Basic optics of vision

Ophthalmology course no. 1

Gen Med Vth y
• Prerequisite • Purpose – as a general
– Anatomy of the eye practitioner you should
– Geometrical optics understand
(highschool) – Image formation
– Ocular optics
– Ammetropias
– Glass Rx
 • There are two types of lenses. These are
converging lenses (like magnifying glasses) and
Lenses diverging lenses (like those used in peep holes
in the front doors). Converging lenses are
thicker in the middle (surface is convex) and
diverging lenses are thicker on the outer edges
(surface is concave). The two names for the
lenses come from what they do to parallel light
rays as they enter the lens.
• Light arriving from a source very, very far away
(like infinitely far away) is made up of parallel
light rays.For purpose of eye modeling, infinite
far may be approximated as 5 m away.
• The point at which parallel light rays, parallel to
the principal axis, converge (or appear to
diverge from in the case of a diverging lense) is
known as the focal point (F). Any parallel rays
which are not also parallel to the principal axis
converge (or appear to diverge from) a point on
a plane which contains F known as the focal
plane (see below). When you use a camera
which uses film to record the image, the film
must be placed in the focal plane when the
subject being photographed is very, very far
away from the lens.
 Gaussian approximation
(paraxial or small angle approximation)
• In the paraxial, or Gaussian approximation,
the image of a point is assumed to be formed
by the rays close to optical axis - paraxial rays -
for which sine of the angle practically equals
the angle itself (in radians). Replacing sine by
the angle simplifies the expressions for
refraction and reflection (Snell’s law), allowing
for quick, yet accurate assessment of basic
spatial and geometric image properties.
 Lenses
The converging lens brings parallel rays
of light onto a single point – the focus.
The diverging lens – rays spread out;
when are extended back, they come
together at the focus.
Geometrical optics – ray tracing
• Basic rules
– Ray coming parallel to the
axis bends and passes
through the focus
– Ray coming through the
optical center does not
bend
• Note that for convex
lenses focus is beyond the
lens; for the concave
lenses focus is in front of
the lens, and you use
virtual ray extension
 The three rules of refraction
Convergent lens
• Any incident ray traveling parallel to the
principal axis of a converging lens will
refract through the lens and travel
through the focal point on the opposite
side of the lens.
• Any incident ray traveling through the
focal point on the way to the lens will
refract through the lens and travel
parallel to the principal axis.
• An incident ray that passes through the
center of the lens will in effect continue
in the same direction that it had when
it entered the lens.
Divergent lens
• Any incident ray traveling parallel to the
principal axis of a diverging lens will
refract through the lens and travel in
line with the focal point (i.e., in a
direction such that its extension will
pass through the focal point).
• Any incident ray traveling towards the
focal point on the way to the lens will
refract through the lens and travel
parallel to the principal axis.
• An incident ray that passes through the
center of the lens will in effect continue
in the same direction that it had when
it entered the lens.
Drawing image – convex lens
 Examples
Note position and magnification
Concave lens

Image is
•Upside – same orientation
as object
•Virtual – obtained by
crossing of ray extensions
•Cannot be projected on a
screen
 The Thin Lens Formula
• Lens diagrams have the main disadvantage that there is uncertainty in precisely where the image
is. Therefore the use of the lens formula is better. The lens formula is:

1/o+1/f=1/i

– [f - focal length; o - object distance; i - image distance; all are expressed in distance units – meters
(International System IS)]

• The magnification is worked out using this simple formula:

M = o/i

• Since o is in metres, and i is in metres, M has no units.

 Power of the lens
• Thicker lenses bend light more, and are therefore
described as more powerful. Powerful lenses have
short focal lengths. The power of a lens is measured
in dioptres (D) and is given by the formula:

Power = 1/focal length

• Unit of power is 1/meter = m-1 = diopter

 Cartesian Sign Convention +/-
• By Cartesian Convention, in diagrams light travels from left to right
• Any distance to the left of the lens is negative; to the right is
positive

• For a convex lens, the focal length is positive as the focus is real
(rays pass through the focus) and is to the right side of the lens on
diagram.
– Power of convex lens is positive (+ diopters)

• For a concave lens, the focal length is negative, because the

principal focus is virtual (ray extensions pass through the focus) and
is to the left side of the lens on diagram.
– Power of concave lens is negative (- diopters)

• If the image position gives a negative value, then the image

is virtual and to the left of the lens.
Problem – hand-held magnifying glass
• Find the position and size of a coin, 2 cm in diameter placed 33 cm from a
converging lens of +2 diopters

• Answer – note that object is between the secondary focus and the lens
• Go to IS units
• H = 2 cm = 2/100 m = 0.02 m
• o = -33cm = -0.33m
• Lens power P= +2dpt → focal distance f=1/P=1/+2.5dpt=0.50 m
• Lens formula 1/o+1/f=1/i
– 1/(-0.33)+1/0.50=1/i
– (-3)+2=1/i
– i= -1m
• Magnification M = o/i = -1/-0.33 = 3
• Therefore the image height is
• Him= M*Hob= 3*0.02m= 66cm
• Note that image is upside, larger and virtual
The human eye
•Functions like a camera
•Cornea and lens = convex
lens
•Retina = photo film

•An object at infinity (5m or

more) is focused clearly on
the retina by an emmetropic
eye = eye with no refractive
error
•Image is real (can be
captured on a screen),
inverted and smaller than the
object itself
 Static refraction
• The overall refractive status of the eye is determined
by four components:
– Corneal power (mean, 43 D)
– Anterior chamber depth (mean, 3.4 mm)
– Crystalline lens power (mean, 21 D)
– Axial length (mean, 24 mm)
• Most important refractive surface – cornea
– Since the indices of refraction for the various refractive
parts of the eye are all very similar (1.34 to 1.4), the largest
change in density occurs for light going from air to the
cornea (n=1 into n=1.38). This bends the light towards the
normal (ie, converges the light).
Static Refraction

• Emmetropia = the eye is in focus, image of an

object at infinite forms on the retina, without
need of active ocular mechanism of
accomodation
 Accomodation
Accommodation is the mechanism by which the eye changes its
refractive power by altering the shape of its crystalline lens. During
accommodation, the ciliary muscle contracts allowing the zonular fibers to
relax. This relaxation causes the equatorial edge of the lens to move away
from the sclera during accommodation resulting in increased lens
convexity (roundness). This increase in roundness primarily occurs on the
front surface of the lens.
a. The Amplitude of Accommodation, also known as the
accommodative response, is the maximum increase in diopter power
obtainable by an eye. The amplitude of accommodation is measured
monocularly.
b. The Range of Accommodation denotes the linear distance
(expressed in centimeters or meters) over which the accommodative
power allows an individual to maintain clear vision. The range lies
between the near point of accommodation and the far point of
accommodation. This is considered the most useful clinical measurement
of accommodation. It helps answer the question as to whether an
individual’s accommodative range comfortably encompasses his visual
needs.
 Ametropia
Ametropia (abnormal refractive state)=Refraction
errors.
parallel rays of light are not brought to a focus on the retina
in an eye at rest. A change in refraction is required to achieve
sharp vision.
 Ametropia
• Emetropia = focus
stands on the retina

• Hyperopia = focus
stands behind the
retina

• Myopia = focus
stands in front of the
retina

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 Myopia
short sightedness - the
optical refractive
power of the eye is
too high so the
parallel rays of light
are brought to a
focus in front of the
retina, (when the eye
is at rest).
causes:
1/↑ ant-post diameter of
the globe= axial
myopia

2/↑ curvature of the

cornea= curvature
myopia

3/↑ refractive index of

the lens= index
myopia

22
Hyperopia
(long sightedness); the optical power is too low so parallel rays of light
converge towards a point behind the retina, (when the eye is at rest).
causes:
1/↓ A-P diameter of the globe= axial hypermetropia.
2/↓ curvature of the cornea= curvature hypermetropia.
3/↓ refractive index of the lens= index hypermetropia.

23
 Emetrope – far/near point
• Far point – infinite (aprox. 5m)
• Near point – function of the range of
accomodation
– Ex. a 40 y old man with an amplitude of
accomodation of 3d has a near point at 33 cm
– Near point is very close to the eye for children,
becomes increasingly remote with age, usually at
60-65 y overlapping the far point at infinite (5m)
 Myope – far/near point

• Far point – closer than

infinite (5m), function
of the power of
myopia
• Near point – closer
then emmetrop’s near
point, as myopic
refraction adds to
accomodation in
focusing at near
 Spectacle correction of myopia by minus
spherical lenses
a. Rays from the far point
are focused on the
retina.
b. A negative lens whose
focal point coincides
with the far point
forms a virtual image
of rays from infinity at
the far point.
c. Rays from the infinity
strike the eye with a
vergence as if from
the far point and are
focused on the retina.

