Red-eye syndrome

Red-eye syndrome

The majority of patients with acute red eye have a

relatively benign condition, such as bacterial,
viral, or allergic conjunctivitis, subconjunctival
hemorrhage, or blepharitis, which poses little or
no threat to vision.
 Conversely a few are at risk of rapid progression
within a few hours or days to severe visual
impairment, even blindness, such as from acute
angle-closure glaucoma, intraocular infection
(endophthalmitis), bacterial, viral, amebic, or
fungal corneal infection, acute uveitis, or scleritis.
 Red-eye syndrome

Pain, rather than discomfort, should be regarded as

inconsistent with conjunctivitis, episcleritis, or
blepharitis.
 It is suggestive of keratitis, intraocular or scleral
inflammation, or raised intraocular pressure, with the
likelihood of a serious cause increasing with increasing
severity.
Associated nausea and vomiting are particularly
suggestive of markedly raised intraocular pressure.
Deep, boring pain, typically waking the patient at
night, is characteristic of scleritis.
Photophobia characteristically occurs in keratitis and
anterior uveitis.
 Red-eye syndrome

Reduced vision, whether reported by the patient

or identified by measurement of visual acuity, in
the absence of a pre-existing explanation, should
also be regarded as inconsistent with
conjunctivitis, episcleritis, or blepharitis, and as
with pain, the greater the severity, the greater is
the likelihood of a serious cause.
Severity of redness is not necessarily a guide to
the seriousness of the underlying condition for
example, despite its bright red appearance,
subconjunctival hemorrhage is a benign entity.
 Red-eye syndrome

Distribution of redness can be helpful;

predominance around the limbus
(circumcorneal) is indicative of intraocular
disease, diffuse redness involving the tarsal
and bulbar conjunctiva is indicative of
conjunctivitis, focal or diffuse redness of the
globe is consistent with episcleritis, and
redness of the eyelid margins is indicative of
blepharitis.
 Red-eye syndrome

Bluish redness (violaceous discoloration) of the globe,

best identified in natural rather than artificial light, is
characteristic of scleritis.
 Vesicles or ulcerations of the lids or periocular skin
are typical of ophthalmic zoster (shingles) and less
commonly varicella or primary herpes simplex virus
infection.
Conjunctivitis usually causes purulent, mucoid, or
watery discharge, and allergic conjunctivitis typically
causes itching.
Profuse purulent discharge is characteristic of
gonococcal conjunctivitis, which requires emergency
treatment.
 Red-eye syndrome
 Any abnormality of the cornea apparent on gross examination, such
as ulceration or focal opacity, which may be due to infection, or
diffuse cloudiness, which may be due to markedly raised
intraocular pressure when it is usually associated with a semi-
dilated unreactive pupil, warrants emergency ophthalmologic
assessment unless it is known to be longstanding (eg, pterygium).
 Instillation of fluorescein facilitates identification of an epithelial
defect, including dendritic ulceration due to herpes simplex virus
keratitis.
 A constricted pupil is suggestive of intraocular inflammation,
typically due to anterior uveitis.

 Hypopyon (pus within the anterior chamber), a feature of

corneal infection, intraocular infection, or acute anterior uveitis
(iritis), necessitates emergency ophthalmologic assessment.
 Red-eye syndrome

 Slitlamp examination facilitates assessment of

distribution of redness; identification of conjunctival
abnormalities, including examination of the superior tarsal
conjunctiva following eversion of the upper eyelid;
 diagnosis of episcleritis and scleritis; characterization of
corneal lesions; and detection of corneal keratic
precipitates, anterior chamber flare and cells, and possibly
hypopyon indicative of anterior chamber inflammation due
to anterior uveitis, intraocular infection, or secondary to
corneal inflammation, including infection.
 In cases of intraocular inflammation, dilated fundal
examination is essential to determine whether there is
involvement of the vitreous, retina, or choroid, which is
important to diagnosis as well as assessment of severity.
 INFECTIONS &
INFLAMMATIONS OF THE
LIDS
 HORDEOLUM

 A hordeolum is an infection of one or more glands of the lid.

