INTRODUCTION TO OPHTHALMOLOGY
FOR
SENIOR MEDICAL STUDENTS
Chi-Wah (Rudy) Yung, M.D.
Course Director
ryung@iupui.edu
Introduction
Welcome to Ophthalmology. You will spend one week with us to learn about Basic
Ophthalmology. The objective of this course is to introduce you to the basic technique of
eye examination and to recognize the signs of common eye diseases.
This handout will aid you in your study. It covers the entire lecture materials and
you final examination will be made up of questions from the lectures. However, I
encourage you to take advantage of our library, which is located on the 3rd floor of the
Rotary Building. You will find excellent audio visual teaching material which will cover a
wide area of general ophthalmology such as ocular emergency or how to handle “pink eye,”
just to name a few.
Your one-week rotation will be spent mainly in one of two general ophthalmology
clinics, the Regenstrief Eye Clinic and the VA Clinic. The faculty and resident staff will
supervise you.
Again, welcome to Ophthalmology and we hope you enjoy your rotation.
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Contents
Section
I.
The Basic Eye Examination
II.
Ocular Emergencies
III.
The Red Eye
IV.
Vision Screening in Infancy
V.
Introduction to Glaucoma
VI.
Diabetic Retinopathy: Diagnosis and Treatment
VII.
Neuro-Ophthalmology for the Primary Care Physician
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Section 1:
The Basic Eye Examination
R. Todd Morason, M.D.
History
A. History of the Present Illness
As with the general medical patient, the fist step in the examination of an
eye patient is obtaining a thorough history. Demographic data, including the
patient’s name, age, race, gender and occupation should be recorded. This is
followed by a brief statement, in the patient’s own words, of the chief
complaint (e.g. “Blurred vision in the left eye for two months”). Then, more
detailed information regarding the history of the present illness is recorded.
This would include time and context of onset, severity, exacerbating or
relieving influences, variation (e.g. daily or seasonal), and laterality (i.e. is one
eye or are both eyes affected). Clarify symptoms when possible. For
instance, if the vision is blurred, determine whether it is more noticeable at
distance, near or both. If eye discomfort is present, have the patient describe
it specifically. Is it a foreign-body sensation (suggestive of corneal pathology)
or is the pain more deep and intense (suggestive of iritis, acute glaucoma or
scleritis)? As you will find, there are numerous potential complaints relating
to the eyes, and these will be discussed in detail in upcoming sections.
B. Past Medical History
As many ocular diseases are manifestations of, or associated with,
systemic disease, it is important to obtain a complete past medical and
surgical history. Consider inquiring about diabetes, hypertension, and
cardiovascular disease. If a patient has diabetes, determine the number of
years it has been present, what medications are used to control it and how well
the patient’s blood sugars are controlled. Obtain additional review of systems
as dictated by the clinical history.
C. Past Ocular History
Inquire regarding the use of eyeglasses or contact lenses, history of
amblyopia, previous use of eye medications, previous eye surgery and prior
eye trauma.
D. Systemic and Ocular Medications
Record all systemic medications. These are sometimes helpful in
revealing medical problems not mentioned in the past medical history.
Record all eye medications separately with their dosages and frequency.
Often patients will not recall the names of their eye drops; however, the color
of the cap on the container will reveal the class of the medication. (Red:
anticholinergic (mydriatic, dilating drops), Green: cholinergic (miotic),
Yellow: Beta-adrenergic blocking agents, Orange: dorzolamide and White:
many medications such as antibiotics, steroids and artificial tears).
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E. Allergies
Inquire regarding allergies to medications, both systemic and topical, as
well as environmental allergies.
F. Family Ocular History
Many eye conditions, such as glaucoma and age-related macular
degeneration, are heritable. Inquire about these as well as any family history
of blindness and its cause. Relevant family medical history should also be
obtained.
Examination
You have likely developed a systematic approach in your physical
examination of medical patients. A similar approach is used, albeit on a much
smaller scale, in examining the eyes. In general, the exam proceeds from the
more anterior ocular structures to the more posterior. It is natural to want to focus
on readily apparent pathology; however, to avoid skipping over less obvious
abnormalities all steps of the basic exam should be performed on all eye patients,
regardless of their presenting signs and symptoms.
A. Overview or “Gestalt”
With some experience, it may be possible to determine the nature of a
patient’s eye problem even before more detailed examination takes place.
During history-taking, one may observe evidence of medical, dermatologic
(e.g. Roseacea) or neurologic disease (e.g. hemi-facial paresis). Be observant
of the patient as a whole before focusing in on the eyes, as this will often
provide useful diagnostic clues.
B. Face and Periorbita
1. Skin
Observe the facial skin for any dermal or vascular changes. Observe the
skin’s color, texture, tone and moisture. Note any lesions or evidence of
trauma.
2. Facial Bones
Note any significant asymmetry in facial bones. Observe for any signs of
old trauma or congenital malformations.
3. Lid Position
The position or the upper and lower eyelids should be fairly symmetric.
Note any drooping (ptosis) or retraction of the eyelids. Assess
effectiveness of eyelid closure and strength of the orbicularis muscles if
appropriate.
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Occluder
C. Visual Acuity
An accurate assessment of visual acuity is perhaps the most important
element of the physical examination of the eye. The vision should be tested
with the patient wearing his or her glasses or contacts, as the goal is to
determine the patient’s “best corrected acuity”. In adults, acuity is most often
tested using a Snellen eye chart. This chart is designed to be read from a
distance of 20 feet. A similar eye chart in pocketsize form is also available;
however, if this chart is used with presbyopic patients (age 40 or greater), they
should be tested while wearing their reading glasses or bifocals.
Near Card - The pocket vision screener is designed to be read at a
distance of 14 inches.
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Each eye is tested separately. The smallest line the patient is able to read
accurately is determined, and this is recorded using Snellen notation. The
notation is expressed as a fraction (e.g. 20/40) where the numerator denotes
the distance between the patient and the eye chart, and the denominator
denotes the distance at which a subject with normal vision can read the same
line. If the patient is unable to identify the largest figure on the chart (usually
20/400), some measure of acuity may still be obtained. The distance to the
chart may be reduced (note the change in testing distance in the Snellen
notation, e.g. if the patient reads the 20/400 figure at 10 feet, the acuity is
recorded as 10/400). Alternatively, the greatest distance at which a patient
can correctly count the fingers of the examiner’s hand is recorded (e.g. CF at 1
foot). If the level of acuity is below the counting-fingers level, the ability to
identify hand motion is assessed. Below this, the ability to perceive light is
recorded (e.g. “light perception” or “no light perception” if the patient is
completely blind). For pre-literate patients, it may be possible to test acuity
using an Allen picture chart. In pre-verbal patients, the ability to fix on and
follow a visual target may be used as a gross estimate of visual acuity (this
ability develops at age 2-3 months). A photophobic response to bright light
may be used in infants prior to this age.
The pinhole test is helpful in determining best-corrected acuity in the
presence of refractive error (myopia, hyperopia or astigmatism). The patient
views the chart through a single pinhole opening in an occluder (one can be
improvised by poking a small hole in a piece of cardboard). As the pinhole
admits only parallel light, which is not refracted by the eye, the effect of
refractive error on vision is circumvented.
C. Pupils
Examination of the pupils is extremely important as it may reveal serious
neurologic or other types of eye disease. When recording pupillary findings,
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the common notation “PERRLA” is not sufficiently specific. Rather, the
millimeter measurements of pupil size should be noted.
The pupils are first examined in ambient light. Their shape and size are
noted. Next, in a darkened room with the patient staring at a distant target, the
size of the pupils is measured with a millimeter ruler or pupil gauge (present
on most pocket eye charts) with minimal, diffuse illumination. A light source,
such as a penlight, is then used to assess the pupillary diameter of each eye
under lighted conditions. If a difference in pupillary size between the two
eyes (anisocoria) is noted, the accommodative reflex should also be examined.
This is done by recording the pupillary sizes with the patient staring at a
distant target, and then with the eyes focused on a near target (e.g. the
patient’s own thumb placed 6 inches in front the eyes). The “swinging
flashlight test” is then performed to detect the presence or absence of a
relative afferent pupillary defect (also called a Marcus Gunn pupil). This test
along with a discussion of various pupillary abnormalities and their causes
appear in the neuro-ophthalmology section.
D. Visual Field Examination
A discussion of visual field testing and assessment is provided in the
neuro-ophthalmology section.
E. Ocular Motility and Alignment
The patient is asked to follow a fixation target in all directions of gaze.
The eye movements are assessed in each eye individually and then in both
eyes simultaneously. The movements should be full in all directions and
should be similar between the two eyes. Document any limitations in eye
movement. A full discussion of motility assessment and alignment testing is
found in the neuro-ophthalmology and pediatrics sections.
F. Slit Lamp Examination
1. Uses of the Slit Lamp
While many external eye abnormalities may be observed with a
penlight examination, the magnified view provided by the slit lamp is
invaluable in revealing subtle ocular pathology. Although the slit lamp
looks a bit intimidating at first, with some practice the medical student
will easily learn to use it to examine the anterior segment of the eye in
detail. In addition, the slit lamp is useful for measuring lesions in the
anterior segment, and, with the Goldmann applanation tonometer
attachment, it may also be used to measure intraocular pressure.