26
 Hyperope – far/near point
• Far point – it is virtual, obtained by tracing ray extensions and located
behind the eye, as rays focusing on retina should reach the eye in a
convergent bundle; it is relayed to infinite as hyperopic refraction is
compensated by accomodation, according to power and age.
• Near point – is further away then the emmetrope’s near point as part of
the accomodation is used for distance vision
• In many cases:
– Young hyperopic sees well at distance and at near
– Old hyperopic needs two pairs of spectacles
 Spectacle correction of hyperopia
by plus spherical lens.
a. The far point lies behind
the eye. Rays converging
to the far point lies
behind the eye. Rays
from the far point are
focused on the retina.
b. A plus lens focuses rays
from infinity at its focal
point, which is coincident
with the virtual far point.
c. Convergent rays strike the
eye and are focused on
the retina.

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 Astigmatism

Paraxial theory indicates that spherical refracting surfaces form point

images because these surfaces have constant curvatures in all
meridians.

Cylinders, conversely, have a maximum curvature along their

circumferential direction and zero curvature along their length, that is,
parallel to the cylinder axis. The zero curvature is 90 degrees to the
maximum curvature. A cylindrical refracting surface will form a line
image of a point parallel to the cylinder axis.

If the cylinder is bent into a doughnut shape, then the meridian that
formerly had zero curvature takes on a curvature. This curvature is less
than the circumferential curvature and is at 90 degrees to the latter.
Thus, a toric surface results, which forms two line images of a point at
right angles to each other and at different distances along the axis.
The distance between these line foci is called the interval of Sturm in
honor of the mathematician who investigated it in 1838.
 Astigmatism
• The bundle of light, as it traverses the interval of Sturm, has its cross-section
transformed from a horizontal line to a horizontal ellipse. Then it becomes circular
in section, and this position is known as the circle of least confusion. As the light
progresses, the section becomes elongated into a vertical ellipse. This narrows to a
vertical line at the end of the interval. The eye becomes astigmatic when any of its
refracting surfaces assume a toroidal shape. The astigmatism is termed regular if
the meridians of maximum and minimum curvature are at right angles to each
other. These meridians are called principal meridians.
Cylindrical lenses
 Cylindrical
refraction

• A line is imaged as a
point when
perpendicular to
the axis of the
cylinder (parallel to
the meridian)
• A line is imaged as a
line when parallel to
the axis
Sphero-cylindrical (toroidal) lenses
 Types of regular astigmatism
1-Simple hyperopic astigmatism.

2-Compound hypermetropic astigmatism

3-Simple myopic astigmatism

4-Compound myopic astigmatism

5-Mixed astigmatism
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 Presbyopia
• Usually at 40 y age
• Amplitutde of acomodation = 3-4 d
• Near point = 33-25 cm
• Need of near vision glasses
 Presbyopia - Principles of correction
• Plus lens depending on
amplitude of
accomodation
• Usually – we correct for
33 cm (3d), but keep in
mind asking patient’s
needs
• Rx = 3d – amplitude of
accom. (function of
age)
 Refractometry
• Method to subjectively or objectively measure
refractive error
• Subjective refractometry – test patient with
corrective lenses until distant vision is clear
• Objective refractometry – manual retinoscopy
or automated refractometry
• Non/cycloplegic refraction – use of topical
medication paralysing ciliary muscle
accomodative response
 Noncycloplegic Refractometry
• Manifest refraction – part of the refractive
error is masked by the accomodative response
– Acceptable for adults
– In most children – not suitable
• Accomodation spasm = false myopia
• Hypermetropia = underestimated; may induce
strabismus
 Cycloplegic refraction
Indications

• Accurate refraction in young children

• Distinguish true myopia from pseudomyopia
• Diagnose accommodative spasm
• All forms of strabismus, particularly esotropia
• Pharmacologic occlusion therapy in amblyopia
• Latent hyperopia
• Mentally disabled or uncooperative patient
• Visual acuity not consistent with manifest refraction
• Suspected malingering or hysteria
• Opacities in the ocular media
• Preoperative refractive laser patients
 Clinical Pearls
• Refractive errors – very important in children
• Uncorrected may induce amblyopia (lazy eye)
• Beware – anisometropic error (refraction significantly
different between the fellow eyes) may extremely
amblyopigenic
• Every child should be screened as early as possible –
ideally earlier then 1y of age
– Screening – paediatric infrared refractometer (Plus Optix,
2Win); good for identifying anisometropia, scans virtually
simultaneous both eyes
– For correction Rx – cycloplegic retinoscopy is mandatory
 Myopia
• Less amblyopigenic – normal visual development
by good near vision
• Should be corrected from 2y age if exceeds -2d
• Always do cycloplegic correction – false myopia
due to ciliary spasm may hide latent hyperopia;
most kids have minus refractometry readings…
• Do not correct refractometry readings, but
correct actual vision impairment
 Hyperopia
• May be amblyopigenic, especially if
anisometropia is present
• May induce squint – esotropia (convergent)
and rapidly induces amblyopia
• Anisometropia – Rx should encompass all the
inter-eye refraction difference
• Convergent squint – Rx = full cycloplegic
refraction
 Astigmatism
• Should always be corrected early during
childhood when exceeds 1d cylindrical power
• May induce meridional amblyopia, may be
astenopic later in life (induces fatigue)
• Later in life – cylindrical Rx may be difficult to
tolerate
http://ophysics.com/l16.html
 Take home message
• Refractive errors – very important early in life
• Uncorrected – may induce strabismus and
amblyopia (lazy eye), a condition which is
irreversible after 10y of age
• After 10 y – refractive errors are not disease;
they should be corrected according to vision
not to refractometry readings; uncorrected,
they do not induce disease but are source of
discomfort and fatigue…
Lids. Ocular surface. Cornea

Ophthalmology course no. 2

Gen Med Vth y
• Prerequisite • Purpose – as a general
– Anatomy of the eye practitioner you should
– Physiology of the eye understand
– Lid, ocular surface and
cornea pathology
– Referral criteria
– Differential of red eye
– Ophthalmic Rx
Lids
Benign nodules and
cysts - chalazion
• A chalazion (meibomian cyst) is a
chronic, sterile, granulomatous
inflammatory lesion caused by
retained sebaceous secretion
leaking from the meibomian or
other sebaceous glands into
adjacent stroma. A chalazion
secondarily infected is referred
to as an internal hordeolum.
• Tx – conservative – antibiotics
and steroids topical (ointment on
the outer surface, drops in the
conjunctival cul-de-sac); some
cases solve spontaneously. Warm
compresses and gentle massage
may help evacuate.
 Chalazion
• Surgery - The eyelid is
everted with a special
clamp, the cyst is
incised vertically and its
contents curetted
through the tarsal plate.
Cyst capsule must be
removed completely in
order to deter
recurrencies
 Other
benign
nodules
B
A

C D

(A) Epidermal inclusion cyst. (B) dermoid cyst; (C) sebaceous cysts; (D)
cyst of Zeis
 External hordeolum (stye)
• An external hordeolum (ie,
stye) is a localized infection or
inflammation of the eyelid
margin involving hair follicles
of the eyelashes.
• A hordeolum usually is painful,
erythematous, and localized. It
may produce edema of the
entire lid. Purulent material
exudes from the eyelash line.
• Tx – never express – risk of
complication – orbital
cellulitis, cavernous synus
thrombosis; instead incise and
evacuate, don’t stitch
Benign pigmented
lesions
• Congenital melanocytic
naevus - are uncommon and
histologically resemble their
acquired counterparts. Large
lesions have potential for
malignant transformation of
up to 15%.
• A kissing or split naevus is a
rare type of congenital naevus
that involves the upper and
lower eyelid and may
occasionally contain numerous
hairs.
• Tx, if necessary, involves
complete surgical excision.
Acquired melanocytic neavus
• Classification, clinical appearance and potential for malignant
transformation of naevi are determined by their histological
location within the skin as follows:
– a. Junctional naevus occurs in young individuals as a uniformly brown
macule or plaque. The naevus cells are located at the junction of the
epidermis and dermis and have a low potential for malignant a
transformation .
– b. Compound naevus occurs in middle-age as a raised papular lesion.
The shade of pigment varies from light tan to dark brown but tends to
be relatively uniform throughout . The naevus cells extend from the
epidermis into the dermis. It has a low malignant potential which is
related to the junctional component.
– c. Intradermal naevus, the most common, typically occurs in old age. It
is a papillomatous lesion, with little if any pigmentation, that may
show dilated vessels and protruding lashes (Fig. 1.10E). Histologically
the naevus cells are confined to the dermis and have no malignant
potential (Fig. 1.10F).
• Histological variants of naevi include balloon cell naevi, halo
b
naevi, Spitz naevi (juvenile melanomas) and dysplastic naevi
(atypical moles). Multiple dysplastic naevi constitute the
dysplastic naevus syndrome (atypical mole syndrome – AMS).
Individuals with AMS are at increased risk of developing
conjunctival and uveal naevi and cutaneous, conjunctival and
uveal melanomas.
• Tx is indicated for cosmetic reasons or concern about
malignancy. Excision must be complete because following
incomplete removal it may be difficult to differentiate
recurrence from melanoma both clinically and histologically. c
 Xanthelasma

