocular Pharmacology, blurring of vision.
5th edition. St. Louis, MO: Butterworth-Heinemann, C. Ointments are most commonly used due to ease of
Elsevier, 2008. application and minimal subjective complaints from
2. Flach AJ and Fraunfelder FW. Chapter 3: Ophthalmic patient use.
Therapeutics, in Vaughan & Ashbury's General D. Ointments have prolonged contact time, allowing for
Ophthalmology, 16th edition. New York, NY: McGraw Hill less frequent dosing of medication.
Companies, 2004.
3. Weitzman S and Caprioli J. Chapter 61, Ocular 5. Addition of local vasoconstrictor epinephrine to
Pharmacology of Antibacterial Agents, in Duane's Clinical lidocaine results in which of the following?
Ophthalmology, 2006 edition. Philadelphia, PA: Lippincott A. Decrease in duration of action
Williams & Wilkins, 2006. B. Decrease in local bleeding
4. Sutphin JE and Wells JM. Chapter 56: Medical Treatment C. Increase in risk for systemic toxicity
of Glaucoma, in Duane's Clinical Ophthalmology, 2006 D. Increase in rate of absorption into the circulation
edition. Philadelphia, PA: Lippincott Williams & Wilkins,
2006. 6. Characteristic of atropine eye drops
5. Sutphin JE and Wells JM. Chapter 61, Ocular A. Is an intermediate-acting cycloplegic agent
Pharmacology of Antibacterial Agents, in Duane's Clinical B. Is used for amblyopia treatment
Ophthalmology, 2006 edition. Philadelphia, PA: Lippincott C. It can cause blurring of vision because of its miotic
Williams & Wilkins, 2006. effect.
D. It can cause bradycardia and asthmatic attacks
218 Self-Instructional Materials in Ophthalmology 12nd Edition

7. Which of the following statements is TRUE regarding 9. Anti-microbial treatment of eye disease
prostaglandin analogues? A. Combination of several antibiotics in a single eye
A. First-line drug for open angle c -e-tt ocular drop preparation is preferred for wide microbial
hypertension coverage.
B. Mechanism of action is dec =poi aqueous B. Eye drops are given twice daily for ocular infections.
production C. Topical administration for ocular surface infection is
C. Prolonged use results in drug :ibiera-ce preferred.
D. The most common side effe..7 oypettnchosis D. Treatment is started once the results of the Gram
stain and culture are available.
8. Characteristic of beta biodcers
A. Dose is once daily Answer to Self-Test on page 223.
B. Drug tolerance develops af-L- - Drponged use
C. Mechanism of action is in ao_eous outflow.
D. Miosis is a side effect
8 SPECIAL TOPICS I 8.5 Ocular Pharmacology 219

CHAPTER 1. ANATOMY OF THE EYE ASE 2
1 A 1. When did the red eye start?
2. C 2. Was there no redness of the left eye?
3. D 3. Do you have tearing, discharge, itchiness, eye pain,
BOV?
4. D
5. C 4. Describe your eye discharge. How much is the
discharge?
6. C
7. C 5. Are your symptoms worsening, same as during the
onset or improving?
8. E
9. C 6. Are there family members or friends with red eye
similar to yours?
10. B
7. Do you have allergies?
8. Do you have previous consultation? If yes, what was
CHAPTER 2. PHYSIOLOGY OF THE EYE
prescribed? What was the response of your eye to the
1. C
medications? How are you applying the medications
2. A
and for how long?
3. True
9. Have you self-medicated? What did you apply and
4. A
what was the response of your eye?
5. A-2, B-3, C-1
6. B
7. A CHAPTER 4. BASIC EYE EXAMINATION
8. C 1. B
9. C 2. B
10. C 3. B,C,D
11. B 4. A
12. False 5. A
13. D 6. C
14. C C,D,F
15. C
CHAPTER 5.1. DISORDERS OF THE CORNEA
CHAPTER 3. EYE SYMPTOMS 1. A
2. C
CASE 1. 3. A
1. When did the blurring of vision (BOV) start? 4. C
2. Is the BOV in one eye or both? If one eye, which eye? 5. D
3. Is the BOV for distance, near or both? 6. C
4. Has the BOV worsened since the onset?Or has there 7. B
been some improvement? 8. D
5. Is the BOV in the whole visual field or in certain 9. C
portions of it only? 10. A
6. Are there associated eye symptoms like pain and 11. D
redness? 12 Ili
7. Do you squint in order to see better?

8. Have you consulted another doctor for this CHAPTER 5.2. CATARACT
problem? What did the doctor prescribe? Was there
10 improvement? 2.
9. Have you worn eyeglasses before? When? Are you 3.
still wearing eyeglasses now? If not why did you 4. D
discontinue? 5.
10. Do you have any other illness? Are you taking
medications or have you taken medicatins prior to
CHAPTER 5.3. RETINA, VITREOUS AND CHAPTER 5.5. DISORDERS
CHOROID OF THE OPTIC NERVE
CASE 1 2_
1. Vitreous hemorrhage OD probably secondary to 3. 6
Proliferative Diabetic Retinopathy / Non Prokferaiine 4. D
Diabetic Retinopathy OS 5. D
B
2. For OD: Vitreous hemorrhage because the retina 7. C
cannot be seen in OD/ negative ROR. This is probably 8 A
due to PDR because the other eye has NMI and she
has been a diabetic for many years with poor s.. -- 1A
control.
CHAPTER 5.6. ERRORS OF REFRACTION
For OS: NPDR because of the ex..:3-f B
hemorrhages and microaneurysms ano oecaLse 2_ C
is diabetic 3, A
4. C
3. I would want to know if she has ever been seen by 5. B
an ophthalmologist and diagnosed to hake diabetic -6_ A
retinopathy, if laser treatment has been done for 00. 7. C
I would also want to know if blurring of OD started 8. A
long before in a milder fours bekwe the sudden
9. C
drastic visual loss a week ago. I mil ask 'she has been
10. A
seeing her endocrinokvist, because blood sugar 11. A
management is necessary_
12. B
13. B
I will need an ocular ultrasound for OD and a 14. B
fluorescein angiogram for 05.
CASE 1
CASE 2 1. Yes
1. Age related macular degeneration wet type OS, 2. Myopia
pseudophakia OU 3. retinoscopy or autorefraction
2. Because OS has subretinal bleeding , poor vision, and CASE 2

because she is 77 years old No
Patient's age, good vision for distance, patient has to
3. I will want to know ishes- 'she takes vitamins, put reading material 50 cm away to be able to read
if she has a famiy history c - - ar retinal problem, if 1.
this has happened to her before, if anyone else in her
famey has the same problem. 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 =
2. A
CHAPTER 5.4. GLAUCOMA 3. D
4. A.
2. E.
5.
3. C 6. A
4. A 7. C
5. E 8. B
6. A
7. A
9. A
10. C
8. A
9. D
10. C
9 ANSWERS TO SELF- TEST Eg