2. Parts of the Slit Lamp
A typical slit lamp is shown in the attached photo. The Haag-Streit
900 is shown, as it is the most commonly encountered model. There are
three basic elements of the slit lamp: The patient-positioning frame (with
chin rest and forehead strap) (1), the illumination arm (2), and the viewing
arm (oculars and magnifying elements) (3). The Goldmann applanation
tonometer is also attached to the viewing arm (4).
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The patient should be positioned comfortably, with his or her chin on
the chin rest (5) and the forehead pressed against the forehead strap (these
should be cleaned prior to examining each patient). There is a knob
below the chin rest to adjust its height (6). The height should be adjusted
so that the lateral canthus (the angle formed by the upper and lower
eyelids) is aligned with the black positioning stripe on the right side of the
positioning frame (7). The height of the chair or slit lamp base may need
to be adjusted to maintain patient comfort. The examiner should wear his
or her spectacle correction or contacts when using the slit lamp. The
oculars should be set for the examiner’s inter-pupillary distance and the
eyepieces set to “0”. After the patient is positioned, the slit lamp is turned
on with a knob below the slit lamp’s base (8).
The viewing and illumination arms are connected to a moving base,
which is locked into position with a knob (9). After releasing the locking
knob, the examiner grasps the joystick (10). The joystick allows the
examiner to shift the position of the viewing and illumination arms right,
left, forward and backward. The knob may be twisted to raise or lower the
light beam. This arrangement allows the view to be adjusted with just one
hand, while keeping the other hand free for other tasks.
The illumination arm is set to project light at an oblique angle toward
the eye being examined. The height of the beam is controlled with a knob
(11) (the beam height is displayed in millimeters on a meter (12) above the
knob, which is useful for measuring lesions of the anterior segment.).
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This same knob, when rotated fully counter-clockwise, switches the
illumination to cobalt blue (which is used in combination with fluorescein
staining to reveal epithelial defects of the cornea and during applanation
tonometry.) The width of the beam is controlled with a separate knob
(13). Just below the millimeter scale is a lever (14) which controls the
brightness of illumination. A lever below the oculars allows adjustment of
magnification (15).
With the illumination adjusted to a comfortable level, the viewing and
illumination arms are moved into position with gross movement of the
base. The beam is positioned on the eye to be examined. While viewing
through the oculars, the examiner is able to adjust the depth of focus with
the joystick. By moving the joystick backward and forward, the depth of
focus is adjusted from the more superficial to more deep structures.
3. Parts of Slit Lamp Examination
a) Lids, lashes and lacrimal system
The lids are examined for any dermal or vascular changes. The lashes
are examined for evidence of blepharitis (inflammation of the eyelids),
such as flakes (“scurf”), collarettes or sleeves on the lashes.
b) Conjunctiva
The conjunctiva is examined for any injection (redness), and if present,
its distribution (diffuse, perilimbal, or focal). Inflammation in the
form of papillae or lymphoid follicles is also noted. Any secretions or
discharge are noted. If a foreign body is suspected, the lower fornix
should be examined by pulling down the lower eyelid with the free
hand. The upper eyelid should also be everted to inspect the superior
fornix. This is performed by placing a cotton swab horizontally
against the upper eyelid at the level of the eyelid crease. The swab is
held by the hand on the temporal side of the eye. The lashes of the
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upper lid are grasped with the other hand. While pressing gently
posterior and downward with the swab, the lashes are drawn outward
and upward, everting the lid. The conjunctiva of the upper eyelid may
then be examined with the slit lamp.
c) Cornea
The cornea is examined for abnormalities in the tear film. Also noted
are any defects in the epithelium (best seen with fluorescein staining
and cobalt blue illumination). The other layers of the cornea,
including Bowman’s layer, the stroma, Descemet’s membrane and the
endothelium are also examined.
d) Anterior Chamber
The anterior chamber is examined to assess its depth. Inflammation in
the form of “flare and cell” is also assessed. When intraocular
inflammation (uveitis) is present, flare results from protein spillage
into the anterior chamber. It has a similar appearance to light beams
streaking through murky water. Cell is the appearance of white blood
cells in the anterior chamber. This finding can be quite subtle, and is
best seen with high magnification. With the level of focus set within
the anterior chamber, white blood cells appear as small specks floating
in the aqueous, similar in appearance to dust particles floating in and
out of a movie projector beam. Pigment cells and red blood cells may
also be seen. Blood in the anterior chamber (hyphema) usually results
from trauma. If present in sufficient amount, the red blood cells may
settle inferiorly forming a flat-topped layer in the bottom on the
anterior chamber. Layering of white blood cells in inferior anterior
chamber (hypopyon) may also occur with severe intraocular
inflammation
e) Iris
The iris is inspected for any nodules, tumors, cysts or
neovascularization, which may occur in severe diabetic disease or
other eye disease.
Lens
The lens is inspected for cataracts, of which there are several types.
Nuclear cataracts are the most common. They result from aging and
appear as a yellow to brown, hazy discoloration of the lens. Posterior
subcapsular cataracts are granular opacifications which appear in the
posterior aspect of the lens. They are sometimes age related, but may
be associated with diabetes, steroid use or intraocular inflammation.
f) Anterior Vitreous
The anterior vitreous is the deepest structure visible with the slit lamp
without additional lenses. Uveitis of the posterior segment of the eye
may be seen in the form of flare and cell in the vitreous.
Further discussion of slit lamp findings is found in the red-eye section.
G. Intraocular pressure
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The measurement of intraocular pressure is discussed in the glaucoma
section.
H.
Fundus
Direct Ophthalmoscope
The direct ophthalmoscope is a useful tool for examining the optic disc
and posterior pole. The best view is achieved when the pupils are dilated. In
adults the most commonly utilized mydriatics are Phenylephrine (Neosynephrine)
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2.5% and Tropicamide (Mydriasil) 1%. One drop of each solution is placed in
each eye. Full dilation usually occurs after 30 minutes. The pupils will
reconstrict after 4-8 hours.
Direct ophthalmoscopy is performed with the eye that corresponds
to the eye being examined. The examiner should wear his or her glasses or
contact lenses during the exam (a rubber pad on the back of the ophthalmoscope
prevents it from scratching the glasses). To begin, the focusing lens is set to zero
and the illumination opening is set to a full spot size. The brightest level of
illumination tolerated by the patient should be used. The patient’s red reflex is
checked from a distance of 2 feet. Often, opacities in the media (e.g. cataracts,
vitreous floaters) may be seen.
While the patient looks straight ahead the examiner approaches the
patient’s eye with the ophthalmoscope. The eye is best examined at a distance of
2-3 cm.
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The examiner then dials the focusing lenses until the image of the retina
becomes clear (note: if the examiner has no refractive error or the error is
corrected with spectacles or contacts, the lens power on the direct
ophthalmoscope that produces a clear view of the retina corresponds to the
patient’s refractive error). Red numbers signify minus lenses (myopic correction)
and green or white numbers signify plus lenses (hyperopic correction). The optic
disc, vessels and macula are then examined. The shape, size and color of the disc
are noted along with the degree of cupping. The emerging vessels are examined
and any pulsation of the vessels is noted. The macula is examined for
abnormalities, such as diabetic retinopathy and hypertensive retinopathy. While
the direct ophthalmoscope provides an excellent, magnified view of the posterior
pole, it is not useful in viewing the peripheral retina, even with complete dilation.
The peripheral retina is best viewed with the binocular indirect ophthalmoscope,
seen in the following picture.
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Further discussion of fundoscopy is found in the retina and glaucoma
sections.
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Section II
Ocular Trauma
Rudy Yung, M.D.
I.
History and Examination:
A. History: Time and location of injury, ask the Ws (when, what, where and
how). Past ocular history is also important.
B.
C.
Ocular Examination:
1.
Visual acuity: Use Snellen chart for distance vision or near card for
near vision. Make sure that patient is wearing proper eye glasses and
check one eye at a time. Knowing visual acuity prior to injury can be
helpful.
2.
External examination: Gross observation to detect any asymmetry,
abnormal facial or periorbital features. Palpation of the bony orbit,
avoid pressure on eye if nature of injury not known or if ruptured globe
is suspected.
3.
Retract upper and lower eyelids with care if foreign body is suspected.
Again avoid this procedure if ruptured globe is suspected.
Pupil examination:
1.
Observe pupil shape and size. Abnormal pupil shape such as tear-drop
pupil is highly suspicious for penetrating eye injury.
2.
Direct pupillary response and consensual response: Afferent pupillary
defect (Fig. 1).
Figure 1
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II.
D.
Motility.
E.
Slit-lamp examination if available.
F.
Intraocular pressure measurement.
G.
Direct Ophthalmoscopy.
Eye Trauma
A. Chemical injury – a true emergency. Need to initiative treatment
immediately. At home, any source of water should be used to irrigate the eye
before going to emergency room. In hospital or office, can irrigate the eye
with any IV fluid before obtaining ophthalmology consultation. Be sure to
look for foreign body by everting the eyelids. Do not waste time to perform
a complete eye examination. Start treatment first, then perform history and
physical. Damage from alkali injuries is usually worse and carries a poor
prognosis(Fig. 2). The most damaging alkaline is Ammonia Hydroxide
followed by Sodium Hydroxide.
Figure 2
B.