• Xanthelasma is a common, frequently bilateral conditionwhich is

usually found in middle-aged and elderly individuals.
• Xanthelasma (and corneal arcus) can be associated with increased
levels of serum cholesterol, especially in young males.
• Histology shows lipid-laden histiocytes in the dermis.
• Signs. Multiple yellowish subcutaneous plaques usually located at
the medial aspects of the eyelids.
• Tx for cosmetic reasons is either by excision or destruction with a
carbon dioxide or argon laser. Patients with the highest recurrence
rate are those with persistently elevated cholesterol levels.
 Basal cell carcinoma
• BCC is the most common human
malignancy and most frequently affects
elderly patients.
• The most important risk factors are fair
skin, inability to tan and chronic
exposure to sunlight.
• Any ulcerated lesion on the lid, non-
healing for more than 1 month should
be considered as a potential carcinoma.
• The tumour is slow-growing and locally
invasive but nonmetastasizing.
• Tumours located near the medial
canthus are more prone to invade the
orbit and sinuses, are more difficult to
manage than those arising elsewhere
and carry the greatest risk of recurrence.
• Tumours that recur following incomplete
treatment tend to be more aggressive.
Squamous (spindle)
cell carcinoma
• SCC is a much less common, but
typically more aggressive tumour
than BCC with metastasis to regional
lymph nodes in about 20% of cases.
Careful surveillance of regional lymph
nodes is therefore an important
aspect of initial management. The
tumour may also exhibit perineural
spread to the intracranial cavity via
the orbit.
• It occurs most commonly in elderly
individuals with a fair complexion and
a history of chronic sun exposure.
• The tumour may be indistinguishable
• clinically from a BCC but surface
vascularization is usually absent,
growth is more rapid and
hyperkeratosis is more often present.
 Lentigo maligna
Melanoma
• Melanoma rarely develops on the
eyelids but is potentially lethal.
Although pigmentation is a hallmark
of skin melanomas, half of lid 1
melanomas are non-pigmented and
this may give rise to diagnostic
difficulties.
• 1. Lentigo maligna (melanoma in
situ) is an uncommon condition that
develops in sun-damaged skin in
elderly individuals. Malignant change
may occur, with infiltration of the
dermis.
• 2. Melanoma - histology shows large
2.a
atypical melanocytes within the
dermis.
– a. Superficial spreading melanoma is
characterized by a plaque with an
irregular outline and variable
pigmentation.
– b. Nodular melanoma is typically a
blue-black nodule surrounded by
normal skin. 2.b
 Ptosis
Ptosis is an abnormally low position of
the upper lid which may be
congenital or acquired.
1. Neurogenic ptosis is caused by an
innervational defect such as 3rd
nerve paresis and Horner syndrome.
2. Myogenic ptosis is caused by a
myopathy of the levator muscle itself,
or by impairment of transmission of
impulses at the neuromuscular
junction (neuromyopathic). Acquired
myogenic ptosis occurs in myasthenia
gravis, myotonic dystrophy and
progressive external
ophthalmoplegia.
3. Aponeurotic ptosis is caused by a
defect in the levator aponeurosis.
4. Mechanical ptosis is caused by the
gravitational effect of a mass or by
scarring.
1. Pathogenesis. Probably failure of neuronal migration
or development with muscular sequelae; a minority
are hereditary.
2. Signs:
• Unilateral or bilateral ptosis of variable severity.
Simple congenital
• Absent upper lid crease and poor levator
function.
• In downgaze the ptotic lid is higher than the
ptosis
normal because of poor relaxation of the levator
muscle. This is in contrast to acquired ptosis in
which the affected lid is either level with or lower
than the normal lid on downgaze.
• Following surgical correction the lid lag in downgaze
may worsen.
3. Associations:
• Superior rectus weakness may be present because
of its close embryological association with the
levator.
• Compensatory chin elevation in severe bilateral
cases.
• Refractive errors are common and more frequently
responsible for amblyopia than the ptosis
itself.
4. Treatment should be carried out during the preschool
years once accurate measurements can be obtained,
although it may be considered earlier in severe cases
to prevent amblyopia. Most cases require levator
resection.
• Involutional ptosis is an age- Involutional ptosis
related condition caused by
dehiscence, disinsertion or
stretching of the levator
aponeurosis, restricting
transmission of force from a
normal levator muscle to the
upper lid. Due to fatigue of the
Müller muscle it frequently
worsens towards the end of the
day, so that it can sometimes be
confused with myasthenic ptosis.
1. Signs
• Variable, usually bilateral, ptosis with a
high upper lid crease and good
levator function.
• In severe cases the upper lid crease
may be absent, the eyelid above the
tarsal plate very thin and the upper
sulcus deep.
2. Treatment options include levator
resection, advancement with
reinsertion or anterior levator repair.
 Ectropion
• Anterior rotation of the lid,
usually inferior lid, which
can cause epiphora,
conjunctival inflammation,
keratinization of the tarsal
conjunctiva, sometime
inferior corneal exposure
• Causes
– Involutional (exagerate laxity)
– Cicatricial (sclerodermia, after
burns)
– Paralytic (ipsilateral facial
nerve palsy)
– Mechanical – lid masses
(tumor, cyst)
Paralytic ectropion. Lagophthalmia
 Entropion
• Posterior rotation of the
lid, usually inferior lid,
generating irritation,
corneal erosions, in severe
cases ulceration and
pannus formation
• Causes
– Involutional – vertical lid
instability due to
attenuation of lid
retractors, overfunction of
orbicularis muscle
– Cicatricial – scarring of
tarsal conjunctiva
Ocular surface
 Symptoms
• Non-specific symptoms
include lacrimation, grittiness,
stinging and burning. Itching is
the hallmark of allergic
disease, although it may also
occur to a lesser extent in
blepharitis and dry eye.

• Significant pain, photophobia

or a marked foreign body
sensation do not belong to
conjunctival inflammation per
se and suggest corneal
involvement.
 Discharge
• 1. Watery discharge is composed
of a serous exudate and tears and
occurs in acute viral or acute
allergic conjunctivitis.
• 2. Mucoid discharge is typical of
chronic allergic conjunctivitis and
dry eye.
• 3. Mucopurulent discharge
typically occurs in chlamydial or
acute bacterial infection.
• 4. Moderately purulent discharge
occurs in acute bacterial
conjunctivitis.
• 5. Severe purulent discharge is
typical of gonococcal infection.
 Signs

• Hyperaemia (‘injection’) that is

diffuse, beefy-red and more intense
away from the limbus is typical of
bacterial infection.
• Haemorrhages may occur with viral
and occasionally bacterial
conjunctivitis.
• Chemosis (conjunctival oedema) may
occur when severe inflammation
produces a translucent swelling
which, if severe, may protrude
through the closed lids. Acute
chemosis usually indicates a
hypersensitivity response whereas
chronic oedema suggests orbital
outflow constriction.
 Signs
• Membranes
– a. Pseudomembranes consist of
coagulated exudate adherent to
the inflamed conjunctival
epithelium. They can be peeled
easily leaving the underlying
epithelium intact.
– b. True membranes involve the
superficial layers of the
conjunctival epithelium so that
attempted removal leads to
tearing.
• Subconjunctival scarring may
occur in trachoma and other
types of cicatrizing conjunctivitis.
Severe scarring is associated with
loss of goblet cells and accessory
lacrimal glands, and can lead to
cicatricial entropion.
• Follicles
– Multiple, discrete, slightly elevated lesions
resembling translucent grains of rice, most
prominent in the fornices. Blood vessels
run around or across rather than within
the lesions.
– Histology shows a subepithelial lymphoid
germinal centre with central immature
lymphocytes and mature cells peripherally.
– Causes include viral and chlamydial
conjunctivitis, Parinaud oculoglandular
syndrome and hypersensitivity to topical
medications.
• Papillae
– can develop only in the palpebral
conjunctiva and in the limbal bulbar
conjunctiva where it is attached to the
deeper fibrous layer.
– In contrast to follicles, a vascular core is
present.
– Histology shows folds of hyperplastic
conjunctival epithelium with a
fibrovascular core and subepithelial
stromal infiltration with inflammatory
cells. Late changes include superficial
stromal hyalinization, scarring, and the
formation of crypts containing goblet cells.
– Causes include bacterial conjunctivitis,
allergic conjunctivitis, chronic marginal
blepharitis, contact lens wear, superior
limbic keratoconjunctivitis and floppy
eyelid syndrome.
 Limphadenopathy

