1A) REFRACTIVE ERRORS

A) HYPEROPIA (Farsightedness)
Definition: In hyperopia, there is a discrepancy between the refractive power and axial length of the eye
such that parallel light rays converge at a focal point posterior to the retina.
Epidemiology:
About 20 of persons between the ages of 20 and !0 have refraction more than "# diopter. $ost newborns
exhibit slight hyperopia %newborn hyperopia&. 'his decreases during the first few years of life. In advanced
age, refraction tends to shift toward the myopic side due to sclerosing of the nucleus of the lens.
Etiology:
'he mechanisms are not fully understood.
(athophysiology:
In farsighted patients, the virtual far point of the eye lies posterior to the retina. )nly convergent incident
light rays can be focused on the retina. 'his is due either to an excessively short globe with normal
refractive power %axial hyperopia& or, less fre*uently, to insufficient refractive power in a normal+length
globe %refractive hyperopia&. Axial hyperopia is usually congenital and is characteri,ed by a shallow
anterior chamber with and well developed ciliary muscle.
--- .yperopic eyes are predisposed to acute angle closure glaucoma because of their shallow anterior
chamber. 'his can be provo/ed by diagnostic and therapeutic mydriasis ---
0pecial forms of refractive hyperopia:
Absence of the lens %apha/ia& due to dislocation
(ostoperative apha/ia following cataract surgery without placement of an intraocular lens.
'o bring the focal point on to the retina, a farsighted person must accommodate even when ga,ing into the
distance. 1lose ob2ects remain blurred because the eye is unable to accommodate any further in near vision.
As accommodation is lin/ed to convergence, this process can result in esotropia %accommodative esotropia
or accommodative convergent strabismus&. %see topic 31&
0ymptoms:
In young patients, accommodation can compensate for moderate hyperopia. .owever, this leads to chronic
overuse of the ciliary muscle. 4eading in particular can cause asthenopic symptoms such as eye pain or
headache, burning sensation in the eyes, blepharocon2unctivitis, blurred vision, and rapid fatigue. As
accommodation decreases with advancing age, near vision becomes increasingly difficult. 5or this reason,
hyperopic persons tend to become presbyopic early.
6iagnosis:
)phthalmoscopy reveals tortuous retinal vascular structures because the retina is too large for the small
eye. 'he ciliary muscle is chronically in tension. 'his overuse leads to latent accommodation in which the
muscle is unable to relax even after the hyperopia has been corrected with plus lenses. 'his latent hyperopia
may be overloo/ed if refraction testing is performed without first completely paraly,ing the ciliary body
with cycloplegic agents such as atropine. 'he full extent of hyperopia includes both this latent hyperopia
and clinically manifest hyperopia.
'reatment:
'he insufficient refractive power must be augmented with converging lenses %plus or convex lenses&. 'he
strongest plus lenses that the patient can tolerate without compromising visual acuity should be given. 1are
should be ta/en to avoid overcorrection.
B) MYOPIA (Shortsightedness)
Definition: A discrepancy between the refractive power and axial length of the eye such that parallel light
rays converge at a focal point anterior to the retina.
Epidemiology:
About 27 of persons between the ages of 20 and !0 have refraction less than +# diopters.
Etiology:
It is not clear. Increased familial incidence suggest genetic factors.
(athophysiology:
8hereas parallel light rays converge at a focal point on the retina in emmetropic eyes, they converge at a
focal point anterior to the retina in myopic eyes. 'his means that no sharply defined images appear on the
retina when the patient ga,es into the distance. 'he myopic eye can only produce sharply defined images of
close ob2ects from which the light rays diverge until they enter the eye. 'he far point % 9 the farthest point
that is still recogni,able in focus& moves closer: in myopia of +# diopter it lies at a distance of # m.
'he far point %distance from the eye 9 A& can be calculated using the formula: A %m& 9 #;6, where 6 is
myopia in diopters.
(ossible causes include an excessively long globe with normal refractive power %axial myopia& and, less
fre*uently, excessive refractive power in a normal+length globe %refractive myopia&.
A difference in globe length of # mm corresponds to a difference of about ! diopters in refractive power.
5orms: 'hese include:
Simple myopia %school+age myopia&: )nset at the age of #0 + #2 years. <sually the myopia does not
progress after the age of 20. 4efraction rarely exceeds = diopters. .owever, a benign progressive also
exists, which stabili,es only after the age of !0.
Pathologic myopia: 'his disorder is hereditary and progresses continuously independently on external
influences.
0ymptoms and diagnosis:
'he diagnosis is based on clinical picture and refraction testing. $yopic patients have very good
near vision. 8hen ga,ing into the distance, they s*uint in an attempt to improve their uncorrected visual
acuity. )lder myopic patients can read without corrective lenses by holding the reading material at about
the distance of the far point.
'he typical morphologic changes occurring in myopia are referred to as myopia syndrome.
(rogressive myopia is characteri,ed by thinning of the sclera. 'he elongation of the globe causes a shift in
the axes of the eye. 'his often simulates esotropia %mar/ed turning inward of the eyes&. 'he anterior
chamber is deep. Atrophy of the ciliary muscle is present as it is hardly used. 'he volume of the vitreous
body is too small for the large eye, and it may collapse prematurely. 'his results in vitreous opacifications
that the patients perceives as floaters. 'he ris/ of retinal detachment is increased in myopia. .owever, it
does not increase in proportion to the severity of the myopia.
'reatment:
'he excessive refractive power of the refractive media must be reduced. 'his is achieved through the use of
diverging enses %minus or concave lenses&. 'hese lenses cause parallel light rays to diverge behind the
lens. 'he refractive power %6& is negative %hence the term minus&.
1orrection with !onta!t enses offers advantages. 'he closer the >minus? lens is to the eye, the wea/er its
refractive power must be to achieve the desired optic defect. $inus lenses should be no stronger than
absolutely necessary. Although accommodation could compensate for an overcorrection, patients usually do
not tolerate this well. Accommodative asthenopia %rapid ocular fatigue& results from the excessive stress
caused by chronic contraction of the atrophic ciliary muscle.
--- $yopic patients have >la,y? accommodation due to atrophy of the ciliary muscle. A very slight
undercorrection is often better tolerated than a perfectly sharp image with minimal overcorrection ---
In certain special cases, re"ova o# the !r$staine ens may be performed to reduce the refractive power
of the myopic eye. .owever, this operation is associated with a high ris/ of retinal detachment and is rarely
performed. 'here is also possibility of implanting an anterior !ha"%er intrao!&ar ens %diverging lens&
anterior to the natural lens to reduce refractive power.
C) ASTI'MATISM
Definition: Astigmatism is derived from the @ree/ word stigma %point& and literally means lac/ of a focal
point. 'he disorder is characteri,ed by a curvature anomaly of the refractive media such that parallel light
rays do not converge at a point but are drawn apart to form a line.
Epidemiology:
A2 of all humans have astigmatism greater or e*ual 0.7 diopters. In about 20, this astigmatism is greater
than # diopter and re*uires optical correction.
(athophysiology:
'he refractive media of the astigmatic eye are not spherical but refract differently along one meridian than
along the meridian perpendicular to it. 'his produces two focal points. 'herefore, a punctiform ob2ect is
represented as a sharply defined line segment at the focal point of the first meridian but also appears as a
sharply defined line segment rotated B0 degrees at the focal point of the second meridian. $idway between
these focal points is what is /nown as the >circle of least confusion?. 'his is the location at which the
image is e*ually distorted in every direction %with the least loss of image&. 'he system lac/s a focal point.
'he combined astigmatic components of all refractive media comprise the total astigmatism of the eye:
'hese media include:
Anterior surface of the cornea
(osterior surface of the cornea
Anterior surface of the lens
(osterior surface of the lens
1lassification and causes:
External astigmatism: Astigmatism of the anterior surface of the cornea.
Internal astigmatism: 'he sum of the astigmatic components of the other media.
Astigmatism can also be classified according to the location of the meridian of greater refraction:
With-the-rule astigmatism %most common&: 'he meridian with the greater refractive power is vertical.
Against-the-rule astigmatism: 'he meridian with the greater refractive power is hori,ontal.
Obliue astigmatism: 'he meridian with the greater refractive power is obli*ue.
<ntil now it was tal/ed about a reg&ar astig"atis" involving only two meridians perpendicular
to each other. 'his is presumably caused by excessive eyelid tension that leads to astigmatic changes in the
surface of the cornea.
In irreg&ar astig"atis", the curvature and the refractive media are completely irregular. 'here
are multiple focal points, which produces a completely blurred image on the retina.
'his condition may be caused by:
1orneal ulceration with resulting scarring of the cornea
(enetrating corneal trauma
Advanced /eratoconus
1ataract
0ymptoms:
(atients see everything distorted. Attempts to compensate by accommodation can lead to asthenopic
symptoms such as burning sensation in the eyes or headache.
6iagnosis:
'he /eratoscope allows gross estimation of astigmatism. 1omputeri,ed corneal topography
%video/eratoscopy& obtains the distribution of refractive values over the entire cornea. An ophthalmometer
measures the central corneal curvature, which determines the refractive power of the cornea.
'reatment:
Early correction is crucial. <ntreated astigmatism in children will lead to uncorrectable amblyopia.
4egular astigmatism : 'he purpose is to bring the >focal lines? of two meridians together at one focal
point. 'his re*uires a lens that refracts in only one plain. 1ylinder lenses are re*uired for this
application.
Irregular astigmatism : 'his form cannot be corrected with eyeglasses. External astigmatism may be
managed with a rigid contact lens, /eratoplasty, or surgical correction of the refractive error. Internal
astigmatism is usually lens+related. In this case, removal of the lens with implantation of an intraocular
lens is indicated.
1B) POSTERIOR (VEITIS (CHOROI)ITIS)
Etiology:
It may be caused by a variety of causes:
Coth iridocyclitis and choroiditis may be caused by: 'oxoplasmosis, sarcoidosis, tuberculosis, syphilis,
sympathetic ophtalmia, borreliosis, brucellosis, yersiniosis, listeriosis, or malignant tumors.
1auses of choroiditis only, include : 'oxoplasmosis, sarcoidosis, syphilis, histoplasmosis, or toxocara.
0ymptoms:
(atients are free of pain %the choroid has no sensory nerves&, although they report blurred vision and
floaters.
6iagnosis:
)phtalmoscopy reveals isolated or multiple choroiditis foci. In acute disease they appear as ill+defined
white dots. )nce scarring has occurred the foci are sharply demarcated with yellowish brown color. Do
cells will be found in the vitreous body in a primary choroidal process. .owever, inflammation proceeding
from the retina %retinochoroiditis& will show cellular infiltration of the vitreous body.
'reatment:
It is treated with antibiotics or steroids, depending on its etiology.
(rognosis:
'he inflammatory foci will heal within 2 to = wee/s and form chorioretinal scars. 'he scars will result in
locali,ed scotomas that will reduce visual acuity if the macula is affected.
S$"*atheti! o*hta"ia
It is a specific bilateral inflammation of the uveal tract due to chronic irritation of one eye, caused
by perforating wound to the eye or intraocular surgery, that produces transferred uveitis in the fellow eye.
Etiology:
It can occur in an otherwise unaffected eye even years after penetrating in2uries or intraocular surgery in the
fellow eye. 'issues in the in2ured eye %uveal tract, lens, and retina& act as antigens and provo/e autoimmune
disorder in the unaffected eye.
0ymptoms:
'he earliest symptoms include limited range of accommodation and photophobia. Eater there is diminished
acuity and pain.
'reatment:
'he in2ured eye, which is usually blind, must be enucleated to eliminate the antigen. .igh+dose topical and
systemic steroid therapy is indicated. 'reatment with immunosuppressives may be necessary.
(rognosis:
'he disorder has a chronic course and may involve complications such as secondary glaucoma, secondary
cataract, retinal detachment, and shrin/age of the eyeball. It can lead to blindness in severe cases.
1C) CA(STIC I+,(RIES A+) B(R+S
Ca&sti! in-&ries
1austic in2uries are chemical in2uries caused by acids or al/alis. 'hey are among the most
dangerous ocular in2uries. 5irst aid at the site of the accident is crucial to minimi,e the ris/ of severe
se*uelae such as blindness.
As a general rule, aci! burns are less dangerous than al/ali burns. 'his is because most acids do
not act deeply. Aci!s differ from al/alis in that they cause immediate coagulation necrosis in the superficial
tissue. 'his has the effect of preventing the acid from penetrating deeper so that the burn is effectively a
self+limiting process. .owever, some acids penetrate deeply li/e al/alis and cause similarly severe in2uries.
1oncentrating sulphuric acid %such as from exploding car battery& draws water out of tissue and
simultaneously develops intense heat that affects every layer of the eye. Al"alis differ from most acids in
that they can penetrate by hydroly,ing structural proteins and dissolving cells. 'his is referred to as
li*uefactive necrosis. 'hey can cause severe intraocular damage by al/ali,ing the a*ueous humor.
0ymptoms include epiphora %excess secretion of tears&, blepharospasm, and severe pain. Acid
burns usually cause immediate loss of visual acuity due to the superficial necrosis. In al/ali in2uries, loss of
visual acuity often manifests itself only several days later.
(roper diagnosis of the cause and severity of the burn is crucial to treatment and prognosis.
$orphologic findings and the resulting prognosis can vary greatly depending on the severity and duration
of exposure. 0light in2uries cause superficial punctate /eratitis with no corneal erosions. 1on2unctival
epithelium remains largely intact, but there is slight chemosis %edematous con2unctival swelling&. 'he
prognosis is good, it heals without loss of function. $oderate to severe in2ury causes moderate to total
corneal erosion and moderate chemosis. 'he corneal stroma appears slightly opacified and there is slight
irritation of the anterior chamber %slight amount of cellular and protein exudates in the anterior chamber&.
'he healing is defect with functional impairment and possibly symblepharon %adhesions between the
palpebral and bulbar con2unctiva&. 0evere in2uries produce total corneal erosion including erosion of the
con2unctival epithelium at the limbus. 'here is severe chemosis and total ischemia of the limbal vessels. All
corneal layers are opacified %so called Fcoo/ed fish eyeF&. 'here is severe irritation of the anterior chamber
with damage to the iris, lens, ciliary body, and angle of the anterior chamber %it can lead to secondary
glaucoma&. (rognosis is poor, defect healing with functional impairment may cause loss of the eye.
0ymblepharon is common.
'reatment: 5irst aid often decides the fate of the eye. Immediate copious irrigation of the eye may
be performed with any water solution of neutral p., such as tap water, mineral water, soft drin/s, coffee,
tea, or similar li*uids. $il/ should be avoided as it increases penetration of the burn by opening the
epithelial barrier. A second person must restrain the severe blepharospasm to allow effective irrigation. A
topical anesthetic is helpful but it is rarely at the scene of the accident. 1oarse particles should be flushed
and removed from the eye. )nly after these actions the patients should be brought to an ophthalmologist.
'he ophthalmologist administers topical anesthesia and everts both eyelids to remove small particles under
a microscope using a moist cotton swab. 'hen he flushes the eye with a buffer solution. Eong term
irrigation using an irrigating contact lens may be indicated. In severe cases, topical cortisone therapy is
initiated, followed by subcon2unctival steroids, the pupil is immobili,ed with atropine. 'he next step is to
administer anti+inflammatory agents systemically, vitamin 1 to neutrali,e cytotoxic radicals, aceta,olamide
reduces intraocular pressure %prophylaxis against secondary glaucoma&, hyaluronic acid promotes re+
epitheliali,ation of the cornea. Administration of topical antibiotics is important. 'he most severe cases can
be treated by con2unctival and limbal transplantation of stem cells, hard contact lens promoting healing,
surgical lysis of symblepharon, plastic surgery of the eyelids, and /eratoplasty.
B&rns
5lames such as from a cigarette lighter, hot vapors, boiling water, and splatters of hot grease or hot
meal cause thermal coagulation of the corneal and con2unctival surface. Cecause of the eye closing reflex,
the eyelids often will be affected as well. In2uries due to explosion also include particles of burned powder.
0ymptoms are similar to those of caustic in2uries %epiphora, blepharospasm, pain&. A topical
anesthetic is administered, and the eye is examined. Immediate opacification of the cornea will be readily
apparent. 'his is due to scaling of the epithelium and tissue necrosis, whose depth will vary with the
severity of the burn. In burns from metal splinters, one will often find cooled metal particles embedded in
the cornea.
'reatment: 'he initial treatment consists of cooling antiseptic bandages %pain relief&, after which
necrotic areas of the s/in, con2unctiva, and cornea are removed under local anesthesia. 5oreign particles
such as embedded ash and smo/e particles in the eyelids are removed by brushing them out with a sterile
toothbrush under general anesthesia. 'his is done to prevent them from growing into the s/in li/e a tattoo.
0uperficial particles in the cornea and con2unctiva are removed under local anesthesia together with an
antibiotic ointment.
(rognosis: the clinical course of a burn is less severe than that of a caustic in2ury. 'his is because
burns, li/e acid in2uries, cause superficial coagulation. <sually they heal well when treated with antibiotic
ointment.
.A) I+F/AMMATORY )ISEASES OF THE EYE/I)S
a) )iseases o# the e$eid gands
#. Hordeo&"
It is a result of an acute bacterial infection of one or more eyelid glands.
Epidemiology and etiology:
0taphylococcus aureus is a common cause of hordeolum. External hordeolum involves infection of the
glands of Geis or $oll. Internal hordeolum arises from infection of the $eibomian glands. .ordeolum
is often associated with diabetes, gastrointestinal disorders, or acne.
0ymptoms:
It presents as painful nodules with a central core of pus. External hordeolum appears on the margin of
the eyelid where the sweat glands are located. Internal hordeolum of a sebaceous gland is usually only
revealed by everting the eyelid and usually accompanied by a more severe reaction such as
con2unctivitis or chemosis of the bulbar con2unctiva. (seudoptosis and swelling of the preauricular
lymph nodes may also occur.
6ifferential diagnosis:
1hala,ion %tender to palpation& and inflammation of the lacrimal glands %rarer and more painful&.
'reatment:
Antibiotic ointments and application of dry heat %red heat lamp& will heal the lesion.
(rognosis:
After eruption and drainage of the pus, the symptoms will rapidly disappear. 'he prognosis is good.
2. Chaa0ion
It is a firm nodular bulb within the tarsus.
Epidemiology and etiology:
1hala,ia occur relatively fre*uently and are caused by a chronic granulomatous inflammation due to
buildup of secretion from the meibomian gland.
0ymptoms: 'he firm painless nodule develops very slowly. Except for the cosmetic flaw, it is usually
asymptomatic.
'reatment and prognosis:
0urgical incision. (rognosis is good except for the chance of local recurrence.
%) )iseases o# the e$eid "argin
11 Se%orrhei! %e*haritis
'his relatively fre*uent disorder is characteri,ed by scaly inflammation of the margins of the
eyelids. Coth eyes are usually affected. 'here are often several contributing causes. 'he s/in constitution,
seborrhea, refractive anomalies, hypersecretion of the eyelid glands, and external stimuli such as dust,
smo/e, and dry air in air+conditioned rooms often contribute to persistent chronic inflammation.
'he margins of the eyelids usually show slight inflammatory changes such as thic/ening. 'he
eyelashes adhere due to increased secretion from the glands of the eyelids, and scaly deposits form. It is
often accompanied by chronic con2unctivitis.
'reatment depends on the cause. 'he scales and crusts can usually be softened with warm olive oil
and then easily removed. In more severe cases treatment include expressing the glands and local
application of antibiotic ointment. 'reatment with topical steroids is indicated under certain conditions. 'he
prognosis is good although the course of the disorder is *uite protracted.
!) S2in diseases o# the e$eids
11 C onta!t e!0e"a
Eight+s/inned patients and patients susceptible to allergy are fre*uently affected. It is caused by
antigen+antibody reaction in patients with intolerance to certain substances such as cosmetics, eye+drops, or
eye ointments. 0ymptoms include reddening, swelling, lichenification, and severe itching of the s/in of the
eyelid initially, followed by scaling with a sensation of tension. 'reatment consists of eliminating the
causative agent. 1orticosteroids usually bring *uic/ relief of symptoms.
.1 Ede"a
Edema is a fre*uently encountered clinical symptom. 6epending on the cause %inflammatory or
noninflammatory edema&, the intensity of swelling in the eyelid will vary. 'he location of swelling is also
influenced by gravity and can vary in intensity. 5or example, it can be more intense in the early morning
after the patient rises than in the evening. (ossible causes of inflammatory edema include hordeolum,
abscess, erysipelas, ec,ema, or it can be associated with paranasal sinus disorders, orbital cellulitis,
dacryoadenitis, and dacryocystitis. 0ymptoms include swelling, reddening, sensation of heat, and pain. It is
usually unilateral. (ossible causes of noninflammatory edema include systemic disorders %heart, /idneys,
and thyroid gland& or allergy. 0ymptoms include swelling and pale and cool s/in. It is usually bilateral and
painless. 'reatment depends on the cause of the disorder.
31 Her*es si"*e4 o# the e$eids
It is an acute, usually unilateral disorder accompanied by s/in and mucous membrane vesicles. It
results when latent herpes simplex viruses present in the tissue are activated by ultraviolet radiation. 'he
virus spreads along sensory nerve fibers from the trigeminal ganglion to the surface of the s/in.
0ymptoms include typical clustered eruptions of painful vesicles filled with serous fluid occurring
fre*uently at the 2unction of mucous membranes and s/in. Eater the vesicles dry and crusts form. Eesions
heal without scarring.
'reatment consists of topical use of virostatic agents. 'he patient should avoid intense ultraviolet
radiation as prophylaxis against recurrence. 'he prognosis is good, although it fre*uently recurs.
51 Her*es 0oster o*hta"i!&s
'he disorder usually affects immunocompromised persons between the ages of A0 and =0 who
have underlying disorders. It is caused by varicella+,oster virus, which initially manifests itself as
chic/enpox. If activation or reinfection occurs, the latent neurotropic viruses present in the body can lead to
herpes ,oster ophtalmicus.
'he incubation period is 3 + #H days, after which severe pain occurs in the area supplied by the
first branch of the trigeminal nerve. (rodromal symptoms of erythema, swelling, photosensitivity, and
lacrimation may occur before the characteristic clear watery vesicles appear. 'he vesicles burst and
brownish scabs form, which are later shed. Clepharitis is also often present.
'reatment includes topical virostatic agents and systemic acyclovir.
Involvement of the nasociliary branch of the ophthalmic nerve can lead to severe intraocular
inflammation.
(rognosis: 'he s/in lesions heal within ! to A wee/s: scars may remain. )ften pain and
hypesthesia may persist.
61 E$eid a%s!esses
It is a circumscribed collection of pus with severe inflammation, swelling, and subse*uent
fluctuation. It can form as a se*uela of minor trauma, insect sting, or spread of inflammation from the
paranasal sinuses.
'he severe inflammation and swelling often ma/e it impossible actively to open the eye.
0pontaneous perforation with pus drainage can occur.
'reatment: )ral or intravenous antibiotics and dry heat are indicated. A stab incision can relieve
tension at the onset of fluctuation. 'he prognosis is generally good. )rbital cellulitis or cavernous sinus
thrombosis can occasionally occur as a se*uela of eyelid abscess. 'his represents a life+threatening
complication.
.B) PE)IATRIC EYE )ISEASES (COMMO+EST SYMPTOMS)
!. Congenita o!&ar a%nor"aities
1ongenital ocular defects fall into 2 main categories:
A. Developmental anomalies due to genetic defects
7. Tissue reactions to intrauterine insults (infections, drugs)
=. 1ongenital anomalies of the globe
5ailure of formation of the optic vesicle results in anophtalmos. 5ailure of closure %incomplete fusion
of the embryonic optic cup& produces colobomas of iris, retina, and choroid. 1ryptophtalmos occurs
when the eyelids fail to separate.
Abnormally small eyes can be divided into nanophtalmos, in which function is normal, and
microphtalmos, in which function is abnormal.
2& Eid abnormalities
1ongenital ptosis is commonly due to dystrophy of the levator palpebrae muscle of the upper lid. )ther
causes are congenital .ornerIs syndrome and third nerve palsy. (alpebral coloboma is a cleft of
usually the upper lid. Earge defects re*uire early repair to avoid corneal ulceration due to exposure.
3. 1orneal defects
'here may be partial or complete opacity of the cornea as found in congenital glaucoma, faulty
development of the corneal endothelium, intrauterine inflammations, or interstitial /eratitis. 'he most
fre*uent cause of opa*ue corneas in infants is congenital glaucoma, in which the eye is often larger
than normal %buphtalmos&.
H. Iris and pupillary defects
$isplaced or ectopic pupils %corectopia& are fre*uently observed. 1oloboma of the iris indicates
incomplete closure of the fetal optic cup and usually occurs inferiorly and nasally. It may be associated
with coloboma of the lens, choroid, and optic nerve. Abnormalities of iris color include albinism, due
to absence of normal pigmentation, and heterochromia, which is a difference in color in the two eyes.
B. Eens abnormalities
'he most common abnormalities include cataract, colobomas, or subluxation, as seen in $arfanIs
syndrome.
Any lens opacity present as birth is a congenital cataract. 1ongenital cataracts are often associated with
other conditions. $aternal rubella during the first semester is a common cause of congenital cataract.
)ther congenital cataracts have hereditary bac/ground.
If the pupillary opening is totally occluded by the cataract, normal sight does not develop, and the poor
fixation may lead to amblyopia and nystagmus. Early surgery %first few wee/s of life& has good visual
results. Apha/ic correction is then achieved with contact lenses that need to be changed fre*uently to
maintain optimal correction.
#0. Jitreous abnormalities
4emnants of the hyaloid artery may be seen on the posterior surface of the lens of on the optic dis/.
(ersistent hyperplastic primary vitreous is an important cause of leuco/oria that must be differentiated
from retinoblastoma, congenital cataract, and retinopathy of prematurity.
##. )ptic nerve
1ongenital anomalies of the optic nerve are relatively common. 'hey are usually benign, but they may
be associated with severe visual loss in the case of optic nerve hypoplasia or the rare central coloboma
of the dis/. )ptic nerve hypoplasia is a ma2or cause of visual loss in children. 'he degree of visual
impairment varies from few visual field defects to no perception of light.
#2. 1ongenital nasolacrimal duct obstruction
1anali,ation of the distal nasolacrimal duct normally occurs before birth or during the first month of
life. As many as !0 of babies will have epiphora during this time. Eacrimal sac massage and
antibiotic treatment of episodes of con2unctivitis will help in ma2ority of those with prolonged
symptoms. Dasolacrimal probing is curative in the remainder of babies.
#!. Postnata *ro%e"s
'he most common ocular disorders in children are external infections of the con2unctiva and the
eyelids %bacterial con2unctivitis, hordeola, blepharitis&, strabismus, ocular foreign bodies, allergic
reactions of the con2unctiva and eyelids, refractive errors %particularly myopia&, and congenital defects.
#A. )phtalmia neonatorum
1on2unctivitis of the newborn may be of chemical, bacterial, chlamydial, or viral origin.
6ifferentiation is sometimes possible according to the timing of presentation, but appropriate smears
and cultures are essential. 'reatment of maternal genital infections should prevent many cases of
neonatal con2unctivitis.
1on2unctivitis due to chlamy!ial infection: see topic #7C, due to viral infection: see topic AA
1on2unctivitis due to chemical trauma: 1hemical con2unctivitis caused by the silver nitrate drops
%prevention against gonococcal infection& instilled into the con2unctival sac at birth is most
apparent during the first or second day of life. It is usually self+limited.
1on2unctivitis due to bacterial infection: Cacterial con2unctivitis, usually due to 0taphylococcus
aureus, .emophilus species, 0treptococcus pneumoniae, Deisseria gonorrhoae, or (seudomonas
aeruginosa %the last two being the most serious because of potential corneal damage& present
between the second and fifth days after birth. (rovisional identification of the causative organism
may be made from con2unctival smears. 5or gonococcal con2unctivitis see topic B1.
#7. 1ongenital posterior uveitis due to toxoplasmosis
'he pathogen, 'oxoplasma gondii, is transmitted transplacentally. 'he children have a macular scar
that significantly impairs visual acuity. 'his often lead to secondary strabismus. 'here is no cure.
#=. 4etinopathy of prematurity
'his condition is estimated to result in 770 new cases of infant blindness each year in the <0A---
4etinal vasculari,ation proceeds from the optic nerve, beginning at the fourth month of gestation.
4etinal vessels normally reach the nasal ora serrata at H month and the temporal ora serrata at B month.
4etinopathy of prematurity develops if this process is disturbed. It is usually bilateral but often
asymmetric. It begins at the 2unction of vasculari,ed and avascular retina, initially as an obvious
demarcation line %stage #&, followed by formation of a distinct ridge %stage 2&, then extraretinal
fibrovascular proliferation %stage !&. Even among patients with stage !, there is a high incidence of
spontaneous regression. 'he cicatrical phase %stages A and 7& is manifested by increasingly severe
retinal detachment.
'he ma2or ris/ factors are decreasing gestational age and low birth weight. 'he cause of
retinopathy of prematurity seems to be supplemental oxygen. 'reatment: cryotherapy or
photocoagulation.
#3. 1ongenital glaucoma
It appears alone or in association with other congenital lesions. Early recognition is essential to prevent
blindness. It is bilateral. 'he most stri/ing symptom is severe photophobia. Early signs are corneal
opacity, increased corneal diameter, and increased intraocular pressure. 'he eyes are large
%buphthalmos&.
#H. 4etinoblastoma
'his rare malignant tumor of childhood is fatal if untreated. It is usually diagnosed before the end
of the third year. In !0 of cases, it is bilateral. 4etinoblastoma is caused by loss of a dominant
protective allele. 'his can occur by mutation, either in somatic retinal cells alone %nonheritable
retinoblastoma + B7& or in the germ line cells as well %heritable retinoblastoma&. In heritable
retinoblastoma, the genetic predisposition is inherited as an autosomal dominant trait: children of
survivors have 70 chance of having the disease: and the tumor is usually bilateral and multifocal. In
sporadic cases, the tumor is usually not discovered until it has advanced far enough to produce an
opa*ue pupil. 4eddened eye, and infiltration of the vitreous body, anterior chamber, and orbit may
occur. A deviating eye may be also the first sign of the tumor. In children of families affected by
retinoblastoma, regular screening is important in the early detection of tumors.
1alcifications fre*uently occur in this tumor. 4adiographs and 1' images that show calcifications
can help to confirm the diagnosis is uncertain cases.
Enucleation is the treatment of choice in extensive unilateral cases. In bilateral case, conservative
therapy with radiotherapy, and photocoagulation are used to preserve the less severely affected eye.
Eeft untreated, a retinoblastoma will eventually metastasi,e to the brain and cause death.
#B. 0trabismus
It is present in 2 of children. Any child with strabismus K ! mo old %before it is normal& must be
referred to an ophthalmologist. Deglect may lead to undesirable cosmetic effect, psychic trauma, and
amblyopia.
20. Amblyopia
It is decreased visual acuity of one eye %uncorrectable with lenses& in the absence of organic eye
disease. Jisual deprivation due to any cause, congenital or ac*uired, during the critical period of
development %until age H years& prevents the establishment of normal vision in the involved eye.
4eversal of this effect becomes increasingly difficult with increasing age of child.
'he most common causes of amblyopia is strabismus %see topic 31&. It is treatable.
.C) A+TIBIOTICS I+ OPHTHA/MO/O'Y
a) T o*i!a anti%ioti! so&tions and oint"ents
Antibiotics are commonly used in the treatment of external ocular infection, including bacterial
con2unctivitis, hordeola, marginal blepharitis, and bacterial corneal ulcers. 'he fre*uency of use is related
to the severity of the condition.
Cacitracin, neomycin, polymyxin, erythromycin, tetracycline, gentamicin, and tobramycin are the most
commonly used topical antibiotics. 'hey are used separately and in combinations as solutions and as
ointments.
2#. Ba!itra!ine
)intment, most gram+positive organisms are sensitive. Dot used systemically because of its nephrotoxicity.
22. Er$thro"$!in
)intment is effective particularly in staphylococcal con2unctivitis. It may be used instead of silver nitrate in
prophylaxis of ophtalmia neonatorum.
2!. +eo"$!in
0olution and ointment. Effective against gram+positive and gram+negative organisms. Deomycin is usually
combined with some other drug %polymyxin, bacitracin& to widen its spectrum.
2A. Po$"$4in B
)intment, suspension. <sually combined with neomycin and bacitracin. Effective against gram+negative
organisms.
%) To*i!a *re*arations o# s$ste"i! anti%ioti!s
'opical use of the antibiotics commonly used systemically should be avoided if possible, because
sensitisation of the patient may interfere with future systemic use. .owever, it is indicated in certain
conditions %e.g. tetracycline in the treatment of trachoma&.
27. Tetra!$!ine
)intment, suspension. Indication: 'rachoma.
2=. 'enta"i!in
0olution, ointment. <sed in serious ocular infections %corneal ulcer caused by gram+negative organisms&.
23. To%ra"$!in
0olution, ointment. Cest reserved for treatment of (seudomonas /eratitis.
2H. Chora"*heni!o
0olution, ointment. Effective against a wide variety of gram+positive and gram+negative organisms.