CHAPTER 6.2. UVEITIS AND SCLERITIS CHAPTER 7.1. DEVIATION OF THE EYE
1 D 1. B
2. C 2. D
3. A 3. A
4. C 4. D
5. C 5. A
6. B 6. B
7. D 7. C
8. C 8. B
9. C 9. E
10. C 10. C
CASE 1. CHAPTER 7.2. PROPTOSIS

1. Chronic uveitis, active or with acute exacerbation, CE
2. Anterior uveitis, specifically iritis or iridocyditis 2. A
3. B-scan ultrasound, due to absence of view through 3. A
the pupil 4. B
S. B
CASE 2.
6_ C
1. anterior segment, specifically the iris, possible 7_ A
involvement of the macula & B
2. recurrent uveitis - assuming that the patient was 9. A
inflammation free during the one year period 10. A
3. Granulomatous type based on the slit lamp
11. B
findings particularly the presentation of the keratic 12. D
precipitates and presence of nodules in the iris.
4. Fluorescein angiography and OCT can be requester
CHAPTER 8.1. RETINOBLASTOMA
to determine involvement of the macula
E
CASE 3.
3. D
1. nodular episcleritis vs. nodular scleritis 4. C
2. Check the following: 5. B
a. Response of the eye to use of vasoconstrictors
6. C
and/or pressure. If blanching occurs, it is more
7. C
likely that the patient has episcleritis rather than 8. D
scleritis.
9. C
b. Presence of tenderness since tenderness 10. D
support diagnosis of scleritis.
c. Check mobility of the nodule. Movable nodule CHAPTER 8.2. OCULAR MANIFESTATIONS
would support the diagnosis of episcleritis over
scleritis. OF SYSTEMIC DISEASES
CHAPTER 6.3. TEARING EVALUATION OF FUNDUS PICTURES

B 1 - dot / blot hemorrhages; 2 - hard
2. B exudates
3. A Picture 2: Scheie Stage 3 hypertensive retinopathy
Picture 3: Hypertension. Abnormal findings: flame-
4. A
shaped hemorrhages, hard exudates,
S. A
altered AV ratio
6. A Diabetes. Abnormal findings:
Picture 4:
7. B pre-retinal hemorrhage, dot hemorrhages,
8. E microaneuryms
Edition
1. A CHAPTER 8.4 OCULAR TRAUMA AND
2. B EMERGENCIES
3. C
4. C 2_ C
5. B 3. C
6. A
4. C
7. D
5. A
8. D
6. A
9. B
7. B
10. C
C
9_ D
CHAPTER 8.3. EYELID MALPOSITIONS D
1. D
2. D
CHAPTER 8.5 . OCULAR PHARMACOLOGY
3. C
4. A
5. D
6. C
7. C
8. D
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
New Old TOTAL
General Clinic 14,506 11,207 25.713
Refraction Clinic 7,695 7.695
Subspecialty C - .:.s 6.542 29,849 36.391
Cataract 343 413 756
Contact Le - s 88 156 244
Cornea-Extemal Diesease 1.292 3,571 4.863

Dry Eye 165 915 1.080
Glaucoma 818 9,650 10,468
Low Vision 11 0 11
Pediatric Optithairboiog), .-a -: 546 3,181 3.727
Strabisrr
Neuro-C - - 176 571 747
Orbit 272 699 971
Plastic Lacrimal 638 1.535 2.173
Retina. Med ,_.
--a 1,557 4,493 6,050
Retina. S _ -- 453 3,619 4,072
Uveieis 183 1,046 1,229
TOTAL 25,444 44,355 69,799
Table 2. TO2 Ciric G: cats Table 3. Top 10 Admissions

n• NIlrnhAr 134
Cataract 3265 29.3 Corneal Perforating Injury 102 8.5

Error o' 1.664 14.8 Sclero-Corneal Perforating injury 79 6.6
Conj 692 62 R e t n o bl a sto m a 74 6.2
Hypee.•:, f 611 5.5 Angle Closure Glaucoma, Primary (PACG) 69 5.7
Pteryg 594 5.3 Corneal Microbial Keratitis, ruptured 58 4.8
Nasola:--f-ai Da: Obstructs°. 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 Nasolacrimal Duct Obstruction. acquire.
42 3.5
complete
311 2.8
Proliferative Diabetic Retinopathy 38 3.2
Presbyoc a 250 2.2
Rhegmatogenous Retinal Detachment 34 2.8
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
Rank Diagnosis Number
Diagnosis Number
1 DTS' mild mixed 39 23.6
Contusion eyeball + commotion retinae ± 512 20.6
orbital wall fracture 2 DTS with MGD, Blepharitis 14 8.5
Conjunctivitis, viral 380 15.3 13 7.9
3 DTS mild evaporative
Conjunctivitis, bacterial 203 8.2 11 6.7
4 DTS with Tear Instability
Corneal Perforating Injury ± cataractous 110 4.4 DTS with Aqueous Deficiency 10 6.1
5
lens + intraocular foreign body
6 DTS mild 6 3.6
Corneal Foreign Body 101 4.1
73 2.9 DTS with Meibomian Gland 4 2.4
Comeal Abrasion 7
Dysfunction
Central Microbial Keratitis 69 2.8
DTS with Nasolacrimal Duct
8 2 1.2
Lid Laceration/Avulsion 64 26 Obstruction
Essentially Normal Findings 61 2.4 No DTS 2 1.2
Subconjunctival Hemorrhage 42 1.7 Mixed Blepharitis 2 1.2
TOTAL NO. OF ER CONSULTS 2,490 9 DTS Moderate Evaporative 1 0.6
ETD 1 0.6
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 Diagnosis Number Rank Diagnosis No.
1 High astigmatism 10 11.4 1 Comeal Perforating Injury (CPI) 96 7.4
2 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
Adherent Leukoma 1 1.1 9 Central Microbial Keratitis, Pseudomonas 21 1.6
Anisometropic amblyopia 1 1.1 Leukoma, Adherent 21 1.6
Contact Lens Related Punctate 10 Conjunctivitis, Adenoviral
1 1.1 20 1.5
Epithelial Erosion
TOTAL NO. OF NEW PATIENTS 1,292
Lenticular Astigmatic Amblyopia 1 1.1
Myopic Astigmatism 1 1.1
Myopia 1 1.1
Traumatic Resorbed Cataract 1 1.1
Table 8. Top10 Diagnosis: Glaucoma Dr: Table 10. Top10 Diagnosis: Plastic Lacrimal Clinic
Rank Diagnosis No. FRank Diagnosis No. X
1 Open Angle Primary 1 Orbital Wall Fracture 108 16.9
2 Angle Closure Glaucoma, Primary • 2 Nasolacrimal Duct Obs•-.. - Acquired 97 15.2
Angle Closure Suspect, Primary 3 Lid Mass 31 4.9
3 Glaucoma Suspect 4 Dacryocystitis 19 3.0
4 Angle Closure, Primary 5 Nasolacrimal Duct Obstruction. Congenital 15 2.4
Absolute Eye secondary tc re; Ptosis 15 2.4
5
glaucoma
6 CN VII Palsy 14 2.2
6 Neovascular Glaucoma 48
7 Entropion 13 20
7 Secondary Angle Closure f"-..ir-r-a.
8 Periorbital Contusion Hematoma 11 1.7
8 Angie Closure Glaucoma_ Cfravic 73 28
9 Lid Laceration. unspecified 10 1.6
Open Angle Glaucoma Sear 73 78
10 Contusion Eyeball 9 1.4
9 Pseudoexfoliative -:
10 Phacomorphic
TOTAL NO. OF IA Mme! SNI
Table 11. Top10 Diagnosis: Neuro-Opnthalmology Clinic