• The most common cause of lymphadenopathy

associated with conjunctivitis is viral infection.
It may also occur inchlamydial and severe
bacterial conjunctivitis (especiallygonococcal),
and Parinaud oculoglandular syndrome.The
preauricular site is typically affected.
 Acute bacterial
conjunctivitis

• Tx – topical +/- systemic

antibiotics
• Complication – corneal
ulcer
 Conjunctivitis
neonatorum
• First 5-7 d postpartum,
vaginal delivery
• Obtain mother genital
culture
• Emergency – risk of
cornea perforation
• Tx – antibiotics local
and systemic; ocular
surface generous saline
irrigation
Viral conjunctivitis
• Frequently epidemic
bursts
• Ocular lubricants
• Antibiotics topical in
case of abundant
mucopurulent secretion
• Frequent complication –
superficial punctate
keratitis; consider
topical steroids
 Allergic conjunctivitis
• Sometime seasonal
• Look for known allergies
• Avoid exposure
• Tx. Antihistamine
medication – topical
and systemic
• In severe cases consider
short time steroids
 Vernal
conjunctivitis
• Seasonal exacerbation
• Ig-E and cell-mediated immune-
allergic response
• Palpebral and limbal involvement
• Corneal involvement
– Superior punctate erosions
– Macroerosions
– Subepithelial scars
• Tx
– Lid hygiene
– Mast cell stabilizers
– Antihistamines
– Steroids – with moderation
– Immunosuppresors – cyclosporine
topical
• A triangular fibrovascular
subepithelial ingrowth of
degenerative bulbar conjunctival
tissue over the limbus onto the
Pterygium
cornea.
• Patients who have been living in hot
climates and may represent a
response to ultraviolet exposure and
possibly to other factors such as
chronic surface dryness.
• Interference with vision by obscuring
the visual axis or inducing
astigmatism.
• Pseudopterygium - a band of
conjunctiva adhering to an area of
compromised cornea at its apex. It
forms as a response to an acute
inflammatory episode such as a
chemical burn, corneal ulcer
(especially if marginal), trauma and
cicatrizing conjunctivitis.
• Tx
– Medical – ocular lubricants
– Surgical – excision +/- conjunctival
autograft, Mitomycin C, amniotic
membrane graft
Cornea
 Bacterial keratitis
• usually only develops when the
ocular defences have been
compromised.
• some bacteria (N. gonorrhoeae,
N. meningitidis,C. diphtheriae,
and H. influenzae) are able to
penetrate a normal corneal
epithelium, usually in association
with severe conjunctivitis.
• the most common pathogens are
the following:
– Pseudomonas aeruginosa –
aggressive, frequently contact lens
related
– Staphylococcus aureus
– Streptococci: S. pyogenes, S.
pneumoniae
 Clinical features
• 1. Presentation is with pain, photophobia,
blurred vision and mucopurulent or purulent
discharge.
• 2. Signs in chronological order:
– An epithelial defect associated with a larger
infiltrate.
– Enlargement of the infiltrate and the
epithelial defect.
– Stromal oedema, folds in Descemet
membrane and anterior uveitis.
– Chemosis and eyelid swelling in severe cases.
– Rapid progression of infiltration with an
enlarging hypopyon.
– Severe ulceration may lead to descemetocele
formation and perforation, particularly in
Pseudomonas infection .
– Endophthalmitis is rare in the absence of
perforation.
– Scarring, vascularization and opacification.
– Improvement is usually heralded by a
reduction of eyelid oedema and chemosis, as
well as shrinking of the epithelial defect and
decreasing infiltrate density.
• Hospital admission should be considered
for patients who are not likely to comply or
are unable to self-administer treatment. It
should also be considered for aggressive
disease particularly if involving an only eye.
Treatment
• Discontinuation of contact lens wear is
mandatory.
• Obtain corneal scraps and cultures
• Initiate empirically, broad spectrum topical
antibiotic – hourly for 24-48h then temper
– Monotherapy – 4th generation floroquinolone
– Combination therapy – 2nd/3rd generation
cephalosporines and aminoglycoside (use
fortified formulas)
– Modify tx according to clinical evolution and
culture results
• Mydriatics – reduce pain, prevent posterior
synechiae formation
• Steroids – comfort, reduce scarring; use
with care, may promote some
microorganisms replication
• Subconjunctival injections – consider when
poor compliance
• Systemic antibiotics – consider when
– Potential for systemic involvement
– Severe corneal thinning
– Scleral involvement
• Etiology
– Yeasts (candida spp)
Fungal keratitis
– Filamentous fungi (Fusarium,
Aspergillus)
• Common predisposing factors are
chronic ocular surface disease, long-
term use of topical steroids (often in
conjunction with prior corneal
transplantation), contact lens wear,
systemic immuno-suppression and
diabetes. Filamentary keratitis may
be associated with trauma, often
relatively minor, involving plant
matter or gardening/ agricultural
tools.
• Presentation is with a gradual onset
of pain, grittiness, photophobia,
blurred vision and watery or
mucopurulent discharge.

Candida keratitis
– Yellow-white densely suppurative
infiltrate
– A collar-stud morphology may be seen.
 Fungal keratitis
Filamentous keratitis
• A grey or yellow-white stromal
infiltrate with indistinct fluffy
margins.
• Progressive infiltration, often
with satellite lesions.
• Feathery branch-like extensions
or a ringshaped infiltrate may
develop.
• Rapid progression with necrosis
and thinning can occur.
• Penetration of an intact
Descemet membrane may occur
and lead to endophthalmitis
without evident perforation.
 Treatment
• Follow steps as for bacterial keratitis
• Topical antifungal – initially hourly for 24-48h then according to
evolution; treat at least 12 weeks (agents are generally fungistatic,
evolution is protracted)
– Amphotericin B, Fluconazol, Econazol, Natamicin
– Consider removing epithelium over the lesion to enhance penetration
of antifungal agents
• Always add broad spectrum antibiotic to prevent bacterial co-
infection
• Cycloplegics
• Subconjunctival fluconazol in severe cases
• Systemic antifungals (voriconazol) in risk of endophthalmitis
• Consider tetracycline/doxicycline for anticollagenase effect when
severe corneal thinning/risk of perforation
 Herpes simplex keratitis
• Most common infectious cause of corneal
blindness in developed countries
• Primary infection
– usually occurs in childhood, spread by droplet
transmission, but uncommon in first 6 month
(maternal antibody protection)
– self limited, mild fever, upper respiratory
simptoms
– ocular involvement – mild, self-limited
conjunctivitis/blepharitis
 Recurrent disease (reactivation)
• Following primary infection, latent virus is incorporated
in host DNA – cannot be eradicated; infection is located
in dermatomal sensory ganglion – eg. trigeminal
ganglion
• Clinical reactivation – trigerred by fever, immune
supression, fatigue, stress, trigeminal trauma,
hormonal change
• Site of reactivation – remote from the site of primary
disease
• Herpetic keratitis is recurrent disease
• Risk factors for severe disease: atopic eye disease,
childhood, immune supression, topical steroid abuse
 Epithelial disease
• Epithelial desquamation results in a
linear-branching (dendritic) ulcer,
most frequent located centrally.
• The ends of the ulcer have
characteristic terminal buds and the
bed of the ulcer stains well with
fluorescein.
• The virus-laden cells at the margin of
the ulcer stain with rose bengal.
• Corneal sensation is reduced.
• Inadvertent topical steroid treatment
may promote progressive
enlargement of the ulcer to a
geographical configuration.
• Mild associated subepithelial haze is
typical.
 Tx
• Treatment of HSV disease is
predominantly with nucleoside
(purine or pyrimidine) analogues that
are incorporated to form abnormal
viral DNA.
• Aciclovir, ganciclovir and trifluridine
have low toxicity and approximately
equivalent effect.
• The majority of dendritic ulcers will
eventually heal spontaneously
without treatment, though scarring
and vascularization may be more
significant with more prolonged
disease.
• Oral antiviral therapy is probably
indicated in most immunodeficient
patients and may also be effective
alternatives to topical treatment
when the latter is poorly tolerated, or
in resistant cases.
 Deep interstitial keratitis
– disciform keratitis
• Following succesive recurrencies
• Active HSV infection of deep stromal layers and
endothelium and/or hypersensitivity reaction to viral
antigen in cornea
• A central zone of stromal oedema often with
overlying epithelial oedema; occasionally the lesion is
eccentric.
• Keratic precipitates underlying the oedema.
• Folds in Descemet membrane in severe cases.
• The IOP may be elevated.
• Reduced corneal sensation.
• Healed lesions often have a faint ring of stromal or
subepithelial opacification and thinning.
• Consecutive episodes may be associated with
gradually worsening subepithelial and/or stromal
scarring and superficial or deep vascularization.
• Mid-stromal scarring can give the appearance of
interstitial keratitis.
 Necrotizing stromal keratitis
• Stromal necrosis and melting,
often with profound interstitial
opacification .
• Anterior uveitis with keratic
precipitates underlying the area
of active stromal infiltration.
• An epithelial defect may be
present.
• Progression to scarring,
vascularization and lipid
deposition is common.
• Tx. – for both disciform and
necrotizing keratitis includes:
– Topical steroids
– Antiviral protection – topical and
systemic
– Consider immunosupresives -
cyclosporine
 Neurotrophic metaherpetic keratitis
• Failure of re-epithelialization
resulting from corneal
anaesthesia, often exacerbated
by other factors such as drug
toxicity.
• A non-healing epithelial defect,
sometimes after prolonged
topical treatment
• Secondary bacterial or fungal
infection may occur.
• Tx
– Facilitate epithelization: lubricants,
trophycs, discontinue antiviral,
temper steroids
– Consider bandage lens,
blepharoraphy
 Herpes zoster
ophthalmicus
• Varicella zoster virus (VZV)
– Chicken pox (varicella)
– Shingles (herpes zoster)
• Primary infection – usually
chicken pox; VZV travels in a
retrograde manner to the dorsal
root and cranial nerve sensory
ganglia, where it may remain
dormant for decades, with
reactivation thought to occur
after VZV-specific cell-mediated
immunity has faded.
• HZO describes shingles involving
the dermatome supplied by the
ophthalmic division of the 5th
cranial (trigeminal) nerve.
1. Direct viral invasion may lead to
conjunctivitis and epithelial keratitis.
2. Secondary inflammation and occlusive
Mechanisms of
vasculitis may cause episcleritis, scleritis,
keratitis, uveitis, optic neuritis and cranial
nerve palsies. Inflammation and
ocular involvement
destruction of the peripheral nerves or
central ganglia, or altered signal
processing in the CNS may be responsible
for postherpetic neuralgia. Cicatrizing
complications may arise following severe
eyelid, periocular skin and conjunctival
involvement.
3. Reactivation causes necrosis and
inflammation in the affected sensory
ganglia, causing corneal anaesthesia that
may result in neurotrophic keratitis.