Subconjunctival hemorrhage – usually benign and self-limited. No
treatment is required, but be aware of rupture globe.
C.
Hyphema – collection of blood in the anterior chamber (Fig.3) Associated
with serious intraocular injury. Check for sickle cell status if patient is
Africa-American. Hyphema may associate with acute rise in intraocular pressure in these patients and needs to be monitored closely.
Hospitalization may be required.
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Figure 3
D. Cornea abrasion – best diagnosed with staining the cornea with fluorescein
(Fig. 4). Symptoms include sharp pain, tearing, photophobia and foreign
body sensation. Treatment includes topical antibiotic, cycloplegic
medications (e.g. Homatropine 5%), and pressure patching. DO NOT treat
patient with topical anesthetics because they are toxic to the corneal
epithelium.
Figure 4
E.
Corneal foreign body – can be removed with topical anesthetic as long as
the foreign body does not extend the entire cornea into the anterior chamber.
Be sure to look under the eyelids for hidden foreign bodies. Suspect
intraocular foreign body if patient exposed to particles, grinding wheel or
chisel, or foreign body propelled by any mechanical force (Fig. 5 and 6).
Obtain facial X-ray if index of suspicion is high.
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Figure 5
Figure 6
F. The open globe
1. Corneal laceration – through and through interruption of the cornea (Fig
7). The anterior chamber usually is shadow. Iris may be incarcerated
into the wound.
2. Corneal-scleral laceration – wound extended into sclera, and may
extend posteriorly (Fig 8).
When suspect an open globe, one shall protect the eye from further injury by
covering the eye with a shield or any device that can protect the eye(Fig 9)
Do not instill any medication to the eye. Do not attempt to remove anything
from the wound (tissue from inside of the eye may look like dirt or mucous).
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Figure 9
G. Eyelid lacerations – check if the eyelid margin is involved. The nasolacrimal drainage system may be involved if injury involves nasal portion of
the eyelid. Need to look for associated occult eye or orbital trauma. The
multiple layers of the lid must be apposed correctly to avoid poor lid
function, which could result in corneal injury or scarring.
H. Bony orbit – fracture of the floor of the orbit most common (blow-out
fracture). Eye movement may be restricted especially up and down gaze.
CT is best to identify extend of the fracture. Medial wall fracture is usually
associated with air in orbit.
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The Red Eye
Fred M. Wilson II, M.D.
Shailaja Valluri, M.D.
I
Blepharitis: a chronic lid-margin inflammation (Fig. 1)
Figure 1
1.
Types
Staphylococcal Blepharitis: occurs at the eyelash line
(anterior margin)
Seborrheic Blepharitis: Meibomian gland dysfunction
(posterior blepharitis), almost always associated with
seborrheic dermatitis.
2.
Clinical Features:
Burning, itching, foreign body sensation and irritation
typically worse in the mornings
Lids can often be stuck together in the mornings (especially
in staphylococcal blepharitis)
Hard fibrinous scales at the base of eye lashes
Collarettes (scales that encircle eye lashes) often present
Loss of lashes (madarosis) or white lashes (poliosis) or
irregular lid margins (tylosis)
3.
Treatment
-
Lid hygiene with diluted Johnson’s baby shampoo twice a
day for one month then decrease to once a day
Ophthalmic antibiotic ointment such as erythromycin or
bacitracin once a day at bedtime for one month
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4.
Prognosis
-
Warm compresses to eyelids twice a day
If there is associated conjunctivitis, use topical ophthalmic
antibiotic solution such as sulfacetamide 10% qid or
polymyxin/trimethoprim qid.
Oral doxycycline or erythromycin if patient has meibomian
gland dysfunction.
Usually an annoyance, however certain complications such
as corneal ulcers, scarring and neovascularization can
occur.
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Chalazion or Internal hordeolum: Inflammation of meibomian gland due to
occluded orifice and extrusion of lipid contents of the gland into the surrounding
area inciting granulomatous inflammation. (Fig. 2)
II
Figure 2
1.
Clinical Features:
Visible or palpable eyelid lump accompanied with pain,
swelling, and erythema.
Patients often have underlying blepharitis and meibomian
gland dysfunction.
2.
Treatment:
-
Warm compresses for 15 to 20 minutes over the lesion with
light massage.
Topical ophthalmic antibiotic (erythromycin or bacitracin)
ointment two to four times a day.
Refer to ophthalmologist if chalazion does not resolve after
several weeks or if patient desires surgical treatment for a
quicker resolution. After resolution a firm, nontender,
localized nodule often remains.
Preseptal Cellulitis: Anterior to the orbital septum. Orbit is not involved.
(Fig. 3)
III
Figure 3
1.
Clinical Features:
Red, swollen eyelids usually without induration.
May be tender
Vision and ocular motility are typically normal
No relative afferent pupillary defect
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-
No evidence of proptosis
No pain on eye movement
2.
Pathogenesis:
Usually occurs following trauma or skin infection
Can also occur as extension from other infectious site
(sinuses, lacrimal sac infections)
Common organisms include S. aureus and Streptococcus
species. In pediatric age group Hemophilus influenzae is a
fairly common pathogen.
3.
Treatment:
-
Gram stain and culture any conjunctival drainage or
discharge.
Mild preseptal cellulitis can be treated with broad-spectrum
oral antibiotic such as a second-generation cephalosporin.
CT scan can be sometimes be useful to differentiate
preseptal from orbital cellulitis,
Moderate to severe preseptal cellulitis and children under
the age of five should be treated aggressively with
intravenous antibiotics.
Tetanus toxoid should be administered if necessary.
Topical ophthalmic ointment or drops for secondary
conjunctivitis.
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IV
Orbital Cellulitis (Fig. 4)
Figure 4
1.
Clinical Features:
Red, swollen, tender eyelids
Hyperemia and chemosis of the conjunctiva
Pain on eye movement with restricted ocular motility
Vision can be decreased
Afferent pupillary defect may be present
Proptosis
Double vision may be present
Fever
2.
Pathogenesis:
Most infections originate from the sinuses especially the
ethmoid sinus.
Dental abscesses, upper respiratory infections, orbital
trauma, eyelid and strabismus surgery, lacrimal sac
infections have been associated with orbital infections.
Common organisms include S. aureus and Streptococcus
species. In pediatric age group Hemophilus influenzae is a
fairly common pathogen.
4.
Treatment:
-
V!
Admit for IV antibiotics and close monitoring.
Consult appropriate services (Ophthalmology, ENT)
CT scan of orbit and sinuses
CBC, blood cultures and culture any conjunctival drainage
or discharge.
Broad-spectrum antibiotics such as second- generation
cephalosporin or ampicillin/sulbactam
Nasal decongestants
In immunocompromised individuals and diabetics one must
also consider the possibility of mucormycosis
Complications include subperiosteal abscess, cavernous
sinus thrombosis, and meningitis.
Nasolacrimal drainage obstruction
1.
Clinical Features
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2.
Treatment
-
-
VII
Persistent tearing and discharge, often associated with
redness
+ Dacryocystitis (infected lacrimal sac): raised, tender,
eythematous, swollen lacrimal sac beneath the medial
canthal tendon
Congenital obstruction (usually due to persistent congenital
membranes in nasolacrimal duct)
Massage lacrimal sac daily
Topical antibiotic solution (10% sulfacetamide qid
for 1-2 weeks) if purulent discharge
Systemic antibiotics if dacryocystitis
Refer to ophthalmologist if no resolution after 6-8
months of age for nasolacrimal duct probing.
Acquired obstruction
Rule out nasal inflammation, polyps, tumors
Systemic antibiotics if dacryocystitis
Nasal decongestants
If chronic and/or recurrent refer to ophthalmologist
Acute Conjunctivitis (referred to as “pink eye” by the layman) (Fig. 5)
Figure 5
1.
Clinical Features
Redness
Itching
Discharge: characteristic of cause
Watery with white, stringy mucous: allergic
Purulent: bacterial
Watery or serous: viral or chemical
Palpable, tender preauricular lymphadenopathy:
characteristic of viral or chlamydial causes. Bacterial
conjunctivitis presents typically without
lymphadenopathy.
2.
Bacterial conjunctivitis
-
Etiology: Staphylococcus sp., Streptococcus sp.,
Hemophilus influenza, Pseudomonas sp.
Treatment
-
Clean lids of discharge
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3.
Topical antibiotics qid x 5-7 days (10% sulfacetamide or
Polytrim) or ophthalmic ointment qid x 7 (bacitracin,
erythromycin, or gentamicin)
Refer to ophthalmologist if not improved in 3-4 days
Hyperacute bacterial conjunctivitis (copious purulent discharge within 12
to 24 hours)
-
Etiology: Neisseria gonorrhea
Critical Signs: profusely purulent discharge (flowing pus);
sometimes prominent lid swelling; chemosis, occasionally
preauricular lymphadenopathy
Treatment
Immediate conjunctival scrapings for Gram’s stain
and for cultures and sensitivities are mandatory.
Ophthalmology consult
Ceftriaxone 1 gm i.m. in a single dose. If corneal
involved then Ceftriaxone 1 gm q12-24 hrs.
Topical ofloxacin or ciprofloxacin q 1 h if cornea is
involved with the infection
Treat for possible co-infection with chlamydia
4.
Viral conjunctivitis
Contagious: commonly occurs in epidemics (adenovirus)
Treatment
No- effective therapy except time (2-6 weeks).