Ta*9. Top10 Dggr *mararta-ccgi
Diagnosis No.
Rank
Rank maim* MB lit 28 15.9
8.6 1 Optic Nerve Atrophy
1 Error of Reird a..)
2 Optic Neuropathy, post traumatic 18 10.2
2 Sensory Exotropia 40 7_3
3 Inter- 7.9^t E. 7.1 3 Optic Neuropathy. 2° to ethambutol 14 8.0
4 Recra.:- • e Pc:: - :/sta Bolo* 33 6.0 4 CN VI Palsy 12 6.8

te 5 Myasthenia Gravis 11 6.3
5 30 5.5
Optic Neuritis 11 6.3
6 -e 29 5.3
6 Optic Neuropathy, Compressive 8 4.5
Ne_rx9c Dealers
27 4.9 7 Cortical Blindness 6 3.4
- .
8 Maim Reera 26 4.8 8 Anterior Ischemic Optic Neuropathy 5 2.8
24 44 CN III Palsy 5 2.8

Space Occupying Lesion 5 2.8
TOTAL NO. OF NEW PATENTS 546
Intracranial Mass 5 2.8
CN III. IV. VI Palsy 2.3
Multiple CN Palsy 4 2.3
10 lschemic Optic Neuropathy 3 1.7
Pituitary Adenoma 3 1.7
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 Table 14. Top10 Diagnosis: Surgical Retina Clinic
Rank Diagnosis No. % Rank Diagnosis No.
1 Thyroid Related Eye Disease 64 23.5 1 Proliferative Diabetic Retinopathy 101 22.3
2 Carotico-Cavernous Fistula 29 10.7 2 Rhegmatogenous Retinal Detachment 89 19.6
3 Anophthalmia 28 10.3 3 Vitreous Hemorrhage 68 15.0
4 Orbital Inflammatory Disease 14 5.1 4 Idiopathic Macular Hole 33 7.3
5 Lacrimal Gland Tumor 13 4.8 5 Endophthalmitis 24 5.3
6 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 8 2.9 Non Proliferative Diabetic Retinopathy,
10 10 22
Severe
Table 13. Top10 Diagnosis: Medical Retina Clinic Table 15. Top10 Diagnosis: Uveitis Clinic
Rank Diagnosis No. Rank 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, 5 Panuveitis 8 4.4

5 64 4.1
Non Neovascular Anterior Uveitis Chronic
6 7 3.8
6 Pathologic Myopia 45 2.9 (Non-Granulomatous)
7 Clinically Significant Macular Edema 32 2.1 7 Nematode Uveitis 6 3.3
Age Related Macular Degeneration, 8 Sclerouveitis 5 2.7

8 31 2.0
Neovascular 9 Endogenous Endophthalmitis 4 2.2
Central Retinal Vein Occlusion, 1.8 Anterior Uveitis Chronic (Granulomatous) 3 1.6
9 28 10
Ischemic
Fuch's Heterochromic Iridocyclitis 3 1.6
Central Retinal Vein Occlusion, 21 1.3
10 3 1.6
Non Ischemic Juvenile Rheumatoid Arthritis
Retinoblastoma 21 1.3 „ Posterior Uveitis 3 1,6
TOTAL NO. OF NEW PATIENTS 1.557 Uveitic Cataract 3 1.6

L
White Dot Syndrome 3 1.6
r
I TOTAL NO. OF NEW PATIENTS 183
REFERENCE
1. Astudillo P. Annual Report of Department of
Ophthalmology and Visual Science 2010
I.-. a. a.' -I • I • 11 I_ 1 I 1..‘ e_l• •