• Hutchinson sign describes involvement of

the skin supplied by the external nasal
nerve, a branch of the nasociliary nerve
supplying the tip, side and root of the
nose. The sign correlates strongly with
ocular involvement although there is no
correlation between the severity of the
rash and the severity of ocular
complications.
 HZO – Acute shingles
• Prodromal phase – fever, malaise,
headache
– Affected dermatome: itching or burning to
sever deep pain; elder patients with large
areas of involvement and severe pain = risk
of postherpetic neuralgia
• Skin lesions – always respect midline
(ddx herpes simplex)
– Erythematous areas with maculopapular
rush
– Within 24h groups of vesicles appear and
become confluent over 2-4 days
– vesicles often pass through a pustular
phase before they crust and dry after 2–3
weeks
– Large, deep haemorrhagic lesions are more
common in immunodeficient patients
– All lesions may leave depigmented scars
Acute eye disease

• Acute epithelial keratitis –

dendritic lesions, with tapered
ends, no terminal buds, stain
better with rose bengal than
with fluorescein.
• Episcleritis and scleritis
• Nummular keratitis - develops
at the site of epithelial lesions
about 10 days after the onset
of the rash; fine granular
subepithelial deposits
surrounded by a halo of
stromal haze
 Acute eye disease
• Stromal keratitis and disciform
keratitis – 5% of cases, usually 3wk
after onset of the rash – direct
stromal invasion/immune mediated
mechanism
• Acute keratouveitis – one third of
patients; accute iris ischaemia and
subsequent sectorial iris atrophy
• IOP elevation – common
• Neurological complications – cranial
nerve palsies, optic neuritis (rare);
beware CNS involvement
 Chronic eye
disease
• Neurotrophic keratitis – 50% of
patients, but usually mild; due
to sensorial denervation of the
cornea (cornea hipo/anestaesia)
• Patchy scleral atrophy
• Eyelid scarring with cicatricial
ectropion / entropion
• Recurrencies
• Post-herpetic neuralgia – up to
75% of patients of 70y; may
impair quality of life
 Tx
• Antiviral
– Topical – acyclovir, gancyclovir p.i.d.
– Systemic – acyclovir 800mg p.i.d
• Steroids – not during active epithelial disease;
consider in late immune-mediated disease,
uveitis, IOP elevation, better in association
with antivirals
• Ocular surface protection – tear substitutes,
ointments in late disease
 Peripheral
ulcerative keratitis
• Primary, idiopathic = Mooren
ulcer
• Secondary – systemic
associations = autoimmune
diseases, collagen vascular
diseases, most frequent –
rheumatoid arthritis
• Progressive peripheral stromal
melting; risk of perforation; may
involve central spread (Mooren)
or limbal inflammation
(systemic)
• Tx – steroids /
immunosuppresive topical or
systemic
• Loss of the trigeminal innervation to
the cornea resulting in partial or Neurotrophic
complete anaesthesia
• Impairment of epithelial healing and
loss of goblet cells, culminating in
keratitis
epithelial breakdown and persistent
ulceration
• Causes
– Acquired damage to trigeminal nerve
or ganglion – stroke, tumour
(accoustic neurinoma), aneurysm
– Ocular disease – herpes (simplex,
zoster), abuse of topical anaesthetic,
chemical burn and refractive corneal
surgery
– Systemic – diabetes, leprosy
– Congenital
• Signs
– Persistent epithelial defect usually
central, with rolled edges
– Asymptomatic stromal melting, rarely
perforation
• Tx – tear substitues and ointments;
in severe cases consider partial
blepharoraphy
• Result of incomplete lid closure
(lagophthalmos) Exposure
• Drying of the cornea despite normal
tear production. keratopathy
• Causes
– Neuroparalytic, especially facial nerve
palsy which may be idiopathic or the
result of surgery for an acoustic
neuroma or parotid tumour.
– Reduced muscle tone as in coma or
parkinsonism
– Mechanical – eyelid scarring (burns,
zoster, cicatricial pemphigoid), tight
facial skin (sclerodermia,
blepharoplasty)
– Severe proptosis (thyroid eye disease
– Graves)
• Signs
– Persistent epithelial defects – usually
inferior
– Stromal melting, risk of perforation
– Secondary infection
• Tx – ocular lubricants and
ointments; partial blepharoraphy in
irreversible exposure
 Corneal ectasia -
• Progressive disorder in which the
cornea assumes a conical shape
keratoconus
secondary to stromal thinning and
protrusion
• Central or paracentral stromal
thinning, accompanied by apical
protrusion and irregular astigmatism.
• Can be graded by keratometry
according to severity as mild (<48 D),
moderate (48–54 D) and severe (>54
D).
• Complication – acute hydrops, scarring
• Tx
– Optical – spectacles, rigid contact lenses
– Pathogenical – corneal collagen
crosslinking
– Intracorneal ring segment implantation
– Keratoplasty
 Take home message
Red eye differentials
• Peripheral hyperaemia
– More severe in the
conjunctival fornices
– Resides in superficial
conjunctival plexus
vasodilation
– Bright red in colour
– Usually ocular surface
disease
 Take home message
Red eye differentials
• Central (perikeratic)
hyperaemia
– More severe near the
limbus
– Resides in deep
conjunctival and
episcleral plexuses
vasodilation
– Dark red in colour
– Usually intraocular
inflammation
 Glaucoma

Ophthalmology course no. 3

Gen Med Vth y
• Prerequisite • Purpose – as a general
– Anatomy of the eye practitioner you should
– Physiology of the eye understand
– Basic notions of fluid – Glaucoma as a blinding
dynamics disease
– Phamacology – Impact of glaucoma on
healthcare
– Follow-up principles
– Antiglaucomatous Rx
 Epidemiology
• Glaucoma = 2nd cause of blindness worlwide
• 8,4 million people blind from glaucoma
• POAG – prevalence 2% in adults over 40
– 2.2 million people in US (2004), will be 3.3 million in
2020
– Large differences between ethnoracial groups
• PACG – high prevalence in Inuit, Chinese and
other Asian ethnoracial groups
– Prevalence 0.7% worldwide, adults over 40 = 20.2
million people, aut of which 15.5 million in Asia
 What is glaucoma?
• Glaucoma = large umbrella diagnosis, multiple
pathological entities which have in common optic
nerve damage with:
– Morphological impairment – loss of nerve fibers
(ganglion cell axons)
• Optic cup enlargement
• Nerve fiber layer defects
– Functional impairment – loss of retinal sensitivity in
midperipheral areas with visual field depression
• IOP rise – is only a risk factor, but lowering IOP is
the only available treatment in order to delay
visual impairment
Acqueos secretion
Acqueos outflow
 Anterior
chamber angle
 Acqueos dynamics
• Fa= Ftrab+Fus(alt)
– Ftrab Pressure dependent
– Fus Pressure independent