Aplastic anemia may occur in long+term therapy-
2B. F&oro7&inoones (!i*ro#o4a!in8 nor#o4a!in)
0olution. Effective against a wide variety of gram+positive and gram+negative ocular pathogens, including
(seudomonas aeruginosa. 'hey are used mainly for the treatment of corneal ulcers but have also been used
in case of resistant bacterial con2unctivitis.
!) S&*hona"ides
'he most commonly used drugs in the treatment of bacterial con2unctivitis. 'hey are effective
against both gram+positive and gram+negative organisms, they are relatively cheap, and their use is not
complicated by secondary fungal infections, as sometimes occurs following prolonged use of antibiotics.
'he commonest sulphonamides used are s&#iso4a0oe, and s&#a!eta"ide sodi&". 'hey are
available as solutions and ointments.
3A) COR+EA/ (/CER1 CA(SE A+) TREATME+T
(rotective mechanisms of the cornea
'he cornea has defensive mechanisms re*uired because of its constant exposure to microbes and
environmental influences. 'he mechanisms include:
4eflective eye closing
5lushing effect of tear fluid %lyso,yme&
Its hydrophobic epithelium forms a diffusion barrier
Epithelium can regenerate *uic/ly and completely
(redisposing factors to corneal infections, pathogens, and pathogenesis:
8hen pathogens succeed in brea/ing the corneal defences through superficial in2uries or minor
epithelial defects, the cornea will respond with /eratitis.
(redisposing factors include:
Clepharitis, infection of the ocular appendages %e.g. dacryostenosis with bacterial infestation of the
lacrimal sac&, changes in the corneal epithelial barrier %e.g. bullous /eratopathy or dry eyes&, contact lenses,
lagophtalmos %an incomplete closure of the palpebral fissure when an attempt is made to shut the eyelids&,
neuroparalytic disorders, trauma, or topical and systemic immunosuppressive agents.
(athogens causing corneal infections may include:
Jiruses, bacteria, acanthamoeba, and fungi.
(athogenesis:
)nce these pathogens have invaded the corneal tissue, a typical chain of events will develop:
!0. 1orneal lesion
!#. (athogens invade and coloni,e the corneal stroma %red eye&
!2. Antibodies will infiltrate the site
!!. As a result, the cornea will opacify and the point of entry will open further
!A. Irritation of the anterior chamber with hypopyon %typically pus will accumulate on the floor of the
anterior chamber&
!7. 'he pathogens will infest the entire cornea
!=. As a result the stroma will melt down to 6escemetIs membrane, which is relatively strong. 'his is
/nown as descemetocele: only 6escemetIs membrane is still intact.
!3. As it progresses, perforation of the 6escemetIs membrane will occur and the a*ueous humor will be
seen to lea/. 'his is referred to as a perforated corneal ulcer and is an indication for immediate surgical
intervention %emergency /eratoplasty + see topic 221&. 'he patient will notice progressive loss of
vision and the eye will be soft.
!H. (rolapse of the iris %the iris will prolapse into the newly created defect& closing the corneal perforation
posteriorly. Adhesions of the iris will produce a white corneal scar.
'he se*uence can vary in speed and severity. It can form within a few hours or days and *uic/ly
progress to corneal ulcer. 'his rapidly progressing form of infectious corneal ulcer %usually bacterial& is
referred to as serpiginous corneal ulcer. It penetrates the cornea rapidly and leads to intraocular
involvement. A serpiginous ulcer is very dangerous as it can lead to loss of the eye.
Ba!teria 2eratitis
Epidemiology:
)ver B0 of all corneal inflammation are caused by bacteria.
Etiology:
'he most common pathogens are Staphylococcus aureus %slow progression, little pain&, epidermidis,
Streptococcus pneumoniae %rapid progression, very painful&, Pseudomonas %rapid, painful, with bluish
green mucoid exudate&, and Moraxella %painless, slow progression&.
--- $ost bacteria are unable to penetrate the cornea as long as the epithelium remains intact. )nly
gonococci and diphteria can penetrate an intact epithelium ---
0ymptoms:
(atients report moderate to severe pain, photophobia, impaired vision, tearing, and purulent discharge.
(urulent discharge is typical for bacterial forms, viral form produce a watery discharge.
'reatment:
Any type of corneal ulcer is emergency ---
Conservative therapy: It is started with broad+spectrum topical antibiotics, until the results of pathogen
testing are /nown. Immobili,ation of the ciliary body and iris by therapeutic mydriasis is indicated in
intraocular irritating %manifested by hypopyon&. .ospitali,ation is indicated in case of advanced ulcer.
0ubcon2unctival A'Cs are re*uired.
Surgery: Emergency /eratoplasty is indicated.
3B) RETI+A/ CHA+'ES I+ )IABETES ME//IT(S %see topic #HC for comparison&
Definition: 6iabetic retinopathy is an ocular microangiopathy
Epidemiology:
6iabetic retinopathy is one of the main causes of ac*uired blindness in the industriali,ed countries.
Approximately B0 of all diabetic patients have retinopathy after 20 years.
(athogenesis and stages of diabetic retinopathy:
6iabetes mellitus can lead to changes in almost every ocular tissue. 'hese include symptoms of
/eratocon2unctivitis sicca, xanthelesma, mycotic orbital infections, transitory refractory changes, cataract,
glaucoma, neuropathy of the optic nerve, oculomotor palsy. .owever, B0 of all visual impairments in
diabetic changes are caused by diabetic retinopathy.
6iabetic retinopathy proceeds by a totally different mechanism than the hypertensive retinopathy.
8hereas hypertension affects the arterioles, diabetes affects the veins +more specifically the venous side of
the capillary bed, as a venous occlusive disease. In fact, the picture in retinal vein occlusion may resemble
that in diabetes. 1linical findings are as follows:
!B. 'he veins become dilated. .ence, there is A;J nic/ing in diabetes as well as in chronic hypertension.
In diabetes, the A;J nic/ing stems from venous dilation, whereas in chronic hypertension it stems from
arteriolar thic/ening.
A0. $icroaneurysms appear on the venous side of the capillary bed in diabetes, as areas of wea/ness and
expansion of the vessel wall. 'hese appear as pinpoint reddish spots, commonly surrounding the foveal
region and may be difficult to distinguish from tiny %>dot?& hemorrhages.
A#. 4etinal venules normally lie deeper in the retina than do arterioles. As a result, hemorrhages in
diabetes, a venous disease, tend to be situated relatively deep in the retina, as roundish >dot? or larger
>blot? hemorrhages. 'hese hemorrhages differ from the superficial >flame+shaped? hemorrhages of
hypertension, which is an arteriolar disease.
A2. Exudates also tend to lie deeper than those in hypertension. 8hereas superficial >cotton wool?
exudates are more characteristic of hypertension, the deeper lying, roundish >hard exudates?,
representing products of cell damage %lipid deposits&, are more characteristic of diabetes.
A!. In diabetes, as a result of retinal ischemia, blood vessels may proliferate as fine networ/s of
neovasculari,ation, which can extend into the vitreous body and bleed.
'he most common international nomenclature used to describe the various changes is distinguishing
nonproliferative stages %#. mild, 2. moderate, !. severe& and proliferative stages %#. non+high+ris/, 2. high+
ris/&.
#hanges in nonproliferative !iabetic retinopathy inclu!e:
$icroaneurysms, intraretinal hemorrhages, hard exudates, retinal edema, venous beading, hemorrhages,
cotton+wool spots %nerve fiber infarctions with soft exudates&, and intraretinal microvascular anomalies.
#hanges in proliferative !iabetic retinopathy inclu!e:
(reretinal neovasculari,ation, vitreous hemorrhage, traction retinal detachment %due to traction of
vitreous scarring&, and rubeosis iridis %neovasculari,ation of the iris that can occlude the angle of the
anterior chamber: this entails the ris/ of acute secondary angle closure glaucoma&.
0ymptoms
It remains asymptomatic for a long time. )nly in the late stages with macular involvement or vitreous
hemorrhage will the patient notice visual impairment or suddenly go blind.
6iagnosis:
6iabetic retinopathy is diagnosed by stereoscopic examination of the fundus with the pupil dilated.
5luorescein angiography is used if laser treatment is indicated. 'he presence of rubeosis iridis is confirmed
or excluded in slit+lamp examination, or by gonioscopy of the angle of the anterior chamber.
6ifferential diagnosis:
1ommonly, diabetic and arteriosclerotic changes are found concurrently: hence, the fre*uent difficulty
in precisely defining the etiology of the underlying pathology. In both diabetes and hypertension there are
hemorrhages, exudates, and A;J nic/ing, but for different reasons.
'reatment:
$acular edema that threatens vision is managed with focal laser treatment. (roliferative diabetic
retinopathy %microaneurysms and neovascular areas& is treated with laser photocoagulation.
(rophylaxis:
All type II diabetics should undergo ophtalmologic examination upon diagnosis of the disorder,
and type I diabetics should undergo examination within 7 years of the diagnosis. 'hereafter, they should be
examined regularly because neglecting exposes the patients to the ris/ of blindness.
(rognosis:
'he ris/ of blindness can be reduced by optimum control of blood glucose, regular ophtalmologic
examination, and timely therapy, but it cannot be completely eliminated. 4ubeosis iridis in the proliferative
stage later results in loss of the eye as it is an irreversible process.
3C) PERFORATI+' I+,(RIES OF THE EYE8 I+TRAOC(/AR FOREI'+ BO)IES
'ogether with severe caustic in2uries, perforating in2uries are the most devastating forms of ocular
trauma. 'hey are caused by sharp ob2ects that penetrate the cornea and sclera. A distinction is made
between penetration with and without an intraocular foreign body. .owever, even blunt trauma can cause
an open+globe in2ury in an eye wea/ened by previous surgery or in2ury where extremely high+energy forces
are involved %such as falling on a cane&.
(erforating in2uries cover the entire spectrum of clinical syndromes. 0ymptoms can range from
massive penetration of the cornea and sclera with loss of the anterior chamber to tiny, nearly invisible
in2uries that close spontaneously. 'he latter may include a fine penetrating wound or the entry wound of a
foreign body. 6epending on the severity of the in2ury, the patientLs visual acuity may be severely
compromised or not influenced at all.
)ne of the most common se*uelae is a traumatic cataract. 'he rupture in the lens capsule allows
a*ueous humor to penetrate, causing the lens to swell. 'his results in lens opacification of varying severity.
Earge defects will lead to total opacification of the lens within hours or a few days. 0maller defects that
close spontaneously often cause a circumscribed opacity.
6epending on the severity of the perforating in2ury, the following diagnostic signs will be present:
'he anterior chamber will be shallow or absent. 'he pupil will be displaced toward the penetration site.
0welling of the lens will be present %traumatic cataract&. 'here will be bleeding in the anterior chamber and
vitreous body. .ypotonia of the globe will be present.
'he rupture of the lens capsule and vitreous hemorrhage often ma/e the examination difficult as
they prevent direct inspection. 'hese cases re*uire radiographs in two planes to determine whether there is
a foreign body in the eye or 1' studies, that permit precise locali,ation of the foreign body and can also
image radiolucent foreign bodies such as plexiglas. A particularly common circumstance that should
generate suspicion of intraocular foreign body involves in2ury incurred when metal hits metal %e.g. hammer
and nail or hammer and chisel&. In these cases, the patient feels a foreign body sensation and pain. 'he
puncture wound may be difficult to see. 'he diagnosis may be confirmed by examining the fundus in
mydriasis and obtaining radiographic studies.
'reatment: irst aid. 8hen perforating trauma is suspected, a sterile bandage should be applied
and the patient referred to an eye clinic for treatment. 'etanus immuni,ation and prophylactic antibiotic
treatment are indicated. Surgical treatment includes suturing the globe and reconstructing the anterior
chamber. Any extruded intraocular tissue %such as the iris& must be removed. Intraocular foreign bodies
should be removed when the wound is repaired %i.e., by vitrectomy&.
Eate conse*uences include: Improper reconstruction of the anterior chamber may lead to adhesions
between the iris and the angle of the anterior chamber, resulting in secondary angle closure glaucoma. A
retinal in2ury can lead to retinal detachment. 5ailure to remove iron foreign bodies can lead to ocular
siderosis, which causes irreparable damage to the receptors and may manifest itself years later. 1opper
foreign bodies cause severe inflammatory reactions in the eye %ocular chalcosis& within a few hours.
0ymptoms range from uveitis and hypopyon to phtisis bulbi %shrin/age and hypotonia of the eyeball&.
)rganic foreign bodies %such as food& in the eye lead to fulminant endophtalmitis.
5A) HERPETIC EYE )ISEASES
AA. Her*es si"*e4 o# the e$eids and Her*es 0oster o*hta"i!&s %see topic 2A&
%) Her*es si"*e4 2eratitis
Epidemiology and pathogenesis:
It is among the more common causes of corneal ulcer. About B0 of the population are carriers of the
herpes simplex virus. A typical feature is an unnoticed primary infection that heals spontaneously. $any
people then remain carriers of the neurotropic virus, which can lead to recurrent infection at any time
proceeding from the trigeminal ganglion. A corneal involvement is always a recurrence. A primary herpes
simplex infection of the eye will present as blepharitis or con2unctivitis. 4ecurrences may be triggered by
external influences %such as exposure to <J radiation&, stress, menstruation, immunologic deficiency, or
febrile infections&.
0ymptoms:
It is usually very painful and associated with photophobia, lacrimation, and swelling of the eyelids. Jision
may be impaired in the presence of central epithelitis.
5orms and diagnosis:
'he following forms are differentiated according to the specific layer of the cornea in which the lesion is
located. 4ecurrences are more fre*uent in the stroma and endothelium.
Den!ritic "eratitis is characteri,ed by branching epithelial lesions. 'hese lesions will be visible after
application of fluorescein dye. 1orneal sensitivity is reduced. It may progress to stromal /eratitis.
Stromal "eratitis: (ure stromal involvement without prior dendritic /eratitis is characteri,ed by intact
epithelium that will not show any defects after application of fluorescent dye. 0lit lamp examination
will reveal central dis/iform corneal infiltrates %dis/iform /eratitis&. 0uperficial or deep vasculari,ation
may be present. 4eaction of the anterior chamber will be accompanied by endothelial pla*ues %protein
deposits&.
En!othelitis $en!othelial "eratitis% is caused by the presence of herpes viruses in the a*ueous humor.
'his causes swelling of the endothelial cells and opacification of the ad2acent corneal stroma.
Involvement of the endothelial cells in the angle of the anterior chamber causes a secondary increase in
intraocular pressure %secondary glaucoma&. )ther findings are endothelial pla*ues and inflamed cells
in the anterior chamber.
'reatment:
Infections involving the epithelium are treated with trifluridine as a superficial virostatic agent. 0tromal and
intraocular infections are treated with acyclovir topically or systemically.
--- 1orticosteroids are contraindicated in epithelial herpes simplex infection but may be used to treat
stromal /eratitis where the epithelium is intact---
!) Her*es 0oster 2eratitis
It refers to /eratitis due to endogenous recurrence of chic/enpox %caused by varicella+,oster virus&.
Etiology:
(roceeding from the trigeminal ganglion, the virus reinfects the region supplied by the trigeminal nerve.
'he eye is only affected when the ophtalmic division of the trigeminal nerve is involved.
6iagnosis and treatment
It also occurs in superficial and deep forms, which are similar to .0 infection of the cornea. 1orneal
sensitivity is reduced or absent. 'he eye is treated with acyclovir ointment, s/in changes are usually treated
with systemic acyclovir. If corneal epithelium is intact, the irritation of the anterior chamber can be treated
with steroids.
d) +eonata !on-&n!tivitis
.0J types # and 2 is the ma2or viral agent causing neonatal /eratocon2unctivitis.
0ymptoms, signs, and diagnosis:
It can occur as an isolated infection or with disseminated or 1D0 infection. 'he onset is on the 7
th
to 3
th
day
of life. It presents as watery blepharocon2unctivitis with corneal involvement. It can be diagnosed by viral
isolation, detecting .0J+# or .0J+2 antigen by immunofluorescence in con2unctival cultures or identifying
.0J in electron microscope.
'reatment: It should be treated by topical %eyedrops or ointments& acyclovir. 0ystemic acyclovir in severe
cases.
e) A!&te in#e!tio&s !on-&n!tivitis %see topic 2!C&
#) Her*es si"*e4 and her*es 0oster retinitis
It is a rare disorder occurring in immunocompromised patients. )ther viral agent causing retinitis in such
patients include 1$J, or rubella virus.
0ymptoms and diagnosis:
(atients report loss of visual acuity and visual field defects. 0lit+lamp examination will reveal cells in the
vitreous body. )phtalmologic findings include retinal necrosis with intraretinal bleeding. 8hen the retinitis
heals, it leaves behind wide+area scarring.
'reatment and prognosis:
.igh doses of an antiviral agents %acyclovir&. Jiral retinitis can be arrested if diagnosed early, but
recurrences are common in immunocompromised patients. Clindness cannot be prevented in case of retinal
necrosis.
5B) APHA9IA8 PSE()OPHA9IA
Apha"ia& apha"ic eye 9 an eye with displaced lens or from which the crystalline lens has been
removed.
Pseu!opha"ia& pseu!opha"ic eye 9 an eye with an artificial lens
A7. A*ha2ia
'here are generally two types of apha/ia:
A=. 6ue to diso!ation
Subluxation %partial dislocation&: 'he suspension of the lens is loose, and the lens is only partially
within the hyaloid fossa.
'uxation %complete dislocation&: 'he lens is torn completely free and has migrated into the vitreous
body or, less fre*uently, into the anterior chamber.
Etiology:
'here are several causes of lens dislocation. $ost fre*uently, it is due to trauma. Eater in life,
pseudoexfoliation may also lead to dislocation of the lens. .ereditary causes and metabolic disease
%homocystinuria, $arfanIs syndrome, or ectopia lentis& produce lens displacement early in life, yet they are
rare.
0ymptoms:
0light displacement may be of no functional significance. $ore pronounced displacement produces severe
optical distortion with loss of visual acuity.
6iagnosis:
'here is tremulous motion of the lens and iris when the eye moves. 'his is detectable under slit lamp
examination.
'reatment:
'he ris/ of secondary angle closure glaucoma from protrusion of the iris and dislocation of the lens into the
anterior chamber are indications for removal of the lens.
A3. Posto*erative apha/ia following cataract surgery without placement of an intraocular lens
'reatment:
Apha/ia produces hyperopia, therefore plus lenses are re*uired to correct it. 'he closer the plus
lens to the retina, the stronger its refractive power must be to converge incident lights at a point on the
retina. 5or this reason, cataract eyeglasses have a refractive power of about #2 diopters, a contact lens about
#A diopters, an anterior chamber ocular lens about 20 diopters, and a posterior chamber lens about 2!
diopters.
1ontact lenses are suitable for postoperative correction of unilateral cataract. .owever, many older
patients have difficulty learning how to cope with contact lenses.
1orrection of unilateral apha/ia with unilateral glasses is usually contraindicated because it results
in anisei/onia %a condition in which the si,e and shape of the ocular image of one eye differ from those of
the other&. 'herefore, it is suitable only for correcting bilateral apha/ia. 1ataract eyeglasses have also the
disadvantage of limiting the field of vision %peripheral and ring scotoma + ring scotoma 9 scotoma
encircling the point of fixation&.
AH. Pse&do*ha2ia
In BH of all cataract extractions, an intraocular lens %I)E& is implanted in place of the natural lens
%posterior chamber lens&. 'he power of the lens re*uired is determined postoperatively by biometry.
'here are 2 types of intraocular lenses:
Mono#o!a IO/s: 'he patient can select whether the strength of the artificial lens is suitable for
distance vision or near vision.
Bi#o!a IO/s: 'hese allow close and remote ob2ects to appear in focus. .owever, bifocal and
multifocal lenses do not achieve the optical imaging *uality of monofocal lenses.
5C) A'E:RE/ATE) MAC(/AR )E'E+ERATIO+
It is a progressive degeneration of the macula in elderly patients.
Epidemiology:
Age+related macular degeneration is the most fre*uent cause of blindness beyond the age of =7 years. It
may also occur in children as a hereditary disorder.
(athogenesis:
'he fovea, a pinpoint, depressed area of the central retina, is the retinal area with greatest visual acuity.
'his area plus the area surrounding it is termed the macula. 6rusen %small, hyaline, globular pathological
growth& develop here, in the retinal pigment epithelium due to accumulation of metabolic products. 'he
peripheral retina is usually spared.
0ymptoms:
(atients notice a gradual loss of visual acuity. 8here macular edema is present, patients complain of image
distortion %metamorphopsia&, macropsia %stage in which seen ob2ects appear magnified&, or micropsia
%stage in which seen ob2ects appear smaller than they actually are&. Although the patient is >legally blind?,
his peripheral, vision is more or less wor/ing and he gets about *uite well.
6iagnosis:
)phtalmoscopic examination can distinguish 2 separate stages that occur in chronological order:
() Early A*+: 6rusen, atrophy %appears pale&, and proliferation of retinal pigment epithelium
,) 'ate A*+: @eographic atrophy of the retinal pigment epithelium. 0erous detachment of the retina
and;or retinal pigment epithelium: hemorrhages. 5ibrous scar.
'reatment:
Do reliable effective therapy is available. Easer therapy may be performed in the early stage %in case there
is lea/age of fluid under the retina& in case there is no neovasculari,ation involving the fovea centralis. <se
of progressively stronger near vision aids such as a hand magnifier or binocular magnifier should be tried.
1linical course and prognosis:
'he course is chronic and lead to progressive loss of visual acuity.
6A) THE )RY EYE (9ERATOCO+,(+CTIVITIS SICCA)
It is a noninfectious /eratopathy characteri,ed by reduced moistening of the con2unctiva and cornea.
Epidemiology:
Meratocon2unctivitis sicca as a result of dry eye is one of the most common eye problems between the
ages of A0 and 70. As a result of hormonal changes in menopause, women are far more fre*uently
affected %H=& than men. It is also more common in regions with high environmental pollution.
Etiology:
It results from dry eyes, which may be due to one or two causes:
AB. *e!uce! tear pro!uction associated with systemic disorders %such as 02NrgenIs syndrome and
rheumatoid arthritis& or as a result of atrophy or destruction of the lacrimal gland.
70. Altere! composition of the tear film can be due to vitamin A deficiency, medications %such as oral
contraceptives and retinoids&, or environmental influences %such as nicotine, smog, or air
conditioning&. 'he tear film brea/s up too *uic/ly and causes corneal drying.
0ymptoms:
(atients complain of burning, reddened eyes, and excessive lacrimation %reflex lacrimation& from only
slight environmental causes such as wind, cold, low humidity, or long reading. A foreign+body sensation
is also present. 'hese symptoms may be accompanied by intense pain.
6iagnosis:
)ften there is a discrepancy between the minimal clinical findings and the intense symptoms
reported by the patient. 4esults from Schirmer tear testing %a strip of litmus paper is inserted into the
con2unctival sac of the temporal third of the lower eyelid and after about 7 minutes, at least #7 mm of
the paper should turn blue due to the al/aline tear fluid: values less than 7 mm are abnormal& usually
show reductions of the watery component of tears, and the tear brea"-up time %which provides
information about the mucin content of the tear film which is important for its stability& is reduced.
Jalues of at least #0 seconds are normal: the tear brea/+up time in /eratocon2unctivitis sicca is less than
7 seconds.
In severe cases the eye will be reddened, and the tear film will contain thin mucus. Any corneal
lesion can be demonstrated with fluorescein dye. In less severe cases the eye will only be reddened. 'he
rose bengal test %dying dead epithelial cells and mucin& is another test useful in evaluation.
'reatment:
Artificial tear solution in varying viscosities are prescribed. 'hese range from eyedrops to high+
viscosity long+acting gels that may be applied every hour. 'he puncta can be temporarily closed with
silicon punctal plugs to at least retain the few tears that are still produced. 0urgical obliteration of the
puncta may be indicated in severe cases. (atients should be also informed about the possibility of
installing an air humidifier in the home.
(rognosis:
'he prognosis is good when treated correctly. .owever, the disorder cannot be completely healed.
6B) CA(SES OF S())E+ /OSS OF VISIO+
)iagnosis;
7#. .istory:
'here are few very important *uestions the patient must be as/ed to be able to diagnose the cause of
sudden loss of vision:
Is the visual loos transient or persistentO
Is the visual loss monocular or binocularO
8hat was the tempoO 6id it occur abruptly, or did it develop over hours, days, or wee/O
8hat are the patientIs age and medical conditionsO
72. Examinations to be performed:
!isual acuity testing: 'he first thing to be determined in evaluating acute visual loss.
Confrontation testing: Dormal visual acuity does not assure that significant vision has not been
lost, because the entire visual field must be considered. 5or instance, a patient who has lost all of
the peripheral vision on one side in both eyes + a homonymous hemianopsia + has normal visual
acuity.
Pupillary reactions: 5or example, the presence or absence of relative afferent pupillary defect %see
topic #3A for details& is often important in the evaluation of monocular visual loss.
"phtalmoscopy: It is the most important examination because it allows direct inspection of the
fundus and an assessment of the clarity of the refractive media.
Penlight examination: It will usually detect corneal disease responsible for acute visual loss.
Tonometry: It helps to confirm angle+closure glaucoma.
Media opacities: 'hese opacities do not cause relative afferent pupillary defect. Acute visual loss
may result from conditions that cause rapid changes in the transparency of these tissues.
Corneal edema: 'he most common cause of corneal edema is increased intraocular pressure.
Jisual loss due to an attac/ of angle+closure glaucoma is usually the result of corneal edema. Any
acute infection or inflammation of the cornea %e.g. herpes simplex /eratitis& may mimic corneal
edema.
#yphema %blood in the anterior chamber&: 0ignificant hyphema reduces vision, and complete
hyphema will reduce vision to light perception only. $ost hyphemas are conse*uences of blunt
trauma: however, abnormal vessels %occurring with tumors, diabetes, or intraocular surgery&
predispose to hyphema.
!itreous hemorrhage: Earge hemorrhages occur after trauma and in any condition causing retinal
neovasculari,ation %e.g. diabetes or retinal vein occlusion&.
Possi%e !a&ses;
7!. 4etinal disease
Retina deta!h"ent %see topic #A1&8 "a!&ar disease %usually bleeding from neovasculari,ation
formed as part of the process of age+related macular degeneration + see topic A1&8 and retina vas!&ar
o!!&sion %see topic BC and #=C& are all associated with sudden loss of vision. .owever, acute visual
loss may develop in any inflammatory process that affects the retina, including infectious
chorioretinitis, vasculitides, and idiopathic inflammation. 'hese conditions may be distinguished by
their ophthalmologic findings.
7A. )ptic nerve disease
1onditions affecting the optic nerve can often result in acute visual loss. Although the optic nerve may
or may not appear normal initially by ophthalmoscopy, pupillary responses are abnormal in unilateral
disease.
It includes o*ti! ne&ritis %retrobulbar neuritis + see topic #B1&, *a*iede"a %see topic #01&, is!he"i!
o*ti! ne&ro*ath$ %see topic #31&, and tra&"a %traumatic optic neuropathy&.
77. Jisual pathway disorders
He"iano*ia
'he cerebral visual pathways are susceptible to involvement by vascular events or tumors. In older
persons, a homonymous hemianopia, defined as loss of vision on one side of both visual fields, may
result from occlusion of one of the posterior cerebral arteries with infarction of the occipital lobe.
)ther vascular events occurring in the middle cerebral artery distribution also may produce
hemianopia, but usually other neurologic signs are prominent. Almost any patient with hemianopia
warrants 1' or $4I examination.
Corti!a %indness
$uch rarer is extensive bilateral damage to the cerebral visual pathways resulting in complete loss
of vision. 'his condition is referred to as cortical, or central blindness. Cecause the pathways serving
the pupillary light reflexes separate from those carrying visual information, a patient who is cortically
blind has normal pupillary reactions. 'his finding, along with a normal fundus, helps in diagnosing
cortical blindness. $ost patients with cortical blindness either improve or will die because of severe
neurological damage.
7=. 5unctional disorders
'he ad2ective >functional? is used in preference to >hysterical? or >malingering? to describe visual loss
without organic basis.
6C) AC(TE A+'/E C/OS(RE '/A(COMA A+) ITS TREATME+T
Definition: Acute episodic increase in intraocular pressure %I)(& to several times the normal value %#0 + 20
mm .g& due to sudden bloc/age of drainage. (roduction of a*ueous humor and trabecular resistance are
normal.
Epidemiology:
'he incidence among persons over the age of =0 is # per #000. 8omen are !x as often affected as men.
Etiology: %see also topic #=A&
Anatomically predisposed eyes with shallow anterior chambers pose a relative restriction to the flow of
a*ueous humor through the pupil. 'his pupillary bloc/ increases the pressure in the posterior chamber. 'he
pressure displaces the iris anteriorly toward the trabecular meshwor/, suddenly bloc/ing the outflow of
a*ueous humor %angle closure&. A typical glaucoma attac/ occurs unilaterally due to widening of the pupil
either in dar/ surroundings and;or under emotional stress. A typical situation is the evening mystery movie
on 'J. Iatrogenic pharmacologic mydriasis and systemic psychotropic drugs can also trigger a glaucoma
attac/.
0ymptoms:
73. Acute onset of intense pain: 'he elevated I)( acts on the corneal nerves to cause dull pain. 'his pain
may be referred to the temples, bac/ of the head, and 2aws via the ! branches of the trigeminal nerve.
7H. -ausea an! vomiting occur due to irritation of the vagus nerve and can simulate abdominal disorders.
7B. Diminishe! visual acuity: (atients notice obscured vision and colored halos around lights in the
affected eye. 'hese symptoms are caused by the corneal edema.
=0. Pro!romal symptoms: (atients report blurred vision prior to the attac/.
--- 'he full clinical syndrome of acute glaucoma will not always be present. 'he diminished visual acuity
may go unnoticed if the other eye has normal vision. (atientsI sub2ective perception of pain can vary
greatly ---
6iagnosis:
'here is a typical triad of symptoms:
=#. .nilateral re! eye /ith con0unctival or ciliary in0ection1 ,) 2ixe! an! !ilate! pupil1 3) 4ar! eyeball
on palpation
)ther findings include:
6ull and steamy corneal edema: the anterior chamber is shallow or completely collapsed.
'he fundus is generally obscured due to opacification of the corneal epithelium. As symptoms subside
and the cornea clears, the optic dis/ will range from normal to hyperemic optic nerve. 'he central
retinal artery will pulse on the optic dis/ as blood can only enter the eye during the systole due to the
high I)(.
Jisual acuity is reduced to perception of hand motions.
6ifferential diagnosis:
5eneral symptoms often predominate and may be mista/en for appendicitis or a brain tumor.
In iritis an! iri!ocyclitis, the eye is also red, but the I)( tends to be decreased.
'reatment:
--- An acute glaucoma attac/ is an emergency. 'he underlying causes of the disorder re*uire surgical
treatment, although initial therapy is conservative.
=2. Medi!a thera*$;
@oals of conservative therapy:
=!. Decrease IOP
)smotic reduction in the volume of the vitreous body is achieved via systemic hyperosmotic solutions.
(roduction of a*ueous humor is decreased by inhibiting carbonic anhydrase %IJ aceta,olamide&.
'he iris is withdrawn from the angle by administering topical miotic agents %pilocarpine&.
=A. Allo/ the cornea to clear %important for subse*uent surgery&
4epetitive indentation of the cornea presses the a*ueous humor into the periphery of the angle of the
anterior chamber, which opens the angle and permit a*ueous humor to drain. 'his also helps clear up the
cornea.
=7. *elieve pain
Analgesic agents, antiemetic agents, and sedatives may be used if necessary.
==. S&rger$ (sh&nt %et<een the *osterior and anterior !ha"%er)1
)nce the cornea is clear, the underlying causes of the disorder are treated surgically by creating a shunt.
-eo!ymium:yttrium-aluminium-garnet laser iri!otomy $nonincisional proce!ure%: 'he Dd:PA@
laser can be used to create an opening in the peripheral iris %iridotomy& without having to open the
globe.
Peripheral iri!ectomy $incisional proce!ure%: A limbal incision is made, through which an iridectomy
is performed. It is rarely performed today.
Coth methods can be used as prophylaxis in patients reporting prodromal symptoms.
(rognosis:
recurrent acute angle closure glaucoma or angle closure persisting longer than AH hours can produce
peripheral synechiae between the root of the iris and the trabecular meshwor/ opposite it. 'hese cases
cannot be treated by laser iridotomy or iridectomy. 5iltration surgery is indicated in these cases.
=A) )ISOR)ERS OF THE /ACRIMA/ )RAI+A'E SYSTEM8 AC(TE A+) CHRO+IC
)ACRYOCYSTITIS1
6acryocystitis is an inflammation of the lacrimal sac. It is the most fre*uent disorder of the lower
lacrimal system. It is usually the result of obstruction of the nasolacrimal duct and is unilateral in most
cases.
=3. A!&te da!r$o!$stitis
Epidemiology:
'he disorder most fre*uently affects adults between the ages of 70 and =0.
Etiology:
'he cause is usually a stenosis within the lacrimal sac. 'he retention of tear fluid leads to infection from
staphylococci, pneumococci, (seudomonas, or other pathogens.