10. 2 Different Types
of Eye Redness
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 tor- -
vessels or blood rod underneath tria
due to eeding or Di of blood foam trk
(Figure 1). Subcor.,,,- :7 • -errerrhage usually -as a
localized well-defined -our any good '.e- as
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

appears IS pc .oca.zea :ne ,.moal area and diminishes
towards the fornices, this is referred to as ciliary congestion
Figure 1 E..
(Figure 3). Since deeper vessels are involved, instillation of
Conjunctival Injection, Congestion. - this instance. injection topical vasoconstrictors and exerting pressure on these vessels
IS more rnarKeo trie tor= and diminishes as the F:•ea and instillation of topical vasoconstrictors will not affect its
is approached (Figure 2). As it is the superficial cc - t-. . a' presentation. Despite its relatively benign appearance, this
vessels that are dilated, one will observe blanch - z- type of redness is frequently associated with vision-threatening
redness with pressure on the eye. This type of redness also conditions such as keratitis, anterior uveitis and acute
responds to topical instillation of vasoconstrictors. Conditions glaucoma. As both these conditions may lead to complications
associated with this type of redness are usually benign and 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.
Sclera! Congestion. The dilated vessels are deeper in (vasculitis) which can cause necrosis of the affected sclera and
location which gives a characteristic purple-colored tinge possibly jeopardize the integrity of the globe. As such, all cases
to the affected area (Figure 4). Scleral congestion will not of scleral congestion should be referred to an ophthalmologist
diminish with pressure, nor respond to topical instillation for appropriate evaluation and management.
of vasoconstrictors or epinephrine. This type of redness is
typical for scleritis, which is also considered as potentially Table 1 summarizes diagnostic characteristics of selected
vision threatening as it involves inflammation of the vessels conditions that present with eye redness.
Table 1. Serious Non-trauma Related Vision Threatening Red Eye Conditions

-sr..
...1111111111111111
CHARACTERISTICS
Condition INN"
Rednei Vision Pain Discharge Puriil 10P,,
Acute Diffuse; most Moderate to Moderate to severe; ^j: Mid-dilated; elevated

Glaucoma prominent around severely reduced; often with headache non-reactive to
the limbus iridescent vision and vomiting light
Anterior Uveitis Diffuse: most Mild to moderately Mild to moderate: No Miotic; irregular normal to
prominent around reduced photophobia shaped: poorly hypotonic
the limbus reactive to light
Keratitis Diffuse; more Moderate to Moderate to severe Yes; if May be affected generally
prominent around severely reduced infectious if associated not affected
the limbus cause with uveitis
Scleritis Focal or diffuse with Normal to mildly Moderate to severe. No Not affected Not affected
purple-tinged color reduced usually tender
Endophthalmitis Diffuse Moderately to Moderate to severe Yes Mid-dilated elevated
severely reduced
10.3 Step-by-Step Diagnosis
of Ocular Emergencies
Teresita R. Castillo MD,
Presented is a simplified ap;.-. .:.3ctillistprimorycare physic The two most common complaints of non-trauma patients
may use when confronted with p1110115 ill die Emergency seek - eye cor -. on an emergency basis would be acute
Room setting. It is assumed t.'- F nallimits seek consult in the visual disturbance (Diagram B) and an acute red eye
ER primarily for conditions that -eamItoracte in onse (Diagram C) Mese form the basis for further distinction of
_ -.hat commonly confronts a physician. Note
Initial distinction that is made is —e presence of a -. 1 -is that generally lead to unilateral visual
history of trauma, hence cistr-,-_- c Discussed inasmuch as bilateral involvement is
non-traumatic ocular C0f1CrtiCri Playmate A) a:-.- stable to non-ocular etiology. Furthermore, as
-_ 3ns fre.:;Jently overlap each other, they may fall under
Ocular trauma ;els to arty in*/ to the eye The injury may several categories.
be due to mechanical trauma art or penetrating), chemical
agents, or physical agents tarchasiadaboa Summarized are Each category of conditions is further discussed in the
additional key features arml aoriesponckig management that subsequent tables. Emphasis is placed on the key points,
each physician should know IMAM conhormed with cases of initial or immediate management for each case and lastly, the
ocular trauma. urgency or need for ophthalmologic consult.
r
(ER CONSULT)
TRAUMA?
YES
NON-TRAUMATIC
NATURE OF
INJURY?
MECHANICAL? SAME
CHEMICAL?
I
4
1 EXTRAOCULAR? VISION?
CONJUNCTIVAL
LESIONS
• CHEMICAL
BURN
iC1
REDUCED
CORNEA INVOLVED
GLOBE INJURY LENS PROBLEMS

SUPERFICIAL iC3)
(1B-1 PERIORBITAL
INJURIES
POSTERIOR SEGMENT 14C1C4
10P?
ORBITAL
OPTIC NERVE IC5 )
FRACTURE
LID LACERATION l• NORMAL HYPOTONIC
CLOSE GLOBE OPEN GLOBE

LID MARGIN I AREA
INJURIES INJURIES
INVOLVED NASAL
TO PUNCTUM
PENETRATION/
CONTUSION —4D1 IE
PERFORATION
1
NO YES LAMELLAR rTh, RUPTURED
LACERATION/ ID2 GLOBE
ABRASION
1183 INTRAOCULAR
HEMORRHAGE ID3 FOREIGN BODY 1E3
Diagram A. Trauma-related Ocular Emergencies

I. OCULAR TRAUMA
KEY Poem ER NIAIRAGEINEINF OPFITHA REFERRAL

CONDITION
IA Chemical Burns Extract information on - ....•• err etc 3r45 :"..;
1. Nature of chemical (acid vs affected epe/eses. ophthalmologist
TRUE OCULAR alkali) 2 wow slier at least 1liter NSS
EMERGENCY 2. Any first aid administeivict &meal solution) using cannula_
Irriptibn 6 done wd chemical has
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 Includes injury r.. Pecr-Jcal 537 L Perla= basic eye exam whenever
Injuries tissues: possble Always start with visual
• cher-css acuity tinting prior to doing any
• COIllt_SOr'S Nenanznra manipulation of the eye_
• laceraccrsavascrs • 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 1_ Complete neurologic and eye exam. Non-urgent referral
• :ar arC . ... Orel sensation of cheek. upper - patients should be
• 'Itsarricm ECIP5. 7_ doope Seed's and gums (compare with seen within 1-2 weeks
• >loss conualaterai side} post trauma (evaluate
• :3,,rairri eriogrerair-vc_ ocoe 2 Palpate orbital rim and eyelid (for for persistent diplopia,
cieptus) enophthalmia)
•-partiwit to esodoollebnialsisimi 3. RequeSt for orbital CThcan-
4_ Ice pack to the orbit for 24-48 hours.
5. Instruct patient to avoid Valsalva
maneuvers (e.g. blowing of nose,
straining, etc.)
3. Lid lacerations An eyelid Lace+ etpu.i should be 1. Examine with magnification to Refer for following:
treated as a case of penetrating assess for any comeaVconjunctival 1. with accompanying
eye injury until proven otherwise. laceration or penetration. Dilated globe trauma or if suspect
fundus examination may be required. intraorbital or intraocular
kik to assess edent of damage 2 Would examination - size and foreign body.
• _id lacerations involving the id depth_ 2. full thickness laceration
3. Superficial lacerations - primary or involvement of the lid
•narcn or those located nasal
to the purictuni will 'equine wound care and repair_ margin
ophthalmologic referral (prior 4_ Tetanus prophylaxis. 3. laceration is nasal to
to repaid. punctum (upper or
lower)
4. extensive tissue loss or
distortion of the anatomy
10 APPENDIX 1103 Step-By-Step Diagnosis Of Ocular Emergencies