Strict hygiene with frequent hand washing
recommended
Refer to ophthalmologist if pain, photophobia,
decreased vision
Artificial tears qid for comfort
5.
Allergic (hayfever) conjunctivitis
Clinical Features:
Itching, burning eyes
Lid swelling
Conjunctival Chemosis
Redness
-
Treatment:
Cool compresses
Avoid allergens
Topical/oral antihistamines (naphazoline gtts qid
prn or Patanol bid)
27
-
6.
Mast cell stabilizers (4% cromolyn qid )
Refer if refractory to treatment
Chemical Conjunctivitis / Chemical burns (Fig. 6)
Figure 6
-
Acid
-
-
Immediate damage/ Ocular Emergency
Stat continuous irrigation with normal saline for
many minutes to hours until pH of tears neutralized
Cycloplegia ( Atropine1% qid or scopolamine
0.25% bid or homatropine 5% bid )
Patch with ophthalmic ointment ( bacitracin,
erythromycin)
Always refer to an ophthalmologist
Alkali
Immediate and delayed damage
Stat continuous irrigation for many minutes to hours
until pH of tears neutralized
Stat referral to ophthalmologist
Potential for serious ocular damage
28
VIII. Subconjunctival hemorrhage (Fig. 7)
Figure 7
Usually spontaneous without known cause. Sometimes associated with
hypertension, valsalva maneuver, and anticoagulants
Patient often presents with bright red eye
Normal vision, no pain, no history of trauma
No treatment except time (2 weeks) and reassurance
IX.
Neonatal conjunctivitis (ophthalmia neonatorum)
1.
Clinical Features
Redness
Discharge
Cutaneous vesicles suggest herpes simplex
2.
Etiology:
Chlamydia (inclusion conjunctivitis), Candida albicans, Neisseria
gonorrhoeae or N. meningitides, Herpes simplex type II, Pseudomonas
aeruginosa, “everyday bacteria” (staph. strep. pneumo.), and chemical
conjunctivitis from silver nitrate prophylaxis .
3.
Treatment:
-
Conjunctival scrapings and cultures are mandatory;
fluorescent-antibody tests are available for chlamydia and
herpes
29
-
3.
Prognosis:
-
Treatment highly variable depending on etiology.
Consider ophthalmology consult whenever appropriate
If Gram stain shows gram positive organisms treat with
erythromycin ophthalmic ointment Q2-4 hours for 5-10
days
If Gram Stain shows Gram negative organisms treat with
tobramycin or gentamicin ophthalmic solution or ointment
q2-4 hours for 5-10 days
If gram stain is suggestive of gonococcus refer to
ophthalmologist immediately
neisserial infections usually require systemic ceftriaxone or
penicillin
herpes simplex may call for systemic acyclovir and topical
trifluorothymidine (Viroptic drops)
Chlamydial infections should be treated with both topical
erythromycin ophthalmic ointment (qid) and systemic
erythromycin (40 –50 mg/kg/day in four divided doses).
Rapid corneal perforation can occur with neisseria or
pseudomonas
acute or chronic keratitis can be caused by herpes or
chlamydia
N. meningitides can be fatal, as can disseminated herpes
simplex or chlamydia (pneumonitis)
Note: Systemic tetracycline should be avoided in pregnant or breast feeding
women and children under the age of eight years
.
X. Dry eyes (keratoconjunctivitis sicca)
1.
2.
4.
Clinical Features
Redness
Burning
“gritty”, foreign-body sensation (symptoms exceed the
signs)
Symptoms typically worse in the evenings
Treatment
Artificial tears instilled frequently (preservative-free)
Lubricating ophthalmic ointment qhs
Protective sun goggles for outdoor wear
If severe, refer to an ophthalmologist
Etiology
Common with aging
30
-
Associated with rheumatoid arthritis, Stevens-Johnson
syndrome, systemic medications (diuretics, antihistamines,
antidepressants, dermatologic drying agents)
XI. Exposure Keratitis
1.
Clinical Features
Redness
Ocular irritation
Symptoms typically worse in the mornings
Inadequate blinking or closure of eyelids leading to corneal
drying
2.
Etiology
-
3.
Treatment
-
XII.
Bell’s palsy (seventh cranial-nerve palsy)
scarred or malpositioned lids
Proptosis (thyroid ophthalmopathy)
Artificial tears, lubricating ointment
Mechanical lid closure (massage, voluntary forced lid
closure, taping lids prn)
Refer if severe
Pinguecula/Pterygium (Fig. 8)
Figure 8
1.
Clinical Features
-
Conjunctival degeneration caused by exposure to sun,
wind, and dust
31
2.
Treatment:
-
Arises from bulbar conjunctiva in interpalpebral fissure
near the limbus (nasal and/or temporal)
Pinguecula: confined to conjunctival tissue
Pterygium: extension onto the cornea, may involve visual
axis
These lesions respond to irritants in the environment (e.g.,
smoke, fumes) and become red and inflamed—thereby
attracting attention
Frequent use of artificial tears...to reduce symptoms
Sunglasses for outdoor wear to prevent progression
Topical ophthalmic solutions with vasoconstrictors qid prn
to alleviate redness
Refer to ophthalmologist if actively growing pterygium is
present or if inflammation is severe
XIII. Episcieritis/scleritis
1.
Clinical Features
Localized redness associated with discomfort and
tenderness
Noninfectious (immunologic) inflammation of sclera/
episclera usually sectoral in distribution; no discharge
Most cases are idiopathic
+ Associated conditions: autoimmune disorders, e.g.,
rheumatoid arthritis
May be vision-threatening with extension into the cornea or
intraocular inflammation
2.
Treatment:
-
Refer to ophthalmologist
Topical Steroids
Oral Non steroidals
Severe cases might need oral steroids and cytotoxic agents
Prognosis:
-
can be chronic
can lead to uveitis, scleral melting, corneal involvement
3.
XIV. Corneal abrasion
1.
Clinical Features
Redness
Tearing
Photophobia
Pain
32
2.
XV.
Treatment
homatropine)
-
Decreased vision
Usually a history of trauma or contact lens wear
Cycloplegic eye drops (1-2% cyclopentolate, 2-5%
Topical ophthalmic antibiotic drops or ointment
Pressure patch (2 eye pads) for at least 24 hours
Do not patch contact lens related abrasions
Oral analgesics with codeine if severe pain
Refer to ophthalmologist in 24-48 hours if not pain-free
Keratitis (corneal inflammation usually caused by infection)
1. Viral
Herpes simplex type I most common
Signs and symptoms: red eye with watery discharge and
foreign-body sensation
Epithelial dendrite or branching figure is characteristic, best
seen with fluorescein stain
Refer to ophthalmologist stat
2. Bacterial
Signs and symptoms: red, painful eye with purulent
discharge and decreased vision
Discrete corneal opacity seen with penlight
Hypopyon may be present
Refer to ophthalmologist stat as there is risk of corneal
perforation, corneal scarring and loss of vision.
XVI. Anterior chamber: vision-threatening conditions
33
1. Hyphema: blood in the anterior chamber
Usually follows blunt trauma
Signs and symptoms: decreased vision, pain, redness, blood
seen grossly layered out in the anterior chamber. Refer to
ophthalmologist stat, risk of other unsuspected ocular
damage, glaucoma, further bleeding
2. Iritis: inflammation in anterior chamber
Signs and symptoms: circumcorneal redness, pain,
photophobia, decreased vision, and small pupil; intraocular
pressure may be abnormal
+ Associated conditions: juvenile rheumatoid arthritis
sarcoidosis, dental abscesses, urethritis, inflammatory
bowel disorders, allergies, tuberculosis, and syphilis
May be seen following blunt trauma to eye; usually delayed
1-3 days
-
Complications: glaucoma and cataract
Recognize and refer to an ophthalmologist
3. Acute glaucoma
Sudden block of aqueous outflow by peripheral iris moving
forward to occlude the trabecular meshwork
Characteristically seen in susceptible individuals who
experience attacks of acute rise in intraocular pressure
when pupil(s) dilate(s)
Precipitating factors: dim light, many pharmacologic
agents (topical and systemic), emotional stress
Signs:
Circumcorneal redness
Mid-dilated (5 mm), nonreactive pupil
Cloudy cornea
Increased intraocular pressure (usually 50
mm Hg or more)
34
-
-
IX.
One or both eyes may be involved
Symptoms:
Severe ocular pain or headache
Blurred vision
Perception of halos around lights
+ Nausea and vomiting
Presents as “a great masquerader”: can be confused with
other conditions, e.g., cerebral aneurysm (headache,
dilated pupil), appendicitis (nausea, vomiting)
Refer to ophthalmologist stat
VISION-THREATENING RED EYE DISORDERS
A. Signs and symptoms
1. Decreased vision
2. Ocular pain
3. Photophobia
4. Circumcorneal redness
5. Corneal edema
6. Corneal ulcers, dendrites
7. Abnormal pupil
8. Elevated intraocular Pressure
B. Conditions
1. orbital cellulitis
2. Episcleritis, scleritis
3. Corneal infection
4. Hyphema
5. Iritis
6. Acute glaucoma
C. Recognize and refer
GENERAL PRECAUTIONS IN TREATING RED EYES
A. Avoid corticosteroids: they mask worsening of conditions, allow
secondary infections, and make primary infections worse, and can cause
glaucoma, cataract, and corneal melting and
perforation
B. Avoid topical anesthetics as treatment: they soon become very toxic to the
eye and retard healing with prolonged use
C. Do not patch infected eyes. Do not patch contact lens related abrasions
D. Do not use irritating and allergenic drugs (neomycin, gentamicin,
tobramycin, antiviral agents) for longer than two weeks
35
Section IV
Vision Screening in Infancy
Joseph C. Paviglianiti, M.D.