0ymptoms:
It includes highly inflamed, painful swelling in the vicinity of the lacrimal sac that may be accompanied by
malaise, fever, and involvement of the regional lymph nodes. 'he pain may be referred as far as the
forehead and teeth. An abscess in the lacrimal sac may form in advanced disorders: it can spontaneously
rupture the s/in and form a draining fistula.
Acute inflammation that has spread to the surrounding tissue of the eyelids and chee/ entails a ris/ of
sepsis and cavernous sinus thrombosis, which is a life+threatening complication-
6iagnosis:
4adiographic contrast studies can visuali,e the obstruction for preoperative planning.
6ifferential diagnosis:
.ordeolum %small, circumscribed, nonmobile inflamed swelling&
)rbital cellulitis %usually associated with reduced motility of the eyeball&
'reatment:
Acute cases are treated with local and systemic antibiotics according to the specific pathogen. 6isinfectant
compresses can be also helpful. (us from a fluctuating abscess is best drained through a stab incision.
'reatment after acute symptoms have subside often re*uires surgery %dacryocystorhinostomy + a direct
connection between the lacrimal sac and the nasal mucosa& for persistent relief.
=H. Chroni! da!r$o!$stitis
Etiology:
)bstruction of the nasolacrimal duct is often secondary to chronic inflammation of the connective tissue or
nasal mucosa.
0ymptoms and diagnosis:
'he initial characteristic is increased lacrimation. 0igns of inflammation are usually not present. Applying
pressure to the inflamed lacrimal sac causes large *uantities of transparent mucoid pus to regurgitate
through the punctum. 1hronic inflammation of the lacrimal sac can lead to a serpiginous corneal ulcer.
'reatment:
0urgical intervention is the only effective treatment. 'his involves either a dacryocystorhinostomy or
removal of the lacrimal sac.
=B. +eonata da!r$o!$stitis
Etiology:
Approximately = of newborns have a stenosis of the mouth of the nasolacrimal duct due to a persistent
mucosal fold. 'he resulting retention of tear fluid provides ideal growth conditions for bacteria, particularly
staphylococci, pneumococci, and streptococci.
0ymptoms and diagnosis:
0hortly after birth %2+A wee/s&, pus is secreted from the puncta. 'he disease continues subcutaneously and
pus collects in the palpebral fissure. 'he con2unctiva is not usually involved.
6ifferential diagnosis:
@onococcal or inclusion con2unctivitis.
'reatment:
6uring the first few wee/s, the infant should be monitored for spontaneous opening of the stenosis. 6uring
this period, antibiotic and antiinflammatory eyedrops and nose drops are administered. If symptoms persist,
irrigation or probing under general anesthesia may be indicated. )ften massaging the region several times
daily will be sufficient to open the obstruction.
=B) T(MORS OF THE EYE/I)S
30. 6enign tumors
11 )&!ta !$sts
'he round cysts of the glands of $oll are usually located in the angle of the eye. 'heir contents are
clear and watery. @ravity can result in ectropion. 'herapy consists in marsupiali,ation. 'he prognosis is
good.
.1 >anthees"a
It is a local fat metabolism disorder that produces lipoprotein deposits. 'hese are usually bilateral
and distributed symmetrically.
(ostmenopausal women are most fre*uently affected. A higher incidence is in patients with
diabetes, increased levels of plasma lipoprotein, or bile duct disorders.
0ymptoms: 'he soft yellow white pla*ues are sharply demarcated. Aside from the cosmetic
problem, the patients are usually asymptomatic. 'he pla*ues can only be removed surgically. 4ecurrence is
high.
31 Mo&s!&" !ontagios&"
'his noninflammatory contagious infection is caused by 6DA viruses. 'he disease usually affects
children and teenagers and is transmitted by direct contact. 'he pinhead+si,ed lesions have typical central
depressions and are scattered near the upper and lower eyelids. 'hese lesions are removed with a curet.
51 C&taneo&s horn
'he yellow+brown cutaneous protrusion consists of /eratin. )lder patients are more fre*uently
affected. It should be surgically removed as 27 can develop into malignant s*uamous cell carcinomas
years later.
61 9eratoa!antho"a
It is a rapidly growing tumor with a central /eratin mass that opens on the s/in surface %can
sometimes be expressed&. 'he tumor may resolve spontaneously, forming a small scar. 6iff. dg. should
exclude a basal cell carcinoma %the margin of /eratoacanthoma is avascular&, and s*uamous cell carcinoma
%excluded by a biopsy&.
=1 He"angio"a
It is a congenital benign vascular anomaly resembling a neoplasm that is most fre*uently noticed
in the s/in and subcutaneous tissues. @irls are most often affected. 5acial lesions most commonly occur in
the eyelids. .emangiomas include capillary or superficial, cavernous, and deep forms. .emangiomas can
be compressed, and the s/in will then appear white.
'reatment: 0pontaneous remission occurs in 30 of cases. 8here there is an increased ris/ of
amblyopia due to the si,e of the lesion, cryotherapy, intralesional steroid in2ections, or radiation therapy
can accelerate regression. (rognosis is generally good.
b% +alignant tumors
11 Basa !e !ar!ino"a
It is a fre*uent, moderately malignant, fibroepithelial tumor that can cause severe local tissue
destruction, but very rarely metastasi,es.
Approximately B0 of all malignant eyelid tumors are basal cell carcinomas. 'heir incidence
increases with age. 'hey are more commonly locali,ed on the lower eyelid. $orbidity in sunny countries is
higher than in Europe. 6ar/+s/inned people are affected significantly less often.
1auses of basal cell carcinoma may include a genetic disposition. Increased exposure to the sunIs
ultraviolet radiation, carcinogenic substances %such as arsenic&, and chronic s/in damage can lead to
increased incidence. Casal cell carcinomas arise from the basal cell layers of the epidermis and the
sebaceous gland hair follicles, where their growth locally destroys tissue.
0ymptoms:
'ypical characteristics include a firm, slightly raised margin with a central crater and superficial
vasculari,ation with an increased tendency to bleed. <lceration is occasionally referred to as an ulcus
rodens %invasive ulcer&.
'reatment and prognosis:
'he lesion is treated by surgical excision. If it is not possible, the only remaining options are radiation or
cryotherapy. 'he earlier a basal cell carcinoma is detected, the easier it is to remove. (rognosis is very good
in case of surgical excision.
.1 S7&a"o&s !e !ar!ino"a
'his is the second most common malignant eyelid tumor. 'he carcinoma arises from epidermis,
grows rapidly and destroys tissue. It can metastasi,e into the regional lymph nodes. 4emote metastases are
rarer. 'he treatment of choice is complete surgical removal.
3#. Adeno!ar!ino"a
'his rare tumor arises from the meibomian glands or the glands of Geis. 'he firm, painless swelling is
usually located in the upper eyelid. In its early stages it can be mista/en easily for a chala,ion. 'he lesion
can metastasi,e into local lymph nodes. 'he treatment of choice is complete surgical removal.
=C) EMER'E+CY I+ OPHTA/MO/O'Y
'rue emergencies are conditions re*uiring therapy within minutes.
It includes:
Acute angle-closure glaucoma %see topic 71&
#hemical in0uries an! burns %see topic #1&
Occlusion of the central retinal artery %see topic BC&
<rgent situations re*uire therapy within a few hours.
It includes:
Penetrating in$uries of the globe need protection of an eye shield. Deither a patch nor an ointment is
advisable. An x+ray of 1' scan of the orbit to chec/ for radiopa*ue foreign bodies should be ordered.
4eferral to an ophthalmologist is indicated.
Con$unctival or corneal foreign %odies re*uire topical anestheti,ation followed by removal of the
ob2ect with irrigation or a cotton+tipped applicator.
Corneal a%rasions: 5irst it is anestheti,ed, grossly examined, and then stained with fluorescein to
enhance the view if necessary. Antibiotics are instilled, followed by short+acting cycloplegic drops for
the relief of pain. A pressure patch to maintain lid closure for 2A hours in case of big abrasion. 0evere
cases are referred to an ophthalmologist.
#yphema can result in elevation of the intraocular pressure- It may also be a sign of globe rupture,
dislocated lens, or retinal detachment. Immediate referral to ophtalmologist is necessary.
& lid laceration can be sutured if not deep and neither the lid margin or the canaliculi are involved:
otherwise, refer to an ophtalmologist.
'adiant energy %urns such as sun burn or snow blindness, re*uire topical anesthesia, examination,
topical antibiotic, cycloplegic agents, and patching.
Traumatic optic neuropathy, although uncommon, should be always considered in patients with cranial
or maxillofacial trauma. (atients have decreased unilateral vision, relative afferent pupillary defect, but
examination reveals no ocular origin. .igh+resolution 1' is indicated. .igh+dose steroids may help if
given in the first H hours. A prompt referral to an ophthalmologist is indicated.
?A) REFRACTIVE ME)IA OF THE EYE
4efraction is defined as the ratio of the refractive power of the lens and cornea %refractive media&
to the axial length of the globe. Emmetropia is distinguished from ametropia.
E""etro*ia %normal sight&: 'he ratio of the axial length of the eye to the refractive power of the
corneal and lens is balanced. (arallel light rays that enter the eye therefore meet at a focal point on the
retina and not anterior or posterior, as is the case in ametropia.
A"etro*ia %refractive error&: 'here is a mismatch between the axial length of the eye and the
refractive power of the lens and cornea. 'he ametropia is either axial, which is common, or refractive,
which is less fre*uently encountered. 'he most common disorders are nearsightedness, farsightedness,
and astigmatism.
Jery few people have refraction of exactly 0.0 diopters. About 77 of persons between the ages of 20 and
!0 have refraction between "# and +# diopters.
Emmetropia is not necessarily identical to good visual acuity. 'he eye may have other disorders
that reduce visual acuity, such as atrophy of the optic nerve or amblyopia.
'he refractive power of an optical lens system is specified in diopters, which are international
units of measure. 4efractive power is calculated according to the laws of geometric optics. 'he maximum
total refractive power of an emmetropic eye is =! diopters with an axial length of the globe measuring 2!.7
mm. 'he cornea accounts for A! diopters and the lens for #0 + 20 diopters, depending on accommodation.
'he refractive power 6 %specified in diopters& of an optical system is the reciprocal of the focal
length of a lens f %specified in meters&. 'his yield the e*uation: 6 9 #;f
Example: 8here a lens focuses parallel incident light rays 0.7 m behind the lens, the refractive power is
#;0.7 m 9 " 2 diopters. 'his is a converging lens. 8here the virtual focal point is in front of the lens, the
refractive power is #;+0.7 9 + 2 diopters. 'his is a diverging lens.
A!!o""odation
'he refractive power of the eye is not a constant value. 'he eyeIs refractive power must alter to
allow visuali,ation of both near and distant ob2ects with sharp contours. 'his accommodation is made
possible by the elasticity of the lens.
Accommodation mechanisms:
32. /ens; 'he elasticity of the lens capsule tends to ma/e the lens assume a spherical shape. .owever, in
the unaccommodated state this is prevented by the pull of ,onule fibers. 'he elasticity of the lens
progressively decreases with age, and the range of accommodation decreases accordingly. (resbyopia
%physiologic loss of accommodation in advancing age& begins when the range of accommodations falls
below ! diopters. 'his causes the near point %the shortest distance that allows focused vision& to move
more far: so that the patientIs arms become >too short for reading?.
3!. @on&e #i%ers: 'hey insert into the e*uator of the lens and connect it to the ciliary body.
3A. Ciiar$ "&s!e: 1onstriction of the ring+shaped ciliary muscle decreases the tension of ,onule fibers.
'he lens can get the spherical shape, which increases the refractive power, and the focus of the eye
shifts to the near field, and close ob2ect ta/e on sharp contours.
'he ciliary muscle is innervated by the short ciliary nerves, postganglionic parasympathetic fibers of the
oculomotor nerve. (arasympatholytics such as atropine inhibit the function of the ciliary muscle
%cycloplegia& and prevent accommodation.
?B) SECO+)ARY '/A(COMA
Definition: @laucomas caused by other ocular diseases, such as inflammation, trauma, tumors, medication,
and physical or chemical influences.
37. Se!ondar$ o*en ange ga&!o"as
'he anatomic relationship between the root of the iris, the trabecular meshwor/, and peripheral cornea
are not disturbed. .owever, the trabecular meshwor/ is congested and the resistance to drainage is
increased.
'he most important forms:
3=. Pseu!oexfoliative glaucoma: 'his form occur in 0candinavian countries. 6eposits of amorphous
material form throughout the anterior chamber and congest the trabecular meshwor/.
33. Pigmentary glaucoma: Poung myopic men typically are affected. It is characteri,ed by release of
pigment granules from the pigmentary epithelium of the iris that congest the trabecular meshwor/.
3H. #ortisone glaucoma: A0 of the population react to ! wee/ steroid therapy by elevated I)(. It is
reversible when the steroids are discontinued.
3B. Inflammatory glaucoma: 'wo mechanisms are involved:
H0. 'he viscosity of the a(ueous humor increases as a result of the influx of protein from inflamed iris
H#. 'he trabecular mesh)or* %ecomes congested with inflammatory cells and cellular debris.
H2. Phacolytic glaucoma: 'his is acute glaucoma in eyes with mature or hypermature cataracts. 6enatured
lens protein passes through the intact lens capsule in the anterior chamber and is phagocyti,ed. 'he
trabecular meshwor/ becomes congested with macrophages and the protein itself.
H!. Se!ondar$ ange !os&re ga&!o"a
As in primary angle closure glaucoma, the increase in I)( is due to bloc/age of the trabecular
meshwor/. .owever, the primary configuration of the anterior chamber is not the causative factor.
'he most important causes:
HA. *ubeosis iri!is: Deovasculari,ation of the iris %rubeosis iridis& draws the angle of the anterior chamber
together li/e a ,ipper %neovascular glaucoma&. Ischemic retinal disorders such as diabetic retinopathy
and retinal vessel occlusion can lead to rubeosis iridis with progressive closure of the angle of the
anterior chamber. )ther forms of retinopathy or intraocular tumors can also cause rubeosis iridis. 'he
prognosis of neovascular glaucoma is poor.
H7. 7rauma: (ost+traumatic presence of blood or exudate in the angle of the anterior chamber and
prolonged contact between the iris and trabecular meshwor/ in a collapsed anterior chamber can lead
to anterior synechiae and angle closure.
Treat"ent o# se!ondar$ ga&!o"as
$edical therapy is usually identical to the treatment of primary chronic open angle glaucoma. .owever,
treatment will generally depend on the etiology of the glaucoma. 'he underlying disorder is best treated
first. 'he prognosis for secondary glaucomas is generally worse than for primary glaucomas.
?C) CO+COMITA+T STRABISM8 AMB/YOPIA8 A+) THEIR MA+A'EME+T
0trabismus is defined as deviation of an eyeIs axis from its normal position.
'here are 2 ma2or types of manifest strabismus:
#oncomitant strabismus: 'he deviating eye accompanies the leading eye in every direction of
movement. 'he angle of deviation remains the same in all directions of ga,e. 'his form of strabismus
may occur as monocular strabismus, in which only one eye deviates or as alternating strabismus, in
which both eyes deviate alternately.
Paralytic strabismus results from paralysis of one or more eye muscles. 'his form differs from
concomitant strabismus in that the angle of deviation does not remain constant in every direction of
ga,e. 5or this reason, this form is also referred to as incomitant strabismus.
Etiology: 'he incidence of strabismus is about 7+3. Esotropia %convergent strabismus& occurs more
fre*uently in Europe and <0A. 1oncomitant strabismus usually occurs in children, whereas paralytic
strabismus primarily affects adults. 'his is because concomitant strabismus is generally congenital or
ac*uired within the first few years of life, whereas paralytic strabismus is usually ac*uired, for example as
a post+traumatic condition.
O!&ar "otiit$;
'he movements of the eyeballs are produced by the following extraocular muscles:
7he four rectus muscles: the superior, inferior, medial, and lateral.
7he t/o obliue muscles: 'he superior and inferior.
6irection of pull of the extraocular muscles: 'he hori,ontal ocular muscles pull the eye in only one
direction: 'he lateral rectus pulls the eye outward %abduction&: the medial rectus pulls it inward %adduction&.
All other extraocular muscles have a secondary direction of pull in addition to the primary one. 6epending
on the path of the muscle, where it inserts on the globe, and the direction of ga,e, these muscles may
elevate or depress the eye, adduct it or abduct it, or rotate it medially %intorsion& or laterally %extorsion&.
'he primary action of the superior rectus and the superior obli*ue is elevation: the primary action of the
inferior rectus and inferior obli*ue is depression.
Derve supply to the extraocular muscles: 'he oculomotor nerve %third cranial nerve& supplies all of the
extraocular muscles except the superior obli*ue, which is supplied by the trochlear %fourth cranial nerve&,
ant the lateral rectus, which is supplied by the abducent %sixth cranial nerve&. 'he extraocular muscle nuclei
are located in the brain stem on the floor of the fourth ventricle and are interconnected to nec/ muscle
nuclei and vestibular nuclei for coordinated movements of the head and globe. Jarious areas in the brain
control eye and ga,e movements.
Con!o"itant stra%is"&s
Epidemiology:
It occurs in children. About 7+3 of all children are affected. In =0+30 of all cases, the disorder manifests
itself within the first two years of life.
Etiology:
Jision at birth is neither focuses nor binocular, and both sensorimotor coordination and binocular vision are
very unstable during the first few years of life. Impairments of the sensory or motor systems or central
processing of visual perceptions that occur during this time can disturb the coordination between the eyes
and lead to strabismus. .owever, the causes are often unclear.
'he possible causes include:
'eneti! #a!tors + About =0 of children with strabismus have a positive family history.
(n!orre!ted re#ra!tive errors are partially responsible for the occurrence of strabismus. 1hildren with
hyperopia tend to have esotropia. 'his is because convergence and accommodation are coupled. 'hese
children have to accommodate without converging when ga,ing into the distance to compensate for
their refractive error. .owever, accommodation always triggers a convergence impulse that can cause
esotropia.
Ins&##i!ient #&sion + 'his can occur in con2unction with anisometropia %une*ual refractive power in
the two eyes& and anisei/onia %une*ual retinal image si,e&. It can also occur in heterophoria %latent
strabismus& after one eye has been covered with a bandage for a prolonged period.
(niatera vis&a i"*air"ent + 0evere myopia, corneal scarring, lens opacities %cataract&, macular
changes, and retinal disorders can cause secondary strabismus.
Other !a&ses: (erinatal lesions such as asphyxia, or cerebral trauma or encephalitis
--- Any initial examination of a patient with strabismus must include examination of the fundus of both
eyes under mydriasis in addition to examination of the anterior segment of the eye ---
(athophysiology:
6eviation of the visual axis of the deviating eye causes ob2ect to be pro2ected to noncorresponding points of
the retina. )ne would expect these patients suffer from constant double vision because the left and right eye
supply different information to the brain. .owever, the central nervous system ulitili,es two mechanisms to
help avoid double vision in concomitant strabismus:
H=. Suppression: A central inhibiting mechanism suppresses the visual stimuli from the deviating eye.
'here are two different types of suppression.
1entral scotoma: 'his visual field defect occurs when the perceived ob2ect is pro2ected to the same
location on the fovea in both eyes but strabismus causes the eyes to perceive it as separate ob2ects. As
this would cause confusion, the ob2ect pro2ected on the fovea of the deviating eye is suppressed.
5ixation point scotoma: 'his visual field defect occurs when the image perceived by the leading eye is
pro2ected to a point next to the fovea in the deviating eye. 'his results in diplopia as the fixation point
does not lie in the fovea as it would in physiologic sight. 'he scotoma occurs at this noncorresponding
point next to the fovea to suppress the diplopia.
H3. Sensory a!aptation: In binocular vision with the ga,e directed straight ahead, the fixation point of the
deviating eye can fall beyond the fovea in the deviating eye. 'his produces anomalous retinal
correspondence as the fixation point in the nondeviating eye always falls on the fovea. 'his means that
the image created in the deviating eye is not as sharply focused as the image in the leading eye and is
suppressed.
Amblyopia secondary to suppression: 1onstant suppression in strabismus can lead to severe, especially in
children below the age of =. If not treated, amblyopia becomes irreversible beyond the age of =+H.
Amblyopia only occurs in unilateral strabismus. In alternating strabismus, fixation or deviation alternates
between so that both eyes learn to see.
)i##erentia diagnosis o# a"%$o*ia;
Amblyopia /ith strabismus: 1ause: 0uppression of the deviating eye. 'reatment: )cclusion therapy.
Deprivation amblyopia: 1ause: )rganic disease, such as ptosis or cataract. 'reatment: Early surgery
and occlusion therapy in applicable cases.
*efractive amblyopia: 1ause: 6ifferent refractive errors. 'reatment: 1orrection of eyeglasses or
contact lenses and occlusion therapy in applicable cases.
6ilateral amblyopia: 1ause: Dystagmus, astigmatism, late correction of refractive errors. 'reatment:
Done.
For"s o# !on!o"itant stra%is"&s
Esotropia: Inward deviation of the visual axis
Exotropia: )utward deviation of the visual axis
4ypertropia an! hypotropia: )cular deviation with one eye higher or lower than the other.
#yclotropia: 'his refers to the rotation of one eye around its visual axis. It is very rare.
HH. Esotro*ia (!onvergent stra%is"&s)
It is one of the most commonly encountered forms of strabismus.
0ymptoms and diagnosis:
'here are three forms of esotropia
HB. #ongenital or infantile: 0trabismus is present at birth or develops within the first = months of life.
'his form is characteri,ed by a large alternating angle of deviation, lac/ of binocular vision, and
intermittent inclination of the head in the direction of the leading eye.
B0. Acuire!: 'wo forms are distinguished:
It manifests itself between the ages #+! %the age of incomplete sensory development&. It is
unilateral. Amblyopia is usually already present.
It manifests itself between the ages ! +3. 'his form of acute late strabismus with normal sensory
development is much less fre*uent. As binocular vision is already well developed, affected
children cannot immediately suppress the image of the deviating eye. As a result, they suffer from
sudden double vision at the onset of strabismus, which they attempt to suppress by closing one
eye. Immediate treatment is indicated to preserve binocular vision.
B#. +icrostrabismus: 'his is defined as unilateral esotropia with a minimal cosmetic effect. As a result, it
is diagnosed late %A+= years&. Cy that time the resulting amblyopia in the deviating eye may be severe.
B2. E4otro*ia (divergent stra%is"&s)
It is less common than esotropia. As it is usually ac*uired, it is encountered more in adults. Exotropia
less fre*uently leads to amblyopia because the strabismus is often alternating. )ccasionally, what is /nown
as >panorama vision? will occur, in which case the patient has an expanded binocular field of vision.
'hese forms are distinguished:
Intermittent exotropia: 'his is the most common form of divergent strabismus. 'he angle of
deviation is present only when the patient ga,es into the distance: the patient has normal binocular
vision in near fixation.
Secon!ary exotropia occurs with reduced visual acuity in one eye resulting from disease or
trauma.
B!. Verti!a deviation (H$*ertro*ia and h$*otro*ia)
It is caused by anomalies in the nerve supply to the rectus and obli*ue muscles. Jertical deviations are
usually associated with esotropia or exotropia.
BA. A%nor"a a!!o""odative !onvergen!eAa!!o""odation
8hen this is abnormal, the angle of deviation may fluctuate depending whether the fixated ob2ect is far
or near. 5or example, in accommodative esotropia, the angle of deviation is larger with close ob2ects
than with distant ob2ects.
6iagnosis:
'here are several types of diagnostic tests %evaluation of ocular alignment with a focused light, preferential
loo/ing test for evaluation of infantile strabismus, unilateral cover test, measuring of angle deviation, or
determination of the type of fixation&.
'reatment:
B7. In chil!ren
'reatment is generally long+term %from the first months of life to about the age of twelve&. 'herapeutic
success is determined not only by the clinical course but also the childIs personality and the parentsI
ability to cooperate. 'he treatment can be divided into ! phases:
B=. It is determined if the cause of strabismus may be treated with eyeglasses %such as hyperopia&.
B3. If it cannot be treated with eyeglasses, the next step is to minimi,e the ris/ of amblyopia by
occlusion therapy %see below&
BH. )nce the occlusion therapy has produced sufficient visual acuity in both eyes, the alignment of
one or both eyes is corrected by surgery. 'he alignment correction is re*uired for normal binocular
vision and also has a cosmetic benefit.
BB. In a!ults
'he only purpose of surgery is cosmetic improvement. A functional improvement in binocular vision
can no longer be achieved.
'reatment and avoidance of strabismic amblyopia:
0trict occlusion therapy by eye patching or eyeglass occlusion is the most effective method.
(rimarily the leading eye is patched. 0evere amblyopia re*uires an eye patch, because eyeglass occlusion
%covering the eyeglass lens of the leading eye with an opa*ue material and being reserved for mild cases of
amblyopia& has a ris/ that the child might attempt to loo/ over the rim of the eyeglasses with the leading
eye. 'his would compromise the effectiveness of occlusion therapy, whose purpose is to train the
amblyopic eye.
Amblyopia must be treated in early childhood. 'he younger the child is, the more favourable and
rapid the response to treatment will be. 'he upper age limit for occlusion therapy is approximately the age
of nine.
'he goal of treatment in infantile strabismus is to achieve alternating strabismus with full visual
acuity and central fixation in both eyes. Cinocular vision is less important here. It is not normally
developed anyway in patients who develop strabismus at an early age and cannot be further improved.
0urgery should be postponed until after amblyopia has been successfully treated. .owever, the
child should undergo surgery prior to entering school so as to avoid the social stigma of strabismus. 'he
procedure involves wea/ening the too strong muscles by releasing them, and strengthening the too wea/
muscles by pulling them.
BA) IMA'I+' I+ OPHTHA/MO/O'Y (A+'IO'RAPHY8 (/TRASO+O'RAPHY8
RA)IO'RAPHY)
A& AD@I)@4A(.P ID )(.'AE$)E)@P
5undus imaging can be enhanced by fluorescein, a dye whose molecules emit green light when
stimulated by blue light. 8hen photographed, the dye highlights vascular and anatomic details of the
fundus. 5luorescein angiography %5EA@& has become very important in the diagnosis of many retinal
conditions. Cecause it is so precise, it is essential for planning laser treatment of retinal vascular disease.
'echni*ue:
'he patient is seated in front of the retinal camera following pupillary dilation. After fluorescein is
in2ected into a vein, it circulates throughout the body. As the dye passes through the retinal and choroidal
circulation, it can be visuali,ed %blue light& and photographed.
Early phased photos document the eyeIs initial rapid, se*uential perfusion of the choroid, the
retinal arteries, and the retinal veins. Eater phase photos may, for example, demonstrate the gradual,
delayed lea/age of dye from abnormal vessels. 'his extravascular dye+stained edema fluid will persist long
after the intravascular fluorescein has exited the eye.
'he dye delineates structural vascular alterations, such as aneurysms or neovasculari,ation.
1hanges in blood flow such as ischemia and vascular occlusion are seen as interruptions of the normal
perfusion pattern. .emorrhage does not stain with dye but rather appears as a dar/, sharply demarcated
void. 'his is due to bloc/age and obscuration of the underlying bac/ground fluorescence.
Isocyanin angiography %I1@& is a method using the isocyanin dye. 'his enhances especially well
the choroidea, and therefore, it is used to visuali,e choroideal affections.
C& <E'4A0)<D6 6IA@D)0'I10 ID )(.'AE$)E)@P
<ltrasonography is used to study structures that may not be directly visible. It can be used to
evaluate either the globe or the orbit. .igh+fre*uency sound waves are emitted from a special transmitter
toward the target tissue. As the sound waves bounce bac/ off the various tissue components, they are
collected by a receiver that amplifies and displays them on a screen.
<ltrasonography can be used to image and differentiate orbital disease or intraocular anatomy of
eyes with opa*ue media. In addition to defining the si,e and location of intraocular and orbital masses, it
can provide clues to the tissue characteristics of a lesion %e.g. solid, cystic, vascular, calcified&.
Cecause sound echoes reflected from two separate locations will reach the probe at different times,
this time separation can be used to calculate the distance between the points, based on the speed of sound in
the tissue medium. 'he most commonly used intraocular measurement is the axial length %cornea to retina&.
'his is important in cataract surgery in order to calculate the power for an intraocular lens implant.
<ltrasound can also be used to *uantify tumor si,e and monitor growth over time.
'he application of pulsed ultrasound and 6oppler techni*ues provides information on the orbital
vasculature. It is possible to determine the direction of flow in the ophtalmic artery and the ophtalmic veins,
reversal of flow in these vessels occurring in internal carotid occlusion and carotid+cavernous fistula.
1& 4A6I)E)@I1 6IA@D)0'I10 ID )(.'AE$)E)@P
(lain Q+rays and 1' scans are useful in evaluation of orbital and intracranial conditions. 1' scan
in particular has become the most widely used method for locali,ing and characteri,ing structural disease in
the extraocular visual pathway. 1ommon orbital abnormalities demonstrated by 1' scan include
neoplasms, inflammatory masses, fractures, and extraocular muscle enlargement associated with @raveIs
disease.
'he intraocular applications of radiology are primarily in the detection of foreign bodies following
trauma and the demonstration of intraocular calcium in tumors such as retinoblastoma. 1' scan is useful
for foreign body locali,ation because of its multidimensional reformatting capabilities and its ability to
image the ocular walls.
BB) )ISEASES OF THE SC/ERA
C asic /nowledge:
'he sclera and the cornea form the rigid outer covering of the eye. All six ocular muscles insert
into the sclera. 'he sclera is a fibrous, whitish opa*ue, and consists of acellular connective tissue. 'he site
where the fibers of the optic nerve enter the sclera is /nown as the lamina cribrosa. In the angle of the
anterior chamber, the sclera forms the trabecular networ/ and the canal of 0chlemm. 'he a*ueous humor
drains from there into the intrascleral and episcleral venous plexus. Deurovascular supply: Jortex veins and
the short anterior and posterior ciliary arteries penetrate the sclera. 'he ciliary nerves course through the
sclera from posterior to anterior.
Examination methods:
'he anterior portion of the sclera can be examined directly with a slit lamp. Evaluation of the
posterior sclera re*uires ultrasound.
1olor changes:
'he sclera is normally dull white li/e porcelain. Altered color suggests one of these changes:
1on2unctival and;or ciliary in2ection and inflammation will give the sclera a red appearance.
A sclera that is very thin will appear blue because of the underlying choroid %this occurs in newborns,
in osteogenesis imperfecta, and following inflammations&
In 2aundice, the sclera turns yellow
In ochronosis %al/aptonuria&, the sclera will ta/e on brownish color.
0taphyloma and ectasia:
#00. Sta*h$o"a refers to a bulging of the sclera in which the underlying uveal tissue in the bulge is
also thinned and degenerated. Cy far the most common form is posterior staphyloma in severe myopia,
a bulging of the entire posterior pole of the eyeball. 0taphyloma can also occur secondary to scleritis.
#0#. E!tasia is a thinning and bulging of the sclera without uveal involvement, as can occur secondary
to inflammation.
Coth staphyloma and ectasia are secondary. Do treatment is available.
'rauma
'he sclera is fre*uently involved in penetrating trauma. 6eep in2uries usually involve the choroid
and retina. 0urgery to treat larger in2uries should also include a retinal repair.
Inflammations:
Inflammations are the most clinically significant scleral changes. 'hey more often involve the
anterior sclera %episcleritis and anterior scleritis& than the posterior sclera %posterior scleritis&.
#lassification: 5orms of scleral inflammation are differentiated as follows:
+ocation: anterior or posterior %i.e., anterior or posterior to the e*uator of the globe&.
Depth: 0uperficial %episcleritis& or deep %scleritis&.
,ature: 6iffuse %usually scleritis&, circumscribed or segmental %episcleritis&, nodular, with formation of
small mobile nodules %scleritis and episcleritis&, necroti,ing, or non+necroti,ing %both scleritis only&.
E*is!eritis
It is a circumscribed, usually segmental, and generally nodular inflammation of the episclera
%connective tissue between the sclera and con2unctiva&.
Epidemiology:
Episcleritis is the most common form of scleral inflammation.
Etiology:
It is rarely due to systemic underlying disorders causing scleritis %see later&, and only occasionally due to
bacterial or viral inflammation. )ften episcleritis has no apparent cause.
0ymptoms:
It can be unilateral or bilateral. It is usually associated with segmental reddening and slight tenderness to
palpation.
5indings:
'he episcleral vessels are arranged radially. In episcleritis, these vessels and the con2unctival vessels above
them are become hyperemic. 'he episclera is infiltrated with inflammatory cells, but the sclera itself is not
swollen. 0mall mobile nodules are typical of nodular episcleritis.
6ifferential diagnosis:
It should be differentiated from con2unctivitis and scleritis. 'he con2unctival blood vessels are the most
superficial: the episcleral vessels lie within 'enonIs capsule and are arranged radially. 8hen
vasoconstrictive eyedrops are applied, the con2unctival in2ection will disappear but not the episcleral
in2ection.
'reatment and prognosis:
It usually resolves spontaneously within # or 2 wee/s. 0evere symptoms are treated with topical steroids
%eyedrops& or with D0AI6s.