Egig
CONDITION KEY POINTS ER MANAGEMENT OPHTHA REFERRAL
IC 1. Conjunctival Vision generally not affected if 1. Assess extent of wound if Refer to ophthalmologist
lesions conjunctiva alone is involved. present. Conjunctival lacerations if wound repair necessary.
Pain or foreign body sensation, may be left unsutured if less than Advise patient to see
however, is usually present. This 5mm in length. Suturing is done ophthalmologist if other
may come in the form of in cases when length is greater symptoms develop,
• laceration than 5 mm. particularly blurring of
• foreign body 2. Foreign body removal is done vision.
• subconjunctival hemorrhage 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.
. Reduced vision Injury to the cornea can lead to 1. Corneal abrasions • Referral required in
with corneal reduced vision primarily if the a. Eye patch or bandage contact cases of penetration or
Involvement lesion involves the visual axis of lenses for large abrasions. presence of retained FB
the patient. Injury may come in b. Topical antibiotic to prevent particularly if organic in
the following forms: secondary infection nature.
• abrasions c. Topical cycloplegic agents • Refer to
• foreign bodies (FB) 2. Corneal foreign bodies ophthalmologist for
• lamellar lacerations a. Foreign body removal with follow-up care to check
(see Section ID2) aid of cotton pledget or small on progress of healing.
• perforating injury gauged needle (g. 25 or Note that corneal
(see Section 1E1) smaller) after instilling topical abrasions should
anesthetic resolve in 24-48 hours
b. Topical antibiotic to prevent if area involved is not
secondary infection large.
• Advise patient to
NOTE: Despite presence of severe see ophthalmologist
eye pain or discomfort, topical immediately should
anesthetics should NEVER be pain or BOV persist
prescribed to the patient. beyond this period.
3. Lens problems Lens involvement comes in 1. Rule out injury to other ocular Urgent referral in
following forms: structures. following instances:
• lens subluxation/dislocation Treatment of sequelae of lens • Severe inflammation
• rupture of the lens injury that may be present (red eye)
• cataract formation (eq. deleted lOP and severe • Elevated lOP
intraocular inflammation)
Follow-up for possible
surgical intervention.
4. Posterior Reduced vision occurs as a resit Any of the conditions listed Urgent referral
segment of following conditions: would require referral to an
problems • vitreous hemorrhage ophthalmologist for further
• retinal contusion evaluation and management.
• retinal detachment
• choroidal rupture
5. Optic nerve Optic nerve contusion or avulsion Referral to ophthalmologist Urgent referral for proper
problems may result from orbital trauma/ for further evaluation and assessment.
injury management.
CONDITION KEY Pawns ER MANAGEMENT OFHMA REFERRAL
ID 1. Contusion Contusion eyebar! — Basic eye examination (to rule out Referral depends on
Eyeball various intrack: _ a- other injuries) extent and nature of
the ccs.-êa 7: injury.
_
see-
• Stioccriurictuai he— -age

Ste sector' C
• -ifore—a see Section 03)
• ;tetra edema' detachment
See Sewn
• Diec vier.e
1e,(.450- see Section ICS)
2. Lamellar :4.:yriera-rc roves 3c aracterized 1. Topical antibiotics to prevent Urgent referral for proper
Laceration/ .74 re wound. secondary infection. assessment.
Abrasions --e. > 31e= .a....crts when due 2. Topical cycloplegic agents.
"Z Bra:: doe= 3. Watch out for development
ar-elar aceation s a form of of hypotony due to leakage of
_ _ry injury bekig partial aqueous from the wound.
wounds of the cornea
scera See aso Section 1C2.
3. Hemorrhage i -lenar--act a bleeding may Hyphema Follow-up consult with

ox-r r anous structures: 1. Restrict physical activity of ophthalmologist within
• S-occrfaxtival hemorrhage patient. 2-6 days (hyphema should
see Sera 1C1) 2. High back rest resolve spontaneously
3. Topical steroids for inflammation within this period)
• -04:rer-a
control due to presence of
• iifIstecus hemorrhage (see
Section C3) 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)
1. Topical and intravenous Urgent referral required

IE 1. Penetrating awl ;Eric/wry rqures are
antibiotics. in ALL instances where
Peristalsis ghee character2ed by the presence of globe integrity is
injuries an enbarce and exit wound. These 2. Eye shield to protect the eye.
3. Tetanus prophylaxis. compromised.
wounds may be accompanied by
injury to ocher structures like the iris 4. Advise patient regarding surgical
and the lens. repair.
2. Ruptured globe Frequently a result of blunt 1. Eye shield to protect the eye. Urgent referral in ALL
trauma, and should be suspected 2. Topical and intravenous instances where globe
in these patients in presence of antibiotics. rupture is suspected.
following: 3. Tetanus prophylaxis.
• severe conjunctival osmosis 4_ Advise patient regarding surgical
• bullous subconjunctival repair.
hemorrhage
• limitation of movement of
EOMs
3. Intraocular A special category of globe 1 Topical and intravenous Urgency of referral
foreign body perforation. E..-- = :7 :S_ dependent on
2. d to protect the eye. accompanying injuries.
3. prophylaxis.
4. Advise patient regarding surgical
repair.
0 APPENDIX 1103 Step-Ety-Step Diagnosis Of Ocular Emergencies Eigi

NON-
TRAUMATIC
VISUAL RED EYE?