1.)
2.)
3.)
4.)
5.)
6.)
7.)
8.)
9.)
Strabismus
Amblyopia
Leukocoria
Cloudy Cornea
Nasolacrimal Duct Obstruction
Ptosis
Nystagmus
Retinopathy of Prematurity
Anisocoria
1.) Strabismus (abnormal ocular alignment)
- esotropia (eye turns in) (ET) (Fig. 1)
- exotropia (eye turns out) (XT) (Fig. 2)
- hypertropia (eye turns up) (HT)
- hypotropia (eye turns down) (hypoT)
Figure 1 Esotropia (ET)
Figure 2 Exotropia (XT)
- approximately 5% of all US children have strabismus
- newborns commonly have strabismus but should grow out of it in a few daysweeks(Nixon 1985, 40% newborns straight, 33% exotropia,
3% esotropia)
- infants often have flat nasal bridges and large epicanthal folds which can have
false appearance of crossing ( To avoid being fooled: shine penlight at eyes;
if light reflex is in center of corneas OU, then eyes are straight, even if it looks
like they are crossed in); called “pseudoesotropia”
- need to check motility to make sure eyes move equally in all fields of gaze
36
-
-
-
-
-
-
Specific Types of Strabismus:
Congenital ET
-eyes cross in before 6 months of age; parents say eyes “always crossed”
since birth
-affects 1-2% of ALL babies born
-large angle (eye is really turned way in)
-usually needs surgical alignment (doesn’t usually fix itself with glasses)
-usually NOT much hyperopia (farsightedness)
-likely will never have good depth perception/fusion even if eyes
surgically aligned early
Refractive ET
-these kids are pretty farsighted, and in their efforts to focus, their eyes
cross in (unlike congenital ET which is not a focusing problem)
-usually mostly cured with glasses
Nonrefractive ET
-eyes cross in after age ~1 but not due to focusing problem; needs surgical
alignment
Infantile XT (eyes go out)
-if newborn presents to office with XT before 6 months of age, (but older
than a few weeks, see above) consider it a brain problem and consider a
scan
Intermittent XT
-occurs after age 6 months usually
-usually maintain good stereo/depth perception
-parents note eye wandering out, initially only briefly, but as kid gets to be
older, they lose control and the eye “stays out” more and more;
-surgery indicated when eye wanders out more than it is straight
Convergence insufficiency
-eyes don’t converge well when trying to focus to read
-c/o headaches, asthenopia (vague eye pains/aches) and diplopia when
reading
-tx c prisms and or surgery
Nerve palsies causing strabismus (trauma is a common cause)
-6th nerve palsy (LR doesn’t work, so medical rectus unopposed, pulls eye
in)
-3rd nerve palsy (MR doesn’t work, so lateral rectus unopposed, pulls eye
out)
-4th nerve palsy- Superior oblique doesn’t work, so inferior oblique (an
elevator) is unopposed and patient presents with ipsilateral hypertropia
and a contralateral head tilt)
-NOTE all patients with their heads tilted (so they don’t see double) have
4th N palsy until proven otherwise.
37
2.) Amblyopia (“Lazy Eye”)
- “lazy eye” means many things to different people and therefore it is a bad
term and us smart medical people should never use it
“my kid’s eyelid droops….it’s a lazy eye” (ptosis)
“my kid’s eye wanders out (or in)…it’s a lazy eye” (eso/exotropic)
“he don’t see so good out of his left eye…it’s a lazy eye” (amblyopia)
- amblyopia defined as reduced visual acuity in a structurally healthy eye
(derived from the Greek word for “dullness of vision”)
- vision out of an amblyopic eye has been described as similar to a shimmer
effect of hot air over a highway – “a continuously wavy motion in the
environment”, “the object of regard fades in and out of focus continuously”;
the vision is not really blurry…it’s more dull, with words and letters blending
together.
- “crowding phenomenon”- amblyopic eye may only be able to read a line at
20/50, but if letters presented individually, can get the 20/30 letters right
- amblyopes therefore “do better” with more time given to read
- some amblyopic eyes actually see better with less light in the room (neural
density filter test-put dark lenses in front of an amblyopic eye and won’t
notice much decrease in vision; vs. will notice decrease in eye with organic
vision loss.
- AMBLYOPIA affects 2-5% US/world population (it’s common and a lot of
kids have it!)
- Causes of amblyopia (decreased vision in one eye)
A) Strabismic-most common. Bad alignment, means one eye is not looking
at the target; over time, that eye shuts off permanently
B) Refractive- usually due to anisometropia (a large refractive difference
between the eyes, such that the eye that is more out of focus, gradually
shuts off). Can also be due to bilateral HIGH hyperopia and myopia
(really, really farsighted or nearsighted)
C) Occlusion – usually due to ptosis (with lid blocking visual input) or
cataract (with lens blocking input). Rarely can be caused by excessive
patching of the good eye while trying to treat amblyopia of the bad eye
(i.e. you patch the good eye so much it becomes the bad eye)
D) Underlying organic etiology - for example, optic nerve hypoplasia (the
vision is ↓ due to the bad nerve, but patch can sometimes get a little of that
vision back)
38
3) Leukocoria (white pupil) (Fig. 3)
Figure 3 Leukocoria
-
-
-
Big differential diagnosis, but most commonly:
congenital cataract (discussed below)
PHPV (persistent hyperplasia of primary vitreous)
Retinoblastoma or other intraocular tumor (discussed below)
Retina detachment (due to trauma or retinopathy of prematurity)
Coats disease – fluid under retina
Toxocariasis (nematode infection) from exposure to puppies or other
uveitis
Large retina coloboma
most commonly picked up by parents in kids photos – one eye has red reflex,
other white
More on congenital cataracts:
- cause 10% of all visual loss worldwide
-1:250 newborns has some form of congenital cataract ranging from
insignificant to vision threatening
- etiology is mostly idiopathic, some familial with auto dominant
inheritance; other causes: intrauterine infection (rubella, herpes, CMV),
metabolic disorders (galactosemia), Lowes, Refsums, Alports, sulfite
oxidase deficiency, Fabry’s), structural abnormalities (microphthalmia,
coloboma, aniridia, PHPV, posterior lenticonus), trauma, radiation,
craniofacial (Hallerman-Streiff, Rubenstein-Taybi.)
More on Retinoblastoma
-the most common intraocular malignancy of childhood
-1:20,000 live births
-there is an inherited form (usually bilateral) and a non-inherited form
(usually unilateral-spontaneous) of retinoblastoma
-retinoblastoma usually presents with leukocoria or strabismus
-loss of recessive suppressor gene on chrom #13, “two hit hypothesis,”
50% of all cases hereditary
-looks like a white mass sitting on the retina or a lesion under the retina
causing a retinal detachment
-usually dx at age 12-24 mo
-if untreated → 100% fatal
-if treated → 90% survival
39
-kids of pts with inherited bilateral Retinoblastoma have 45% chance of
developing Retinoblastoma (takes two hits – so one parent contributes a
bad gene, one a good gene therefore 50% x 90% penetrance => 45%)
-kids of patients with spontaneous unilateral retinoblastoma have ~ 5%
chance of developing Retinoblastoma)
-treatment options:
-enucleation: curative if tumor has not left the eye (which it does
via optic nerve)
-XRT
-Focal (plaque) brachytherapy
-Chemo
-Cryotherapy
3.) Cloudy Cornea (Fig 4)
Figure 4 Cloudy Cornea
- think congenital glaucoma until proven otherwise. Glaucoma is increased
pressure in the eye: presentations include: tearing, photophobia, cloudy
cornea, megalocornea; Treatment: glaucoma drops and surgery to either ↑
outflow or ↓ production of fluid from the anterior chamber of the eye
- Other causes of a cloudy cornea: STUMPED
-Sclerocornea – the white of the eye covers the cornea
-Tears in corneal endothelium – birth trauma, congenital glaucoma
-Ulcers of cornea (herpes, rubella)
-Metabolic – mucopolysaccharidosis, lipidoses, tyrosinosis
-Peters anomaly (posterior corneal defect)
-Endothelial dystophies
-Dermoid
- Infections - trachoma
- endemic, over 250 million people worldwide have it
- by far the MOST common cause of corneal scarring and blindness in the
world
40
4.) Nasolacrimal Duct Obstruction (NLDO)
- an obstruction in nasolacrimal system, most likely at Valve of Hasner where
drainage system empties into nose beneath the interior turbinate
- Symptoms: crusty, yellow matting/tearing of eyelids/lashes, usually from
birth
- tx: 90% resolve on own by age 1 yr: in meantime, treat symptomatically with
antibiotic eye drops and NLD massage.
- Otherwise, can probe open the system; if malformed, can do
dacryocystorhinostomy (DCR) to create a new plumbing system into the nose.