S!eritis
It is a diffuse or locali,ed inflammation of the sclera. 0cleritis is classified according to location:
Anterior %inflammation anterior to the e*uator of the globe&
Posterior %inflammation posterior to the e*uator of the globe&
Anterior scleritis is further classified according to its nature:
-on-necroti8ing anterior scleritis %nodular or diffuse&
-ecroti8ing anterior scleritis %with or without inflammation&
Epidemiology:
0cleritis is far less fre*uent than episcleritis. (atients are generally older and women are affected more than
men.
Etiology:
70 of cases %which have severe clinical course& are attributable to systemic autoimmune or rheumatic
disease, or as a result of immunologic processes associated with infection. 'his applies especially to
anterior scleritis. (osterior scleritis is usually not associated with any specific disorder. As with episcleritis,
scleritis is only occasionally due to bacterial or viral inflammation.
2reuent systemic !iseases that can cause scleritis include rheumatoid arthritis, polymyositis,
dermatomyositis, an/ylosing spondylitis, spondylarthritis, vasculitis, 8egenerIs granulomatosis,
herpes ,oster ophtalmicus, syphilis, and gout&.
*are causes include tuberculosis, lues, borreliosis, and 4eiterIs syndrome.
0ymptoms and findings:
All forms except for scleromalacia perforans are associated with severe pain and general reddening of the
eye.
Anterior non-necroti8ing scleritis $no!ular form%: 'he nodules consist of edematous swollen sclera
and are not mobile %in contrast to episcleritis&
Anterior non-necroti8ing scleritis $!iffuse form%: 'he inflammation is more severe than in the nodular
form.
Anterior necroti8ing scleritis /ith inflammation: 1ircumscribed reddening of the eyes is a typical
sign %in2ection of the deep scleral blood vessels&. As it progresses, the sclera thins and the underlying
choroid shows through. 'he inflammation gradually spreads from its primary focus. <sually it is
associated with uveitis.
Anterior necroti8ing scleritis /ithout inflammation $scleromalacia perforans%: 'his form typically
occurs in female patients with rheumatoid arthritis. It is usually asymptomatic and begins with a
yellow necrotic patch on the sclera. As it progresses, the sclera also thins. 'his is the only form of
scleritis that may be painless.
Posterior scleritis: 0ometimes there is no abnormal finding in the anterior eye: and pain will be the
only symptom. Associated inflammation of the orbit may result in exophtalmos and impaired ocular
motility due to myositis of the ocular muscles. Intraocular findings include exudative retinal
detachment and;or choroid detachment.
6ifferential diagnosis:
1on2unctivitis and episcleritis
'reatment:
Anterior non-necroti8ing scleritis: 'opical or systemic nonsteroidal antiinflammatory agents.
Anterior necroti8ing scleritis /ith inflammation an! posterior scleritis: 0ystemic steroid therapy is
re*uired to control pain. In more severe cases, immunosuppressive agents may be used.
Anterior necroti8ing scleritis /ithout inflammation $scleromalacia perforans%: As no effective
treatment is available, grafts of preserved sclera or lyophili,ed dura may be re*uired to preserve the
globe.
BC) ORBITA/ T(MORS
All orbital tumors displace the globe and cause exophtalmos that is associated with limited ocular
motility. 0ome tumors also cause specific additional symptoms.
#02. He"angio"a
.emangiomas are the most common benign orbital tumors in both children and adults. 'hey usually
appear in a nasal superior location. 1apillary hemangiomas are more common in children %they swell when
the child screams&, and cavernous hemangiomas are more common in adults. 'reatment is only indicated
where the tumor threatens to bloc/ the visual axis with resulting amblyopia or where there is a ris/ of
compressive optic neuropathy. 1apillary hemangiomas in children may be treated with cortisone or low+
dose radiation therapy.
#0!. )er"oid and e*ider"oid !$st
'hese lesions are the most common orbital tumors in children. Etiologically, they are dermal or
epidermal structures that have been displaced into deeper layers. .owever, they usually are located anterior
to the orbital septum %and therefore are not in the orbit itself&. Eesions located posterior to the orbital
septum usually become clinically significant only in adults. 'reatment consists of complete removal.
#0A. Meningio"a
A meningioma can be from the optic nerve %meningioma of the optic nerve sheath& or from within the
cranium %sphenoid meningioma&. 0ymptoms vary according to the location. Exophtalmos, limited motility,
and compressive optic neuropathy can result. .yperostoses are fre*uent findings on Q+ray. 'reatment
consists of neurosurgical removal of the tumor. 'he average age of patients is !2-
#07. Histio!$tosis >
'his is a generic form for the proliferation of EangerhansI cells of undetermined etiology.: all ! of the
following types can cause exophtalmos in case of ocular involvement: Eetterer+0iwe disease %malignant&,
.and+0chuller+1hristian disease %benign&, and eosinophilic granuloma %rare and benign&.
#0=. / $"*ho"a
Eymphomas can occur in isolation or in systemic disease. 'he disorder may be treated by radiation or
chemotherapy. 'hey are usually slightly malignant. 'he highly malignant Cur/ittIs lymphoma, which has a
high affinity for the orbital cavity, is a notable exception.
#03. Rha%do"$osar!o"a
'his is the commonest primary malignant tumor in children. 'he tumor often growth very rapidly.
Cecause of the accompanying inflammation, a differential diagnosis should exclude orbital cellulitis. 8ith
modern treatment programs, such as chemotherapy and radiation therapy, treatment is possible in many
cases.
#0H. Metastases
In children, the incidence of metastasis is higher in the orbital cavity than in the choroid. In adults,
it is exactly the opposite. 'he most common orbital metastases in children originate from neuroblastomas.
$alignant tumors from ad2acent tissue can also invade the orbital cavity.
CA) PAI+ I+ A+) ARO(+) THE EYE
Acute eye pain and headaches attributed to the eyes are very common.
.eadache and asthenopia %eye wea/ness, pain, eyestrain& is the most common human complaint,
and there is an association with common refractive errors, such as hyperopia or astigmatismus %see topic
#A&. $yopic patients never have headache or asthenopia because of their refractive error-
Eye pain, on the other hand, most often reflects an eye in2ury or disease locali,ed in the eye. An
exception is the deep bilateral discomfort associated with viremia and fever, which represents the local
ophthalmic myalgic response of a more generali,ed systemic process.
Eye pain may be superficial or !eep. 0uperficial discomfort is most often caused by irritation or
fran/ in2ury of the corneal epithelium or con2unctiva. 'he cornea is richly supplied with pain nerve fibers,
which are very close to the surface. 'he superficial discomfort associated with a foreign body, corneal
abrasion, actinic /eratitis, or hypoxic /eratitis is usually completely relieved by a topical anesthetic + a
useful point in the differential diagnosis. 'he deep pain of iritis and acute glaucoma, on the other hand, is
not.
#0B. Cornea #oreign %od$ %see topic 22C&
##0. Cornea erosion %see topic 22C&
###. A!tini! 2eratitis
Etiology:
It is possible for the cornea, li/e for other epithelial tissue, to be >sunburnt?. Affected persons
usually present with symptoms = to #2 hours after extensive exposure to ultraviolet light, so that this is
a common night+time emergency department presentation. Except for natural sunlight, sun lamps may
also be responsible. >0un+blindness? is caused by the exposure of the cornea to the sunlight reflected
off snow on the ground in high mountains.
0ymptoms:
'ypically the patient is in acute distress %feeling >acute blindness?&, fre*uently having been
awa/ened from sleep by severe burning eye pain, usually bilateral. Although the pain may be mild, it is
most often very severe, with tearing, in2ection, and photophobia resulting in mar/ed blepharospasm.
'here is a dramatic and welcome relief achieved by topical anesthetic. 0lit+lamp examination after
fluorescein dyeing reveals upta/e in the area defined by the width of the palpebral fissure.
'reatment:
'his disorder is best treated with short+acting cycloplegic agent and antibiotic ointment. 'he
patient should be instructed that the symptoms will resolve completely within 2A to AH hours. 'he
patient should be at rest, in a dar/ened room, and eye movements should be avoided.
##2. Conta!t ens 2eratitis (h$*o4i! 2eratitis)
'he cornea is avascular, therefore, it receives most of its nutrition and oxygenation via its coating of
tear fluid. Interference with this tear film results in hypoxia. 'he clinical syndrome is most often seen
with hard contact lenses. 'ypically, the patient was wearing his contact lenses for an unusually long
period, thus causing prolonged tear film interruption. 'he effect is, that the cornea >suffocates?.
5ollowing a latent period of = to #0 hours after removal, the patient presents with bilateral eye pain
ranging from mild foreign body sensation to severe pain with blepharospasm and tearing.
Examination shows in2ected eyes, relief with topical anesthesia, and fluorescein upta/e in the centre of
the cornea, corresponding to the area covered by the lens.
'reatment:
Ei/e actinic /eratitis. 'he lenses should not be worn until symptoms are entirely gone.
##!. A!&te iritis %anterior uveitis& %see topic 2#A and #HA&
##A. A!&te ange !os&re ga&!o"a %see topic 71&
CB) OCC/(SIO+ OF THE CE+TRA/ RETI+A/ ARTERY
It refers to a retinal infarction due to occlusion of an artery in the lamina cribrosa or a branch
retinal artery occlusion.
Epidemiology:
4etinal artery occlusion occurs significantly less often than vein occlusion.
Etiology:
Emboli are fre*uently the cause. Eess fre*uent causes include inflammatory processes such as temporal
arteritis %accompanied by headache&.
0ymptoms:
In central retinal artery occlusion, the patient generally complains of sudden, painless unilateral blindness.
In branch retinal artery occlusion, the patient will notice a loss of visual acuity or visual field defects.
6iagnosis:
It is made by ophtalmoscopy. In the acute stage of central occlusion, the retina appears grayish
white due to edema of the layer of optic nerve fibers and is no longer transparent. )nly the fovea centralis,
which contains no nerve fibers, remains visible as a >cherry red spot? because the red of the choroid shows
through at this site. 'he column of blood will be seen to be interrupted. 4arely one will observe an
embolus. Atrophy of the optic nerve will develop in the chronic stage of central retinal artery occlusion.
In branch retinal artery occlusion, a retinal edema will be found in the affected area of vascular
supply.
(erimetry %visual field testing& will reveal a total visual field defect in central occlusion and a
partial defect in branch occlusion.
6ifferential diagnosis:
Eipid+storage diseases that can also create a cherry red spot such as 'ay+0achs disease, Diemann+(ic/
disease, or @aucherIs disease should be excluded.
'reatment:
Emergency treatment is often unsuccessful even when initiated immediately. )cular massage, medications
that reduce intraocular pressure, or paracentesis are applied in an attempt to drain the embolus in a
peripheral retinal vessel. 1alcium antagonists or hemodilution are applied in an attempt to improve vascular
supply.
1linical course and prognosis:
'he prognosis is poor because of irreparable damage to the inner layers of the retina occurs within one
hour. Clindness usually cannot be prevented in central occlusion. 'he prognosis is better when only a
branch of the artery is occluded unless a macular branch is affected.
CC) +EO+ATA/ CO+,(+CTIVITIS
##7. +eonata gono!o!!a !on-&n!tivitis
Epidemiology and etiology:
'he incidence of neonatal gonococcal con2unctivitis %also called gonorrheal ophtalmia or ophtalmia
neonatorum due to D. gonorrhoae& in the <0A is 2 to !;#0,000 live births. It is caused by Deisseria
gonorrhoae ac*uired from infected mother during parturition.
0ymptoms:
It produces an acute purulent con2unctivitis that appears 2 to 7 days after birth. 'he infant has severe eyelid
edema followed by chemosis and profuse purulent discharge that may accumulate under the tight and
swollen eyelids. 8hen the babyIs eyes are opened, the pus can s*uirt out under pressure and cause
dangerous con2unctivitis in the examinerIs own eyes. 'herefore, the examiner should always wear eye
protection in the presence of suspected gonococcal infection- @onococci can penetrate the eye even in the
absence of a corneal defect and lead to loss of the eye-
6iagnosis:
'he first procedure should be a culture and @ram stain of a con2unctival specimen. @onococcal infection is
suggested microscopically by intracellular gram+negative, coffee bean+shaped diplococci.
6ifferential diagnosis: %#0 of the newborn have con2unctivitis ---&
)ther possible causes of ophtalmia neonatorum %neonatal con2unctivitis& include:
Cha"$dia %see below&
Her*es si"*e4 vir&s %see topic AA + .erpetic eye diseases&
Other %a!teria s&!h as Pse&do"onas8 Sta*h$o!o!!&s8 Stre*to!o!!&s8 or He"o*hi&s in#&en0ae +
'he onset is in the A
th
+ 7
th
day of life, the discharge is mucopurulent, @ram+positive or @ram+negative
organisms are identified.
To4i! %silver nitrate + 1redeIs prophylaxis& + 'he onset is within hours, it is characteri,ed by hyperemia
and slight watery to mucoid discharge&
)ther causes of purulent discharge:
+eonata da!r$o!$stitis + It only becomes symptomatic 2 to A wee/s after birth, with reddening and
swelling of the region of the lacrimal sac and purulent discharge from the puncta.
(rophylaxis:
<se of # silver nitrate %1redeIs method&, antibiotic ophtalmic ointments or drops instilled into each eye
after delivery are recommended. Done of these agents prevent 1hlamydial ophtalmia ---
'reatment:
'opical administration of broad+spectrum antibiotics %gentamicin eyedrops every hour& and systemic
penicillin %penicillin @ IJ& or cephalosporin in the presence of penicillinase+producing strains.
##=. +eonata !on-&n!tivitis !a&sed %$ Cha"$dia
Epidemiology and etiology:
1hlamydia ophtalmia is caused by 1hlamydia trachomatis ac*uired during parturition. It occurs in 2 to A
of live births and may account for !0 to 70 of neonatal con2unctivitis. About A0 of infants born to
affected women develop con2unctivitis and about #7 develop pneumonia.
0ymptoms:
It usually occurs 7 to #A days after birth. It may range from mild con2unctivitis with minimal mucopurulent
discharge to severe eyelid edema with copious drainage and pseudomembrane formation. 5ollicles are not
present in the con2unctiva, as they are present in older children and adults.
6iagnosis:
It is best diagnosed in tissue culture. 'he direct monoclonal antibody tests detecting chlamydiae in smears
and EEI0As detecting chlamydiae in con2unctival cultures are very sensitive.
6ifferential diagnosis: %see topic ##C + )phtalmoblenorrhea&
'reatment:
0ystemic and topical erythromycin eyedrops 7 times daily. It is essential to examine the parents and include
them in therapy.
1DA) A+ATOMY A+) F(+CTIO+ OF THE OPTIC +ERVE A+) VIS(A/ PATHEAY
a) O*ti! nerve
'he optic nerve consists of an intraocular, an intraorbital, and an intracranial portion. 'he
intraocular portion is visible on ophtalmoscopy as the optic dis/. All retinal nerve fibers merge into the
optic nerve here, and the central retinal vessels enter and leave the eye here. 'he complete absence of
photoreceptors at this site creates a gap in the visual field /nown as the blind spot. 'here is a wide range of
physiologic variability in the si,e of the optic dis/. 'he normal color is yellowish orange. 'he margin of the
dis/ is sharply defined and readily distinguished from the surrounding retinal tissue. 'he normal optic dis/
is not prominent.
)ptic cup is the slightly eccentric cavitation of the optic nerve. It is the brightest part of the optic
dis/. Do nerve fibers exit from it. 'he si,e of the optic cup correlates with the si,e of the optic dis/.
Cecause enlargement of the optic cup means a loss of nerve fibers, it is particularly important to document
the si,e of the optic cup. 'his is specified as the ratios of cup to dis/ diameter %cup;dis/ ratio&.
1entral retinal artery and vein enter the eye slightly nasal to the centre of the dis/. Jisible
pulsation in the vein is normal. Arterial pulsation is always abnormal. 'he optic dis/ receives its blood
supply from the ring of Ginn, an anastomotic ring of small branches of the short posterior ciliary arteries
and the central retinal artery.
'he intraorbital portion begins after the nerve passes through scleral connective tissue, the lamina
cribrosa. After the nerve passes through the optic canal, the intracranial portion begins. Ei/e the brain, the
intraorbital and intracranial portions are surrounded by dura mater, pia, and arachnoid.
%) Vis&a *ath<a$
'he anatomy of the visual pathway may be divided into = separates parts:
##3. Optic nerve: 'his includes all of the optic nerve fibre bundles of the eye
##H. Optic chiasm: 'his is where the characteristic crossover of the nerve fibers of both optic nerves
occurs. 'he fibers from the temporal halves of the retinas do not cross the midline but continue into the
optic tract of the ipsilateral side. 'he fibers of the nasal halves cross the midline and there enter the
contralateral optic tract.
##B. Optic tract: 'his includes all of the ipsilateral optic nerve fibers and those that cross the midline.
#20. 'ateral geniculate bo!y: 'he optic tract ends here. 'he third neuron connects to fourth here,
which is why atrophy of the optic nerve does not occur in lesions beyond the lateral geniculate body.
#2#. Optic ra!iations $geniculocalcarine tracts%: 'he fibers of the inferior retinal *uadrants pass
through the temporal lobes: those of the superior *uadrants pass through the parietal lobes to the
occipital lobe and from there to the visual cortex.
#22. Primary visual area %striate cortex or CrodmannIs area #3 of the visual cortex&: 'he nerve fibers
diverge within the primary visual area: the macula lutea accounts for most of these fibers. 'he macula
is represented on the most posterior portion of the occipital lobe. 'he central and intermediate
peripheral regions of the visual field are represented anteriorly. 'he temporal part of the visual field,
only present unilaterally, is represented farthest anteriorly.
)ther connections extend from the visual cortex to associated centres and oculomotor areas
%parastriate and peristriate areas&.
Aside from the optic tract there is also another tract /nown as the retinohypothalamic tract. 'his
tract is evolutionarily older and diverges from the optic chiasm. It transmits light impulses for metabolic
and hormonal stimulation to the diencephalon and pituitary gland system and influences the circadian
rhythm.
1DB) )IFFERE+TIA/ )IA'+OSIS OF THE FRE) EYEF ( see aso to*i! .3B)
A primary care physician fre*uently encounters patients who complain of a red eye. 'he condition
of the red eye is often a simple disorder such as subcon2unctival hemorrhage or an infectious con2unctivitis.
'hese conditions either will resolve spontaneously or can be treated easily by the primary care physician.
)ccasionally, the condition is a more serious disorder and the patient re*uires immediate attention of an
ophthalmologist.
6isorders associated with a red eye:
#2!. Acute+angle closure glaucoma
An uncommon form of glaucoma due to sudden and complete occlusion of the anterior chamber angle
by iris tissue: serious. 'he more common chronic open+angle glaucoma causes no redness of the eye.
#2A. Iritis or iridocyclitis
An inflammation of the iris alone or of the iris and ciliary body: often manifested by ciliary in2ection:
serious.
#27. .erpes simplex /eratitis
An inflammation of the cornea caused by the herpes simplex virus: common, potentially serious: can
lead to corneal ulcerations.
#2=. 1on2unctivitis
.yperemia of the con2unctival blood vessels. 1ause may be bacterial, viral, allergic, or irritative:
common, often not serious.
#23. Episcleritis
An inflammation of the episclera: uncommon, without discharge, not serious, possible allergic,
occasionally painful.
#2H. 0cleritis
An inflammation of the sclera: uncommon, often protracted, usually accompanied by pain: may
indicate serious systemic disease such as collagen+vascular disorder: potentially serious to the eye.
#2B. Adnexal disease
Affects the eyelids, lacrimal apparatus, and orbit: includes dacryocystitis, hordeolum, and blepharitis.
4ed eye can also occur secondary to lid lesions %such as basal cell carcinoma, s*uamous cell
carcinoma, or molluscum contagiosum&, thyroid disease, and vascular lesions in the orbit.
#!0. 0ubcon2unctival hemorrhage
An accumulation of blood in the potential space between the con2unctiva and the sclera: rarely serious.
It usually clears in about 2 wee/s.
#!#. (terygium
An abnormal growth consisting of a fold of tissue that advances progressively over the cornea, usually
from the nasal side: usually not serious. $ost cases occur in tropical climates. 0urgical excision is
indicated if the pterygium starts to grow in the visual axis.
#!2. Meratocon2unctivitis sicca
A disorder involving the con2unctiva and sclera resulting from lacrimal deficiency: usually not serious.
#!!. Abrasions and foreign bodies
.yperemia can occur in response to corneal abrasions or foreign+body in2ury.
#!A. 0econdary to abnormal lid function
CellIs palsy, thyroid ophthalmopathy, or other lesions causing ocular exposure, such as that which
occurs in some comatous patients, can result in a red eye: potentially serious.
1DC) PAPI//E)EMA
It is a bilateral optic dis/ edema secondary to increased intracranial pressure.
Etiology:
A full explanation of the papilledema is lac/ing. It is thought that increased intracranial pressure
and impeded axonal plasma flow through the narrowed lamina cribrosa cause nerve fiber edema. .owever,
there is no definite correlation between intracranial pressure and prominence of the papilledema. 0evere
papilledema can occur within a few hours of increased intracranial pressure, such as in acute intracranial
hemorrhage. 'herefore, papilledema is a conditional, unspecific sign of increased intracranial pressure that
does not provide information of the cause or location of a process.
In =0 of all cases, the increased intracranial pressure with papilledema is caused by an
intracranial tumor: A0 of cases are due to other causes such as hydrocephalus, meningitis, brain abscess,
encephalitis, malignant hypertension, or intracranial hemorrhages. 'he patient should be referred to
neurologists, neurosurgeon, or internist for diagnosis of the underlying cause.
(apilledema cannot occur where there is atrophy of the optic nerve, as papilledema re*uires intact
nerve fibers to develop.
Special forms:
oster -ennedy syndrome: 'his refers to isolated atrophy of the optic nerve due to direct tumor
pressure on one side and papilledema due to increased intracranial pressure on the other side.
#ypotension papilledema: 'his refers to a nerve fiber edema due to ocular hypotension. (ossible
causes may include penetrating trauma or fistula secondary to intraocular surgery.
0ymptoms and diagnosis:
Jisual function remains unimpaired for long time. 'his significant discrepancy between morphologic and
functional findings is an important characteristic in differential diagnosis. Early functional impairments
include reversible obscurations. (erimetry testing may reveal an increase in the si,e of the blind spot.
1entral visual field defects and concentric narrowing of the visual field are late functional impairments that
occur with atrophy of the optic nerve.
7he follo/ing phases may be !istinguishe! by ophtalmoscopy:
.arly phase: 5irst the nasal margin and then the superior and inferior margins of the optic disc are
obscured because of the difference in the relative densities of the nerve fibers. 'he optic cup is initially
preserved. 'he optic dis/ is hyperemic due to dilation of the capillaries, and there is no pulsation in the
central retinal vein.
&cute phase: 'his is characteri,ed by increasing elevation of the optic dis/ %disc elevation and small
cup si,e are, alone, not reliable signs of papilledema, as they can be found normally: however, if these
findings are asymmetrical, being present in one eye but not in the other, pathology is suspected&, radial
hemorrhages around the margin of the optic dis/ and grayish white exudates. 'he optic cup is no
longer apparent. 'he color of the optic dis/ will be red or grayish red.
'he papilledematous disc loo/s li/e the reverse of the glaucomatous dis/. In papilledema, the pressure
is elevated outside the eye, in glaucoma, inside the eye. In papilledema, the disc loo/s >angry? with
dilated blood vessels and is elevated, with a small cup. In glaucoma, the disc is pale and depressed,
containing a large scooped out optic cup.
Chronic phase: 0ignificant optic dis/ edema is present. 'he optic cup is obliterated, and the hyperemia
subsides.
&trophic phase: (roliferation of astrocytes results in atrophy of the optic nerve.
6ifferential diagnosis:
(seudopapilledema, optic dis/ drusen, abnormalities of the optic dis/ without functional impairment, optic
dis/ edema with hypertension, and optic neuritis.
'reatment:
Intracranial pressure should be reduced by treating the underlying disorder. )nce intracranial pressure has
been normali,ed, the papilledema will resolve within a few wee/s. <sually atrophy of the optic nerve will
remain
11A) THYROI) EYE )ISEASE + see topic 2#1
11B) C/ASSIFICATIO+S OF '/A(COMAS
Definition: @laucoma is a disorder in which increased intraocular pressure damages the optic nerve. 'his
eventually leads to blindness in the affected eye.
#& Pri"ar$ ga&!o"a refers to glaucoma that is not caused by other ocular disorder.
2& Se!ondar$ ga&!o"a may occur as the result of another ocular disorder or as side effect of medication
or other therapy.
Epidemiology:
It is the second most fre*uent cause of blindness in developed countries after diabetes mellitus. 20 of
blind persons lost their eyesight as a result of glaucoma. About #0 of the population over A0 has increased
intraocular pressure %I)(&. Early detection of glaucoma is one of the highest priorities for the public health
system.
Cassi#i!ation %according to pathophysiology&:
--- 'he many various types of glaucoma are nearly all due to increased resistance to outflow and not to
heightened secretion of a*ueous humor ---
#!7. O*en ange ga&!o"a
#!=. (rimary: It includes over B0 of all glaucomas. )n gonioscopy %see below& the angle is
completely open and structures appear normal. 'he outflow restriction is in the trabecular meshwor/.
#!3. 0econdary: 2 + A of all glaucomas. )n gonioscopy, the angle is completely open. 'rabecular
meshwor/ and secondary occluding cells may be visible. 'he outflow is bloc/ed by erythrocytes,
pigment, and inflammatory cells occluding the trabecular meshwor/.
#!H. Ange !os&re ga&!o"a
#!B. (rimary %pupillary bloc/ glaucoma&: About 7. )n gonioscopy, the angle is occluded. Do angle
structure is visible. 'he iris tissue occludes the trabecular meshwor/.
#A0. 0econdary : 2 + A . 'he angle is occluded. 'here is no angle structure visible. 'he occluding
structures are visible. 'he trabecular meshwor/ is occluded by anterior synechiae, scarring, and
neovasculari,ation of the iris.
#A#. ,&venie ga&!o"a
# of all glaucomas. 'he angle is open on gonioscopy. )ccluding embryonic tissue and lac/ of
differentiation of the trabecular meshwor/ is visible.
#A2. A%so&te ga&!o"a
'his is not a separate form of glaucoma. It describes a painful eye blinded by glaucoma.
)iagnosis o# ga&!o"a;
#A!. )bli*ue illumination of the anterior chamber
In eyes with an anterior chamber of normal depth, the iris is uniformly illuminated. 'his is a sign of a
deep
anterior chamber with an open angle. In eyes with a shallow anterior chamber and closed angle, the
iris
protrudes anteriorly and is not illuminated uniformly.
#AA. 0lit +lamp examination
An anterior chamber that is less than ! times as deep as the thic/ness of the cornea in the centre with a
peripheral depth less than the thic/ness of the cornea suggests a narrow angle.
#A7. @onioscopy
'he angle of the anterior chamber is evaluated with a gonioscope placed directly on the cornea. It is
the examination of choice for identifying specific forms of glaucoma %see 1lassification&.
#A=. $easuring I)( %see topic #=A&
#A3. )ptic dis/ ophtalmoscopy
In the presence of persistently elevated I)(, the optic cup becomes enlarged and gets pale
discoloration. 'he optic nerve is the eyeIs >glaucoma memory?. Evaluating this structure will tell the
examiner whether damage from glaucoma is present and how far advanced it is. (rogressive
glaucomatous changes in the optic dis/ are closely associated with increasing visual field defects.
#AH. Jisual field testing
6etecting glaucoma re*uires documenting glaucomatous visual field defects %method 9 1omputeri,ed
static perimetry&. 6ocumented findings are important in follow+up to exclude any enlargement of the
defects. @laucomatous visual field defects initially manifest themselves in the superior paracentral
nasal visual field.
11C) VITREO(S BO)Y
C asic /nowledge:
'he vitreous body stabili,es the globe although the eye can remain intact without the vitreous
body. It also prevents retinal detachment. 'he gelatineous vitreous body consists of BH water and 2
collagen and hyaluronic acid. It fills the vitreous chamber, which accounts for 2;! of the total volume of the
eye. 'he connections between the vitreous body and retina are generally loose although there may be focal
adhesions. 'hese firmer focal attachments cause problems during vitreous detachment. 'he focal adhesions
between the vitreous body and retina produce focal traction forces that act on the retina and can cause
retinal tears and detachment. 'he vitreous body contains neither blood vessels nor nerves. As a result,
pathogens can multiply undisturbed for a relatively long time.
Examination methods:
'he anterior part can be examined with a slit lamp. An additional contact lens is re*uired to
examine posterior portions. Indirect ophtalmoscopy or retroillumination is used to examine the entire
vitreous body. )pacities will appear as dar/ shadows. <ltrasound is also an alternative.
a) Aging !hanges
11 S$n!h$sis
'he regular arrangement of collagen fibers gradually deteriorates in middle age. 'he fibers
condense to flattened filamentous structures. 'his process, /nown as li*uefaction, creates small fluid+filled
lacunae in the central vitreous body that initially are asymptomatic %patients may report floaters&. .owever,
once li*uefaction has progressed beyond a certain point, the vitreous body can collapse and detach from the
retina.
.1 Vitreo&s deta!h"ent
It is a complete or partial detachment of the vitreous body from its underlying tissue. 'he most
common form is posterior vitreous detachment: anterior or basal detachment is much rarer %e.g. where
strong forces act on the globe as in ocular trauma&.
Epidemiology:
=7 of all patients between the ages of =7 and H7 have posterior vitreous detachment. (atients with axial
myopia have a predisposition to early vitreous detachment. (resumably the vitreous body collapses earlier
in these patients because it must fill a >longer? eye with a large volume.
Etiology:
Ei*uefaction causes collapse of the vitreous body. 'his usually begins posteriorly where the attachments to
the underlying tissues are least well developed.
0ymptoms and findings:
1ollapse of the JC leads to vitreous densities that the patient perceives as mobile opacities. 'hese floaters
%also /nown as flies or cobwebs& may ta/e the form of circular or serpentine lines or points. 'he JC may
detach partially or completely from the retina. An increased ris/ of retinal detachment is present only with
partial vitreous detachment. In this case, the vitreous body and retina remain attached, and eye movements
in this region will place traction on the retina. 'he patient perceives it as flashes of light. If the traction on
the retina becomes too strong, it can tear. 'his increases the ris/ of retinal detachment and vitreous bleeding
from in2ured vessels.
'reatment:
'he symptoms of vitreous detachment resolve spontaneously once the JC is completely detached.
1omplications accompanying partial detachment %retinal tears, retinal detachment, and vitreous
hemorrhage& re*uire treatment.
%) A%nor"a !hanges in the vitreo&s %od$
11 Persistent #eta vas!&at&re (deveo*"enta ano"aies)
'he embryonic vascular system in the vitreous body and lens normally disappear completely,
leaving only the hyaloid canal. (ersistence of the vascular system is referred to as persistent fetal
vasculature. It comprises several clinical units. 'he most important is (.(J.
Persistent h$*er*asti! *ri"ar$ vitreo&s (PHPV)
Definition: (ersistence of the embryonic primary vitreous %hyaloid arterial system including the
posterior tunica vasculosa lentis&. %'he main function of the primary vitreous is normally to supply the
developing lens with nourishment: in /eeping with this function, it consists mainly of a vascular plexus, the
anterior and posterior tunica vasculosa lentis, that covers the anterior and posterior surfaces of the lens&.
Epidemiology:
'his developmental anomaly is rare.
0ymptoms and findings:
<sually the disorder is unilateral.
Anterior variant o# PHPV; 8ith this more fre*uent variant, a white pupil %leu/ocoria or amaurotic catIs
eye& typically will be discovered shortly after birth. 'his is caused by the whitish plate of connective tissue
posterior to the lens. 6epending on the severity, it will be accompanied by changes in the lens leading to
impaired vision. In extreme cases, the lens resembles an opacified membrane %membranous cataract&.
@rowth of the eye is retarded. 'his results in microphtalmos unless drainage of the a*ueous humor is also
impaired, in which case buphtalmos %hydrophtalmos& will be present.
Posterior variant o# PHPV: 4etinal detachment and retinal dysplasia can occur. Eeu/ocoria will not be
present. 'he reduction in visual acuity is present in severe retinal changes.
6ifferential diagnosis: )ther causes of leu/ocoria %see topic 22A&
'reatment:
'he decreased visual acuity cannot be improved. 0urgery is indicated in case of complications, where the
goal is to save the eye and maintain existing visual acuity.
.1 Vitreo&s he"orrhage
It is a bleeding into the vitreous chamber or a space created by vitreous detachment.
Epidemiology:
'he annual incidence is 3 cases per #00 000.
Etiology:
It may involve one of the ! possible pathogenetic mechanisms:
#AB. Cleeding from normal retinal vessels as can occur as a result of mechanical vascular damage in
acute vitreous detachment or retinal tear.
#70. Cleeding from a%normal retinal vessels as can occur as a result of retinal neovasculari,ation in
ischemic retinopathy or retinal macroaneurysms.
#7#. /nflux of %lood from the retina or other sources such as the subretinal space or the anterior
segments of the eye.