DISTURBANCE?
LATERALITY?
UNILATERAL
RAPIDITY?
SEVERITY?
CONDITIONS GENERALLY
PRESENT WITH
SYSTEMIC ASSOCIATION
_I NEUROLOGIC CAUSE RAPID ACUTE
JONCOLOGIC CAUSE
J DIABETES
PERSISTENT? JREQUIRES MINIMAL

EVALUATION IN ER
JREFER TO OPHTHA FOR
FURTHER EVALUATION
VASCULAR
AT A FUTURE TIME
PAINFUL EYE? CAUSE
AMAUROStS
FUGAX
YES NO
• CENTRAL RETINAL
ARTERY OCCLUSION
- I1A7
EYE DISCHARGE?
VASO-OCCLUSIVE 1•••••
CONDITIONS
CENTRAL RETINAL
VEIN OCCLUSION illAs
YES NO
/-- OPTIC NEURITIS (llA9)

(11A1 ENDOPHTHALMITIS OPTIC NERVE
DISORDERS
CORNEAL ULCER
ACUTE ISCHEMIC )
OPTIC NEUROPATHY IlAio
(11,1/43\4— P
RESEPTAL I
ORBITAL CELLULITIS
RETINAL
DETACHMENT 1 4-,11A1
I1A4 Hi- ACUTE GLAUCOMA VITREOUS

HEMORRHAGE 11Al2
IIA5 I*- UVEITIS (ANTERIOR)

UVEITIS (POSTERIOR) IIA13
Diagram B. Non-trauma Ocular Emergencies associated with G

II. NON TRAUMATIC EMERGENCIES
CONDITION KEY Po 'vs ER MANAGEMENT OPIITHA REFERRAL
1. Endophthalmitis Suspected in t _ --:,rough history and eye Urgent reTer'a to

IIA
• Previous intraocuiar gage" examination with particular ophthalmologist for
(cataract surgery or ilerirg attention to previous ocular further evaluation and
operation often less dor one history and general health management.
month prior) status of the patient.
• I mmunocornpronsed parients 2. Broad spectrum topical and
intravenous antibiotics.
In addition to vtaon iloSi patients
may also present mion a earful
red eye_
2. Corneal ulcer • Primary considealion in 1. Thorough history and eye Urgent referral to
(keratitis) paiinnes•olih hiMory of conaixt examination with particular ophthalmologist for
ienswer- attention to history of contact further evaluation and
• Palos inairabo poem lens use. management.
Ina kkaorjrafpior suisna 1 Broad spectrum topical
or bream bodyerweing the antibiotics.
e)e, thanes not plena*
seen bya physidarby
aPhillubliblocfist
Cannonlyanournesed in Thorough history and eye Urgent referral to
3. Preseptal!
examination with particular ophthalmologist for
Orbital cellulitis
attention to infection of further evaluation and
adjacent tissues management.
2. Broad spectrum intravenous
antibiotics.
3. Referral to pediatrician for co-
management.
4. Acute Glaucc — a • IlluipappensisviehOthet eye 1. Thorough history and eye Immediate referral to
examination. Eye Exam shows ophthalmologist for
• =laudations indude • red eye (ciliary injection) further evaluation and
• onmareambanal headache • hazy cornea management as this may
Oviddlogsanieside) and on • mid-dilated, unreactive lead to permanent loss of
minim nausea and vomiting. pupil vision if left untreated.
• elevated 10P
2. May give patient analgesics
to assist in relieving pain and
headache.
5. Uveitis Antenof • Pain is precipitated by intense Thorough history and eye Urgent referral to
fight Illumination or sunlight examination. History should focus an ophthalmologist
(photophobia). on systemic symptoms and illnesses (within 24 hours) for
• May have systemic as well. Eye exam will show further evaluation and
associations depending on • red eye (ciliary injection) management
etiology of the inflammation. • irregularly-shaped small,
unreactive pupil
• lOP normal or low
6. Amaurosisfugax Visual loss usually lasts seconds to

Thorough history and eye None provided all eye
minutes only, but may last up to
examination.
two hours. Vision subsequently exam findings normal.
2. Referral to a neurologist/
returns to normal. cardiologist
10 APPENDIX 1 103 Step-By-Step Diagnosis Of Ocular Emergencies Egg

ER MANAGEMENT OPHTHA REFERRAL
CONDITION KEY POINTS
Thorough history and eye Immediate referral to an
Central retinal Marked loss of vision of very sudden ophthalmologist for further
7. examination focusing on exact
artery occlusion onset evaluation and institution of
onset of the condition. Eye exam
will show management.
TRUE OCULAR • Relative Afferent Pupillary
EMERGENCY Defect (RAPD)
• Pale retina with cherry red spot
May institute measures to improve
circulation (vasodilation)
8. Central retinal vein Patients predisposed if Thorough history and eye examination Urgent referral to an
occlusion • elderly (increasing age: focusing on history of diabetes or ophthalmologist for further
• hypertensive hypertension. Fundus exam shows large evaluation and management.
• diabetic mew of hemorrhage
9. Optic neuritis • Loss of vision may occur crier Thorough history and eye examination Urgent referral to an
period of hours to days. which reveals (aside from BOV) ophthalmologist for further
• Pain may be noted with eye • RAPD evaluation.
movement. • swollen, edematous disc
10. Acute ischemic Differs from optic neuritis since Thorough history and eye Urgent referral to an
neuropathy condition is often associated with emamination. ophthalmologist for further
systemic findings: Referral to a neurologist/ evaluation.
• temporal headaches or sc caedolooist
tenderness
• generalized muscle pain anckw
1
11. Retinal Detachment Most common cause is a pietisposing 1. Thorough history required, Urgent referral to an
retinal defect as seen in high mopes focusing on patient's refractive ophthalmologist particularly.
history as well as accurate onset of
Patient may present with a hisaory
of flashes or floaters. MstMl defect Es the problem.
often described astuilain tie 2- 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)
12. Vitreous More commonly seen it padentsvials 1. Thorough history and eye Referral to ophthalmologist
hemorrhage following systemic conditions examination with particular not urgent but patient
1. diabetes attention to previous ocular history should be advised to consult
2. hematologic cisordeis and general health status of the at a future time.
patient.
Often accompanied by ocher mind
2. Referral to internal medicine
Problems
specialist for systemic evaluation.
13. Uveitis (Posterior) more marked effeu on 116110111 MI 1. Thorough history and eye Urgent referral to an
comparison to anterior wefts. examination. History should ophthalmologist for further
Patients may also piesera with focus on systemic symptoms and evaluation and management.
systemic finctings since underiping illnesses as well.
cause frequently with systemic 2. Eye exam may reveal vitreous
associations. condensations and other retinal
findings such as retinal vasculitis,
macular edema and focal areas of
retinal detachment.
NON-
I RAUMATIC
1
VISUAL
B RED EYE?
DISTURBANCE!?
l'AINrUL
RYE?
4
1 yes NO
I)Itt 11411111110N
ABNORMAL HI URRED
LIDS? 1)InClIA14(41
VISION?
LID INFECTIONS LOCALIZED