5.) Ptosis (droopy eyelid) (Fig. 5)
Figure 5 Ptosis
-
is it congenital or acquired?
if congenital, usually due to an underdeveloped levator palpebrae muscle,
though congenital eyelid tumor or 3rd nerve palsy could also be implicated;
also congenital Horner’s from a forceps delivery
if acquired, need to closely evaluate pupil to rule out Horner’s (ptosis, miosis,
and anhidrosis) (unfortunately, a guaranteed board question); also need to
consider myogenic causes such as myasthenia or chronic progressive external
ophthalmoplegia; look for a change in ptosis related to chewing or sucking
(Marcus-Gunn jaw wink); also consider lid masses (e.g. neuroblastoma,
neurofibromatosis) or any history of trauma
6.) Nystagmus
- What is Nystagmus?
- involuntary spasmodic motion of the eye due to disruption of the normal
mechanisms for fixation or gaze stability
- normally, the brain uses 3 different mechanisms to keep the eyes trained on a
target
a) “fixation” in primary position involves correction of retinal drift
& suppression of unwanted saccades
b) vestibulo-oculoreflex- maintains fixation while your head moves
c) neural integrator- unknown location in brain serves to overcome
the forces that want to pull the eye back into primary position.
41
-
-
-
-
How should physicians describe nystagmus?
a) jerk (fast and slow phases) vs. pendular (sinusoidal waveform;
equal speed in both directions)
b) horizontal? vertical? torsional?
in general, any new-onset nystagmus requires neuroimaging
any newborn who does not have a partially focused image on the retina (e.g.
due to bilateral cataracts, high bilateral refractive errors) by the age of 3
months will develop IRREVERSIBLE nystagmus
additionally, nystagmus may be the presentation of optic nerve problems
(colobomas, glaucoma, optic nerve hypoplasia, etc); the eye is trying to see
but, due to a faulty nerve, none of the information can get communicated to
the brain => develop nystagmus
in summary, if the newborn brain doesn’t start receiving “eye input” by the
approximate age of 2-3 months, irreversible nystagmus develops- think of it
like the brain telling the eyes “I’m not seeing anything yet, so start looking
around for stuff to see” and a wandering, searching nystagmus begins
Types of Nystagmus
A. Idiopathic Congenital Motor Nystagmus
! usually present early in infancy – onset age 2-3 months
! usually horizontal, dampens with convergence
! usually has a null point where nystagmus is least
! causes:
- idiopathic
- albinism
- aniridia
- Leber’s congenital amaurosis
- achromotopsia
! ddx
- spasmus nutans (nystagmus appearing at age 6months
through 3 years & resolving between ages2 & 8 yrs., with
head bobbing and torticollis
B. Latent Nystagmus
! occurs when you cover an eye, the viewing eye gets nystagmus
with fast phase toward side of viewing eye; usually in patients
with history of strabismus
C. Acquired Nystagmus (the kid definitely didn’t have it yesterday, but
today he does)
! usually present Fridays at 4 p.m.
! etiologies include trauma, stroke, medications, demyelination,
tumors (sometimes the locations of some of these problems can
be guessed at by the type of nystagmus that presents itself):
• seesaw nystagmus – one eye rises and intorts while the
other descends and extorts
! think of chiasm or 3rd ventricle
42
•
•
•
•
•
•
•
•
convergence retraction nystagmus- poor upgaze, eyelid
retraction, large unreactive pupils, with convergencelike movements on upgaze
! think dorsal midbrain or pineal gland
upbeat nystagmus – fast phase beats “up” in primary
position
! think brainstem or cerebellar vermis
! note: if upbeat nystagmus only happens
when pt looks up: think of drug etiology
rebound nystagmus- over/undershoot when trying to
change gaze
! think cerebellum
gaze-evoked nystagmus-not present when eyes straight
ahead, but is present when eyes look to side
! think EtOH, sedatives, cerebellar
problems
downbeat nystagmus – fast phase “down” in primary
position
! think cervico-medullary junction (e.g.
Arnold-Chiari)
periodic alternating nystagmus – fast eye mvts in one
direction for about 60-90 seconds, then fast eye mvts in
the other direction for 60-90 seconds; cycle repeats
continuously
! think cervico-medullary junction or
blindness
vestibular nystagmus – usually has a rotary component
! can be associated with vertigo, tinnitus,
deafness
opsoclonus – random bursts of nystagmus which
switches directions
! think of neuroblastoma or encephalitis in
kids; drugs or strokes in adults
7.) Retinopathy of Prematurity (ROP)
- the vessels of the retina begin to develop out from the optic nerve at about 16
weeks of gestation and reach the ora serrata by about 40-42 weeks of gestation
- in selected preemies, the normally developing blood vessels are damaged and
begin to grow irregularly and proliferate; scar tissue and gliosis follow, along
with hemorrhage of the new, tenuous vessels; the scar tissue can cause
traction on the retina, thus leading to the blinding condition of bilateral retinal
detachments
- related to the birth weight of the baby and the amount of supplemental oxygen
received (low birth weight babies on a ventilator for a long time are more
likely to get ROP)
43
-
there are many other factors which are not really understood (vitamins,
antenatal steroids, post gestational health etc)
- currently all preemies born before 32 weeks of gestational age and/or born
LESS than 1250 g are screened for ROP
- the location of the abnormal vessels is followed closely
o the retina is divided into zones, centered around the optic nerve
o the amount of retinopathy of prematurity is described in stages
o the additional finding of “plus” disease (vascular tortuosity) is also a
bad sign
o when a certain amount of ROP is found within the correct zones, then
the peripheral retina is lasered via a DIODE laser, in the hopes of
causing regression of the abnormal blood vessels; most of the time it
works, sometimes it doesn’t
- ROP is still a significant problem today, with an unacceptably high percentage
of preemies going blind despite proper care and management
8.) Anisocoria (Fig. 6)
Figure 6 Anisocoria
-note that 10-20 % of ALL adults and children have a small amount of anisocoria
(Physiologic anisocoria)
-looking at old photos can be very reassuring and save an expensive workup
-many times a parent will “discover” their child to have unequal pupils one day,
but old close-up photos verify the anisocoria has been there a long time
-common causes of anisocoria
-secret use of miotic or mydriatic eye drops
-HORNER’S – ptosis, miosis, anhydrosis (can use 10% cocaine and
hydroxyamphetamine to differentiate between a 2nd or 3rd order Horners
-Argyll-Robertson pupil- accommodates but doesn’t react to light; check
FTA-ABS for syphilis
-Adie’s tonic pupil – a dilated pupil that doesn’t constrict much to light or
accommodation, but really constricts with a weak miotic agent
-trauma or previous eye surgery
44
-third nerve palsy (also, note whether eye muscles and eye lids are
involved)
-probably best to refer most cases of anisocoria to ophthalmology, unless
anisocoria is known and has been worked up previously
45
Section VI
Diabetic Retinopathy: Diagnosis and Treatment
Ronald Danis, M.D., Thomas Ciulla, M.D.
Diabetic retinopathy is the most prevalent cause of blindness among working age (20 –
64 years old) Americans. About 25% of diabetics have some form of retinopathy, and
about 5% have the more severe type of disease (proliferative diabetic retinopathy).
Onset
Type 1 Diabetes
-Generally free of retinopathy for the first five years after diagnosis
-After 15 years duration of diabetes, the prevalence of retinopathy is over 95%
-After 20 years duration of diabetes, more than half will have proliferative disease
Type 2 Diabetes
-Frequently will have retinopathy at the time of diagnosis
-After 15 years of diabetes, about 2/3 will have retinopathy
For both types of diabetes, the severity and prevalence of retinopathy correlates with 1.,
the duration of disease, and 2., glycemic control. The Diabetes Complications and
Control Trial (DCCT) demonstrated a greater than 60% reduction in the progression of
retinopathy in patients with very tight metabolic control compared to patients with good
blood sugar control. Hypertension and smoking may be aggravating factors in some
patients. Women with pre-existing diabetes who become pregnant occasionally develop
aggressive acceleration of retinopathy, usually associated with poor glycemic control and
pre-eclampsia.
X.
Pathogenesis
-Retinal capillary basement membrane thickening and pericyte loss with eventual
capillary closure
-Blood-retinal barrier breakdown from endothelial cell dysfunction, leading to retinal
edema, which causes retinal neuronal dysfunction and vision loss
-Progressive retinal ischemia leading to neovascularization, which causes fibrovascular
proliferation out from the retina and optic nerve head into the vitreous gel.
Complications such as bleeding (vitreous hemorrhage) and retinal detachment occur
because of the contractile nature of the fibrous component of the proliferation with
subsequent traction on the vessels (bleeding) or on the retina itself (detachment).
XI.
Clinical Stage of Retinopathy
Two major sub-groups: Non-proliferative (background) and Proliferative
46
Non-proliferative (background)
Mild non-proliferative retinopathy:
-Consistent with good vision
-Few scattered microaneurysms, intraretinal hemorrhages
Moderate non-proliferative retinopathy
-More microaneurysms and hemorrhages
-May develop retinal edema with “hard” exudates
-May have micro-infarcts (“cotton-wool spots”)
-May have focal areas of non-perfusion (not clinically apparent)
47
Severe non-proliferative retinopathy
-Intraretinal microvascular abnormalities (IRMAs)
-Venous caliber irregularities (“beading”)
-Often severe edema or large areas of ischemia are apparent
50% risk of proliferative retinopathy within 1 year
Proliferative Diabetic Retinopathy
Early proliferative retinopathy
-Neovascularization of the optic nerve head and/or retina
-With or without vitreous hemorrhage
48
Late proliferative retinopathy
-Severe intraocular fibrovascular proliferation with tractional retinal detachment and/or
vitreous hemorrhage (the usual cause of blindness in diabetic patients).