$ore fre*uent causes of vitreous hemorrhage include:
(osterior vitreous detachment with or without retinal tears %!H&
(roliferative diabetic retinopathy %!2&
Cranch retinal vein occlusion %2&
Age+related macular degeneration %2&
4etinal macroaneurysms %2&
Eess fre*uent causes include retinal vascular tumors or penetrating trauma.
0ymptoms:
(atients report the sudden occurrence of blac/ opacities that they may describe as >swarms of blac/ bugs?
or >blac/ rain?. 'hese are different from the brighter and less dense floaters seen in synchysis and vitreous
detachment. 0evere bleeding can reduce visual acuity.
6iagnosis:
.emorrhages into the vitreous body spread diffusely and coagulation occurs *uic/ly. It re*uires
examination with an ophtalmoscope or contact lens. <ltrasound is indicated in severe bleedings. Cleeding
in the tissues ad2acent to the vitreous body can produce a characteristic fluid meniscus.
'reatment and prognosis:
(atients should be placed in an upright resting position %the bleeding stops spreading and the blood will
settle more *uic/ly. Dext the cause of the hemorrhage should be treated. Jitrectomy is re*uired to drain
hemorrhage that is not absorbed. 0pontaneous absorption is a long process.
31 Vitritis and endo*hta"itis
'his refers to acute and chronic intraocular inflammation due to microbial or immunologic causes.
In the strict case, any intraocular inflammation is endophtalmitis. .owever, in clinical usage,
endophtalmitis refers only to microbial inflammation involving the vitreous body %vitritis&. )n the other
hand, isolated vitritis is not possible due to the avascularity of the vitreous chamber.
Epidemiology:
It occurs most fre*uently as a result of penetrating trauma. 4arely it is a complication of surgery.
Etiology:
Cecause the vitreous body consists of only few cells, inflammation is only possible when the inflammatory
cells gain access to the chamber from the uveal tract or retinal blood vessels. 'his may occur via:
Mi!ro%ia *athogens %bacteria, fungi, or viruses& enter the chamber either through direct
contamination %trauma or surgery& or metastatically as a result of sepsis %common in
immunocompromised patients, especially fungal + 1andida&. 'he virulence and the individualIs
immune status influence whether an acute, subacute, or chronic inflammation will develop. Cacterial
inflammation is far more fre*uent than viral or fungal.
In#a""ator$ ("i!ro%ia or a&toi""&ne) *ro!esses in str&!t&res ad-a!ent to the vitreo&s %od$8
such as uveitis or retinitis can precipitate a secondary reaction in the vitreous chamber.
--- Acute endophtalmitis is a serious syndrome that can result in loss of the eye within a few hours ---
0ymptoms:
Acute inflammation or en!ophtalmitis: It includes acute loss of visual acuity accompanied by deep dull
ocular pain that responds only minimally to analgesics. 0evere reddening of the con2unctiva is present. In
contrast to bacterial or viral, mycotic endophtalmitis begins subacutely %slowly worsening visual
impairment&. 6ays later, this will also be accompanied by severe pain.
#hronic inflammation an! en!ophtalmitis: 'he course is far less severe, and loss of visual acuity is
moderate.
6iagnosis:
Acute: 0lit+lamp examination will reveal massive con2unctival and ciliary in2ection accompanied by
hypopyon %collection of pus in the anterior chamber&. )phtalmoscopy will reveal yellowish+green
discoloration of the vitreous body. If the view is obscured, ultrasound can help in evaluation.
#hronic: Examination reveals moderate ciliary and con2unctival in2ection. 0lit+lamp reveals infiltration of
the vitreous body by inflammatory cells.
A con2unctival smear, vitreous aspirate, and blood cultures will identify the pathogen.
'reatment:
Micro%ial inflammations re*uire pathogen+specific systemic, topical, and intravitreal antimicrobial therapy.
Secondary inflammations: 'he underlying disorder should be treated.
(rophylaxis:
Intraocular surgery re*uires extreme care to avoid contamination. ---6ecreased visual acuity and eye pain
in substance abusers and patients with indwelling catheters suggest 1andida endophtalmitis---
1linical course and prognosis:
5or acute course, the prognosis depends on the virulence of the pathogen and *uic/ therapy. Extremely
virulent pathogens and delayed treatment causes decreased visual acuity. 8ith postoperative inflammation,
an immediate vitrectomy can improve the course. 'he prognosis is better for chronic forms.
#72. The roe o# the vitreo&s %od$ in vario&s o!&ar !hanges and #oo<ing !atara!t s&rger$;
#7!. *etinal !etachment: 'he close connection between the vitreous body and retina can result in
retinal tears in vitreous detachment, which in turn can lead to rhegmatogenous retinal detachment.
'hese retinal defects provide an opening for cells from the retinal pigment epithelium to enter the
vitreous chamber. 'hese pigments cells migrate along the surface of the retina. As they do so, they act
similarly to myofibroblasts and lead to the formation of subretinal and epiretinal membranes and cause
contraction of the surface of the retina. 'his clinical picture is referred to as proliferative
vitroretinopathy %(J4&. 'he rigid retinal folds and vitreous membranes in (J4 complicate
reattachment of the retina. 'his re*uires modern techni*ues of vitreous surgery.
#7A. *etinal vascular proliferation: It can occur in retinal ischemia in disorders such as diabetic
retinopathy, retinopathy in preterm infants, or central or branch retinal vein occlusion. @rowth of this
retinal neovasculari,ation into the vitreous chamber usually occurs only where vitreous detachment is
absent or partial because these proliferations re*uire a substrate to grow on. (reretinal proliferations
often lead to vitreous hemorrhage. 5ibrotic changes produce traction of the retina resulting in a
tractional retinal detachment.
#77. #ataract surgery: (ostoperative inflammation in the anterior segment can progress through the
hyaloid canal to the posterior pole of the eye and macular edema can develop. 'his complication
occurs particularly following cataract surgery in which the posterior lens capsule was opened with
partial loss of vitreous body.
#7=. S&rgi!a treat"ent; Vitre!to"$
It is surgical removal and replacement of the vitreous body with 4ingerIs solution, gas, or silicone oil.
Indications:
<nabsorbed vitreous hemorrhage
'ractional retinal detachment
(roliferative vitroretinopathy
4emoval of intravitreal displaced lenses or foreign bodies
0evere postoperative or post+traumatic inflammatory vitreous changes
(rocedure:
'he vitreous body cannot simply be aspirated from the eye as the vitreoretinal attachments would also
cause retinal detachment. 'he procedure re*uires successive, piecemeal cutting and aspiration with a
vitrectome %a speciali,ed cutting and aspirating instrument&. Aspiration is accompanied by
simultaneous infusion to prevent the globe from collapsing. 'he three instruments %infusion cannula,
light source, and vitrectome& are introduced into the globe through the pars plana, which is why the
procedure is referred to as pars plana vitrectomy. 'his site has the least ris/ of iatrogenic retinal
detachment. In many cases, such as with unabsorbed vitreous hemorrhage, the eye is filled with
4ingerIs solution following vitrectomy. In case of complicated retinal detachment, filling the eye with
4ingerIs solution is not sufficient and the detached retina must be flattened and held with a tamponade
of fluid with a very high specific gravity. Eater, these >heavy? li*uids must be replaced by gases or
silicone oil. .owever, silicone oil leads to cataract formation and therefore, it must be removed in a
second operation.
1. A) A+OMA/IES OF THE EYE/I) POSITIO+
#73. Entro*ion
Entropion is characteri,ed by inward rotation of the eyelid margin. 'he margin of the eyelid and
eyelashes or even the outer s/in of the eyelid are in contact with the globe instead of the con2unctiva.
'he following forms are differentiated according to their origin:
#7H. #ongenital ectropion
#7B. Spastic ectropion
#=0. #icatrical ectropion
Etiology:
#=#. #ongenital entropion: It occurs more fre*uently among Asians but is rare in Europeans,
in whom the spastic and cicatrical forms are more commonly encountered. It results from fleshy
thic/ening of the s/in and orbicularis oculi muscle near the margin of the eyelid. <sually the
lower lid is affected. 'he condition may persist into adulthood.
#=2. Spastic entropion: 'his affects only the lower eyelid. 0everal pathologic factors are
usually involved:
'he structures supporting the lower eyelid %palpebral ligaments, and tarsus& may become lax
with age, causing the tarsus to tilt inward.
'his causes displacement of the fibers of the orbicularis oculi muscle resulting in permanent
contact between the eyelashes and the eyeball. 'his intensifies the blepharospasm.
0enile enophtalmos, usually occurring in old age as a result of atrophy of the orbit fatty tissue,
further contributes to instability of the lower eyelid.
#=!. #icatrical entropion: 'his form of entropion is fre*uently the result of postinfectious or
post+traumatic tarsal contracture %such as trachoma, burns and chemical in2uries&. 1auses can also
include allergic and toxic reactions %pemphigus, 0tevens+Rohnson syndrome&.
0ymptoms:
1onstant rubbing of the eyelashes against the eyeball %trichiasis& represents a permanent foreign+
body irritation of the con2unctiva which causes a blepharospasm that in turn exacerbates the entropion.
'he chronically con2unctiva is reddened, and the eye fills with tears. )nly congenital entropion is
usually asymptomatic.
'reatment:
#=A. #ongenital entropion: Either not re*uired or surgical
#=7. Spastic an! cicatrical entropion: 0urgical.
An adhesive bandage may be applied to increase tension on the eyelid for temporary relief of
symptoms.
(rognosis:
1ongenital entropion often resolves within the first few months of life. 'he prognosis of spastic and
cicatrical entropion is good with prompt surgical intervention. Eeft untreated, there is a ris/ of damage
to the corneal epithelium with superinfection which may progress to a serpiginous corneal ulcer.
#==. E!tro*ion
It is a condition in which the margin of the eyelid is turned away from the eyeball. It almost always
affects the lower eyelid. 'he following forms are differentiated:
#=3. #ongenital ectropion
#=H. Senile ectropion
#=B. Paralytic ectropion
#30. #icatrical ectropion
Etiology:
#3#. #ongenital: It is very rare and usually associated with other developmental anomalies of
the eyelid and face.
#32. Senile: 'he palpebral ligaments and tarsus may become lax with age, causing to sag
outward. It is the most prevalent form.
#3!. Paralytic: 'his is caused by facial paralysis with resulting loss of function of the
orbicularis oculi muscle that closes the eyelid.
#3A. #icatrical: Ei/e cicatrical entropion, this form is usually a se*uela of infection or in2ury.
0ymptoms:
Eeft untreated, incomplete closure of the eyelids can cause desiccation of the cornea including
ulceration from lagophtalmos. At the same time, the eversion of the punctum causes tears to flow down
across the chee/ instead of draining to the nose. 8iping away the tears increases the ectropion. 'his
results in chronic con2unctivitis and blepharitis.
'reatment:
1ongenital, senile, and cicatrical ectropion re*uire surgery.
(aralytic ectropion: Artificial tear solutions, eyeglasses with anatomic lateral protection, or a
>watch glass bandage may prevent desiccation of the cornea. In severe cases, surgery is re*uired.
(rognosis:
It is favorable when treated promptly. 0ometimes several operations will be re*uired.
#37. Ptosis
It is paralysis of the levator palpebrae muscle with resulting drooping of one or both upper eyelids.
5ollowing forms are differentiated:
#3=. #ongenital ptosis
#33. Acuire! ptosis
Paralytic
Sympathetic
Myotonic
Traumatic

Etiology:
#3H. #ongenital: It is usually hereditary. 'he cause is aplasia in the core of the oculomotor
nerve %neurogenic& that supplies the levator palpebrae muscle: less fre*uently it is due to
underdeveloped levator palpebrae muscle %myogenic&.
#3B. Acuire!:
,eurogenic causes: )culomotor palsy %paralytic ptosis&. Eesions in the sympathetic nerve
%sympathetic ptosis& is .ornerIs palsy %ptosis, miosis, and enophtalmos&.
Myogenic ptosis: myasthenia gravis, and myotonic dystrophy.
Traumatic ptosis: can occur after in2uries.
0ymptoms:
'he drooping of the upper eyelid may be unilateral %usually sign of neurogenic cause& or bilateral
%usually sign of myogenic cause&. A characteristic feature of the unilateral form is that the patient
attempts to increase the palpebral fissure frowning %contracting the frontalis muscle&. 1ongenital ptosis
usually affects one eye only.
6iagnosis:
#H0.#ongenital ptosis: 'he affected eyelid is underdeveloped. 'he s/in of the upper eyelid is thin and
smooth. 8hen the patient glances down, the upper eyelid does not move. In case of the upper
eyelid drooping over the center of the pupil always increases the ris/ of amblyopia-
#H#.Acuire! ptosis: (aralytic ptosis in oculomotor palsy is usually unilateral with the drooping eyelid
covering the whole eye. In external oculomotor palsy, only the extraocular muscles are affected,
whereas in complete oculomotor palsy, the inner ciliary muscle and the sphincter pupilae are also
affected. $yasthenia gravis %myogenic ptosis that is often bilateral& is associated with abnormal
fatigue of the striated extraocular muscles. (tosis typically becomes more severe as the day goes
on. 4apidly opening and closing of the eyelids provo/es ptosis in myasthenia gravis and simplifies
the diagnosis.
'reatment:
#H2.#ongenital: 0urgery as *uic/ly as possible to prevent a visual impairment as a result of the ptosis.
#H!.Acuire!: (alsies often resolve spontaneously. 0pecial eyeglasses help in some cases. In more
severe cases, surgery is re*uired.
#HA. Be*haros*as"
It is an involuntary spasmodic contraction of the orbicularis oculi muscle supplied by the facial nerve.
Etiology:
In addition to photosensitivity and increased tear production, blepharospasm will also accompany
inflammation or irritation of the anterior chamber. 1auses of the disorder include extrapyramidal
disease such as encephalitis or multiple sclerosis. 'rigeminal neuralgia or psychogenic causes may also
be present.
0ymptoms:
0pasmodically narrowed or closed palpebral fissures and lowered eyebrows.
'reatment:
'his depends on the cause of the disorder. $ild cases can be controlled by muscle relaxants. 0evere
cases may re*uire transsection of the fibers of the facial nerve. Eocal in2ections of botulinum toxin may
be helpful in some cases.
(rognosis:
It is good where a cause+related treatment is possible. Essential blepharospasm doesnIt respond to
treatment.
1.B) PARA/YTIC STRABISM(S
)phtalmoplegia can affect one or more ocular muscles at the same time. 'he condition may be
partial %paresis, more common& or complete %paralysis, less common&. 'he result is either ga,e palsy or
strabismus %paralytic strabismus&, depending on the cause and severity.
'a0e *as$: Impairment or failure of coordinated eye movements.
Para$ti! stra%is"&s: 0trabismus due to:
+ Isolated limited motility in one eye.
+ Asymmetrical limited motility in both eyes.
'he angle of deviation does not remain constant in every direction of ga,e %as in concomitant strabismus&
but increases in the direction of pull of the paraly,ed muscle. 'his is referred to as an incomitant angle of
deviation.
Etiology and forms:
Congenita o!&ar "otiit$ dist&r%an!es may be due to:
(renatal encephalitis, aplasia of the ocular muscles, birth trauma
A!7&ired o!&ar "otiit$ dist&r%an!es may be due to:
6$, multiple sclerosis, intracranial tumors, arteriosclerosis, central ischemia, AI60, trauma, and other
causes.
)cular motility disturbances are either neurogenic, myogenic, or due to mechanical causes.
#H7. -eurogenic: 'hese are distinguished according to the location of the lesion:
Eesions of the nerves supplying the ocular muscles : 'his condition is referred to as an infranuclear
ocular motility disturbance and is the most common cause of paralytic strabismus.
Eesions of the ocular muscle nuclei : 'his condition is referred to as a nuclear ocular motility
disturbance. 'he oculomotor nuclei supply both sides but the nerves are not close together.
'herefore, bilateral palsy suggests a nuclear lesion, whereas unilateral palsy suggests a lesion of
one nerve.
Eesions of the ga,e centres : 'his condition is referred to as a supranuclear ocular motility
disturbance. It very often causes ga,e palsy.
#H=. +yogenic ocular motility disturbances are rare. 'hese include palsies due to the following cases:
@raveIs disease is the most common cause of myogenic disturbance. Cecause it alters the
contractility of the ocular muscles, it can result in significant motility disturbances.
)cular myasthenia gravis : 'ypical symptoms include fluctuating wea/ness of any muscles. 'he
wea/ness typically increases in severity during the course of the day with fatigue.
1hronic progressive external ophtalmoplegia is usually bilateral, gradually progressive paralysis
of one or more extraocular muscles. In the final stages it result in complete paralysis of both eyes.
Cecause the paralysis is symmetric, the patient does not experience strabismus or double vision.
)cular myositis is inflammation of one or more extraocular muscles.
#H3. +echanical: 'hese include palsies due to:
5ractures: In a blow+out fracture for example, the fractured floor of the orbit can impinge the
inferior rectus. 'his can interfere with upward ga,e and occasionally produce strabismus.
.ematomas
0welling in the orbit or facial bones, such as can occur in an orbital abscess or tumor.
0ymptoms:
0trabismus: (aralysis of one or more ocular muscles can cause its respective antagonist to dominate.
'his results in typical strabismus that allows which muscle is paraly,ed to be determined.
@a,e palsy : 0ymmetrical paralysis of one or more muscles of both eyes limits ocular motility in a
certain direction.
6ouble vision: Eoss of binocular coordination between the two eyes due to ophtalmoplegia leads to
double vision. As the onset of paresis is usually sudden, double vision is the typical symptom that
ma/es the patient to consult a physician. 0ome patients learn to suppress one of the two images within
a few hours, days, or wee/s. )ther patients suffer from persistent double vision.
1ompensatory head posture : 'he patient can avoid diplopia only by attempting to avoid using the
paraly,ed muscle. 'his is done by assuming a typical compensatory head posture in which the ga,e lies
within the binocular visual field: the patient tilts his head and turns it toward the shoulder opposite to
the paraly,ed eye.
)cular torticollis : 'he compensatory head posture in trochlear nerve palsy is the most pronounced and
typical of all cranial nerve palsies. 1ongenital trochlear nerve palsy can lead to what is /nown as
ocular torticollis.
Incomitant angle of deviation : 'he angle of deviation in paralytic strabismus varies with the direction
of ga,e and is not constant as in concomitant strabismus. 'he angle of deviation is greatest when the
ga,e is directed in the direction of pull of the paraly,ed muscle.
6iagnosis of ophtalmoplegia:
Examination of the nine diagnostic positions of ga,e: 'he patient is as/ed to follow the movements of the
examinerIs finger with his eyes only. 'he six cardinal directions of ga,e %right, upper right, lower right, left,
upper left, lower left& provide the most information: upward and downward movements, and straight are
performed with several muscles and therefore do not allow precise identification of the action of a specific
muscle.
'reatment:
0urgery for should be postponed for at least # year to allow possible spontaneous remission. 0evere
diplopia may be temporarily managed by alternately patching the eyes until surgery. 1are must be ta/en to
correctly gauge the angle of deviation. 'he goal of surgery is to eliminate diplopia in the normal visual
field, i.e., with head erect, in both near and distance vision. It will not be possible to surgically eliminate
diplopia in every visual field.
Procedure: 'he antagonist of the respective paraly,ed muscle can be wea/ened. 4esecting or doubling the
paraly,ed muscle can additionally reduce the angle of deviation.
1.C) SEE TOPIC 5C
13A) CO/OR VISIO+8 CO+'E+ITA/ A+) ACG(IRE) )EFECTS OF CO/OR VISIO+
'he perception of color is a cortical response to specific physical stimuli received by the retina. A
narrow band of the electromagnetic spectrum, wavelength between A00 and 300 nm, is capable of being
absorbed by visual pigments contained in cone photoreceptors. 'here are three cone photopigments: blue,
green, and red. A minimal re*uirement for color discrimination is the presence of at least two /inds of cone
photopigment, and normal color vision re*uires the presence of all three.
1olor vision defects are either congenital or ac*uired. 8hile hereditary congenital color defects
are almost always >red+green?, affecting H of males and 0.7 of females, ac*uired defects are more often
of the >blue+yellow? variety and affects males and females e*ually. 1ongenital color defects affect both
eyes e*ually, while ac*uired color defects fre*uently affect one eye more than the other. $ost congenital
color vision defects are Q+lin/ed recessive and are constant in type and severity throughout life. Ac*uired
defects generally vary in type and severity, depending upon the location and source of the usually
ophtalmoscopically observable ocular pathology.
6ichromats are individuals whose cone receptors contain only two of the three cone
photopigments. (ersons with a red+green color deficiency related to red+sensitive pigment loss were
historically described first, and the condition is therefore referred to as protanopia. A second type of red+
green deficiency involving green+sensitive pigment loss is /nown as !euteranopia. Clue+yellow color
blindness is the third form and is referred to as tritanopia. 8hile a color vision defect is present, there is no
acuity loss in these patients.
'he most common color vision deficit is that of anomalous trichromats. 'hese individuals re*uire
three pigments for matching an un/nown color but + unli/e normal trichromats + use them in >anomalous?
amounts.
'here are two forms of monochromatism. In ro! monochromatism, the individual is born without
functioning cones in the retina, and such loss accounts for the associated symptoms of low visual acuity,
absent color vision, photophobia, and nystagmus. 'his condition is can be demonstrated by the
electroretinogram. In cone monochromatism, affected individuals with this extremely rare condition have
no hue discrimination but do have normal acuity and no photophobia and nystagmus. 1one monochromats
do have cone photoreceptors, but all the cones contain the same visual pigment.
1olor vision testing
Dormal color vision re*uires healthy function of the macula and optic nerve. 6epressed color
vision may be a sensitive indicator of certain /inds of ac*uired macular or optic nerve disease. 5or example
in optic neuritis or optic nerve compression %e.g. by a mass&, abnormal color vision is often an earlier
indication than visual acuity.
'he most common testing techni*ue utili,es a series of polychromatic plates. 'he plates are made
up of dots of the primary colors printed on a bac/ground mosaic of similar dots in a confusing variety of
secondary colors. 'he primary dots are arranged in simple patterns %numbers or geometric shapes& that
cannot be recogni,ed by patients with deficient color perception.
13B) CORRECTIO+ OF REFRACTIVE ERRORS
#HH. E$egass enses
11 Mono#o!a enses
'here are two basic types:
Spherical lenses refract light e*ually along every axis.
7oric lenses %/nown as cylindrical lenses& refract light only along one axis.
0pherical and toric lenses can be combined where indicated.
.1 M&ti#o!a enses
#HB. $ultifocal lenses differ from the monofocal lenses of uniform refractive power in that
different areas of the lens have different refractive powers. 'hese lenses are best understood as
combinations of two or more lenses in a single lens.
6ifocals: 'he upper and middle portion of the lens is for the distance correction: the lower portion
is for the near+field correction. (atients are able to view distant ob2ects in focus and read using one
pair of eyeglasses, eliminating the need to constantly change glasses. 'he near+field correction can
be placed in a different part of the lens for special applications.
7rifocals: 'hese lenses include a third refractive correction between the distance and near+field
portions. 'his intermediate portion sharply images the intermediate field between distance vision
and reading range without any need for accommodation.
Progressive a!!ition lenses: 'hese lenses were developed to minimi,e abrupt image changes
when the ga,e moves through the different correction ,ones of the lens while maintaining a sharp
focus at every distance. 'hese eyeglasses also offer cosmetic advantages.
0ub2ective refraction testing for eyeglasses:
8hile the patients loo/s at vision charts, the examiner places various combinations of lenses in front of the
patientIs eye. 'he patients reports which of lenses produces the sharpest image. 'his method identifies the
optimal correction. 4efraction testing is performed either with a series of test lenses from a case or with a
(horoptor, which contains many lenses that can be automatically or manually placed before the patientIs
eye.
'he examination has ! steps:
Monocular testing: 'he optimal refraction is determined separately for each eye. 'he wea/est possible
minus lens is used in myopic patients, and the strongest possible plus lens in hyperopic patients.
0inocular testing: 'he aim of this step is to achieve a balance between both eyes.
,ear point testing: 'he final step determines the patientIs near visual acuity, and, if necessary, the
presbyopic addition.
Cefore the lenses are fitted into the frame, the distance between the pupils must be measured to ensure that
the lenses are properly centred. 'he centre of the lens should be in front of the pupil. Eccentric lenses might
otherwise cause asthenopic symptoms such as headache or a burning sensations in the eyes.
#B0. Conta!t enses
Advantages and characteristics:
1ontact lenses are in immediate contact with the cornea. 1ontact lenses differ from the eyeglasses in
that they correct the refractive error closer to the location of its origin. 5or this reason, the *uality of the
optical image through contact lenses is higher than that viewed through eyeglasses. Eenses do not cloud up
in rainy weather or steam, and peripheral distortion is minimi,ed. 'he cosmetic disadvantage of thic/
eyeglasses is also eliminated. 0evere anisometropia %difference in refractive power between the two eyes&
re*uires correction with contact lenses to minimi,e anisei/onia %the si,e difference of two images&.
'he cornea re*uires oxygen from the precorneal tear film. 'o ensure this supply, contact lenses
materials must be oxygen+permeable. 1ontact lenses may be manufactured from rigi! or flexible materials.
11 Rigid !onta!t enses
'hese lenses have a stable shape. (atients ta/e time to become used to them. 'he well fitting
lenses float on the precorneal tear film. Every time the patient blin/s, the lens is displaced superiorly and
then returns to its central position. 'his permits circulation of the tear film.
'oday, highly oxygen+permeable materials such as silicone copolymers are available. 'his
eliminates the limit for daily wearing. 'hese lenses may also remain in the eye overnight in special cases,
such as apha/ic patients.
4igid contact lenses can be manufactured as spherical lenses and toric lenses. 0pherical lenses can
compensate for astigmatism of less than 2.7 diopters. $ore severe astigmatism re*uires correction with
toric lenses. 'hese lenses can even correct severe /eratoconus.
.1 So#t !onta!t enses
'he material, such as hydrogel, is soft. (atients find these lenses significantly more comfortable.
'he higher the water content of the lens, the better the oxygen permeability. .owever, it is typically lower
than that of rigid lenses. 'he material is more permeable to foreign substances, which can accumulate in it.
'he lens is often supported by the limbus. 'he lens is often displaced only a few tenths of a millimetre
when the patient blin/s. 'his greatly reduces the circulation of tear film under the lenses. 'his limits the
maximum daily period that the patients are able to wear them and they have to be removed at night to allow
regeneration of the cornea.
#B#. S*e!ia !onta!t enses
Therapeutic contact lenses: In the presence of corneal erosion, soft ultra+thin lenses act as a bandage
and thereby accelerate epitheliali,ation of the cornea. 'hey also reduce pain. 'hey may also be used in
patients receiving topical medication as they store medication and only release it very slowly.
/ris print lenses: 'hese colored lenses with a clear central pupil are used in patients with aniridia and
albinism.
0ifocal lenses: 'hese lenses allow the use of contact lenses in presbyopic patients. 'he near+field
portion is located at the bottom because the lens is heavier there. 8hen the patient ga,es down to read,
the lens aligns with the pupil and becomes effective. It is also possible to correct one eye for the distant
vision and the fellow eye for near vision. Another possibility %diffraction& allows production of two
images, a distant refractive and a near+field diffractive image. 'he patient chooses the image that is
important at the moment.
6isadvantages of contact lenses:
$echanical influences on the cornea can lead to transient changes in refraction. 'his results in
eyeglassesI blur after removing the lens and putting eyeglasses. 1ontact lenses must be cleaned daily and
disinfected. 'his is time+consuming and more expensive than eyeglass care and is particularly important
with soft lenses. 'he lens material can absorb proteins, brea/down products, medications, disinfectants, and
bacteria and fungi. 'hey also interfere with corneal metabolism. 1ontact lenses are not suitable for patients
with symptoms of /eratocon2unctivitis sicca.
1omplications: %occurring mainly with soft lenses&
/nfectious *eratitis caused by bacteria, fungi, and proto,oans % --- Acanthamoeba /eratitis is a serious
complication often re*uiring corneal transplantation ---&
1iant papillary con$unctivitis: Allergic reaction of the palpebral con2unctiva.
Corneal vasculari2ation: As the result of insufficient supply of oxygen to the cornea.
Severe chronic con$unctivitis: 'his usually ma/es it impossible to continue wearing contact lenses.
!) S&rgi!a re#ra!tive !ornea *ro!ed&res
#B2. Photorefractive *eratectomy
(rinciple: 'issue is ablated to change the corneal curvature and to achieve a refractive correction.
5lattening the corneal curvature corrects myopia, whereas steepening the curvature corrects hyperopia.
'he amount of tissue removed at different sites can be varied with layer+by+layer excimer laser
ablation. 'his ma/es it possible to correct for myopia, by removing more tissue from the centre of the
cornea, or for hyperopia, by removing more tissue from the periphery.
Indications: Cest results are achieved in correcting myopia of less than = diopters.
#B!. 'adial *eratotomy
(rinciple: 1orrection of myopia by flattening the central dome of the cornea with A + #= radial
incisions extending through B0 of the thic/ness of the cornea. 'his increases the steepness of the
corneal periphery and lowers the centre of the cornea, reducing its refractive power. 'his method does
not include the optical centre of the cornea.
Indications: 'he method is suitable for myopia less than = diopters. A disadvantage is refractive
fluctuations of up to #.7 diopters during the course of the day.
#BA. Photorefractive *eratectomy correction of astigmatism
(rinciple: 0urgical reduction of severe regular astigmatism by flattening the steep meridian in the
centre of the cornea by increasing the steepness of the corneal periphery. Irregular astigmatism cannot
be corrected.
Indication: 0evere regular astigmatism
#B7. #olmium laser correction of hyperopia
(rinciple: 'he laser is focus on the corneal stroma to create shrin/age effect. (lacing these areas
symmetrically steepens the central cornea, which can correct severe hyperopia.
Indication: .yperopia correction up to H diopters.
#B=. .pi*eratopha*ia
(rinciple: 0evere myopia and hyperopia are corrected by suturing specially prepared hyperopic or
myopic corneal grafts on to the recipientIs cornea. 'his involves special preparation of the recipients
cornea. 'he donor graft is then fitted into the prepared cornea and sutured in place.
Indications: Any severe hyperopia and myopia.
#B3. .xcimer laser in situ *eratomileusis (+&S/-)
(rinciple: A superficial corneal flap is created with a micro/eratome. 'hen the /eratome is ta/en away,
the flap is hold aside, and the exposed underlying corneal stroma is ablated with an excimer laser to
correct myopia. 'hen the flap is repositioned on the cornea and fixed in place by its own adhesion.
Indication: Even severe myopia %up to #0 +#2 diopters& can be corrected by this method.
13C) SEE TOPIC 3B
15A) )E'E+ERATIVE COR+EA/ )ISEASES1 A+OMA/IES OF COR+EA/ C(RVAT(RE
#BH. )egenerative !ornea diseases
#BB. Ca!i#i! %and 2erato*ath$
After many years of chronic inflammation of the anterior chamber %chronic uveitis and /eratitis& with
shrin/age of the eyeball. 1alcific deposits occur in CowmanIs layer, causing a transverse ,one of
opacification in the region of the palpebral fissure. 'his change significantly impairs vision. 'he
opacification will be completely removed and vision restored with a sodium E6'A solution
200. Peri*hera #&rro< 2eratitis
'his includes a heterogenous group of disorders in terms of morphology and etiology. All are
noninfectious and lead to thinning and melting of the peripheral cornea that may progress to perforation.
Etiologic factors include: Autoimmune processes %e.g. collagenosis&, trophic !ysfunctions %pitting due to
lac/ of tear film&, and un"no/n !egenerative processes) 'hese corneal changes are most fre*uently
observed in patients with rheumatoid arthritis. 'reating the underlying disorder is essential in these cases.
20#. 9erato"aa!ia
It is a special form of the disorder in which vitamin A deficiency causes xerosis of the con2unctiva and
cornea combined with night blindness. 1orneal ulceration with secondary infection is common. 'his
disorder is one of the most fre*uent causes of blindness in the developing countries in which malnutrition is
prevalent.
202. B&o&s 2erato*ath$
It is a condition caused by edema of the cornea, resulting from function failure of the corneal
endothelium.
Epidemiology: It is among the most fre*uent indications for corneal transplants.
Etiology:
'he transparency of the cornea largely depends on a functioning endothelium with a high density of
endothelial cells. 8here the endothelium has been severely damaged by inflammation, trauma, or ma2or
surgery in the anterior eye, the few remaining endothelial cells will be unable to prevent a*ueous humor
from entering the cornea. 'his results in hydration of the cornea with stromal edema.
0ymptoms:
'he gradual loss of endothelial cells causes slow deterioration of vision. 'he patient will typically have
poorer vision in the morning than in the evening, as corneal swelling is greater during the night with the
eyelids closed.
'reatment:
8here damage to the endothelial cells is not too far advanced, hyperosmolar solutions can improve vision
by removing water. .owever, this only a temporary solution. Eater, a corneal transplant is indicated.
%) Ano"aies o# !ornea !&rvat&re
20!. 9erato!on&s
It is a conical, usually bilateral central deformation of the cornea with parenchymal opacification and
thinning of the cornea.
Epidemiology:
It is the most common deformation of the cornea. )ccurrence is familial, although women are more li/ely
to be affected than men. It is progressive and begins between ages #0 to 20.