• Ftrab=(IOP-Pv)/Rtrab
• Ftrab=(IOP-Pv)*Ctrab
• Ctrab=1/ Rtrab
IOP
IOP
Gonioscopy
Angle anatomy
Angle grading
Indentation gonioscopy
Optic nerve head (ONH)
Normal optic disc
C/D ratio variability – normal ONH
C/D=0.2 C/D=0.8, large physiological
Histopathology – nerve fiber damage

*
Progression
Vertical C/D ratio
End-stage glaucomatous cupping
RNFL defect (retinal nerve fiber layer)
 OCT- ONH
Optical Coherence Tomography
Glaucoma analisys report
Perimetry
Goldmann kinetic
perimetry
Static automated perimetry (SAP)
 POAG - DISEASE DEFINITION
Primary open angle glaucoma

• Primary open-angle glaucoma (POAG) is a

chronic, progressive optic neuropathy in
adults in which there is a characteristic
acquired atrophy of the optic nerve and loss
of retinal ganglion cells and their axons. This
condition is associated with an open anterior
chamber angle by gonioscopy.
• (AAO 2015 – PPP)
Primary open-angle glaucoma is a chronic ocular disease process that is progressive,
generally bilateral, but often asymmetric. It is associated with the following
characteristics:
• Evidence of optic nerve damage from either, or both, of the following: Œ
– Optic disc or retinal nerve fiber layer (RNFL) structural abnormalities ƒ
• Diffuse or focal narrowing, or notching, of the optic disc rim, especially at the inferior or superior poles, which
forms the basis for the ISNT rule.ƒ
• Progressive narrowing of the neuroretinal rim with an associated increase in cupping of the optic disc.
• Diffuse or localized abnormalities of the parapapillary RNFL, especially at the inferior or superior poles .
• Disc rim, parapapillary RNFL, or lamina cribrosa hemorrhages ƒ
• Optic disc neural rim asymmetry of the two eyes consistent with loss of neural tissue ƒ
• Large extent of parapapillary atrophy Œ
• Reliable and reproducible visual field abnormality considered a valid representation of
the subject’s functional status ƒ
– Visual field damage consistent with RNFL damage (e.g., nasal step, arcuate field defect, or paracentral
depression in clusters of test sites) ƒ
– Visual field loss across the horizontal midline in one hemifield that exceeds loss in the opposite
hemifield (in early/moderate cases) ƒ
– Absence of other known explanations (e.g., optic disc drusen, optic nerve pit) ‹
• Adult onset ‹
• Open anterior chamber angles ‹
• Absence of other known explanations (i.e., secondary glaucoma) for progressive
glaucomatous optic nerve change (e.g., pigment dispersion, pseudoexfoliation
[exfoliation syndrome], uveitis, trauma, and corticosteroid use)
 RISK FACTORS ‹
• Higher IOP
• Older age
• Family history of glaucoma
• African race or Latino/Hispanic ethnicity
• Thinner central cornea
• Lower ocular perfusion pressure
• Type 2 diabetes mellitus
• Myopia
• Lower systolic and diastolic blood pressure
• Disc hemorrhage
• Larger cup-to-disc ratio
• Higher pattern standard deviation on threshold visual field
testing
Tx
 Laser trabeculoplasty
• ALT – thermal effect
• SLT – biological complex effect, repeatable
 Incisional glaucoma surgery
• Trabeculectomy – gold standard
• Acqueos shunts
• Non-penetrating surgery
– Deep sclerectomy
– Viscocanalostomy
• Ab interno surgery – trabectome, ABIC
 PACG – disease definition
Primary angle closure is appositional or synechial closure of the
anterior chamber angle - multiple mechanisms:
• Pupillary block is a key element in the pathogenesis of most
instances of PAC. The pressure in the posterior chamber is higher
than in the anterior chamber due to blockage of aqueous humor
flow from the posterior chamber at the pupil, causing an anterior
bowing of the iris that crowds the angle in predisposed eyes.
• Additional mechanisms - the relative position and thickness of the
ciliary body, the location of the iris insertion into the ciliary body,
and the volume of the iris.
• Certain anatomical features can increase this pressure disparity
between the two chambers (e.g., pupil dilation and the crystalline
lens size, shape, position, and thickening with age), which then
results in iris apposition to the anterior chamber angle structures.
In a minority of cases, this can happen acutely, resulting in acute
angle closure.
 PAC
• Prolonged or repeated
contact of the peripheral iris
with the trabecular
meshwork may lead to
functional damage of the
trabecular meshwork and
the development of PAS.
• Angle closure may or may
not be associated with
elevated IOP or
glaucomatous optic
neuropathy, and it may
occur in either an acute or
chronic form.
 Primary Angle Closure and Primary
Angle-Closure Glaucoma

• Any eye that has at least 180

degrees of ITC and an elevated IOP
or PAS with no secondary cause for
the PAS is classified as having PAC.
• The presence of high IOP and/or
PAS suggests that ITC noted during
gonioscopy may be causing
permanent histopathologic changes
to the eye.
• When glaucomatous optic
neuropathy is present (as defined in
the Primary Open-Angle Glaucoma
PPP), the eye has progressed from
PAC to primary angle-closure
glaucoma (PACG).
 Acute Angle-
Closure Crisis
If the anterior chamber angle is
obstructed suddenly, the IOP can rise
rapidly to high levels. The
characteristic clinical signs and
symptoms include
• pressure-induced corneal edema
(experienced as blurred vision and
occasionally as multicolored haloes
around lights)
• middilated pupil
• vascular (i.e., conjunctival and
episcleral) congestion
• eye pain, headache, nausea, and/or
vomiting.
Acute angle-closure crisis may be self-
limited and resolve spontaneously or
it may recur. Untreated, may cause
permanent vision loss or blindness.
The fellow eye is also at high risk of
AACC.
 Tx
• In PACS and PAC
– Obtain patent laser
periheral iridotomy
(LPI)
– Asses IOP
– Medical tx as
needed
• In AACC
– Lower IOP – systemic and topical medication
– When IOP<40 mmHg
• Pilocarpine
• Obtain LPI
 Uveitis

Ophthalmology course no. 4

Gen Med Vth y
• Prerequisite • Purpose – as a general
– Anatomy of the eye practitioner you should
– Physiology of the eye understand
– Basic notions of – Ocular inflammation
immunology – Systemic associations
– Basic notions of – Follow-up principles
microbiology – Tx
– Phamacology
 Definition
• Uvea = the vascular
layer of the eye (iris,
ciliary body, choroid)
• Uveitis = inflammation
of the uveal tract
(stricto sensu), usually
describes many forms
of intraocular
inflammation, including
retina and its vessels
• Anterior uveitis may be subdivided into:
– Iritis in which the inflammation primarily
involves the iris. Topography
– Iridocyclitis in which both the iris and the
pars plicata of the ciliary body are involved.
• Intermediate uveitis is defined as
inflammation predominantly involving
the pars plana, the peripheral retina and
the vitreous.
• Posterior uveitis involves the fundus
posterior to the vitreous base.
– Retinitis with the primary focus in the
retina.
– Choroiditis with the primary focus in the
choroid.
– Vasculitis which may involve veins, arteries
or both.
• Panuveitis implies involvement of the
entire uveal tract without a
predominant site of inflammation.
• Endophthalmitis implies inflammation,
often purulent, involving all intraocular
tissues except the sclera.
• Panophthalmitis involves the entire
globe, often with orbital extension.
 Clinical definitions
1. Onset may be sudden or insidious.
2. Duration of an attack may be either limited, if 3 months
or less in duration, or persistent, if longer.
3. Acute uveitis describes the course of a specific uveitis
syndrome characterized by sudden onset and limited
duration.
4. Chronic uveitis describes persistent inflammation
characterized by prompt relapse (in less than 3 months)
after discontinuation of therapy.
5. Recurrent uveitis is characterized by repeated episodes
of uveitis separated by periods of inactivity
without treatment lasting at least 3 months.
6. Remission refers to inactive disease for at least 3
months after discontinuation of treatment.
7. Resistant
• To steroids if there is no clinical improvement
despite 2 weeks of treatment with maximal dose.
• To immunosuppressives if there is no clinical
improvement despite 3 months of treatment.
 Acute anterior
uveitis (AAU)
1. Presentation is typically with sudden
onset of unilateral pain, photophobia
and redness, which may be associated
with lacrimation. Occasionally patients
may notice mild ocular discomfort a few
days before the acute attack when
clinical signs are absent.
2. Visual acuity is usually good at
presentation except in eyes with severe
hypopyon.
3. External examination shows ciliary
(circumcorneal) injection which has a
violaceous hue.
4. Miosis due to sphincter spasm may
predispose to the formation of
posterior synechiae unless the pupil is
pharmacologically dilated.
 AAU
5. Endothelial dusting by
a myriad of cells is
present early and gives
rise to a ‘dirty’
appearance.