XII.
Vision Loss
Macular edema can occur and cause vision loss in any stage except mild nonproliferative
retinopathy. Vision loss from macular edema may be mild or, if severe and chronic, can
cause legal blindness (acuity <= 20/200). Vision loss is usually gradual over a period of
months and usually is described as simply “blurring”. Macular ischemia can also cause
irreversible vision loss in the more severe stages of retinopathy.
Vision loss from vitreous hemorrhage is characteristically abrupt. It may range from a
few specks or lines in the vision (“floaters”), which may resolve over a few days to
severe profound vision loss to the bare light perception level. Retinal traction and
detachment may cause gradual or sudden vision loss, sometimes coincident with vitreous
hemorrhage.
XIII. Diagnosis
Patient education: when patients present with vision loss, it is often TOO LATE to do
anything to improve the vision. Vision loss from macula edema, vitreous hemorrhage or
retinal detachment may not be reversible and is definitely more manageable when these
complications are detected early. Routine ophthalmoscopic evaluation is key.
Examination with the direct ophthalmoscope through an undilated pupil is VERY
INSENSITIVE. Neovascularization often occurs peripheral to the field within view with
the direct ophthalmoscope. Macular edema may be manifest only by retinal thickening,
which cannot be resolved with the monocular view of the direct ophthalmoscope.
Severely ischemic retinas are sometimes ophthamoscopically unimpressive because
without patent vessels, there is no hemorrhage or exudation. Neovascular vessels may be
very hard to resolve due to lack of contrast in the retina and difficulty in distinguishing
them from retinal vessels.
49
Macular edema is best appreciated with slit-lamp biomicroscopy through a dilated pupil.
Neovascularization near the macula can be seen with the direct ophthalmoscope in a
dilated eye or with slit-lamp biomicroscopy. Peripheral neovascularization and vitreous
hemorrhage may only be seen with the indirect ophthalmoscope.
XIV. Treatment
Macular edema
The Early Treatment of Diabetic Retinopathy Study (ETDRS), a randomized prospective
multicenter trial, demonstrated that macular laser photocoagulation could reduce the rate
of moderate vision loss from macular edema by more than 50%. Milder macular edema
is more easily treated and controlled than severe macular edema. The laser treatment
consists of a fine grid of 50 or 100-micron mild laser spots to areas of retinal thickening
in a grid pattern or focally to treat individual microaneurysms (focal/grid laser treatment).
There is generally no pain involved with this type of treatment and risks consist
principally of inadvertent foveal burns with vision loss (fortunately, very rare) and
corneal abrasion from the contact lens used to focus the laser beam. Occasionally,
multiple treatments are performed in the same eye if it is poorly responsive, and vision
loss may still inexorably occur.
Macular edema may be influenced by systemic factors. Fluid retention from cardiac or
renal failure contributes. Diuresis can sometimes influence the vision in such patients.
Proliferative Retinopathy
The Diabetic Retinopathy Study (DRS) and the later ETDRS established to optimal
timing and role of scatter or pan-retinal laser photocoagulation (PRP) in the control of
proliferative retinopathy. Rates of severe vision loss can be decreased to around 1% per
year if patients are treated in the early stages of proliferative retinopathy. Even patients
who present with more advanced PDR can benefit from PRP treatment with a more than
50% reduction in the rate of blindness. This style of laser treatment consists of placing
more than 1,200 laser burns to the mid-periphery of the retina, outside of the macular
arcades. This is often done in more than one treatment session. Surprisingly, only about
10% of patients have any visual side effects from this treatment, and, generally, these are
mild. If performed without anesthesia, most patients can tolerate the laser treatment with
some discomfort. Some patients will experience pain with the laser treatment and require
a retrobulbar anesthetic block to get them through the treatment.
Particularly if patients present late, with advanced PDR, severe vitreous hemorrhage and
retinal detachment may still occur despite laser treatment. Sometimes, the vitreous
hemorrhage will spontaneously clear over a period of weeks or months, and no further
treatment may be necessary. For non-clearing vitreous hemorrhage or retinal detachment
affecting the macula, vitrectomy surgery by a retina specialist may be performed. This
involves introduction of microsurgical instruments into the vitreous cavity (fiber-optic
light source, pneumatic cutter-aspirator, micro scissors, cautery, laser). Depending on the
specifics of the case, the prognosis for visual recovery varies greatly.
50
XV.
Referral for Eye Exam
• Type 1 DM – refer 5 years after diagnosis
• Type 2 DM – refer at the time of diagnosis
• Refer patients that are pregnant or are considering pregnancy
• Follow-up examinations are determined by the stage of the disease
Immediate referrals for diabetics with persistent decrease in vision or new onset of
floaters.
51
Section V
Glaucoma
Louis Cantor, M.D., Darrell WuDunn, M.D., Ph.D.
I.
Introduction and Definition
A.
Glaucoma is a group of disorders characterized by progressive optic
neuropathy (often characterized by excavation) accompanied by
corresponding defects in visual function. Elevated intraocular pressure is a
prominent risk factor.
B.
Primary glaucomas are not associated with known ocular or systemic
abnormalities that may cause glaucoma. Primary glaucomas are usually
bilateral and may be inherited.
C.
Secondary glaucomas have associated ocular or systemic disorders that
cause or contribute to the development of glaucomatous optic neuropathy.
Secondary glaucomas are often unilateral and familial occurrence is less
common.
II.
Epidemiology
A.
In USA
1. 10 million at risk due to elevated IOP
2. 2 million affected
3. About half are undiagnosed
4. 116,000 blind
B.
Worldwide
1. 100 million at risk due to elevated IOP
2. 3 million blind
III.
Hereditary Factors
A.
Prevalence 1.5-2.0% in general population; 10-15% in first degree
relatives.
B.
Genetics – numerous genes associated with glaucoma have been identified
IV.
Classification of Glaucoma
A.
Open Angle Glaucoma: outflow through trabecular meshwork is impaired
1. Primary
2. Normal tension glaucoma
3. Secondary
a. Increased resistance to trabecular meshwork outflow associated
with other conditions:
i. Pigmentary dispersion
ii. Pseudoexfoliation
iii. Phacolytic
iv. Steroids
b. Increased resistance posterior to trabecular meshwork
secondary to increased episcleral venous pressure (e.g. carotid
cavernous sinus fistula)
52
B.
C.
D.
Angle Closure Glaucoma: resistance to outflow is increased because
peripheral iris obstructs the trabecular meshwork
1. Primary – pupillary block
2. Primary – plateau iris
3. Secondary – pupillary block (phacomorphic, secluded pupil)
4. Secondary – without papillary block (neovascular glaucoma)
Combined Mechanism Glaucoma – combination of two or more forms of
glaucoma
Childhood Glaucoma
V.
Clinical Evaluation
A.
History – importance in diagnosis and management of glaucoma
1. Ocular history
2. General medical and surgical history
3. Family history
B.
Examination
1. Refraction
2. Pupils
3. Anterior segment (Slit Lamp biomicroscopy)
4. Tonometry (intraocular pressure measurement)
5. Gonioscopy
6. Ophthalmoscopy especially optic disc and retinal nerve fiber layer
C.
Visual Fields
VI.
Primary Open-Angle Glaucoma
A.
Epidemiology
1. prevalence
a) 1.3-2.1% in general white population
b) 3 to 4 times higher in general black population
2. risk factors
a) IOP (normal range 10-21 mmHg)
b) Age, black race, family history
c) Diabetes, systemic hypertension, migraine?
B.
Glaucoma Suspect
1. Glaucomatous optic nerve appearance with or without elevated IOP
but normal visual fields
2. The higher the baseline IOP, the greater the risk of developing
glaucoma; however, most individuals with elevated IOP never develop
glaucoma
C.
Normal tension glaucoma
1. Characteristic glaucomatous optic neuropathy and visual field loss but
with IOP consistently in normal range
VII.
Secondary Open-Angle Glaucoma
A.
Pseudoexfoliation glaucoma
B.
Pigmentary glaucoma
53
C.
D.
E.
F.
Traumatic glaucoma
Neovascular glaucoma (early)
Steroid-induced glaucoma
Others
VIII. Acute Angle Closure Glaucoma
A.
Epidemiology
1. prevalence - <0.1% in USA
2. risk factors
a. family history
b. hyperopia (far-sightedness)
c. ethnic background (Eskimos)
B.
Clinical features
1. Symptoms
a. Eye pain and/or headache
b. Blurred vision
c. Seeing halos around lights
d. Red eye
e. Nausea/vomiting
2. Signs
a. Injected conjunctival vessels
b. Edematous cornea
c. Fixed and mid-dilated pupil
d. Markedly elevated IOP (>50 mmHg)
e. Optic disc swelling
XVI. Medical Management of Glaucoma
A.