Etiology:
It is probably a genetic disorder. It has varying paths of hereditary transmissions. 0ometimes it is associated
with 6own syndrome, atopic dermatitis, and other connective tissue disorders %e.g. $arfanIs syndrome&.
0ymptoms:
'he increasing protrusion of the cornea usually produces bilateral irregular myopic astigmatisms. Eeft
untreated, /eratoconus can cause tears of 6escemetIs membrane due to the continuous stretching. 'he
entire cornea can then buldge out at this site. 'his is referred to as /eratoconus. 0ymptoms of acute
/eratoconus include sudden loss of visual acuity accompanied by intense pain, photophobia, and increased
tearing.
6iagnosis: It is made by /eratoscope or ophtalmometer %reflex images will be irregular&.
'reatment:
6egeneration of visual acuity can be corrected initially with eyeglasses: hard contact lenses are re*uired as
the disorder progresses. 'hen the only possibility is penetrating /eratoplasty %transplantation of a corneal
graft from a donor to the patientIs eye&.
(rognosis: 'he prognosis of transplantation is good because the cornea is avascular.
20A. Other !&rvat&re ano"aies o# the !ornea;
9eratogo%&s is a rare congenital deformation resulting in hemispherical protrusion that produces
myopia. 5lattening of the cornea %!ornea *ana& produces hyperopia.
15B) )ACRYOA)E+ITIS (AC(TE A+) CHRO+IC)
207. A!&te da!r$oadenitis
It is an acute inflammation of the lacrimal gland is a rare disorder characteri,ed by intense
inflammation and extreme tenderness to palpation.
Etiology:
'he disorder is often attributable to pneumococci and staphylococci. 'here may be a relationship between
the disorder and infectious diseases such as mumps, measles, scarlet fever, diphteria, and influen,a.
0ymptoms and diagnosis:
It usually occurs unilaterally. 'he inflamed swollen gland is especially tender to palpation. 'he upper eyelid
exhibits a characteristic 0+curve.
6ifferential diagnosis:
Internal hordeolum %smaller and circumscribed&
Eyelid abscess %fluctuation&
)rbital cellulitis %usually associated with reduced motility of the eyeball&
'reatment:
'his will depend on the underlying disorder. $oist, heat, disinfectant compresses, and local antibiotics are
helpful.
1ourse and prognosis:
It is characteri,ed by a rapid clinical course and spontaneous healing with H to #0 days. 'he prognosis is
good.
20=. Chroni! da!r$oadenitis
Etiology:
'he chronic form of inflammation of the lacrimal gland may be the result of an incompletely healed acute
dacryoadenitis. 6iseases such as tuberculosis, sarcoidosis, leu/emia, or lymphogranulomatosis can be
causes of chronic dacryoadenitis. Cilateral chronic inflammation of the lacrimal and salivary glands is
called $i/ulic,Is syndrome.
0ymptoms and diagnosis:
<sually there is no pain. 'he symptoms are less pronounced than in the acute form. .owever, the 0+curve
deformity of the palpebral fissure resulting from swelling of the lacrimal gland is apparent.
'reatment:
'his depends on the underlying disorder. 0ystemic corticosteroids may be effective in unspecific forms.
(rognosis:
It is good when the underlying disorder can be identified and treated.
15!) retina deta!he"ent and its "anage"ent
4etinal detachment refers to the separation of the neurosensory retina from the underlying retinal
pigment epithelium, to which normally it is loosely attached. 'his can be classified into A types:
203. *hegmatogenous retinal detachment results from a tear, i.e., a brea/ in the retina.
20H. 7ractional retinal detachment results from traction, i.e., from vitreous strands that exert tensile
forces on the retina.
20B. Exu!ative retinal detachment is caused by fluid. Clood, lipids, or serous fluid accumulates
between the neurosensory retina and the retinal pigment epithelium. 1oatIs disease is a typical
example.
2#0. 7umor-relate! retinal detachment.
(rimary 46 usually results from a tear. 0econdary 46 may also result from a tear due to other disorders or
in2uries. (roliferative vitreoretinopathy fre*uently develops from a chronic retinal detachment %see topic
##1&.
Epidemiology:
Although 46s are relatively rare, they are significant as they can lead to blindness if not treated
immediately.
*hegmatogenous 46 %most fre*uent form&: Approximately 3 of adults have retinal brea/s. 'he
incidence of this finding increases with advanced age. 'he pea/ incidence is between the 7
th
and 3
th
decades of life. 'he annual incidence is # per #0 000 persons. 'here is a /nown family predisposition,
and 46 also occurs in con2unction with myopia.
Exu!ative1 tractional1 an! tumor-relate! 46s are far less fre*uent.
Etiology:
*hegmatogenous 46: 'his disorder develops from an existing brea/ in the retina. <sually this brea/
is in the peripheral retina, rarely in the macula. 2 types of brea/s are distinguished:
2##. 'ound %rea*s: A portion of the retina has been completely torn out due to a posterior
vitreous detachment.
2#2. #orseshoe tears: 'he retina is only slightly torn.
Dot every retinal brea/ leads to 46. 'his occurs only where the li*uefied vitreous body separates, and
vitreous humor penetrates beneath the retina through the tear. 'he 46 occurs when the forces of adhesion
can no longer withstand this process. 'ractional forces of the vitreous body %usually vitreous strands& can
also cause 46 with or without synchysis %see topic ##1&. In this and every other type of 46, there is a
dynamic interplay of tractional and adhesive forces. 8hether the retina will detach depends on which of
these forces is stronger.
7ractional *D: 'his develops from tractional forces exerted on the retina by preretinal fibrovascular
strands %see topic ##1& especially in proliferative retinal diseases such as diabetic retinopathy.
Exu!ative *D: 'he primary cause of this type is the brea/down of the inner or outer blood+retina
barrier, usually as a result of a vascular disorder such as 1oatsI disease. 0ubretinal fluid accumulates
between the neurosensory retina and the retinal pigment epithelium.
7umor-relate! *D: Either the transudate from the tumor vasculature or the mass of the tumor
separates the retina from its underlying tissue.
0ymptoms:
46 can remain asymptomatic for a long time. In the stage of acute posterior vitreous detachment,
the patient will notice flashes of light %photopsia& and floaters, blac/ points that move with the patientIs
ga,e. A posterior vitreous detachment that causes a retinal tear may also cause avulsion of a retinal vessel.
Clood from this vessel will then enter the vitreous body. 'he patient will perceive this a >blac/ rain?,
numerous slowly falling small blac/ dots. Another symptom is a dar/ shadow in the visual field. 'his
occurs when the retina detaches. 'he patient will perceive a falling curtain or a rising wall, depending on
whether the detachment is superior or inferior. A brea/ in the centre of the retina will result in a sudden and
significant loss of visual acuity, which will include metamorphopsia %image distortion& if the macula is
involved.
6iagnosis:
'he lesion is diagnosed by stereoscopic examination of the fundus with the pupil dilated. 'he
detached retina will be white and edematous and will lose its transparency. In rhegmatogenous 46, a
bright red retinal brea/ will also be visible. 'he tears in rhegmatogenous 46 usually occur in the superior
half of the retina. In tractional 46, the bullous detachment will be accompanied by preretinal grey strands.
In exu!ative 46, one will observe the typical picture of serous detachment: the exudative 46 will
generally be accompanied by massive fatty deposits and often by intraretinal bleeding.
'he tumor-relate! 46 %as can occur with a malignant melanoma& either leads to secondary 46
over the tumor or at some distance from the tumor in the inferior peripheral retina %this is a sign that the
tumor is malignant&. <ltrasound can help in diagnosis.
6ifferential diagnosis:
6egenerative retinoschisis is the primary disorder that should be excluded. A 46 may also be
confused with a choroidal detachment.
'reatment:
4etinal brea/s with minimal circular 46 can be treated with argon laser coagulation. 'he retina
surrounding the brea/ is fused to the underlying tissue whereas the brea/ itself is left open. 'he scars
resulting from laser are sufficient to prevent any further detachment. $ore extensive detachments are
treated with a retinal tampona!e /ith an elastic silicone sponge that is sutured to the outer surface of the
sclera, so called budding procedure. 'his indents the wall of the globe at the retinal brea/ and brings the
portion of the retina in which the brea/ is located bac/ into contact with the retinal pigment epithelium. 'he
indentation also reduces the traction of the vitreous body on the retina. An artificial scar is created to
stabili,e the restored contact between the neurosensory retina and retinal pigment epithelium. 'his is
achieved with a cryoprobe. After a successful operation, this scar prevents recurring retinal detachment.
8here there are several brea/s or the brea/ cannot be located, a silicone cerclage is applied to the globe as
a circumferential buc/ling procedure. 'he procedures described until now are good for uncomplicated
retinal detachments %i.e., without proliferative vitroretinopathy&. In complicated 46s %with proliferative
vitroretinopathy&, the vitroretinal proliferations are excised, and a vitrectomy is performed, in which the
vitreous body is replaced with 4ingerIs solution, gas, or silicone oil. 'hese fluids tamponade the eye from
inside.
(rophylaxis:
.igh+ris/ patients above the age of A0 with a positive family history and severe myopia should be
regularly examined by an ophtalmologist.
1linical course and prognosis:
B7 of rhegmatogenous 46s can be treated with surgery. 8here there has been macular
involvement %i.e., the initial detachment included the macula&, a loss of visual acuity will remain. 'he
prognosis for the other forms of 46 is usually poor, and they are often associated with significant loss of
visual acuity.
16a) *&*i8 dr&g:ind&!ed !hanges o# the *&*i8 a##erent and e##erent *&*iar$ de#e!ts
P&*i
'he pupil refers to the central opening of the iris. It improves the *uality of the resulting image by
controlling the amount of light that enters the eye.
P&*iar$ ight re#e4;
'his reflex arc consists of an afferent path that detects and transmits the light stimulus and an efferent path
that supplies the muscles of the iris.
Afferent path: 'his path begins at the light receptors of the retina, continues along the optic nerve, the
optic chiasm where some of the fibers cross to the opposite side. 'he path continues along the optical
tracts until shortly before the lateral geniculate body. 'here the afferent reflex path separates from the
visual pathway and continues to the pretectal nuclei and from there to both Edinger+8estphal nuclei.
Each of the two pretectal nuclei conducts impulses to both Edinger+8estphal nuclei. 'his bilateral
connection has several conse*uences:
Coth pupils will normally be the same si,e %isocoria& even when one eye is blind.
Coth pupils will narrow even when only one eye is illuminated %consensual light reflex&.
Efferent parasympathetic path.: 'his path begins in the Edinger+8estphal nucleus. Its nerve fibers
form the parasympathetic part of the oculomotor nerve and travel to the ciliary ganglion in the orbit.
(ostganglionic nerve fibers pass through the short ciliary nerves to the effector organ, the sphincter
pupillae muscle. (erliaIs nucleus and the Edinger+8estphal nuclei are also responsible for the near
reflex, which consists of accommodation, convergence, and miosis.
Efferent sympathetic nerve supply to the pupil: 'hree neurons connected by synapses supply the
pupil:
'he central first neuron begins in the posterior hypothalamus, passes the brain stem and the
medulla oblongata to the ciliospinal centre %CudgeIs centre& in the cervical spinal cord.
'he preganglionic second neuron extends from the ciliospinal centre through the white rami
communicantes and sympathetic trun/ to the superior cervical ganglion. It is vulnerable to certain
lesions such as (ancoast tumors because it is immediately ad2acent to the tip of the lung.
'he postganglionic third neuron extends from the superior cervical ganglion as a neural plexus
along the internal carotid artery, ophtalmic artery, and long ciliary nerves to the effector organ, the
dilator pupillae muscle.
+or"a *&*iar$ si0e;
(upil si,e ranges from # mm %miosis& to H mm %mydriasis&.
(upils tend to be larger in teenagers and in dar/ness. 'hey are also wider with 2oy, fear, or surprise due
to increased sympathetic tone, and the person inhales deeply.
(upils tend to be narrower in the newborn due to parasympathetic tone, in the elderly, in light, during
sleep, and when the person is fatigued %due to decreased sympathetic activity&.
In#&en!e o# *har"a!oogi! agents on the *&*i
2#!. Mioti!s
2#A. (arasympathomimetics
Direct parasympathomimetics: Act on acetylcholine receptors of the sphincter pupillae
muscle %miosis& and the ciliary muscle %increased accommodation&. 'hey are used as
glaucoma therapy.
A!et$!hoine has an extremely short duration %several minutes&, therefore, it is not good
as eyedrops because of its rapid brea/down. It is used in intraocularly during cataract
surgery.
Pio!ar*ine is effective for 7+3 hours. 0tandard medication in glaucoma therapy.
Car%a!ho is effective for 3+B hours and has stronger miotic effect than pilocarpine.
0tandard medication in glaucoma therapy.
S In!irect parasympathomimetics: Act by inhibiting acetylcholine esterase. It is used in
glaucoma therapy, but it has important side effects %cataract, higher ris/ of retinal
detachment&.
(hysostigmin is effective for 2 to ! days
(rostigmin is effective for # day
2#7. M$driati!s
2#=. (arasympatholytics: Act by bloc/ing acetylcholine receptors of the sphincter pupillae
muscle %mydriasis& and the ciliary muscle %accommodation paralysis&.
Tro*i!a"ide is effective for A to = hours %shortest acting mydriatic&. <sed for diagnostic
purposes.
C$!o*entoate is effective for #2 to 2A hours and is more cycloplegic than mydriatic.
<sed diagnostically for ob2ective measurement of refraction and therapeutically to relax
the ciliary body %in iritis&.
Ho"atro*ine is effective for # to 2 days. <sed therapeutically %in iritis&.
S!o*oa"ine is effective for # wee/. <sed therapeutically in iridocyclitis or following
surgical repair of retinal detachment.
Atro*ine is effective for # wee/ %longest acting mydriatic&. <sed as scopolamine.
2#3. 0ympathomimetics:
Direct sympathomimetics: Act on the adrenaline receptors of the dilator pupillae muscle. It is
used primarily for diagnostic purposes.
E*ine*hrine is only slightly effective: it is rapidly bro/en down. <sed in diagnosis of
.ornerIs syndrome and in intraocular application %better mydriasis during surgery&.
Phen$e*hrine is effective for = hours. <sed for diagnostic purposes. It has an important
advantage: It does not cause accommodation paralysis.
S In!irect sympathomimetics: Inhibit reabsorption of norepinephrine. used for diagnostic
purposes.
Co!aine 5H is effective for = hours. <sed as eyedrops for diagnostic purposes %e.g.
.ornerIs syndrome&.
--- 6rug+induced mydriasis is contraindicated in patients with a shallow anterior chamber due to the ris/ of
acute angle closure glaucoma ---
P&*iar$ "otor d$s#&n!tion
Isocoria with constricted or dilated pupils is primarily of interest to the neurologist and less to the
ophtalmologist. 'hese disorders will not be discussed here.
Examination methods:
Direct light reflex: 'he examiner first covers both of the patientIs eyes, then uncovers one eye.
Dormally, the pupil will constrict after about 0.2 seconds. 'he other eye is tested in the same manner.
In!irect or consensual light reflex: 'he examiner separates the patientIs eyes by placing his hand on
the patientTs nose. 'he examiner then illuminates one eye while observing the reaction of the other,
non+illuminated eye. Dormally, both pupils will constrict, even the non+illuminated eye.
Evaluating the near reflex: 'he near reflex triad consists of convergence of the visual axis,
accommodation, and constriction of the pupils %miosis&. 'he near ob2ect is tested by having the patient
focus on a distant ob2ect and then on an ob2ect in the near field. 'he near reflex is intact if both eyes
continuously converge with accommodation and miosis as the ob2ect is moved to the near field.
a& A55E4ED' (<(IEEA4P 6E5E1'0
2#H. Iso!oria <ith nor"a *&*i si0e
a) Reative a##erent *&*iar$ de#e!t1
1auses: <nilateral sensory disorder such as retinal detachment, neuritis of the optic nerve, atrophy of the
optic nerve, or retinal vascular occlusion.
6iagnosis:
6irect light reflex is decreased or absent in the affected eye.
'he consensual light reflex in the affected eye is wea/ or absent but normal in the unaffected eye.
Dear reflex is normal.
<nilaterally reduced visual acuity and;or field of vision.
--- <nilateral blindness %afferent defect& does not produce anisocoria ---
%) Biatera a##erent *&*iar$ de#e!t
1auses: Cilateral sensory disorder such as maculopathy or atrophy of the optic nerve.
6iagnosis:
6elayed direct and consensual light reflexes.
Dear reflex is normal.
Cilaterally reduced visual acuity and;or field of vision.
b& E55E4ED' (<(IEEA4P 6E5E1'0
2#B. Aniso!oria <ith diated *&*i in the a##e!ted e$e
220. Co"*ete o!&o"otor *as$
1auses: (rocesses in the base of the s/ull such as tumors, aneurysms, inflammation, or bleeding.
6iagnosis:
6irect and consensual light reflexes without constriction in the affected eye %fixed pupil&.
Dear reflex miosis is absent.
Impaired motility and double vision.
--- 0udden complete oculomotor palsy %loss of motor and parasympathetic function& is a sign of a
potentially life+threatening disorder. In unconscious patients, unilateral mydriasis is often the only clinical
sign of this ---
%) Toni! *&*i
1auses: (ostganglionic damage to the parasympathetic pathway, presumably in the ciliary ganglion, that
fre*uently occurs with diabetes mellitus, alcoholism, viral infection, and trauma.
6iagnosis:
6irect and consensual light reflexes show delayed reaction.
6ilation is also significantly delayed.
Dear reflex is slow but clearly present.
$otility is unimpaired.
(harmacologic testing with 0.# pilocarpine: 0ignificant miosis in the affected eye %denervation
hypersensitivity&, no change in the pupil of the unaffected eye %too wea/&.
--- 'onic pupil is relatively fre*uent and completely harmless cause of unilateral mydriasis ---
22#. Aniso!oria <ith a !onstri!ted *&*i in the a##e!ted e$e
222. HornerIs s$ndro"e
1auses: 6amage to the sympathetic pathway.
#entral $first neuron%: 'umors, encephalitis, diffuse encephalitis
Peripheral $secon! neuron%: 0yringomyelia, diffuse encephalitis, trauma, goiter, aneurysm, processes
in the tip of the lung
Peripheral $thir! neuron%: Jascular processes, internal carotid aneurysm
1linical picture:
22!. Miosis due to failure of the dilator pupillae muscle
2. Ptosis due to failure of the muscle of $ller
!. Eno*hta"os
6iagnosis:
6irect and consensual light reflexes are intact, which distinguishes this disorder from a
parasympathetic lesion, but the pupil dilates more slowly.
Dear reflex is intact
(harmacologic testing with cocaine eyedrops: )n the affected side, there is slight mydriasis. )n the
unaffected side, there is significant mydriasis.
16%) !ha"$dia e$e diseases %see topic B1 as well&
'rachoma is a chronic con2unctivitis caused by 1hlamydia trachomatis and characteri,ed by
progressive excerbations and remissions, with con2unctival follicular hyperplasia, corneal
neovasculari,ation, and scarring of the con2unctiva, cornea, and eyelids.
Epidemiology:
'he disease is endemic in poor countries of Dorth America, the $iddle east, India, and 0outheast Asia. It is
most contagious in its early stages and is transmitted by eye+to+eye contact, by hand+to+eye contact, by eye+
see/ing flies, or by sharing contaminated articles. 'he causative organism is 1. trachomatis serotypes A, C,
and 1.
0ymptoms and signs:
After an incubation period of about 3 days, con2unctival hyperemia, eyelid edema, photophobia, and
lacrimation gradually appear, usually bilaterally. 0mall follicles develop in the upper tarsal con2unctiva and
gradually increase in si,e and number for A wee/s. Inflammatory papillae appear and corneal
neovasculari,ation begins from the limbal vessels. 'his stage may last more than a year, depending on the
therapy. 'he entire cornea may ultimately be involved, reducing vision.
<nless ade*uate treatment is given, the scarring stage follows. 'he follicles and papillae gradually shrin/
and are replaced by scar tissue that often causes entropion and lacrimal duct obstruction. Entropion leads to
further corneal scarring and neovasculari,ation. 0econdary bacterial infection is common. 'he corneal
epithelium becomes dull and thic/ened and corneal ulcers may appear. )n healing, the extent of residual
corneal opacity and vision loss varies.
6iagnosis:
1. trachomatis can be isolated in culture. 'he presence of basophilic cytoplasmic inclusions within
con2unctival epithelial cells differentiates trachoma from acute con2unctivitis. Inclusion bodies are also
found in adult inclusion con2unctivitis, but the clinical picture distinguishes it from trachoma.
'reatment:
5or individual cases, doxycycline for A wee/s %erythromycin for children& can be given. In endemic areas,
tetracycline or erythromycin ophtalmic ointment should be applied for = months. Entropion should be
treated surgically.
16!) o*ti! atro*h$
It is an irreversible loss of axons in the region of the third neuron %from the retinal layer of
ganglion cells to the lateral geniculate body&.
$orphology and pathologic classification:
'he following forms are distinguished on the basis of ophtalmoscopic findings:
Primary atrophy of the optic nerve
Secon!ary atrophy of the optic nerve
5laucomatous atrophy of the optic nerve
5orms of the primary atrophy may be further classified according to their pathogenesis:
Ascending atrophy in which the lesion is located anterior to the lamina cribrosa in the ocular portion of
the optic nerve or retina
6escending atrophy in which the lesion is located posterior to the lamina cribrosa in a retrobulbar or
cranial location.
Etiology:
22A. Etioog$ o# *ri"ar$ atro*h$ o# the o*ti! nerve:
'he most important causes are as follows:
Ascen!ing atrophy %after 2 to A wee/s&:
<sually vascular, such as central retinal artery occlusion or anterior ischemic optic neuropathy.
Descen!ing atrophy %after A to = wee/s&:
227. 1ompressive, such as from an orbital or intracranial mass or hydrocephalus.
22=. 'raumatic, such as avulsion, compression of the optic nerve in a fracture, or hematoma in
the optic nerve sheath
223. Inflammatory, such as retrobulbar optic neuritis, arachnoiditis of the optic chiasm, or
syphilis.
7oxic:
22H. 1hronic abuse of low+grade tobacco and alcohol
22B. Eead, arsenic, or thalium
2!0. $ethyl alcohol
2!#. $edications, such as ethambutol, chloramphenicol, gentamicin, isonia,id, vincristine, etc.
#ongenital or here!itary
Systemic !isor!ers
2!2. .emorrhagic anemia or pernicious anemia
2!!. Eeu/osis
2!A. Etioog$ o# se!ondar$ atro*h$ o# the o*ti! nerve;
'he most important causes are as follows.
Papille!ema
Anterior ischemic optic neuropathy
Papillitis
--- 'he etiology of any atrophy of the optic nerve should be determined to exclude possible life+threatening
intracerebral causes such as a tumor---
0ymptoms:
'he spectrum of functional defects is broad. 'hese range from small peripheral visual field defects in
partial optic atrophy to severe concentric visual field defects or blindness in total optic atrophy.
6iagnosis:
6etailed history, ophtalmoscopy, and perimetry testing. 1olor vision testing and visual evo/ed potential in
beginning optic atrophy.
2!7. Primary optic atrophy: )phtalmoscopy will reveal a well defined, pale optic dis/. 'he pallor can
cover the entire optic dis/, or it may be partial. 'he neuroretinal rim is atrophied, which causes the
optic dis/ to flatten out. 'he diameter of the retinal vessels will be decreased.
2!=. Secon!ary atrophy of the optic nerve: )phtalmoscopy will reveal a pale optic dis/. 'he dis/ is
slightly elevated due to proliferation of astrocytes, and the margin is blurred. 'he optic cup will be
obscured. 'he retinal vessels will be constricted.
'reatment:
It is an irreversible damage to the nerve fibers. Do treatment is available.
(rognosis:
Early identification of timely management of a treatable cause such as a tumor or pernicious anemia can
stop the progression. 8here this is not the case, the prognosis for vision is poor.
1=a) the #or"ation and o&t#o< o# the a7&eo&s h&"or8 intrao!&ar *ress&re8 "eas&re"ents o# io*
'he average normal intraocular pressure of #7 mm .g in adults is significantly higher than the
average tissue pressure in almost every organ. 0uch high pressure is important for the optical imaging and
help ensure several things:
<niformly smooth curvature of the corneal surface
1onstant distance between the cornea, lens, and retina
<niform alignment of the photoreceptors of the retina and the pigmented epithelium
'he a*ueous humor is formed by the ciliary processes and secreted into the posterior chamber of
the eye. 'he a*ueous humor passes through the pupil into the anterior chamber. As the iris lies flat along
the anterior surface of the lens, the a*ueous humor cannot overcome the pupillary resistance %first
physiologic resistance& until sufficient pressure has built up to lift the iris off the surface of the lens.
'herefore, the flow of the a*ueous humor from the posterior chamber into the anterior chamber is not
continuous but pulsatile.
Any resistance to pupillary outflow %pupillary bloc/& leads to an increase in the pressure in the
posterior chamber: the iris inflates anteriorly on its root li/e a sail and presses against the trabecular
meshwor/. 'his is the pathogenesis of angle closure glaucoma.
5actors increasing resistance to pupillary outflow and predispose to angle closure glaucoma:
2!3. Increase! contact bet/een the margin of the pupil an! lens /ith:
Small eyes
+arge lens %increased volume& due to age, or diabetes mellitus %osmotic swelling&
Miosis due to age %atrophy of the sphincter and dilator muscles&, medications, iritis,
diabetic iridopathy %thic/ening of the iris&
Posterior synechiae %adhesions between lens and iris&
2!H. Increase! viscosity of the aueous humor /ith:
/nflammation %protein, cells, or fibrin in the a*ueous humor&
0leeding %erythrocytes in the a*ueous humor&

'he a*ueous humor flows out of the angle through 2 channels:

'he trabecular meshwor/ receives about H7 of the outflow, which then drains into the canal of
0chlemm. 5rom here it is conducted by radial collecting channels into the episcleral venous plexus.
A uveoscleral vascular system receives about #7 of the outflow, which 2oints the venous blood.
'he trabecular meshwor/ is the second source of physiologic resistance. 'he trabecular meshwor/ is a
body of loose sponge+li/e avascular tissue. Increased resistance is present in open angle glaucoma.
Meas&re"ent o# intrao!&ar *ress&re
2!B. Palpation: 1omparative palpation of both eyeballs is a preliminary examination.
2A0. Schi9t8 in!entation tonometry: 'his examination measures the degree to which the cornea can be
indented in the supine patient. It does not provide fully exact results, because it is dependent on the
rigidity of the sclera %e.g. rigidity of the sclera is reduced in myopic eyes&.
2A#. Applanation tonometry: 'his method is the most common method of measuring intraocular
pressure. A measurement is obtained on a sitting patient within few seconds or on a supine patient.
Applanation %flattening& of the cornea is done by a flat tonometer tip. In this case, unli/e in 0chiUt,
indentation tonometry, it does not depend on the rigidity of the sclera, thus eliminating possible error.
'he external pressure re*uired for applanation of the cornea is directly proportional to intraocular
pressure.
Intraocular pressure of 22 .g mm is regarded as suspicious.
2A2. Pneumatic non-contact tonometry: 'he
electronic tonometer directs a ! ms blast of air against the cornea. 'he tonometer records the deflection
of the cornea and calculates the intraocular pressure on the basis of the deformation.
Advantages: <se of topical anesthetic is not needed. 4is/ of infection is eliminated.
6isadvantages: 6ifficult calibration. 1annot be used in the presence of corneal scarring. Examination
is unpleasant. 'he instrument is more expensive.
2A!. +easuring the ,: hour pressure-curve: 'his examination analyses fluctuations of the pressure
level over a 2A+hour period in patients with suspected glaucoma. I)( fluctuates in a rhythmic pattern.
'he highest values occur at night and in early morning. (ressure is measured at = a. m., noon, = p.m., B
p.m., and midnight.
2AA. 7onometric self-examination: (atients measure their I)( at home. .owever, this device re*uires a
certain degree of s/ill, therefore it is most appropriate for young and well motivated patients.
1=B) OCC/(SIO+ OF THE CE+TRA/ RETI+A/ VEI+
It occur as a results of circulatory dysfunction in the central retinal vein or one of its branches.
Epidemiology:
4etinal vein occlusion is the second most fre*uent vascular retinal disorder after diabetic retinopathy. 'he
most fre*uent underlying systemic disorders are arterial hypertension and diabetes mellitus: the most
fre*uent underlying ocular disorder is glaucoma and retinal vasculitis.
Etiology:
)cclusion of the central vein of the retina or its branches is fre*uently due to local thrombosis at sites
where sclerotic arteries compress the veins. In central retinal vein occlusion, the thrombus lies at the level
of the lamina cribrosa: in branch retinal vein occlusion, it is fre*uently at an arteriovenous crossing.
0ymptoms:
(atients only notice a loss of visual acuity if the macula or optic dis/ are involved.
6iagnosis:
It can be diagnosed where linear or punctiform hemorrhages are seen to occur in all four *uadrants of the
retina. )ften one will find distended and increasingly meandering veins. In branch retinal vein occlusion,
intraretinal hemorrhages will occur at the area of vascular supply: this bleeding may occur in only one
*uadrant. 1otton wool spots and retinal or optic disc edema may also be present. 1hronic occlusion may
also be accompanied by lipid deposits. )ne differentiates between non+ischemic and ischemic occlusion
depending on the extent of capillary occlusion. Ischemic occlusion is diagnosed with the aid of fluorescein
angiography.
'reatment:
In the acute stage, hematocrit should be reduced to !7 + !H by hemodilution. Easer treatment is performed
in ischemic occlusion that progresses to neovasculari,ation or rubeosis iridis. 5ocal laser treatment is
performed in macular edema when visual acuity is reduced.
(rophylaxis:
Early diagnosis and prompt treatment of underlying systemic and ocular disorder is important.
1linical course and prognosis:
Jisual acuity improves in #;! of all patients, remains unchanged in #;!, and worsens in #;! despite therapy.
1omplications include preretinal neovasculari,ation, retinal detachment, and rubeosis iridis with angle
closure glaucoma.
1=C) T(MORS OF THE (VEA
(vea "eano"a
8ith an incidence of # per #0.000, malignant uveal melanoma is the most common primary intraocular
tumor. It usually occurs as a choroidal melanoma, and is almost always unilateral. 'umors in the iris
are detected earlier than tumors located in the ciliary body and the choroid.
Iris melanomas: 'hese tumors are initially asymptomatic. .owever, metastatic melanoma cells in
the angle of the anterior chamber can lead to secondary glaucoma. 1ircumscribed iris melanomas
are removed by segmental iridectomy.
#iliary bo!y melanoma: 0ymptoms include changes in accommodation and refraction resulting
from displacement of the lens. 1iliary body melanomas are resected whole at once.
#horoi!al melanomas: 'hese tumors become symptomatic when involvement of the macula
reduces visual acuity or the patient notices a shadow in his field of vision as a result of the tumor
and the accompanying retinal detachment. 'he diagnosis is confirmed by transillumination,
ultrasound, and fluorescein angiography. 1horoidal tumors are treated by radiation. Enucleation is
indicated for large tumors
.veal metastases most fre*uently develop from carcinomas of the breast or lung.
1?a) vis&a #ied8 the diagnosti! i"*ortan!e o# vis&a #ied de#e!ts
@ross screening of the peripheral field vision can be *uic/ly performed using confrontation
testing. right eye fixes on the examinerIs left eye.
'he examiner then briefly shows several fingers of one hand peripherally in one of the four
*uadrants. 'he patient must identify the number of fingers while maintaining straight+ahead fixation. 0ince
patient and the examiner are staring eye to eye, any loss of fixation by the patient will be noticed. 'he
upper and lower temporal and the upper and lower nasal *uadrants are all tested in the fashion for each eye.
If the examiner closes the right eye while the patient covers the left eye + and if targets %fingers&
are presented at a distance halfway between the patient and the examiner + their respective peripheral fields
should be the same. 'his allows comparison of the patientIs field with the examinerIs own.
5ocal visual field defects are called scotomas. 1onsistent defects indicate gross deficiencies in the
*uadrant tested, as seen with retinal detachments, optic nerve abnormalities, and ischemic or mass in2uries
to the intracranial pathway. 'ransient loss of peripheral vision is fre*uently due to circulatory changes
anywhere along the pathway from the retina to the occipital cortex. Examples would be amaurosis fugax
%see topic 7C& or migrainous scotoma.
Peri"etr$
(erimetry is used to examine the central and peripheral visual fields. 'his techni*ue, which is
performed separately for each eye, measures the combined function of the retina, the optic nerve, and the
intracranial visual pathway. It is used clinically to detect or monitor field loss due to disease at any of these
locations. 6amage to specific parts of the neurologic visual pathway may produce characteristic patterns of
change on serial field examination.
'he sensitivity of vision is greatest in the centre of the field %corresponding to the fovea& and least
in the periphery. (erimetry relies on sub2ective patient responses, and the results will depend on the patient
psychomotor as well as visual status. (erimetry must always be performed and interpreted with this in
mind.