True keratic
precipitates (KP)
usually appear only
after a few days and
are usually
nongranulomatous.
6. Aqueous cells indicate
disease activity and
their number reflects
disease severity . This
AAU
must be performed
before mydriasis
because in normal eyes
cells and pigment
clumps may develop
after pupillary
dilatation.
7. Anterior vitreous cells
indicate iridocyclitis.
8. Aqueous flare reflects
the presence of protein
due to a breakdown of
the blood–aqueous
barrier. Flare may be
graded clinically by
observing the degree
of interference in the
visualization of iris.
 AAU
9. Aqueous fibrinous exudate typically
occurs in HLAB27-associated AAU.

10. Hypopyon is a feature of intense

inflammation in which cells settle in the
inferior part of the anterior chamber
(AC) and form a horizontal level.

• In AAU associated with HLA-B27 the hypopyon

has a high fibrin content which makes it dense,
immobile and slow to absorb.
• In patients with Behçet syndrome the hypopyon
has minimal fibrin and therefore shifts according
to the patient’s head position and may disappear
quickly.
• Hypopyon associated with blood may occur in
herpetic infection and in eyes with associated
rubeosis iridis.
 AAU
11. Posterior synechiae may develop quickly and
must be broken down before they become
permanent
12. Low intraocular pressure (IOP) may occur as
a result of reduced secretion of aqueous by
the ciliary epithelium. Occasionally the
intraocular pressure may be elevated
(hypertensive uveitis) as in herpetic uveitis
and Posner–Schlossman syndrome.
13. Fundus examination is usually normal, but
should always be performed to exclude
‘spillover’ anterior uveitis associated with a
posterior focus, notably toxoplasmosis and
acute retinal necrosis.
14. Duration. With appropriate therapy the
inflammation tends to completely resolve
within 5–6 weeks.
15. The prognosis is usually very good.
Complications and poor visual prognosis are
related to delayed or inadequate
management. Steroid-induced hypertension
may occur but glaucomatous damage is
uncommon.
 Chronic anterior uveitis (CAU)
• Less common then AAU
• Persistent inflammation, promptly relapses
(<3months) after discontinuation of therapy
• Inflammation
– Granulomatous
– Non-granulomatous
• Bilateral involvement – more common
 CAU
• Presentation – insidious; almost lack of symptoms
until complications (cataract, band keratopathy)
• Need for careful screening, especially in juvenile
idiopathic arthritis
• External examination – white eye; occasionaly
discrete ciliary flush during exacerbations
• Aqueous cells – vary, but even when numerous,
symptoms may lack
• Aqueous flare – may be more marked than cells,
may act as indicator of disease activity
Keratic precipitates
(KP)
• KP - Aggregates of inflammatory
cells on the corneal endothelium
- epithelioid cells, lymphocytes
and polymorphs; their size,
aspect and distribution indicate
probable type of uveitis.

• Large KP in granulomatous
disease have a greasy (‘mutton-
fat’) appearance. They are often
more numerous inferiorly and
may form in a triangular pattern
with the apex pointing up (Arlt
triangle) – gravity and thermal
gradient
 KP
• Resolved mutton-fat KP
leave behind a
groundglass appearance
(ghost KP), which is
evidence of previous
granulomatous
inflammation.

• Long-standing non-
granulomatous KP may
become pigmented and
less dense centrally.
 CAU
• Dilated iris vessels
(pseudorubeosis) are
occasionally seen in long-
standing cases and resolve
with treatment.
• Iris nodules typically occur
in granulomatous disease.
– Koeppe nodules are small and
situated at the pupillary
border.
– Busacca nodules involve the
iris stroma.
– Large pink nodules are
characteristic of sarcoid
uveitis.
 CAU
• Iris atrophy – patchy
(herpes simplex), sectoral
(herpes zoster), diffuse
(Fuchs heterochromic
uveitis)
• Duration – prolonged
(months-years), with
frequent relapses
• Prognosis – guarded due
to complications –
cataract, band
keratopathy, glaucoma,
hipotony
Posterior uveitis (PU)
• Retinitis may be focal (solitary),
multifocal, geographic or diffuse.
Active lesions are characterized
by whitish retinal opacities with
indistinct borders due to
surrounding oedema. As the
lesion resolves, the borders
become better defined.

• Choroiditis may also be focal,

multifocal, geographic or diffuse.
It does not usually induce vitritis
in the absence of concomitant
retinal involvement. Active
choroiditis is characterized by a
round, yellow nodule.
 PU
• Vasculitis may occur as a primary
condition or as a secondary
phenomenon adjacent to a focus
of retinitis.
• Both arteries (periarteritis) and
veins (periphlebitis) may be
affected although venous
involvement is more common.
• Active vasculitis is characterized
by yellowish or grey-white,
patchy, perivascular cuffing that
may be associated with
haemorrhage.
• Quiescent vasculitis may leave
perivascular scarring, which
should not be mistaken for active
disease.
 Intermediate uveitis (IU)
• IU is an insidious, chronic, relapsing disease in which the vitreous is
the major site of inflammatory signs.
• The condition may be idiopathic or associated with a systemic
disease.
• Pars planitis (PP) is a subset of idiopathic IU in which there is
‘snowbanking’and/or ‘snowball’ formation.
 IU
• Presentation is with the insidious
onset of blurred vision often
accompanied by vitreous floaters.
• Anterior segment - few cells and
small scattered KP, occasionally
have a linear distribution in the
inferior cornea; some forms may
have severe anterior disease

• Vitreous - Vitreous cells with

anterior predominance are
universal; vitreous condensation
and haze in more severe cases.
Vitreous snowballs are usually
most numerous in the inferior
peripheral vitreous
 IU
• Posterior segment
– Peripheral periphlebitis
is common, particularly
in patients with MS
– Snowbanking is
characterized by a grey-
white fibrovascular
plaque which may occur
in all quadrants, but is
most frequently inferior
 Complications
• CMO occurs in 30% of cases
and is the major cause of
impaired visual acuity.
• Macular epiretinal formation is
common.
• Cataract and glaucoma
• Retinal detachment -
tractional, rhegmatogenous
and occasionally exudative;
retinoschisis has also been
described
• Vitreous haemorrhage may
occur from the snowbank or
disc new vessels, particularly
in children with PP.
Systemic associations
Systemic associations
Systemic associations
 Principles of treatment
• Treatment of immune-mediated uveitis
involves predominantly the use of anti-
inflammatory and immunosuppressive agents.
• Antibiotic therapy for infectious diseases
should be considered for specific diseases.
• It is important to keep in mind that drugs used
to treat uveitis have potential side-effects, and
this should always be weighed against the
decision to treat.
 Mydriatics
1. Short-acting
a. Tropicamide (0.5% and 1%) has
a duration of 6 hours.
b. Cyclopentolate (0.5% and 1%) Indications
has a duration of 24 hours. • To promote comfort by
c. Phenylephrine (2.5% and 10%) relieving spasm of the ciliary
has a duration of 3 hours but muscle and pupillary sphincter
no cycloplegia. • To break down recently
2. Long-acting formed posterior synechiae
a. Homatropine 2% has a • To prevent formation of
duration of up to 2 days. posterior synechiae
b. Atropine 1% is the most
powerful cycloplegic and
mydriatic with a duration of up
to 2 weeks.
 Topical steroids
1. Treatment of AAU is usually relatively straightforward.
• Initial therapy involves instillation either hourly
or even more frequently according to severity of
inflammation.
• Once the inflammation is controlled the frequency
should be carefully tapered to 2-hourly, followed
by 3-hourly, then four times a day and eventually
reduced by one drop a week. The drops are often
discontinued altogether by 5–6 weeks.
2. Treatment of CAU is more difficult because long-term
therapy is often required with the risk of complications
such as cataract and steroid-induced elevation of
intraocular pressure.
 Periocular steroid injection
• Therapeutic concentrations behind the lens may be
achieved.
• A prolonged effect can be achieved with ‘depot’
preparation such as triamcinolone acetonide.
• Indications
– In unilateral or asymmetrical intermediate or posterior
uveitis, periocular injections should be considered as first-
line therapy to control inflammation and macular oedema.
– In bilateral posterior uveitis either to supplement systemic
therapy or when systemic steroids are contraindicated.
– Poor compliance with topical or systemic medication.
– At the time of surgery in eyes with uveitis.
 Intraocular steroids
• Injection
– Triamcinolone acetonide (Vitreal S) is an option in
the treatment of posterior uveitis and CMO
unresponsive to other forms of therapy.
• Slow-release implants
– appear to be useful in patients with posterior
uveitis who do not respond to, or are intolerant
to, conventional treatment.
– fluocinolone acetonide, dexamethasone (Ozurdex)
 Systemic steroids
• Intermediate uveitis unresponsive to posterior
sub-Tenon injections.
• Sight-threatening posterior uveitis or
panuveitis, particularly with bilateral
involvement.
• Rarely, anterior uveitis resistant to topical
therapy.
• Occasionally prior to intraocular surgery as
prophylaxis against worsening inflammation.
 Immunosupressive medication
Indications
• Sight-threatening uveitis, which is usually bilateral, non-infectious,
reversible and has failed to respond to adequate steroid therapy.
• Steroid-sparing therapy in patients with intolerable side-effects
from systemic steroids or those with chronic relapsing disease
requiring a high doses of steroids
• Once a patient has been started on an immunosuppressive drug
and the appropriate dose ascertained, treatment should continue
for 6–24 months, after which gradual tapering and discontinuation
of medication should be attempted over the next 3–12 months.
However, some patients may require long-term therapy for control
of disease activity.
Antimetabolites: azathioprine, methotrexate, mycophenolate
Calcineurin inhibitors: cyclosporine, tacrolimus
 Biological blockers
• Interleukin receptor antagonists such as
daclizumab and anakinra.
• Tumour necrosis factor alpha antagonists
such as infliximab and adalimumab.