.. 118 1 YES 14—
L LID MALPOSITION LID

KERAT ITIS
I1A2)4— CORNEAL ULCER ABNORMALITY? SUBCONJUNCTIVAL 1
1vi!; 4- 41/—
8 HEMORRHAGE
CONJUNCTIVITIS 11—
KERATITIS ID3
*4-- CORNEAL ULCER L NO 14—
0
LID INFECTION
al=1114.
A7=0--
IIA4)-4—ACUTE GLAUCOMA
1
UVEITIS
011104--- 1-6
(11AE)46- UVEITIS
[ NO
SUBCONJUNCTIVAL
HEMORRHAGE 1D3)
SCLERITIS
(iiB2 4-- SCLERITIS
CONJUNCTIVITIS 1-411B3
r
;
N.)
Diagram C. Non-trauma Ocular Emergencies associated with acute eye redness
ER MANAGEMENT OPHTHA REFERRAL
CONDITION KEY POINTS
1. Hordeolum Non-urgent conditions
1. Lid infections Problems involving the lids
IIB
and Malpositions associated with red eye are also a. Warm compress Ophthalmologic consult
generally accompanied by foreign b. Topical antibiotic ointment for hordeolum only
body sensation. On occasion (may use steroid-antibiotic if it does not resolve
infections may present with pain combination) despite completion of
and discharge. These conditions c. Analgesics medication.
can further be subdivided into d. Antipyretic if accompanied by Ophthalmologic consult
fever for lid malpositions
1. Hordeolum (Stye)
2. Entropion for possible surgical
2. Blepharitis a. Tape lids to evert them correction.
3. Entropion b. Topical lubricants and artificial
Ectropion tear preparations
4.
3. Ectropion
5. Preseptal cellulitis
a. Tape lids to effect closure
(see Section iiA3)
when sleeping
6. Orbital cellulitis b. Topical lubricants and artificial
(see Section IIA3) tear preparations
2. Scleritis Redness may be diffuse or 1. Thorough history and basic eye Urgent ophthalmologic
localized; may be accompanied exam. Focus on presence of referral for further
by nodule. systemic conditions that can evaluation and
cause scleritis. management.
Usually associated with systemic
conditions, most common of 2. Topical steroid preparations
which is rheumatoid arthritis.
3. Conjunctivitis 1. Pain may or may not be 1. Thorough history assists in Non-urgent conditions
present. ascertaining etiology. Also ask Refer to ophthalmologist
2. Classified according to about specific symptoms that are if
etiology associated with specific types of
• mucoid to
• Bacterial - with conjunctivitis
mucopurulent eye
2. Specific treatment dependent
mucopurulent discharge discharge present
• Viral - generally with on etiology. Refrain from
• recurrent condition
serous discharge prescribing topical steroid
• Allergic - associated preparations if infection has not
been ruled out.
with itchiness; frequently
bilateral
• Chemical - history of
exposure to specific
substances
REFERENCES
1. BMJ Publishing Group. Eye Trauma in Best Practice. June 6. Pramanik, Sudeep. Assessment and Management of
7, 2011: http://bestpractice.bmicom/best-practice/ Ocular Trauma, June 28, 2008: http://webeye.ophth .
monograph/961/ (accessed October 29, 2011). uiowa.edu/eyeforum/tutorials/trauma.htm (accessed
2. Classification of ocular trauma, June 21, 2011: httpsi/ October 29, 2011).
vodvos.com/classification-of-ocular-trauma/ (accessed 7. Sherry Eugene. Electronic Textbook Injuries Chapter 23
October 29, 2011).
Eye.
3. Eye Emergency Manual An Illustrated Guide, 2nd ed. New 8. The WorldOrtho Textbook of Orthopaedics, Trauma and
South Wales: NSW Department of Health, May, 2009. Sports Medicine, 2007: http://www.worldortho.com/dev/
4. Khare, GD, Symons, DV. Common Ophthalmic (accessed October 29, 2011).
Emergencies. Int J Clin Pract. 2008;62(11): 1776-1794.
5. Pokhrel, PK and Loftus. SA. Ocular Emergencies. Amer
Fam Physician. 2007; 76(6): 829-836.
10.4 Eye Care Rules
to Remember
1. Always take and record your petiesies visual acuity 7. Corneal abrasions should heal in 24 to 48 hours.
Every effort must be taker __ , _ _ := a • Daily follow-up of patient is ideally done until the
patient prior to any further _ corneal abrasion is completely healed.
This is done regardless of ho," - ±- eye Cover patient with topical antibiotic drops to prevent
may appear. secondary infection.
If vision improves with patie- _ a 2,- e,
the patient's blurring of visicr "• OUt = a- 8. A penetrating eye injury requires urgent care.
error of refraction. Gentle transport is of utmost importance.
Place an eye shield over the patient's injured eye to
2. Pupil examination: Suspect NNW andlilliews for protect it.
corresponding findings If treatment is delayed, give the patient systemic
pupil - - sargery antibiotics and anti-tetanus injections.
Dilated pupil - Acute gtauarre- -ersoe nassv crf
associated with history of heat 9. Consider the presence of intraocular foreign
• Constricted pupil - Ir s- Horne- 1- bodies if
• Relative Afferent P c elect f3i - fetinal artery • Mechanism of injury is o,e to hammering or nigh-
occlusion; optic - velocity in nature.
• Presence of a possible entry wound in the cornea or
3. Irrigate chemical burns. sclera
co , _4:rously with water for at least
15 minutes 10. In the presence of trauma with a black eye, consider
Instill a local anesthett net and swab the eye presence of globe rupture unless otherwise ruled
lids. out.'
Consider a ruptured globe if
Immediately refer tc "7".`
Patient complains of diplopia or there is
limitation of EOMs
4. Any sudden onset of Marring of vision requires
Patient presents with a bullous subconjunctival
prompt investigation.
=- --;7.-1- s accompanied by hemorrhage
----
Patient has a hypotonic eye
- Anterior chamber is completely filled with blood
Orbital floor fracture should be ruled out if the patient
5. Beware of ungateral eye redness
complains of diplopia or presents with enophthalmia
Trauma (sunken eye).
=-.7.,Fr • aY
11. Never use anesthetic drops for continued pain
uveitis (Iritis) relief.
- 7 -_ siromeal ulcer Use of topical anestnetic crops snouid be limited to
above cases reg._ _ 7 7. !72. to facilitating examination of painful lesions or as part of
:::-thalmologTs for fur e _.a and performing a diagnostic procedure.
e-r%ent. Anesthetic drops should never be prescribed to
patients.
6. Leave some foreign bodies alone.
'• - - .-..odies that are deep
central cor- intra-ocular or intra-orbital. These
cases should be referred to an ophthalmologist.
is the most common eye
12- Always advise patientsthat steroids are potentially 15. Cataract surgery
dangerous. operation.
5terolus con activate a dormant infection (e.g. Herpes oavised when symptoms affect a patient's daily
simplex) life activities.
Prolonged use can lead to the following: It is generally performed as an out-patient procedure
- Glaucoma (day surgery) under local anesthesia.
- Cataract formation Laser is not a treatment option for cataract surgery.
Steroid should be used with caution if Yag laser capsulotomy may be used at a later time
- Any break in the integrity of the globe is for post-cataract surgery patients when posterior
suspected capsule opacification occurs.
- Patient has an ocular infection Cataract does not recur.
- Patient is immunocompromised (e.g. diabetics,
patients on immunosuppressant therapy) 16. Not all red eyes are"sore eyes"(viral conjunctivitis).
Urgent referral to an ophthalmologist is warranted
13. Refer all children noted to have squint or eye if patient presents with
deviation. Severe eye pain
Squint may be a sign of an underlying life- Reduced vision
threatening or vision-threatening condition such as Mucopurulent eye discharge
retinoblastoma or congenital glaucoma. • Prolonged duration
Children with poor vision in one eye often develop
deviation of the involved eye. In very young children 17. Hospital admission is considered if the patient has
it is important to institute measures to correct vision • Hyphema
as this may lead to development of amblyopia. • Hypopyon
• Penetrating/peforating ocular injuries
14. Conjunctivitis is almost always bilateral. • Severe chemical burns
• Viral conjunctivitis is often accompanied by pre- • Acute glaucoma
auricular lymphadenopathy.
• Allergic conjunctivitis is always accompanied
by itchiness which can be relieved by use of ice REFERENCE
compress. Always advise patients to avoid scratching 1 Calvin JL• Reich JA. 35 Golden Eye Rules. http://www.eyeandeatorg.au/
their eyes as this will just aggravate the itchiness. EYELectures/35_Golden_Eye_Rules.pdf (accessed August, 2008).
• All cases of prolonged conjunctivitis should be
referred to an ophthalmologist.
242 Self-Instructional Materials in 0ohthalmoloov I Mel Friitinn