'he principles of testing:
As the patientIs eye fixates on a central target, test ob2ects are randomly presented at different
location throughout the field. If they are seen, the patient responds either verbally or with hand+held
signalling device. Jarying the targetIs si,e or brightness permits *uantification of visual sensitivity of
different areas in the field. 'he smaller or dimmer the target seen, the better the sensitivity of that location.
'here are two basic methods of target presentation. In static perimetry, different locations
throughout the field are tested one at a time. A difficult test ob2ect, such as a dim light, is first presented at a
particular location. If it is not seen, the si,e or intensity of the light is increased until it is detected. 'his is
called >threshold? sensitivity level at this location. 'his se*uence is performed in other locations, so that he
light sensitivity of multiple points in the field can be evaluated to form a profile of the visual field.
In "inetic perimetry, the sensitivity of the entire field to one single test ob2ect is first tested. 'he
ob2ect is moved slowly toward the centre from a peripheral area until it is first spotted. Cy moving the same
ob2ect inward from multiple different directions, a boundary called >isopter? can be mapped out which is
specific for that target. 'he isopter outlines the area within which the target can be seen and beyond which
it cannot be seen. 'hus, the larger the isopter, the better the visual field of that eye. Cy repeating the test
using ob2ects of various si,e or brightness, multiple isopters can then be plotted for a given eye. 'he
smaller or dimmer test ob2ects will produce smaller isopters.
'oday, computeri8e! automate! perimeters are the most sophisticated and sensitive e*uipment
available for visual field testing.
1?%) !atara!t e4tra!tion
1ataract surgery is the most fre*uently performed procedure in ophthalmology.
Indications:
In the presence of unilateral cataract, the surgery is postponed as long as vision in the healthy eye is
sufficient.
In the presence of %ilateral cataract, the eye with the worse visual acuity should undergo surgery when
the patient feels visually handicapped.
In the presence of a mature cataract, it is important to do the surgery as soon as possible.
A detailed history of the patientIs other ocular disorders and vision prior to development of the cataract
should be obtained before surgery to be able to ma/e a prognosis for the patient.
0urgical techni*ues:
2A7. Intracapsular cataract extraction: 'oday it is used only with subluxation or dislocation of the
lens. 'he entire lens is fro,en in its capsule and removed from the eye through a large cornea incision.
2A=. Extracapsular cataract extraction: It is now the method of choice. 'he anterior capsule is opened,
then only the cortex and nucleus are removed: the posterior capsule and ,onule suspension remain
intact. 'his provides a stable base for implantation of the posterior chamber intraocular lens. 'oday
phacoemulsification %emulsifying and aspirating the nucleus of the lens with a ultrasonic needle& is the
preferred techni*ue for removing the nucleus. 'hen the softer portion of the cortex are removed by
suction. 'he posterior capsule is then polished, and an intraocular lens %I)E& is implanted in the empty
capsular bag. 'his method re*uires an incision only ! to = mm in length.
Advantages: It maintains the integrity of the anterior and posterior chambers of the eye, and the
vitreous body cannot prolapse anteriorly as after intracapsular extraction. 'he incidence of retinal
detachment is #0x less than after intracapsular extraction.
Se!ondar$ !atara!t;
About !0 of all cataract patients develop a secondary cataract after extracapsular cataract extraction.
Etiology:
Extracapsular extraction removes only the anterior central portion of the capsule and leaves epithelial cells
of the lens intact along with remnants of the capsule. 'hese epithelial cells are capable of reproducing and
can produce a secondary cataract in the posterior capsule that diminishes the visual acuity.
'reatment:
A Dd:PA@ laser can incise the posterior capsule in the visual axis without re*uiring invasive eye surgery.
'his immediately improves vision.
1?!) is!he"i! o*ti! ne&ro*ath$
'he following forms of ischemic optic neuropathy are distinguished according to the cause of the disorder:
2A3. Arteriosclerotic
2AH. Arteritic
2AB. Arterios!eroti! is!he"i! o*ti! ne&ro*ath$
It is an acute disruption of the blood supply to the optic dis/, i.e., optic dis/ infarction, resulting from
vascular changes in arteriosclerosis.
Epidemiology:
It is a common cause of sudden loss of visual acuity. 'he greatest incidence of this disorder is between the
ages of =0 and 30. In contrast to arteritic, it can also occur in adults below the age of =0.
Etiology:
'he causes of the disorder lie in acute disruption of the blood flow through the lateral branches of the short
posterior ciliary arteries and the ring of Ginn due to severe arteriosclerosis. A narrow scleral canal %a small
optic dis/& is a predisposing factor.
0ymptoms:
(atients report a sudden unilateral loss of visual acuity. 'his is due to segmental or complete infarction of
the anterior portion of the optic nerve. 0everity is variable. 'he patient may present with wedge+shaped or
hori,ontal visual field defects that correlate with segmental nerve fibre edemas. 0evere concentric defects
progressing to total blindness can also occur. Jision may or may not be impaired. An afferent pupillary
defect is always present.
6iagnosis:
'he patient usually has a history of hypertension, diabetes mellitus, or hyperlipidemia.
)phtalmoscopy will reveal edema of the optic dis/, whose margin will be accordingly obscured. )bscured
segments of the margin of the optic dis/ that correlate with visual field defects are typical for I)D.
'reatment and prognosis:
It is nearly impossible to treat. Attempted methods include hemodilution and systemic steroid to control the
edema. 6iagnosis of the underlying cause is important. It is usually poor even where therapy is initiated
early.
270. Arteriti! is!he"i! o*ti! ne&ro*ath$
It is an acute disruption of the blood supply to the optic dis/ due to inflammation of medium+si,ed and
small arterial branches.
Epidemiology:
It occurs almost exclusively after the age of =0. 8omen are affected slightly more than men.
Etiology:
@iant cell arteritis is a fre*uently bilateral granulomatous vasculitis that primarily affects the medium+si,ed
and small arteries. 1ommon sites include the temporal arteries, ophtalmic artery, short posterior ciliary
arteries, central retinal artery, and the proximal portion of the vertebral arteries, which may be affected in
varying combinations.
0ymptoms:
(atients report sudden unilateral blindness or severe visual impairment. )ther symptoms include
headaches, painful scalp and tenderness to palpation in the region of the temporal arteries, pain while
chewing, weight loss, reduced general health and exercise tolerance.
6iagnosis:
'he ophtalmologic findings are the same as in arteriosclerotic I)D. )ther findings include increased
sedimentation rate, an increased level of 1+reactive protein, leu/ocytosis, and iron+deficiency anemia.
'he temporal arteries are prominent, painful to palpation, and have no pulse. 'he diagnosis is confirmed by
biopsy. @iant cell arteritis should be considered in every patient presenting with I)D---
'reatment and prognosis:
Immediate high+dosage systemic steroids is indicated. A maintenance dose is re*uired for several months.
'he prognosis for the affected eye is poor even where therapy is initiated early. Immediate steroid therapy
is absolutely indicated because in 37 of cases the fellow eye is affected within a few hours and cerebral
arteries may also be at ris/.
1Ba) di##erentia diagnosis o# a!&te irido!$!itis and a!&te ange !os&re ga&!o"a %for more details see
topic 2#A + Anterior uveitis and 71 + Acute angle closure glaucoma&
A!&te iritis %AI& x A!&te ga&!o"a %A@&:
Symptoms: AI; 6ull pain and photophobia: A'; Intense pain and vomiting
#on0unctiva: AI; 1ombined in2ection: A'; 1ombined in2ection
#ornea: AI; 1lear: A'; )pacified, edematous
Anterior chamber: AI; Dormal depth, cells and fibrin are present: A'; 0hallow
Pupil: AI; narrowed %reactive miosis&: A'; 6ilated, not round
5lobe: AI; Dormal pressure: A'; 4oc/ hard
1BB) THE F(+)(S I+ ARTERIA/ HYPERTE+SIO+
(athogenesis:
'he severity of vascular damage from hypertension depends partly on the level of hypertension,
and partly on how long it has been present. 'he degree of damage is also dependent on the patient, as
certain individuals appear more prone to vascular damage than others.
0ome hypertensive changes in the fundus relate to the height of hypertension %>acute changes?&
and may occur immediately, if the blood pressure is very high. )ther changes are chronic and ta/e years to
develop.
Acute changes are the result of general and focal arterial constriction, possibly representing an
increase in muscle tone. 'he arterioles appear narrow and tortuous. 0evere vascular constriction presses on
veins at sites where artery and vein cross, causing arteriovenous %A;J& nic/ing. Ischemia and vascular
permeability occur. 6amaged optic axons swell in the local area of damage, forming soft, fluffy >cotton
wool? exudates. 0eepage of red blood cells and hemorrhages occur. 0uch hemorrhages are commonly
>feathery? or >flame+shaped?: they outline the optic fibers that extend toward the optic disc. 8hen
hypertension is severe, the optic disc %papilla& may become edematous and surrounded by hemorrhages and
exudates %papilledema&.
Acute hypertensive changes are classified in A stages:
Stage I: Darrowed, constricted, tortuous arterioles
Stage II: 0evere vascular constriction and narrowing and A;J nic/ing
Stage III: 4etinal hemorrhages, cotton+wool spots, retinal edema
Stage I;: (apilledema
#hronic hypertension also affects the arterioles, but differently than in acute hypertensive
retinopathy. 'he arteriolar media %the central layer of the arteriole& thic/ens, thus gradually obscuring
visuali,ation of the blood through the normally transparent vascular wall. 'he normal arteriolar light
reflection first broadens. As the arteriole thic/en arteriovenous %A;J& nic/ing results. 8ith further
thic/ening the arteriole changes color, producing >copper wiring? %copper colored arterial reflex& and
finally >silver wiring? %silver colored arterial reflex&, in which the blood column is totally obscured.
1hronic arteriosclerotic changes are classified in A stages:
Stage I: Croadening of arteriolar reflexes
Stage II: A;J nic/ing
Stage III: 1opper+wire arteries
Stage I;: 0ilver+wire arteries
0ymptoms:
(atients with high blood pressure fre*uently suffer from headache or eye pain. Impaired vision or loss of
visual acuity only occurs in stage III or IJ hypertensive vascular changes. Arteriosclerosis does not exhibit
any ocular symptoms.
6iagnosis:
.ypertensive and arteriosclerotic changes in the fundus are diagnosed by ophtalmoscopy. 1hanges in the
retinal vasculature are fre*uent findings.
6ifferential diagnosis:
)phtalmoscopy should be performed to exclude other vascular retinal disorders such as diabetic
retinopathy. 6iabetic retinopathy is primarily characteri,ed by parenchymal and vascular changes.
'reatment:
'reating the underlying disorder is crucial. Clood pressure should be reduced below #A0;B0 mm .g.
5undus changes due to atherosclerosis are untreatable.
1linical course and complications:
0e*uelae of arteriosclerotic and hypertensive vascular changes include retinal artery and vein occlusion and
the formation of macroaneurysms that can lead to vitreous hemorrhage. In the presence of papilledema, the
subse*uent atrophy of the optic nerve can produce loss of visual acuity.
(rognosis:
In some cases, the complications are unavoidable despite well controlled blood pressure.
1B!) !orti!osteroids in o*hta"oog$8 their o!&ar side e##e!ts
'opical corticosteroid therapy is indicated for inflammatory conditions of the anterior segment of
the globe. 0ome examples are allergic con2unctivitis, uveitis, episcleritis, scleritis, superficial punctate
/eratitis, interstitial /eratitis, and vernal con2unctivitis.
'he duration and treatment will vary with the type of lesion and may extend from few days to
several months.
Initial therapy for a severely inflamed eye consists of instilling drops every # or 2 hours while
awa/e. 8hen a good response is observed, gradually reduce the dosage and discontinue as soon as
possible.
#aution: 'he steroids enhance the activity of the herpes simplex virus, as shown by the fact that
perforation of the cornea occasionally occurs when they are used in the eye for treatment of herpes simplex
/eratitis %corneal perforation was an extremely rare complication of herpes simplex /eratitis before the
steroids came into general use&. )ther side effects of local steroid therapy are fungal overgrowth, cataract
formation %usual&, and open+angle glaucoma %common&. 'hese effects are less common with systemic
steroid therapy. Any patient receiving local corticosteroids or long+term systemic corticosteroid therapy
should be under care of an ophtalmologist.
Available topical steroids include:
.ydrocortisone %ointment&, prednisolone %suspension, solution&, dexamethasone %suspension, ointment&,
medrysone %suspension&, and fluorometholone %suspension&.
Mi4t&res o# !orti!osteroids and anti:in#e!tive agents
'here are many commercial products containing corticosteroids and one or more anti+infective
agents. 'hey are used by ophthalmologists to treat conditions in which both agents may be re*uired, e.g.
marginal /eratitis due to a combined staphylococcal infection and allergic reaction or
blepharocon2unctivitis. 'hey are also used postoperatively. 'hese mixtures should not be used to treat
con2unctivitis or blepharitis due to un/nown causes.
1CA) OPHTA/MOSCOPY1 THE +ORMA/ EYE 'RO(+)
In!irect ophtalmoscopy is usually performed by the ophtalmologist and produces a inverted image
of the fundus. A condensing lens is held approximately #! cm from the patientIs eye. 'he fundus appears in
two to six+power magnification.
Eess experienced examiners will prefer !irect ophtalmoscopy. .ere, the ophtalmoscope is held as
close to the patient as possible. 4efractive errors in the patientIs eye and the examinerIs eye are corrected
by selecting the ophtalmoscope lens re*uired to bring the retina into focus. 'he examiner views the
patientIs right eye with his or her own right eye so that their noses do not interfere with the examination.
'he examiner sees an erect, #= power magnified image of the retina. 'he examination should be performed
in a slightly dar/ened room with the patientIs pupil dilated.
Advantages of !irect ophtalmoscopy
'he high magnification permits evaluation of small retinal findings such as diagnosing retinal
microaneurysms.
6isadvantages of !irect ophtalmoscopy
'he image of the fundus is highly magnified but shows only small portion of the fundus. 4otating the
ophtalmoscope can only partially compensate for this disadvantage. 6irect ophtalmoscopy also produces
only a two+dimensional image.
Advantages of in!irect ophtalmoscopy
It provides a good stereoscopic, optimally illuminated overview of the entire fundus in binocular system.
6isadvantages of in!irect ophtalmoscopy
$agnification is significantly less than in direct ophtalmoscopy. It re*uires practice and experience.
+or"a #&nd&s
'he retina is normally completely transparent without any intrinsic color. It receives its uniform
bright red color from the vasculature of the choroid. 'he vessels of the choroid themselves are obscured by
the retinal pigment epithelium. Eoss of transparency of the retina is a sign of an abnormal process %for
example in retinal edemas, the retina appears whitish yellow&. 'he optic dis/ is a sharply defined structure
with vital coloration %yellowish orange: in young children it is paler& at the level of the retina and may have
a central excavation %optic cup&. 'he central vein lies lateral to the artery: venous diameter is normally #.7
times greater than arterial diameter. Each vascular structure should be of uniform diameter, and there
should be no vascular constriction where vessels overlap. A spontaneous venous pulse is normal: an arterial
pulse is abnormal. Eight reflection on the inner limiting membrane will normally produce multiple light
reflexes on the fundus. Pounger patients will also have a foveal and macular light reflex, and the retina will
have a reddish color.
1C%) e*ide"i! 2erato!on-&n!tivitis
It is an acute con2unctival inflammation caused by adenovirus.
Etiology:
Adenoviruses cause epidemic /eratocon2unctivitis %serotypes H, #B, !3, and 7&.
0ymptoms and signs:
After an incubation period of about 7 to #2 days, symptoms include con2unctival hyperemia, watery
discharge, ocular irritation, and eyelids that are stuc/ together on awa/ening. 0ymptoms are usually
bilateral and begin in one eye. $any patients have had contact with someone with con2unctivitis and;or
recent upper respiratory tract infection.
'he bulbar and tarsal con2unctivae are hyperemic. 1on2unctival follicles are present on the palpebral
con2unctiva. 'he preauricular lymph node is often enlarged and painful.
In severe cases, patients complain of photophobia and foreign+body sensation. 'hese patients may have
pseudomembranes and focal corneal inflammation. Even after the con2unctivitis has resolved, residual
corneal scarring may be present.
'reatment:
Adenoviral con2unctivitis is highly contagious and spreads by droplet, fomites, and hand+to+eye
inoculation. 'he patient should be told to wash his hands after touching his eyes or nasal secretions to avoid
infection of the noninfected eye. It is self+limiting, lasting # wee/ in mild cases and ! wee/s in severe
cases. Do treatment is needed or available. 0evere con2unctivitis associated with pseudomembranes or
scarring may need topical corticosteroids.
1CC) OPTIC +E(RITIS
Definition: )ptic neuritis is an inflammation of the optic nerve that may occur within the globe %papillitis&
or posterior to it %retrobulbar neuritis&.
Epidemiology:
)ptic neuritis occurs most fre*uently in adults between the ages of 20 and A7. 8omen are more fre*uently
affected than men. 20+A0 of all patients with optic neuritis develop diffuse encephalitis %multiple
sclerosis&.
Etiology:
27#. Papillitis
/nflammatory processes: 'hese include infectious diseases such as Eyme disease, malaria, and
syphilis, and manifestations in the optic nerve of inflammation of the orbit, paranasal sinuses, or
s/ull base.
&utoimmune disorders: 'hese include lupus erythematosus, polychondritis, regional enteritis
%1rohnIs disease&, ulcerative colitis, nodular panarteritis, and 8egenerIs granulomatosis.
Toxic damage due to agents such as methanol, lead, and chloramphenicol. In 30 of these cases,
the cause is not determined.
272. *etrobulbar neuritis
'he primary causes of this disorder are demyelinating diseases of the 1D0 such as diffuse
encephalitis. .owever, a differential diagnosis should always also consider the other causes of papillitis
mentioned above.
0ymptoms:
'he cardinal symptom is sudden loss of vision, which may be accompanied by fever. 'he field of
vision is impaired by central scotoma %scotoma 9 an island+li/e blind gap in the visual field: central
scotoma 9 scotoma involving the point of fixation&, paracentral scotomas, and wedge+shaped visual field
defects up to complete blindness. )ther symptoms include pain that increases when pressure is applied to
the globe, and reduced perception of color intensity.
6iagnosis:
)phtalmoscopic findings in papillitis include edema and hyperemia of the head of the optic nerve. 'his
flattens the optic cup and obscures the margin of the optic dis/. Cleeding at the margin of the optic dis/
may or may not be present. 'he elevation of the optic dis/ is considerable less than in papilledema.
'he optic dis/ will appear normal in retrobulbar neuritis. In retrobulbar optic neuritis, the patient sees
nothing %due to a central scotoma&, and the physician sees nothing %the fundus appears normal&.
)ther findings include afferent pupillary defect, red+green color vision defect, and delayed latency in
the visual evo/ed potential.
6ifferential diagnosis:
Papilledema: Initially there is no loss of function.
/schemic optic neuropathy: 'he central scotoma is lac/ing, and patients are usually over the age of =0.
'reatment:
'his depends on the underlying disorder. 4etrobulbar neuritis with severe loss of vision may be treated with
high doses of steroids.
(rognosis:
'his depends on the underlying disorder. 0evere permanent loss of visual acuity is possible, as are
significant spontaneous improvements. 4etrobulbar optic neuritis in diffuse encephalitis usually improves
spontaneously. .owever, some functional defects such as reduced visual contrast and reduced perception of
color intensity will always remain. $orphologic findings always include a pale optic dis/ as a result of
complex atrophy of the optic nerve.
.Da) anato"i!a str&!t&re o# the retina and its #&n!tion
'he retina is the innermost of ! successive layers of the globe. It has 2 parts:
27!. A photoreceptive part $pars optica retinae%, comprising the first B of the #0 layers listed below.
27A. A nonreceptive part $pars caeca retinae% forming the epithelium of the ciliary body and iris.
'he pars optica retinae merges with the pars caeca retinae at the ora serrata.
Embryology:
'he retina develops from a diverticulum of the forebrain %proencephalon&. )ptic vesicles develop
which then invaginate to form a double+walled bowl, the optic cup. 'he outer wall becomes the pigment
epithelium, and the inner wall later differentiates into the B layers of the retina. 'he retina remains lin/ed to
the forebrain throughout life through a structure /nown as the retinohypothalamic tract.
Eayers of the retina: $oving inward along the path of incident light, the individual layers of the retina are:
277. Inner limiting membrane %glial cell fibers separating the retina from the vitreous body&
27=. 'ayer of optic nerve fibers %axons of the third neuron&
273. 'ayer of ganglion cells %cell nuclei of the multipolar ganglion cells of the third neuron: >data
ac*uisition system?&
27H. Inner plexiform layer %synapses between the axons of the second neuron and dendrites of the third
neuron&
27B. Inner nuclear layer %cell nuclei of the bipolar nerve cells of the second neuron, hori,ontal cells,
and amacrine cells&
2=0. Outer plexiform layer %synapses between the axons of the first neuron and dendrites of the second
neuron&
2=#. Outer nuclear layer %cell nuclei of the rods and cones 9 first neuron&
2=2. Outer limiting membrane %sieve+li/e plate of processes of glial cells through which rods and
cones pro2ect&.
2=!. 'ayer of ro! an! cones %the actual photoreceptors&
2=A. *etinal pigment epithelium %a single cubic layer of heavily pigmented epithelial cells&
2=7. 6ruch<s membrane %basal membrane of the choroid separating the retina from the choroid&
$acula lutea:
'he macula lutea is a flattened oval area in the centre of the retina approximately !+A mm %#7
degrees& temporal to and slightly below the optic dis/. Its diameter is roughly e*ual to that of the optic dis/
%#.3 + 2 mm&. 'he macula appears yellow when examined under green light, hence the name macula lutea
%yellow spot&. Eocated in its centre is the avascular fovea centralis, the point at which visual perception is
sharpest. 'he fovea centralis contains only cones %no rods& each with its own neural supply, which explains
why the region has such distinct vision. Eight stimuli in this region can directly act on the sensory cells
%first neuron& because the bipolar cells %second neuron& and ganglion cells %third neuron& are displaces
peripherally.
Jascular supply to the retina:
'he inner layers of the retina %the inner limiting membrane through the inner nuclear layer& are
supplied by the central artery of the retina. 'his originates at the opthalmic artery, enters the eye with the
optic nerve, and branches on the inner surface of the retina. 'he central artery is a terminal artery
%occlusion will lead to retinal infarction ---& without anastomoses and divides into A main branches.
'he outer layer %outer plexiform layer through the pigment epithelium& contain no capillaries.
'hey are nourished by diffusion primarily from the richly supplied capillary layer of the choroid.
'he retinal arteries are normally bright red, have bright red reflex strips that become paler with
advancing age, and do not show a pulse %pulsation is a sign of abnormality---&. 'he retinal veins are dar/
red with a narrow reflex strip, and may show spontaneous pulsation on the optic dis/.
'he walls of the vessels are transparent so that only the blood will be visible on ophtalmoscopy. In
terms of their structure and si,e, the retinal vessels are arterioles and venules, although they are referred to
as arteries and veins. ;enous !iameter is normally #.7 times higher than arterial !iameter. 1apillaries are
not visible.
Derve supply to the retina:
'he neurosensory retina has no sensory supply. 6isorders of the retina are painless because of the
absence of sensory supply.
Eight path through the retinal layers:
8hen electromagnetic radiation in visible light spectrum %wavelengths of !H0 + 3=0 nm& stri/es
the retina, it is absorbed by the photopigments of the outer layer. Electric signals are created in a multi+step
photochemical reaction. 'hey reach the photoreceptor synapses as action potentials where they are passed
to the second neuron. 'he signals are passed to the third and fourth neurons and finally reach the visual
cortex.
.D%) verna !atarrh
It is a bilateral, recurrent con2unctivitis with concurrent cornea epithelial changes, probably
allergic in origin, with recurrence in spring and fall. It is most common in males aged 7 to 20.
0ymptoms and signs:
Intense itching, lacrimation, photophobia, con2unctival hyperemia, and a mucoid discharge containing
numerous eosinophils are characteristic. <sually the palpebral con2unctiva is involved, but the bulbar
con2unctiva is only sometimes affected. In the palpebral form, s*uare, hard, flattened, pale+pin/ to greyish
>cobblestone? papillae are present, chiefly in the upper tarsal con2unctiva. In the bulbar form, the
circumcorneal con2unctiva becomes hypertrophied and greyish. 0ymptoms usually disappear during the
cold months and become milder over the years.
'reatment:
'opical antihistamine ; vasoconstrictors are useful for mild cases. 'opical mast cell inhibitors and D0AI6s
indicated in more severe cases. 'opical corticosteroids may be used in the most persistent cases.
.D!) to4i! o*ti! ne&ro*ath$ (To4i! a"%$o*ia)
%see also topic #31 + )ptic atrophy&
6efinition: A reduction of visual acuity or dimness of vision %amblyopia& believed to be due to a toxic
reaction in the orbital portion of the optic nerve.
Etiology:
It is usually bilateral and most often seen in patients who use alcohol or tobacco excessively. In case of
alcohol use, malnutrition may be the actual underlying cause. 'here is a reduced ris/ in patients with high
dietary inta/e of animal products and C+complex vitamins, suggesting that an interaction between
nutritional deficits and environmental toxins may be responsible. Eead, methanol, digitalis, ethambutol, and
many other chemicals can also damage the optic nerve.
0ymptoms and signs:
Jisual dimness, photophobia, and ocular discomfort develop over days to wee/s. An initially small central
or pericentral scotoma slowly enlarges, typically to involve both the fixation and the blind spot,
progressively interfering with vision. It may lead to blindness. Abnormalities are usually not seen in
ophtalmoscopy until later in the course.
'reatment:
Jision may improve when the cause is removed immediately, unless the optic nerve has atrophied.
1helation therapy is indicated in lead poisoning. In idiopathic case, treatment with C vitamins before
amblyopia becomes severe may reverse the condition.
.1A) anterior &veitis
Inflammations of the uveal tract are classified according to the various portions of the globe:
Anterior uveitis %iritis&
Intermediate uveitis %cyclitis&
(osterior uveitis %choroi!itis&
.owever, some inflammations involve the middle portions of the uveal tract such as i ri!ocyclitis
%inflammation of the iris and ciliary body& or panuveitis %involving the whole segment&.
2==. A!&te iritis and irido!$!itis
Epidemiology:
Iritis is the most fre*uent form of uveitis. It usually occurs in combination with cyclitis. About !;A of all
iridocyclitis cases have acute course.
Etiology:
Iridocyclitis is often due to immunologic causes such as allergic reaction to bacterial toxins. In some cases
%an/ylosing spondylitis, 4eiterIs syndrome, regional enteritis, ulcerative colitis, or psoriasis& it is /nown to
be fre*uently associated with .EA+C23. Iridocyclitis can also be a symptom of systemic disease such
rheumatic arthritis, sarcoidosis, tuberculosis, syphilis, or leprosy. Infections are less fre*uent and occur
secondary to penetrating trauma or sepsis %bacteria, viruses, mycosis, or parasites&. (hacogenic
inflammation, possibly with glaucoma, can result when the lens becomes involved. 0ome cases are
idiopathic.
0ymptoms:
6ull pain in the eye or forehead accompanied by impaired vision, photophobia, and excessive tearing. In
contrast to choroiditis, acute iritis or iridocyclitis is painful because of the involvement of the ciliary
nerves.
6iagnosis: 'ypical signs include:
#iliary in0ection: 'he episcleral and perilimbal vessels may appear blue and red.
#ombine! in0ection: 'he con2unctiva is also affected.
'he iris is hyperemic %the iris vessels will be visible in a light+colored iris&. 'he structure appears
diffuse and reactive miosis is present.
Jision is impaired because of cellular infiltration of the anterior chamber and protein and fibrin
accumulation %visible as 'yndall effect 9 opacification of a*ueous the humor by proteins observed in
the slit lamp examination when the eye is illuminated with a lateral focal beam of light&. Exudate
accumulation on the floor of the anterior chamber is referred to as hypopyon. Jiral infections may be
accompanied by bleeding into the anterior chamber %hyphema&.
6ifferential diagnosis: see topic 2#A
1omplications:
Secon!ary open angle glaucoma with an increase in intraocular pressure.
Adhesions between the iris and posterior surface of the cornea %anterior synechiae&.
Adhesions between the iris and lens %posterior synechiae&.
'reatment:
'opical, and in some cases, systemic antibiotic or antiviral therapy is indicated for iridocyclitis due to a
pathogen %with a corneal ulcer, penetrating trauma, or sepsis&. 'herapeutic mydriasis %atropine,
scopolamine, epinephrine eyedrops&& with steroid therapy %eyedrops, subcon2unctival in2ections& is
indicated to minimi,e the ris/ of synechiae. 0econdary open glaucoma is treated by beta bloc/ers in
eyedrops or aceta,olamide.
(rognosis:
0ymptoms usually improve within few days when treated properly. 'he disorder can progress to a chronic
stage.

2=3. Chroni! iritis and irido!$!itis
Epidemiology: About #;A of all iridocyclitis cases are chronic.
Etiology, symptoms, and diagnosis: see acute iridocyclitis
6ifferential diagnosis: Acute glaucoma, con2unctivitis, and /eratitis.
1omplications:
'otal obliteration of the pupil by posterior synechiae is referred to as pupillary bloc/. Cecause the a*ueous
humor can no longer circulate, secondary angle closer glaucoma with iris bomb occurs. Occlusion of the
pupil also results in fibrous scarring in the pupil. This can lead to secondary cataract.
'reatment:
In pupillary bloc/, a Dd:PA@ laser iridotomy may be performed to create a shunt to allow the a*ueous
humor from the posterior chamber to circulate into the anterior chamber. In secondary cataract, a cataract
extraction may be performed.
(rognosis:
Cecause of the chronic course, it fre*uently involves complications such as synechiae or cataract that may
lead to blindness from shrin/age of the eyeball.
.1%) "edi!a treat"ent o# ga&!o"a
$edical therapy is the treatment of choice for primary open angle glaucoma. 0urgery is indicated only
where medical treatment fails. 'he general rule of medical therapy is to try to use the wea/est possible
medications re*uired to achieve normal pressure over a 2A+hour period: as much as necessary, and as little
as possible.
Available drugs:
2=H. Paras$"*atho"i"eti! agents
2=B. Direct parasympathomimetic agents + cholinergic agents %*io!ar*ine8 !ar%a!ho8
a!e!idine&
'hese agents improve drainage of a*ueous humor in primary open angle glaucoma. 'he effect is
probably purely mechanical via contraction of the ciliary muscle and tension on the trabecular
networ/ and scleral spur. In acute angle closure glaucoma, the forced narrowing of the pupil and the
extraction of the iris from the angle of the anterior chamber are most important.
0ide effects:
Pounger patients do not tolerate the myopia due to contraction of the ciliary muscle.
$iosis with worsening of the night vision and narrowing of the peripheral field of vision.
230. In!irect parasympathomimetic agents - cholinesterase inhibitors %neostig"ine&
'hese agents improve drainage. 1ontraction of the ciliary muscle and sphincter pupillae muscle is
more pronounced than with other miotic agents. It is indicated in primary open angle glaucoma if
other miotic agents are no longer effective.
0ide effects:
'hese agents are no longer routinely used because of their side effects. they are only used in
isolated cases such as when other medications fail to be effective.
23#. )ire!t s$"*atho"i"eti! agents
'hese agents improve drainage of a*ueous humor and reduce production of a*ueous humor. 'hey
are used in combination with pilocarpine and carbonic anhydrase inhibitors. 'he indication is
primary open angle glaucoma.
0ide effects: 0ome patients develop an allergy.
)i*ive#rin %epinephrine derivative&
0ide effects: metabolic products can form deposits in the con2unctiva and can lead to
obstruction of the canaliculus.
Conidine reduces I)( primarily by vasoconstriction without influencing the si,e of the pupil
and accommodation. It is particularly useful for young patients with primary open angle
glaucoma.
0ide effects: Eowers blood pressure.
A*ra!onidine also reduces a*ueous humor production. In contrast to clonidine, it does not
reduce systemic blood pressure. It is very good in I)( reduction in decompensated glaucoma.
Bri"onidine improves drainage of a*ueous humor by reducing episcleral venous pressure
and reducing a*ueous humor production by decreasing ciliary body perfusion.
Indication: as with apraclonidine.
232. S$"*atho$ti! agents
23!. Direct sympatholytic agents - =-bloc"ers %ti"oo8 %eta4oo8 !arteoo8 evo%&noo8
"eti*ranoo&
'hese agents reduce pressure by decreasing production of a*ueous humor without influencing
pupil si,e and accommodation. Indications: (rimary and secondary open angle glaucoma,
secondary angle closure glaucoma.
0ide effects:
4educe heart rate and increase bronchospasms in asthma patients.
1ontraindications:
Ceta bloc/ers should be used carefully in patients with 1)(6, cardiac insufficiency, or
arrhythmias.
23A. In!irect sympatholytic agents %g&anethidine&
'hese agents decrease a*ueous humor production, but reduce pressure only slightly.
0ide effect: 4ed eyes.
237. Prostagandin anaog&es (atano*rost)
'hese agents increase uveoscleral a*ueous humor drainage. 'hey are suitable for patients with primary
open angle glaucoma. 'hey are used as ad2unctive therapy together with other agents. Do /nown side
effects.