• Probably of good value in systemic immune

diseases – e.g. Behcet
 Lens

Ophthalmology course no. 5

Gen Med Vth y
• Prerequisite
– Anatomy of the eye
– Physiology of the eye
– Basic notions of physics
• Optics
• Ultrasound
• Fluid dynamics
• Purpose – as a general
practitioner you should
understand
– Classification of cataract
– Grading of cataract
– Systemic associations
– Surgical indication
– Surgical results
– Surgical referral and
follow-up
Crystalline lens
Anatomy
Anatomy
Lens epithelium
Lens fiber
Lens sutures
Age related
cataract
Posterior subcapsular cataract
Nuclear cataract
Nuclear cataract
Cortical cataract
Christmas tree cataract
 Intumescent cataract
Phacomorphic glaucoma
Mature cataract
Hypermature cataract
Morgagnian
cataract
Phacolytic glaucoma
 Pathologic cataract
• Cataract in systemic
diseases
– Diabetes
– Thyroid disfunction
– Cushing
– Prolonged steroid
treatment (iatrogenic
Cushing)
– Chronic alcohol abuse
– Myotonic distrophy
– Atopic dermatitis
 Complicated
cataract
• Cataract in ocular diseases
– Uveitis
– Acute angle closure
glaucoma
– Hereditary fundus
distrophies
– After ocular surgery –
vitrectomy, trabeculectomy
– Ocular trauma
Congenital cataract
Congenital cataract
Biometry
Surgery - incision
Capsulorhexis
Capsulorhexis
Phacochop
Quadrant removal
Epinucleus
Cortical cleaning
IOL in the bag
Ophthalmology Course No. 6

OCULAR TRAUMA
Ocular traumatology

IMPORTANCE
Q.o.L.
Vision loss
Organ loss
Social Costs – Young age
Hospitalization
Social reinsertion
Wellfare
BETT – Birmingham Eye Trauma
Terminology

Ferenc Kuhn
Trauma does not tolerate dogma…
Cesare Forlini

Pole to pole surgery

Minimally invasive surgery
Multiple gauge surgery
Eyewall

 Anatomy – 3 coats

 Traumatology
 Eyewall = sclera + cornea
External trauma (closed globe)
 Subconjunctival haemorrhage

 Conjunctival FB

 Conjunctival laceration
External trauma (closed globe)
 Corneal erosion

 Corneal FB
External trauma (closed globe)
 Corneal oedema

 Corneal partial thickness laceration

Blunt trauma – closed globe
injury
Mechanism of action – indirect
Equatorial expansion
Anterior trauma
 Hyphema
Anterior trauma
Iris trauma
Pupillary changes
-transient miosis – Vossius ring (direct action – imprinting)

-traumatic mydriasis (reversible/irreversible)

Anterior trauma
Iris trauma
 Sphincter ruptures
Anterior trauma
Iris trauma
 Iridodialysis
Angle anatomy
Angle recession
Ciclodyalisis cleft
Lens trauma

 Traumatic cataract
Lens trauma

 Zonular dehiscence

 Anterior/posterior lens luxation

IOP disturbances – early / late onset

- Hypertonia - hyphema resorbtion

- inflammation
- trabecular lesions
- Vs.
- Hypotonia - transient ciliary stop
- occult open globe?
- suprachoroidal space open
Penetrating injuries
 Direct mechanism – lacerations
 Location – at the point of impact
 Only entry port(s)
Stiches required
Penetrating injury IOFB
Penetrating injury IOFB
IOFB
 Location – any , from AC to subretinal
Perforating injury (orbital FB)

Entry port Exit port

Ruptures – blunt trauma
 Anatomical weak points – muscle insertions
(material fatigue)
 Acquired weak points – surgical incisions
Burns
Emergencies
Require action in seconds / minutes
 Retina

Ophthalmology course no. 5

Gen Med Vth y
• Prerequisite • Purpose – as a general
– Anatomy of the eye practitioner you should
– Physiology of the eye understand
– Basic notions of – Diabetic retinopathy
biochemistry and – Age-related macular
glucose metabolism degeneration
• Emergency and
periodic referral
• Follow-up patterns
 Diabetic retinopathy (DR)
• Diabetes mellitus is a group
of metabolic diseases
characterized by
hyperglycemia resulting
from defects in insulin
secretion, insulin action, or
both.
• The chronic hyperglycemia
of diabetes is associated
with long-term damage,
dysfunction, and failure of
various organs, especially
the eyes, kidneys, nerves,
heart, and blood vessels.
 DR
• Predominantly a microangiopathy
• Mechanisms of cellular damage
– Intracellular sorbitol accumulation
– oxidative stress due to free radical
excess
– accumulation of advanced glycation
end products
– excessive activation of several protein
kinase C isoforms
• Capillaropathy is characterized by
death of pericytes
– Leakage
– Capillary drop-out and occlusion
• Neovascularization is caused by
capillary nonperfusion – retinal
hipoxia
– Imbalance between angiogenic and
antiangiogenic factors: VEGF /
antiVEGF
Pathophysiology
 Nonproliferative DR (NPDR)
• Complication of
diabetes
• Directly due to the
systemic disease and
associated
hyperglycemia and
other metabolic
alterations
• May be prevented by
good metabolic control
NPDR - microaneurysms
 NPDR - haemorrhages
Deep dark haem. (haemorrhagic
Deep dot/blot haem. microinfarcts)
 NPDR - haemorrhages
Nerve fiber layer haem. Histologycal aspect
NPDR – hard exudates
Diabetic macular edema
Cystoid macular edema (CME)
CMO - treated
Ischemic maculopathy
 NPDR
Cotton-wool spots
(soft exudates) Venous changes
Severe NPDR (preproliferative)
IRMA
 Proliferative DR (PDR)
New vessels on the disk (NVD)
PDR – New vessels elsewhere (NVE)
AFG – NVD/NVE
 Treatment - DME
Focal macular photocoag Grid macular photocoag
 Treatment PDR
Panretinal photocoag (PRP) -
recent PRP - complete
 Advanced diabetic eye disease
Retrohialoydal haem. Intravitreal haem.
 Advanced diabetic eye disease
Tractional retina detachment Rubeosis iridis
 Age-related macular degeneration
(AMD)
Pelli-Robson chart (contrast
Snellen/LogMAR acuity chart sensitivity)
Amsler grid
Amsler grid
OCT
 Age related maculopathy
Hard drusen Soft drusen
 Age related maculopathy
Coalescent soft drusen
Drusenoid RPE detachment Calcified drusen
 Dry (non-exudative) AMD
Drusen and RPE atrophy Geographic atrophy
OCT – drusen and drusenoid PED
OCT – RPE atrophy
Exudative (wet) AMD - RPE
detachment
Haemorrhagic RPE detachment
RPE tear
Choroidal neovascularization (CNV)
Extensive lipid deposition Subretinal bleeding
 CNV
Disciform scarring Exudative retinal detachment
Occult CNV - subRPE
Classic CNV - subretinal
 CNV

intraretinal
subretinal
fluid