Ophtha SIM 2nd Ed

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OPHTHALMOLOGY SECOND EDITION

Marissa N. Valbuena MD, MHPEd, Editor

Teresita R. Castillo MD, MHPEd, Assistant Editor

Publication authorized by the University of the Philippines

Published by UP-PGH Ophthalmology Residence Association, Inc.

Marissa N. Valbuena MD, MHPEd, Editor

Book Design: mervin concepcion vergara

1 ANATOMY OF THE EYE

2 PHYSIOLOGY OF THE EYE

5.1 Disorders of the Cornea

66 5.3 Disorders of the Retina, Choroid and Vitreous

98 5.6 Errors of Refraction

6 RED EYE, TEARING AND DISCHARGE

6.2 Uveitis and Scleritis

Self-Instructional Materials in Ophthalmology I 2nd Edition n

139 7.1 Strabismus

150 7.2 Proptosis

161 8.1 Retinoblastoma

167 8.2 Ocular Manifestations of Systemic Diseases

186 8.3 Eyelid Malpositions

197 8.4 Ocular Trauma and Emergencies

207 8.5 Ocular Pharmacology

220 9 ANSWERS TO SELF- TEST

224 10.1 Patient Census of the Department of Ophthalmology

229 10.2 Different Types of Eye Redness

10.3 Step-By-Step Diagnosis Of Ocular Emergencies

241 10.4 Eye Care Rules To Remember

Self-InstTuetional Materials in Ophthalrn010,3y 1 Ztit1ECIII1011

Norman M. Aquino, MD Franklin P. Kleiner, MD

Teresita R. Castillo, MD, MHPEd Ruben LimBonSiong, MD

Leo D. P. Cubillan, MD, MPH Andrea Kristina Monzon-Pajarillo, MD

Raul D. Cruz, MD Juan Ma. Pablo R. Nanagas, MD, MPH, MSNA

Rolando Enrique D. Domingo, MD Mary Rose L. Pe-Yan, MD

Prospero Ma. C. Tuano, MD Marissa N. Valbuena, MD, MHPEd

Alexander D. Tan, MD Pearl T. Villalon, MD

Rolando Enrique D. Domingo, MD

Self-Instructional Materials in Ophthalmology I 2nd Edition

n the Organ System Integration Curriculum of the UP College of Medicine, the

Marissa N. Valbuena MD, MHPEd

smmnstructional Materials in Ophinalmolonv I 2nd Edition

After the completion of this instructional material, the student is expected to

Ill. Extraocular muscles

IV. Ocular adnexae

ROOF OF THE ORBIT

FLOOR OF THE ORBIT

Figure 1. Walls of the left orbit

ORBITAL WALLS (FIGURE 1)

The conjunctiva is a thin transparent mucous membrane 3. SCLERA AND EPISCLERA

1) Epithelium : 5-6 layers of cells, continuous with the 5. UVEAL TRACT

1. Pars plicata: 2 mm wide; The ciliary processes arise

Anterior ciliary vessels

Vessels of ciliary body

Figure 5. Blood supply of the eye

1 ANATOMY OF THE EYE Ei

Antenor chamber angle

Trabecular meshwork 1. internal limiting membrane

GANGLION CELL 3 - GANGLION CELL LAYER

4 - INNER PLEXIFORM LAYER

BIPOLAR CELL - INNER NUCLEAR LAYER

7 - OUTER NUCLEAR LAYER

8 - EXTERNAL LIMITING MEMBRANE

10 - RETINAL PIGMENT EPITHELIUM