23=. Car%oni! anh$drase inhi%itors (a!eta0oa"ide8 dor0oa"ide8 di!hor*hena"ide)
'hey reduce a*ueous humor production. 0uitable for acute glaucoma and surgeries increasing I)(.
0ide effects: Eong therapy causes malaise, nausea, depression, anorexia, weight loss, and decreased
libido.
233. Os"oti! agents ("annito8 g$!erine)
'hese agents decrease I)( by producing an osmotic pressure gradient by means of the hyperosmotic
substances released into the blood stream. 'his draws water from fluid+filled spaces, especially from
the vitreous body and a*ueous humor. 'hey are exclusively indicated in acute increase in I)( such as
angle closure glaucoma due to its short duration of action %only a few hours&.
.1!) in#a""ator$ diseases o# the or%it

23H. Or%ita in#a""ation
Cecause of the close proximity of the orbital cavity to the paranasal sinuses, which are particularly
susceptible to inflammation, orbital inflammation represents the second most fre*uent group of orbital
disorders after @ravesI disease. )rbital cellulitis is the most severe of these.
23B. Or%ita !e&itis
It is an acute inflammation of the contents of the orbital cavity with the cardinal symptoms of limited
motility and general malaise. It is the most fre*uent cause of exophtalmos in children.
Etiology:
It is usually an inflammation that has spread from surrounding tissue. )ver =0 of cases are
originating in the sinuses, especially the ethmoidal air cells and the frontal sinus. In infants, tooth germ
inflammations may be the cause. Eess fre*uently, it occurs in association with facial furuncles, erysipelas,
hordeolum, panophtalmitis, orbital in2uries, and sepsis.
0ymptoms: (atients report severe malaise, occasionally fever and pain exacerbated by eye movement.
6iagnosis:
'ypical symptoms include exophtalmos with severe chemosis, eyelid swelling, and significantly
limited ocular motility %>cemented? globe&. (atients may have leu/ocytosis and increased sedimentation.
6ifferential diagnosis:
(reseptal %anterior to the orbital septum& cellulitis, which is more common, should be excluded
%chemosis " limited motility are absent&. 4arer conditions include: orbital pseudotumor, orbital periostitis,
orbital abscess.
'reatment:
'his consists of high+dose i.v. antibiotic therapy. 'reatment of underlying sinusitis is indicated if
present.
1linical course and complications:
It can lead to optic neuritis with subse*uent atrophy and loss of vision. (urulent thrombophlebitis of
the orbital veins can result in life+threatening situation + cavernous sinus thrombosis with meningitis,
cerebral abscess, or sepsis.
2H0. Caverno&s sin&s thro"%osis
It is a rare but severe acute clinical syndrome in which the spaces of the cavernous sinus posterior to
the orbital cavity become thrombosed, usually in the presence of ad2acent purulent processes. 'his is not an
orbital disorder in the strict sense.
Etiology: 'hese are purulent inflammations that have spread from the middle ear, petrous bone, orbital
cavities, or from the facial s/in via the angular vein.
0ymptoms: (atients present with acute clinical picture with headache, stupor, fever, and vomiting.
1linical findings:
'here will usually be bilateral exophtalmos and episcleral and con2unctival venous stasis in
combination with multiple pareses of the cranial nerves. Deurogenic paralysis of all ocular muscles is
referred to as total ophtalmoplegia. 8here the optic nerve is also involved, the condition is referred to as
orbital apex syndrome. 'he limited motility of the globe is primarily neurogenic and due to damage to the
nerves in the cavernous sinus as opposed to the mechanical limitation of motility due to the orbital
inflammation in orbital cellulitis.
6iagnosis and treatment:
'his lies in the hands of ED' specialists, neurosurgeons, and internists. .igh+dose systemic
antibiotic therapy and anticoagulation are indicated.
2H#. Or%ita *se&dot&"or
It is a lymphocytic orbital tumor of un/nown origin.
0ymptoms and findings:
(ainful, moderately severe inflammatory reaction with eyelid swelling, chemosis, and unilateral or
bilateral exophtalmos. Involvement of the ocular muscles results in limited motility with diplopia.
6iagnosis: 'he 1' and $4I images will show diffuse soft tissue swelling. A biopsy is re*uired to confirm
it.
'reatment: .igh+dose systemic cortisone. 4adiation therapy or surgery are indicated in resistant cases.
2H2. Or%ita invove"ent in a&toi""&ne diseases; 'ravesI disease
It is an autoimmune disorder with orbital involvement fre*uently associated with thyroid dysfunction.
.istologic examination reveals inflammatory infiltration of the orbital cavity.
Epidemiology:
8omen are affected H times as often as men. =0 of all patients have hyperthyroidism. It is the
most fre*uent cause of both unilateral and bilateral exophtalmos.
Etiology:
It is not fully clear. 'here is lymphocytic infiltration of the orbital cavity. 'he ocular muscles are
particularly severely affected. 5ibrosis develops after the acute phase.
An autonomous adenoma of the thyroid gland is not associated with @ravesI disease. 0ome
patients with @ravesI disease never exhibit any thyroid dysfunction during their entire life.
0ymptoms:
'he onset of this painless disorder is usually between the ages of 20 and A7. (atients complain of
reddened dry eyes with a sensation of pressure and of cosmetic problems. )cular motility is also limited,
and patients may experience double vision.
6iagnosis:
1ardinal symptoms include exophtalmos, usually bilateral, retraction of the upper eyelid with
visible sclera superior to the limbus %this can lead to exposure /eratitis&, difficult eversion of the upper
eyelid %due to eyelid edema&, con2unctival in2ection, and fixed ga,e. 'hic/ening of the muscles and
subse*uent fibrosis lead to limited motility and double vision. Elevation is impaired.
'hic/ening of the muscles is identified in ultrasound or 1' studies.
6ifferential diagnosis:
)rbital tumors and orbital pseudotumors.
'reatment:
In the acute stage, it includes management of the thyroid dysfunction, systemic cortisone, and
radiation therapy of the orbital cavity. 0urgical decompression of the orbital cavity is indicated in recurrent
cases that do not respond to treatment to avoid compressive optic neuropathy. Exposure /eratitis %due to
inability to close the eye& should be treated with artificial tears or tarsorrhaphy %partial or complete suture
closure of the upper and lower eyelid&. In the postinflammatory stage, eye muscle surgery may be
performed to correct strabismus.
1linical course and prognosis:
Jisual acuity will remain good if treatment is initiated promptly. Exophtalmos often persists
despite the fact that the underlying disorder is well controlled.
..a) !a&ses o# e&!o2oria
'eu"ocoria > 8hite or abnormal pupillary reflex: presenting as white pupil. %Eight is normally reflected
off the fundus as red when it is examined through the ophthalmoscope: leu/ocoria is a white reflex that
may signify one of the following conditions: %8hite reflex may be first noticed in photos-&
6ifferential diagnosis:
2H!. #ongenital cataract %A + H : 20.000&: Early infancy, unilateral or bilateral, normal globe si,e. %topic
2C&
2HA. *etinoblastoma %#:20.000&: Infancy, normal globe si,e, unilateral %2;!& or bilateral %#;!&,
calcification in tumor. %topic 2C&
2H7. *etinopathy of prematurity1 stage ? %#:20.000&: Early infancy, usually bilateral, no
microphtalmos, occurring in preterm infants receiving oxygen therapy %topic 2C&
2H=. Exu!ative retinitis $#oat<s !isease%: 1hildhood, unilateral.
2H3. Persistent hyperplastic primary vitreous: <sually unilaterally, usually microphthalmos, leu/ocoria
discovered shortly after birth. %topic #!1&
2HH. 7umors: Astrocytoma, medulloepithelioma.
2HB. Exu!ative retinal !etachment: In toxocarosis, angiomatosis retinae %von .ippel+Eindau tumor&,
diffuse choroidal hemangioma.
2B0. Other causes: 4etinal dysplasia, vitreous abscess, myelini,ed nerve fibers, coloboma of the optic
dis/, foreign bodies in the vitreous chamber
4etinoblastoma is the most important in differential diagnosis of leu/ocoria. 'herefore, leu/ocoria should
be regarded as a retinoblastoma until proven otherwise- It can be excluded on the basis of 1' or ultrasound
+ these studies will reveal an intraocular mass with calcifications.
..%) s&*er#i!ia in-&ries o# the anterior seg"ent o# the e$e and their "anage"ent
a) E$eid in-&r$
Etiology:
Eyelid in2uries can occur in practically every facial in2ury.
1linical picture:
'he highly vasculari,ed and loosely textured tissue of the eyelid causes them to bleed profusely when
in2ured. .ematoma and swelling will be severe. Abrasions usually involve only the superficial layer of the
s/in, whereas punctures, cuts, and eyelid avulsions due to blunt trauma %such as a fist& fre*uently involve
all layers. Cite wounds %such as dog bites& are often accompanied by in2uries to the lacrimal system.
'reatment:
0urgical repair of eyelid in2uries, especially lacerations with involvement of the eyelid margin, should be
performed with care. 'he wounds should be closed in layers and the edges properly approximated to ensure
a smooth margin without tension to avoid later complications, such as cicatrical ectropion.
%) In-&ries to the a!ri"a s$ste"
Etiology:
Eacerations and tears in the medical canthus %such as dog bites or glass splinters& can divide the lacrimal
duct. )bliteration of the punctum and lacrimal canaliculus is usually the result of a burn or chemical in2ury.
In2ury to the lacrimal sac or lacrimal gland usually occurs in con2unction with severe craniofacial trauma
%such as a /ic/ from a horse or a traffic accident&. 6acryocystitis is a common se*uela, which often can
only be treated by surgery %dacryocystorhinostomy&.
1linical picture:
5or dacryocystitis see topic =A.
'reatment:
Eacrimal system in2uries are repaired under an operating microscope. A ring+shaped silicone stent is
advanced into the canaliculus using a special sound. 'he silicone stent remains in situ for ! months and
then is removed.
2B#. Con-&n!tiva a!eration
Epidemiology:
6ue to its exposed position, thinness, and mobility, the con2unctiva is susceptible to lacerations, which are
usually associated with subcon2unctival hemorrhage.
Etiology:
1on2unctival lacerations most commonly occur as a result of penetrating wounds %such as bending over a
spi/ed+leaf palm tree or from a branch that snaps bac/ on to the eye&.
0ymptoms and diagnosis:
'he patient has a foreign body sensation. <sually this is mild. Examination will reveal con2unctival
reddening or subcon2unctival hemorrhage in the in2ured area. )ccasionally only application of fluorescein
dye to the in2ury will reveal the si,e of the con2unctival gap.
'reatment:
$inor con2unctival in2uries do not re*uire treatment as the con2unctiva heals *uic/ly. Earge lacerations
with mobile edges are approximated with absorbable sutures.
--- 'he possibility of a perforating in2ury should be considered in con2unctival in2uries---
2B2. Cornea and !on-&n!tiva #oreign %odies
Epidemiology and etiology:
It is the commonest ocular emergency encountered. It usually involves airborne foreign bodies and metal
splinters becoming lodged in the con2unctiva or cornea.
0ymptoms and diagnosis:
'he patient experiences a foreign body sensation with every blin/ of the eye. 'his is accompanied by
epiphora %tearing& and blepharospasm. 1on2unctival or cilliary in2ection will be present few hours later. 'he
bodies themselves are often so small that they are visible only under loupe magnification. 8here there is no
visible foreign body but fluorescein dye reveals corneal striations, the foreign body will be beneath the
tarsus.
'reatment:
If there is significant blepharospasm, topical anesthesia should be induced. 'he body is ta/en out of its bed
with a fine needle or cannula. 'he defect created by the body will be often contaminated with rust or
infiltrated with leu/ocytes. 'his defect is cleaned and treated with an antibiotic ointment and bandaged if
necessary. After everting the upper and lower eyelids, subtarsal foreign bodies are removed with a moist
cotton swab.
2B!. Cornea erosions
Etiology:
'his follows initial trauma to the surface cornea, such as the fingernail of a child carried in the parentIs
arms, a spi/ed+leaf palm tree, or a branch snapping bac/. (roperly treated, this epithelial defect usually
heals within # to 2 days. .owever, occasionally, the epithelial cells do not properly adhere to CowmanIs
layer so that the epithelium repeatedly ruptures. 'his characteristically occurs in the morning when the
patient wa/es up and suddenly opens his eyes.
0ymptoms and diagnosis:
Immediately after the in2ury, the patient experiences a severe foreign body sensation associated with
tearing. Cecause there is actually a defect in the surface of the cornea, the patient has the sub2ective
sensation of a foreign body within the eye. 'he epithelial defect causes severe pain, which elicits
blepharospasm. Additional symptoms include immediate eyelid swelling and con2unctival in2ection.
5luorescein dye will reveal the defect.
'reatment:
1ontinued topical anesthesia is not recommended because it slows healing and predisposes the anesthetised
cornea to further in2ury. An antibiotic ointment eye bandage is used. 4ecurrent corneal erosion often
re*uires hospitali,ation. Cilateral bandages are placed to ensure that the eyes are completely immobili,ed.
..!) 2erato*ast$
2BA. Penetrating 2erato*ast$
'his is a corneal surgical procedure that involves replacement of diseased corneal tissue with a full+
thic/ness donor graft of corneal tissue. A clear, regularly refracting button of donor cornea is sutured with a
continuous single or double suture or with interrupted sutures.
(enetrating /eratoplasty can be performed as an elective procedure to improve visual acuity or as an
emergency procedure %emergency /eratoplasty&. Emergency /eratoplasty is indicated to treat a perforated
or non+healing corneal ulcer to remove the perforation site and save the eye.
Indications:
1orneal diseases that affect the full thic/ness of the corneal stroma %corneal scars, dystrophy, or
degeneration& or curvature anomalies such as /eratoconus or /eratoglobus with or without central corneal
opacification.
Allograft re2ection %1omplications&:
'he bodyIs immune system can respond with a chronic focal allograft re2ection or a diffuse allograft
re2ection. 'he graft will become opacified.
2B7. /a"ear 2erato*ast$
'his involves replacement of a superficial stromal opacification with a partial+thic/ness donor graft of
clear corneal tissue.
'his surgery re*uires the corneal endothelium, 6escemetIs membrane, and the deeper layers of the
cornea to be intact and healthy as it is only suitable for removing superficial opacifications down to about
the middle of the cornea. 'he donor corneal button is then sutured with one or two continuous sutures or
with interrupted sutures.
Indications:
1orneal opacifications and scars affecting the superficial corneal stroma %post+traumatic, degenerative,
dystrophic, or post+inflammatory opacifications&. 'his method is not suitable for treating corneal ulcers.
Allograft re2ection %1omplications&:
It is less fre*uent than in the case of penetrating /eratoplasty. 'here is also less danger of infection
as lamellar /eratoplasty does not involve the globe.
.3a) deter"ination o# vis&a a!&it$1 !o""on !a&ses o# vis&a *ro%e"s
a) S&%-e!tive "ethods
Jisual acuity, the sharpness of near and distance vision, is tested separately for each eye. )ne eye
is covered with a piece of paper or the palm of the hand.
'he general practitioner can perform an approximate test of visual acuity. It is measured with a
display of different+si,ed targets shown at a standard distance from the eye. 5or example, the familiar
>0nellen chart? is composed of a series of progressively smaller rows of random letters used to test distance
vision. Each row is designated by a number corresponding to the distance, from which a normal eye can
read all the letters of the row. 5or example, the letters in the >#0 ? row are large enough for the normal eye
to see from #0 meters away. Cy convention, distance vision is measured at a distance = meters.
'he eye charts must be clean and well illuminated for the examination. 'he >illiterate E? chart is
used to test small children or if there is a language barrier. >E? figures are randomly rotated in each of four
different orientations throughout the chart. 5or each target, the patient is as/ed to point in the same
direction as the three >bars? of the E. $ost children can be tested this way at about age !.7.
'he sharpness of vision measured is expressed as a fraction:
actual distance
++++++++++++++++++++ 9 visual acuity.
standard distance
-ormal visual acuity is =;=, or #.0 as a decimal number, where the actual distance e*uals the standard
distance.
An example of !iminishe! visual acuity: 'he patients sees only the biggest symbol and none of
the smaller symbols on the chart at a distance of = meters %actual distance&. A normal+sighted person would
be able to recogni,e the biggest symbol at a distance of =0 meters %standard distance&. Accordingly, the
patient has a visual acuity of =;=0 or 0.#.
<ncorrected visual acuity is measured without glasses or contact lenses. 1orrected visual acuity
means that these aids were worn. 0ince poor uncorrected distance acuity may be due to refractive error,
corrected visual acuity is a more relevant assessment of ocular health.
If the patient cannot recogni,e the symbols on the eye chart at a distance of = meters, the examiner
shows the patient the chart at a distance of # meter. If the patient is still unable to recogni,e any symbols,
the examiner as/s the patient to count fingers, recogni,e the direction of hand motion, and recogni,e the
direction of a point light source.
%) O%-e!tive "ethods
It is unavoidable when the patient is unable to provide sub2ective information %for example with
infants& or when this information is unreliable.
2B=. Retinos!o*$ %shadow testing&: 'he retina is illuminated through the pupil. 'he examiner observes
the optical phenomena in the patientIs pupil while moving the light source.
2B3. Re#ra!to"etr$; 'he principle is based on ophtalmologic observation of a test image pro2ected on
the patientIs retina. 'he distance between the test figure and the eye is changed %or various lenses are
placed in the path of the light beam& until the image appears in focus on the retina. 4efraction can be
then calculated from the measured values.
Co""on !a&ses o# vis&a *ro%e"s
'he most common are refractive errors and cataracts. Cut in this topic you can tal/ about almost
any other eye disease of this topic list that is less common than these 2.....
.3%) a!&te in#e!tio&s !on-&n!tivitis
Con-&n!tivitis : genera notes
1on2unctivitis is an inflammatory process involving the surface of the eye and characteri,ed by
vascular dilation, cellular infiltration, and exudation. 2 forms are distinguished:
2BH. A!&te + )nset is abrupt and initially unilateral with inflammation of the second eye within # wee/.
6uration is less than A wee/s.
2BB. Chroni! + 6uration is longer than A wee/s.
Epidemiology:
It is one of the most fre*uent eye disorders.
Etiology:
1auses of con2unctivitis fall into 2 main categories:
!00. In#e!tio&s + bacterial, viral, parasitic, or mycotic
!0#. +on:in#e!tio&s + from a persistent irritation %such as lac/ of tear fluid or uncorrected refractive
error&, allergic, toxic %due to irritants such as smo/e, dust, etc.&, or as a result of another disorder %such
as 0teven+Rohnson syndrome&
0ymptoms:
'ypical symptoms include reddened eyes and stic/y eyelids in the morning due to increased secretion. Any
con2unctivitis also causes swelling of the eyelid, which appear partially closed %pseudoptosis&. 5oreign+
body sensation, a sensation of pressure, and a burning sensation are usually present, although these
symptoms may vary. Intense itching suggests an allergic reaction. (hotophobia and lacrimation %epiphora&
may also be present. 0imultaneous presence of blepharospasm suggests corneal involvement
%/eratocon2unctivitis&.
6iagnosis:
'here are many causes of con2unctivitis and the clinical picture may vary. 'o ma/e accurate diagnosis, we
have to evaluate following signs:
4yperemia: 4eddened eyes are a typical sign. 'he con2unctival in2ection is due to increased filling of
the con2unctival blood vessels. .yperemia is present in all forms of con2unctivitis. .owever, the
visibility of the hyperemic vessels and their location and si,e are important criteria for differential
diagnosis.
'he following types of in2ection are distinguished:
Con-&n!tiva in-e!tion %bright red, clearly visible distended vessels, decreasing toward the
limbus&:
1auses: con2unctival disorders, con2unctivitis.
Peri!ornea in-e!tion %superficial vessels, circular in the vicinity of the limbus&:
1auses: con2unctival disorders near the cornea: rosacea, corneal lesions near the limbus, foreign body,
herpetic /eratitis
Ciiar$ in-e!tion %not clearly visible, brightly colored vessels in the episclera near the limbus&
1auses: disorders of deeper tissues and intraocular structures: episcleritis, scleritis, disciform /eratitis,
iritis,
cyclitis
Co"*osite in-e!tion %fre*uent&
1auses: corneal disorders with intraocular irritation, corneal ulcerations
)ther signs to be evaluated for accurate diagnosis include: !ischarge, chemosis %con2unctival swelling&,
epiphora %excessive tearing&, follicles %lymphocytes accumulation&, papillae %polygonal >cobblestone?
con2unctival pro2ections + typical sign of allergic con2unctivitis&, membranes an! pseu!omembranes
%con2unctival reactions to severe infectious or toxic con2unctivitis: a pseudomembrane can be easily
removed without bleeding, a true membrane leaves behind a bleeding surface when removed&, s/ollen
lymph no!es %sign of viral con2unctivitis&, pannus formation %con2unctival or vascular ingrowth between
CowmanIs layer and the corneal epithelium&, and granulomas %inflamed nodes of con2unctival stroma with
circumscribed areas of reddening + sign of tuberculosis, sarcoidosis, or exogenous + foreign body, post+
operative&.
A!&te in#e!tio&s !on-&n!tivitis
'he normal con2unctiva contains microorganisms. Inflammation usually occurs as a result of
infection from direct contact with pathogens %such as from finger, towel, or swimming pool& but also from
complicating factors %such as compromised immune system or in2ury&.
Epidemiology:
It is very fre*uent.
Etiology:
0taphylococcus, streptococcus, and pneumococcus infections are most common in temperate countries.
6iphteric, pseudomonadal, gonococcal, .emophilus influen,ae, and moraxella con2unctivitis are less
common. .erpes simplex virus con2unctivitis and herpes ,oster ophtalmicus are also common.
0ymptoms:
'ypical symptoms include severe reddening, swelling, and purulent discharge that leads to formation of
yellowish crusts.
Staphylococcal con0unctivitis is subacute, with purulent discharge, and thic/ening of the con2unctiva at the
limbus. Streptococcal c. is subacute, with watery mucoid discharge, and pseudomembranes formation.
Pneumococcal c. is acute, moderately purulent with chemosis, and multiple subcon2unctival hemorrhages.
Diphteric c) is acute, moderately purulent, with membranes formation. Pseu!omonas c) is hyperacute with
purulent discharge and corneal involvement %the bacterium secrets an en,yme that can penetrate the cornea
within # day-& Infection may be spread by unsterile eye+drop bottles and contact lenses. 4emophilus
influen8ae c. is subacute, with serous, mucopurulent discharge. It is especially common in children.
+oraxella c) is subacute, with minimal discharge. 1orneal ulceration may occur. 4erpetic infections are
acute or mild with watery discharge.
'reatment:
It responds well to antibiotics. $ost of them are supplied as ointments %longer acting and suitable for
overnight therapy& and as eyedrops for topical therapy. (reparations that combine an antibiotic and
cortisone alleviate more rapidly sub2ective symptoms. .owever, such treatment has to be closely
monitored- In severe, uncertain, or persistent cases re*uiring microbiological examination to identify the
pathogen, treatment with broad+spectrum antibiotics is indicated and should begin immediately before
microbiology results.
1linical course and prognosis:
It responds well to treatment and remits within few days.
.3!) see to*i! 1C !
.5a) senie and !o"*i!ated !atara!ts
A) senie !atara!t
Definition of cataract: A cataract is present when the transparency of the lens is reduced to the point that
the patientIs vision is impaired.
@eneral symptoms:
6evelopment of the cataract and its symptoms is generally an occult process. (atients experience various
symptoms such as seeing only shades of grey, visual impairment, blurred vision, distorted vision, glare or
star bursts, monocular diplopia, altered color perception, etc. to varying degrees, and these symptoms will
vary with the specific type of cataract.
Senie !atara!t
Epidemiology:
It is by far the most fre*uent form of cataract %B0&. About #0 of all H0+year+olds suffer from a cataract
re*uiring surgery.
Etiology:
'he precise cause is not identified. 'he occurrence is often familial.
1lassification and forms of senile cataracts:
!02. #lassification accor!ing to maturity $!egree of visual impairment%
)eveo*ing !atara!t + Jisual acuity still full
I""at&re !atara!t + Jisual acuity reduced
)eveo*ed !atara!t + Jisual acuity severely reduced
Mat&re and H$*er"at&re !atara!t + Eight and dar/ perception, perception of hand movements in
front of the eye.
!0!. +orphologic classification:
+&!ear !atara!t: In the A
th
decade of life, the pressure of peripheral lens fibre production causes
hardening of the entire lens, especially the nucleus. 'he nucleus ta/es on a yellowish brown color.
Cecause they increase the refractive power of the lens, nuclear cataracts lead to lenticular myopia.
Duclear cataract generally develop very slowly. 6ue to lenticular myopia, near vision %even without
eyeglasses& remains good for a long time. Eyesight in twilight is often better than in daylight because
the mydriasis in dar/ness allows light past the opacity.
Corti!a !atara!t: Duclear cataract are often associated with changes in the lens cortex. It is
interesting that patients with cortical cataract tend to have ac*uired hyperopia in contrast to patients
with nuclear cataracts, who tend to be myopic. 8hereas changes in nuclear cataracts are due to
hardening, cortical changes are characteri,ed by increased water content. 1ortical cataracts progress
more rapidly than nuclear cataracts.
Posterior s&%!a*s&ar !atara!t: 'his is a special form of cortical cataract that begins in the visual
axis. Ceginning as a small cluster of opacities, this form of cataract expands peripherally in a dis/+li/e
pattern. As opacity increases, the rest of the cortex and the nucleus become involved. (osterior
subcapsular cataract leads to early, rapid, and severe loss of visual acuity. Dear vision is usually
significantly worse than distance vision. 6ilating eyedrops can improve visual acuity in this form of
cataract.
Mat&re !atara!t: 'he lens is diffusely white due to complete opacification of the cortex. 8here water
content is increased, a lens with mature cataract can swell and the capsule is under pressure. 'he
increasing thic/ness of the lens increases the resistance of the pupil and with it the ris/ of angle closure
glaucoma. Jision is reduced to perception of light and dar/, and the interior of the eye is no longer
visible. 1ataract surgery is re*uired to restore visual acuity.
H$*er"at&re !atara!t: If a mature cataract progresses to the point of complete li*uefaction of the
cortex, the dense nucleus will subside within the capsule. 'he pressure in the lens capsule decreases
and the capsule becomes wrin/led. 'his condition is the final stage that has usually developed over the
course of two decades. (rompt cataract extraction not only restores visual acuity but also prevents
development of phacolytic %phacolysis 9 lens dissolution& glaucoma %when the lens becomes
permeable for li*uefied lens substances, it will loose volume due to lea/age: the capsule will become
wrin/led: the escaping lens proteins will cause intraocular irritation and attract macrophages that then
cause congestion of the trabecular networ/ 9K phacolytic glaucoma&. Emergency extraction of the
hypermature cataract is indicated in phacolytic glaucoma to save the eye.
B) OTHER ACG(IRE) CATARACTS
!0A. Catara!t <ith s$ste"i! disease such as diabetes mellitus, galactosemia, renal insufficiency,
mannosidosis, 5abryIs disease, 8ilsonIs disease, myotonic dystrophy, tetany, and s/in disorders.
!07. Dia%etic cataract
It is rare in young diabetic patients. 'ransient metabolic decompensation promotes snowfla/e pattern
of cortical opacities. 6iabetic cataract progresses rapidly. 0enile cataracts are observed 7x as often in
older diabetics as in normal patients. 'hese cataracts also occur earlier %2 to ! years& than in normal
patients.
!0=. 1alactosemic cataract
'his deep posterior cortical opacity occurs after birth. If the disorder is diagnosed promptly and the
child is maintained on a galactose+free diet, the opacities of the first few wee/s of life will be
reversible. It is the only form of cataract that responds to conservative therapy.
!03. Co"*i!ated (se!ondar$ !atara!ts); 'his form can occur as a complication of any long+lasting
intraocular inflammation, especially chronic iridocyclitis, retinal vasculitis, and retinitis pigmentosa.
'he result is posterior subcapsular cataract that progresses toward the nucleus.
!0H. Posto*erative !atara!ts: $ost fre*uently following vitrectomy, silicone oil retinal tamponade,
and filtering operations.
!0B. Tra&"ati! !atara!ts: It includes contusion cataract, infrared radiation cataract %common in
glassblowerIs&, and cataract from ioni,ing radiation.
!#0. To4i! !atara!t; (rolonged topical or systemic corticosteroid therapy can result in posterior
subcapsular opacity. )ther less fre*uent toxic cataracts can result from chlorproma,ine or
cholinesterase inhibitors.
.5%) o*en ange ga&!o"a
Pri"ar$ o*en ange ga&!o"a %for secondary open angle glaucoma see topic 3C&
It begins in middle+aged and elderly patients with minimal symptoms that progressively worsen. 'he angle
of the anterior chamber characteristically remains open throughout clinical course of the disorder.
Epidemiology:
It is by far the most common form of glaucoma %over B0&. 'he incidence increases beyond the age of A0,
reaching a pea/ between the ages of =0 + 30. 'here appears to be a genetic predisposition.
Etiology:
'he precise cause is not /nown, although it is /nown that drainage of the a*ueous humor is impeded. 'he
primary lesion occurs as compression neuropathy of the optic nerve.
0ymptoms:
'he ma2ority of patients do not have any sub2ective symptoms for years. 'herefore, regular examination by
an ophtalmologist is crucial for early diagnosis- A small number of patients have occasional unspecific
symptoms such as headache, a burning sensation in the eyes, or blurred vision. 'he patient may also
perceive rings of color around light sources at night.
--- 8here increased I)( remains undiagnosed or untreated for years, glaucomatous optic nerve damage and
the associated visual field defect will reach blindness ---
6iagnosis:
+ +easurement of IOP: Elevated I)( in a routine examination is an alarming sign %K 22 mm .g&.
5luctuations in I)( may occur over a 2A+hour period.
+ 5onioscopy: 'he angle is open and appears normal.
+ Ophtalmoscopy: Examination of the optic nerve reveals whether glaucomatous cupping has already
occurred and how far advanced the glaucoma is.
+ Perimetry: Jisual field defects are characteri,ed by arcuate+shaped scotomas and a contraction of the
peripheral field, usually sparing the central vision until late. It is suitable as a screening test as it ma/es the
patient aware of scotomas. 0pecial programs reveal the earliest and more advanced glaucomatous changes.
6ifferential diagnosis:
!##. Ocular hypertension: (atients with ocular hypertension have increased I)( for years without
signs of glaucomatous optic nerve changes or visual field defects. 0ome patients in this group will
continue to have increased I)( but will not develop glaucomatous lesions: the others will develop
primary open angle glaucoma.
!#2. 'o/-tension glaucoma: (atients with low+tension glaucoma have typical progressive
glaucomatous changes without increased I)(. 'hese patients may have further worsening of the visual
field due to a drop in blood pressure.
'reatment:
0ee topics 2#C
(rophylaxis:
Do prophylactic action can be ta/en. Early diagnosis is crucial and can be only made by an ophtalmologist.
Cy the age of A0 at the latest, patients should have their I)( measured regularly.
(rognosis:
It depends on the stage at which it is diagnosed. @enerally, therapy is more effective the earlier it is
initiated.
.5!) %&nt in-&ries o# the e$e and adne4a
)cular contusions resulting from blunt trauma such as a fist, ball, champagne cor/, stone, and
falling on the eye are very common. 0ignificant deformation of the globe can result where the diameter of
the blunt ob2ect is less than that of the bony structures of the orbit.
1linical picture: 6eformation exerts significant traction on intraocular structures and can cause
them to tear. )ften there will be blood in the anterior chamber, which prevents the examiner from
evaluating the more posterior intraocular structures which can only be examined in mydriasis after a wee/
to ten days because medications that act on the pupil should not be administered as there is a ris/ of
irreversible mydriasis from a sphincter tear, and pupillary movements increase the ris/ of bleeding.
Initial treatment involves immobili,ing the eye, to allow intraocular blood to settle, because
subse*uent bleeding ! or A days after the in2ury is common.
(ossible in2uries resulting from blunt trauma include traumatic aniridia %total avulsion of the iris&
or iridodialysis %avulsion of the root of the iris& resulting in increased glare. 0uture of the base of the iris or
sun glasses are indicated in such cases. Avulsion of the ,onule fibers causes subluxation of the lens
resulting in lens dislocation and decreased visual acuity. 4emoval of the lens and implantation of a
prosthetic lens is indicated. Jitreous detachment %separation of the base of the vitreous body& causes a
patient to see floaters. Avulsion of the globe out of the orbit is fre*uently associated with avulsion of the
optic nerve: immediate blindness occurs and enucleation is necessary. 4etrobulbar hematoma results from
in2ury to retrobulbar vasculature, leading to orbital bleeding, eyelid hematoma, or exophtalmos. .yphema
%bleeding in the anterior chamber& causes blurred vision. .yphema resolves spontaneously. Jitreous
hemorrhage causes loss of visual acuity and it is identified by the lac/ of red reflex on retroillumination
during ophtalmoscopy. )rbital fracture %blow+out fracture& is a fracture of the floor of the orbit with
displacement into the maxillary sinus resulting in diplopia and elevation or depression deficit. 'reatment
consist of surgical repair.
Eate se*uelae of blunt trauma include secondary glaucoma, retinal detachment, and cataract. It
may occur years after the in2ury.