Beta-adrenergic Antagonists
1. Non-selective (timolol, levobunolol, carteolol, metipranolol)
2. Beta-1 selective (betaxolol)
3. Action: reduce aqueous inflow
4. Side effects
a. Bronchospasm
b. Bradycardia
c. Low blood pressure
d. Impotence
e. Confusion
f. Fatigue
g. Hallucinations
B.
Adrenergic Agonists
1. Non-selective (epinephrine, dipivefrin)
2. Alpha-2 selective (apraclonidine, brimonidine)
3. Action: reduce aqueous inflow and increase uveoscleral outflow
4. Side effects
a) Alpha-1 effects:
a. Mydriasis
54
C.
D.
E.
IX.
b. Lid retraction
c. Vasoconstriction
d. Increased heart rate and blood pressure
b) Alpha-2 effects:
a. Miosis in some
b. Hypotension
c. Fatigue
Parasympathommimetic agents (miotics)
1. Cholinergic agents (pilocarpine, carbachol)
2. Anticholinesterases agents (physostigmine, demecarium,
echothiophate)
3. Action: increase aqueous outflow through trabecular meshwork
4. Side effects:
a) brow ache
b) miosis
c) blurred vision
d) retinal detachment
e) prolonged paralysis following anesthesia (irreversible
anticholinesterase agents)
Carbonic Anhydrase Inhibitors
1. Oral (acetazolamide, methazolamide)
2. Topical (dorzolamide, brinzolamide)
3. Action: reduce aqueous inflow
4. Side effects
a) Oral
a. nausea
b. depression
c. parasthesias
d. fatigue
e. skin rash
f. aplastic anemia
g. renal stones
b) Topical
a. local irritation
b. same side effects possible as with oral
Prostaglandin Analogues
1. Latanoprost (prostaglandin F2alpha analogue)
2. Action: increase uveoscleral outflow
3. Side effects
a) iris pigmentation/lash changes
b) inflammation/cystoid macular edema
Surgical Therapy of Glaucoma
A.
Open Angle Glaucoma
55
1.
2.
3.
4.
5.
6.
B.
Surgery indicated with intraocular pressure cannot be maintained
low enough to prevent further progressive damage to the optic
nerve
Reasons for lack of control
a) failure of medical therapy
b) medical therapy not tolerated
c) compliance problems
d) progressive optic nerve cupping and visual field loss
Laser Surgery - Argon Laser Trabeculoplasty
Filtering procedures (trabeculectomy)
Glaucoma tube implant surgery
Ciliary body ablation
Angle Closure Glaucoma
1. Acute angle closure glaucoma (pupillary block) is a medical
emergency and needs to be treated promptly to prevent/minimize
vision loss
2. Initially, IOP should be lowered medically
a. Beta-adrenergic antagonists
b. Alpha-2 agonists
c. Oral carbonic anhydrase inhibitors
d. Osmotic agents
e. Topical steroid for inflammation
f. Pilocarpine 1% to constrict pupil
3. Laser surgery
a. Laser peripheral iridectomy – created alternate route for
aqueous to pass from posterior chamber to anterior chamber
b. Laser peripheral iridoplasty – constricts peripheral iris away
from trabecular meshwork
4. Glaucoma filtering surgery is IOP remains uncontrolled
5. Treatment of fellow eye – prophylactic laser treatment to prevent
attack in fellow eye
56
Section VII
Neuro-Ophthalmology for the Primary Care Physician
Robert D. Yee, M.D.
XVII. A.
Definition and Symptoms
Disorders of optic nerve, brain or other cranial nerves damage vision, produce
abnormal appearance of pupils, cause misalignment of the eyes or generate
abnormal eye movements.
Common chief complaints include blurred vision, scotomas, unequal pupils
(anisocoria), double vision, illusory motion of objects (oscillopsia).
XVIII. B.
Examination
1. History
- onset and course of deficit - eye pain, headache
- neurologic symptoms - systemic diseases - medications
2. Ocular
- best corrected visual acuity
- color vision
- visual fields
patient's description
confrontation tests
- pupils
size and reactivity
"swinging flashlight test"(relative afferent defect)
- ocular motility
misalignment (tropia)
ductions (patterns of cranial nerve palsies)
nystagmus
- ophthalmoscopy
optic disc (color, margins, elevation)
nerve fiber layer
macula
retinal blood vessels (emboli)
3. Neurologic
-
coordination, motor function, sensorium
Visual Pathway Diseases
1. Patterns
-
Optic Nerve
usually monocular
decreased visual acuity
57
color vision loss
afferent pupillary defect
central scotoma
+ or – disc swelling acutely, atrophy later
-
Optic Chiasm
binocular
bitemporal hemianopsia, esp. red object
border long vertical meridian
mild optic atrophy
-
Optic Tract
binocular
homonymous hemianopsia (asymmetric)
mild optic atrophy
2. Optic Nerve Diseases
- Optic Neuritis
young adults
sudden onset
eye pain or headache, esp. on eye movement
worsening over few days
spontaneous recovery
initially disc may be normal (retrobulbar optic neuritis) or
swollen (papillitis)
atrophy later
risk of developing multiple sclerosis
treatment with intravenous corticosteroids
-
Anterior Ischemic Optic Neuropathy (AION)
older (systemic vascular diseases)
sudden onset
no pain
lower ½ visual field
pale swelling optic disc with splinter heme
no recovery
2 types: non-arteritic and giant cell arteritis. Patients with
GCA are at high risk for bilateral blindness. Need
Westergren sedimentation rate urgently. Treated with
Steroids
While awaiting temporal artery biopsy
- compression by mass
gradual onset with progression
disc may be normal, swollen or pale
58
-
Toxicity
binocular
gradually progressive
cecocentral scotoma with decreased color vision
optic atrophy later in course
digitals, tobacco-alcohol, nutritional def., anti-TB drugs
-
Amaurosis Fugax (transient visual loss)
3. Ischemia
Carotid Artery Atherosclerosis
monocular, curtain-like
2-5 minutes
look for emboli in retinal vessels
Vertebrobasilar insufficiency
binocular
10-20 minutes
transient vestibular, brainstem symptoms
Papilledema (increased intracranial pressure)
monocular or binocular
few seconds
precipitated by change of body or head
position and Valsalva
Visual aura of migraine
scintillating scotoma with spread over 20 minutes
+ and – associated severe, long-lasting headache
-
Central Retinal Artery Occlusion
sudden, painless, monocular visual loss
whitening of neurosensory retina
cherry red spot in macula
embolus from carotid artery, heart valve
emergency treatment
breathe increased CO2 paper bag, Carbogen
retrobulbar anesthetic injection
digital ocular massage
paracentesis
59
4. Optic Disc Swelling (differential diagnosis)
-Papilledema
increased intracranial pressure
acute stage
bilateral with normal acuity
swollen, hyperemia
no spontaneous venous pulsations
opacified retinal nerve fiber layer
splinter hemorrhages, exudates
cotton wool spots, retinal folds
chronic stage (optic atrophy)
decreased visual acuity and field
decreased disc swelling
disc pallor and decreased nerve fiber layer
permanent visual loss
causes: brain tumor, meningitis, hydrocephalus,
hypertensive, encephalopathy, pseudotumor cerebri
-
Pseudopapilledema crowded hyperopic disc drusen (buried or
surface)
-
Papillitis
-
AION
Ocular motor disorders
1. Cranial Nerve Palsies
- Symptoms
diplopia
limited range of ductions
-
3rd Nerve Palsy
ptosis
exotropia and hypotropia
+ and – dilated, non-reactive pupil
limited adduction, supraduction, infraduction
pupil-spared-possible diabetes, hypertension with
spontaneous recovery
pupils involved with severe pain – possible aneurysm,
tumor
60
-
4th Nerve Palsy
hypertropia
excyclotorsion (torsional diplopia)
limited infraduction in adduction
often caused by head trauma
6th Nerve Palsy
esotropia
limited abduction
2. Internuclear Ophthalmoplegia
Limitation of adduction
Better adduction with convergence
Slow abducting saccade (medial rectus)
Nystagmus of abduction eye (lateral rectus)
Bilateral INO – suspect multiple sclerosis
Unilateral INO – suspect ischemia
-
3. Nystagmus
-
-
Oscillopsia or blurred vision
Characteristics
direction
waveform (jerk, pendular)
effects of eccentric gaze
Acquired forms from many CNS locations
brainstem, cerebellum vestibular system
Congenital nystagmus
no oscillopsia
horizontal, even in vertical gaze
high frequency
jerk or pendular
patient might not have been aware of long-standing
nystagmus
Pupil Abnormalities
1. Afferent Pupillary Defect (Marcus-Gunn pupil)
- Swinging flashlight test
bright hand-light
fixation at distant target
3 sec on first eye, rapidly to second eye for 3 sec.,
back to first eye and repeat
watch for initial constriction of pupils
watch for dilation of pupil as light half on eye
61
-
sensitive sign of optic nerve disorder, even mild
marked pupillary defect not found with suppression
amblyopia, macular disorders, optic tract or posterior visual
pathway
disorders
-
Physiologic anisocoria of 1 mm is common
-
Pharmacologic fixed, dilated pupil
2. Anisocoria
inadvertent or intentional cycloplegic drop to eye does not
constrict to drop of pilocarpine 1%
-
3rd Nerve Palsy
extraocular muscle paresis present
constricts to pilocarpine
62