 When the meibomian glands are involved, it is called an internal
hordeolum.
 An external hordeolum (stye) is an infection of a gland of Zeis or Moll.
 Pain, redness, and swelling are the principal symptoms.
 An internal hordeolum may point to the skin or to the conjunctival
surface.
 An external hordeolum always points to the skin.
 Most hordeola are caused by staphylococcal infections, usually
Staphylococcus aureus.
 HORDEOLUM

 Treatment consists of warm compresses several times a

day for 10–15 minutes.

 If the process does not begin to resolve within 48 hours,
incision and drainage of the purulent material is indicated.

 Antibiotic ointment is routinely applied to the site.

 Systemic antibiotics are indicated if cellulitis develops.
 CHALAZION

 A chalazion is a sterile, focal, chronic inflammation of the lid that

results from obstruction of a meibomian gland.
 It is commonly associated with rosacea and posterior blepharitis.
 Symptoms begin with mild inflammation and tenderness that
persists over a period of weeks to months.
 It is differentiated from a hordeolum by the absence of acute
inflammatory signs.
 Most chalazia point toward the conjunctival surface, which may
be slightly reddened or elevated.
 If sufficiently large, a chalazion may press on the globe and cause
 astigmatism.
 Intervention is indicated if the lesion
is not amenable to a warm compress
regimen, distorts the vision,
or is aesthetically unacceptable.
 CHALAZION

Intralesional steroid injections alone may be

useful for small lesions and in combination
with excision for more chronic cases.
 ANTERIOR BLEPHARITIS

Anterior blepharitis is a common, chronic bilateral

inflammation of the lid margins.
There are two main types: staphylococcal and
seborrheic.
Staphylococcal blepharitis may be due to infection
with
S aureus, Staphylococcus epidermidis.
Often, both types of blepharitis are present (mixed).
 ANTERIOR BLEPHARITIS

The chief symptoms are irritation, burning, and itching

of the eyes and lid margins.
The eyes are “red-rimmed.” Many scales or scurf can
be seen clinging to the lashes of both the upper and
lower lids.
 In the staphylococcal type, the scales are dry, the lids
are erythematous, the lid margins may be ulcerated,
and the lashes tend to fall out.
 In the seborrheic type, the scales are greasy,
ulceration does not occur, and the lid margins are less
inflamed.
 Seborrhea of the scalp, brows, and ears is also
frequently found.
 ANTERIOR BLEPHARITIS

 In the more common mixed type, both dry

and greasy scales are present with lid margin
inflammation.
Staphylococcal blepharitis may be
complicated by hordeola, chalazia, epithelial
keratitis of the lower third of the cornea, and
marginal keratitis.
Both forms of anterior blepharitis predispose
to recurrent conjunctivitis.
 ANTERIOR BLEPHARITIS

 Treatment consists of lid hygiene, particularly in the

seborrheic type of blepharitis.
 Scales must be removed daily from the lid margins by
gentle mechanical scrubbing with a damp cotton applicator
and a mild soap such as baby shampoo.
 Staphylococcal blepharitis is treated with
antistaphylococcal antibiotic or sulfacetamide ointment
applied on a cotton applicator once daily to the lid margins.
 Both types may run a chronic course over a period of
months or years if not treated adequately.
 Associated staphylococcal conjunctivitis or keratitis usually
disappears promptly following local antistaphylococcal
medication.
 POSTERIOR BLEPHARITIS

Posterior blepharitis is inflammation of the

lids secondary to dysfunction of the
meibomian glands.
 Like anterior blepharitis, it is a bilateral,
chronic condition.
Anterior and posterior blepharitis may
coexist.
 Seborrheic dermatitis is commonly
associated with meibomian gland dysfunction.

 POSTERIOR BLEPHARITIS

Posterior blepharitis is manifested by a broad spectrum of

symptoms involving the lids, tear film, conjunctiva, and
cornea.
Hordeola and chalazia may also occur.
The lid margin demonstrates hyperemia and
telangiectasia and may become rounded and rolled
inward as a result of scarring of the tarsal conjunctiva,
causing an abnormal relationship between the precorneal
tear film and the meibomian gland orifices.
 POSTERIOR BLEPHARITIS

 Posterior blepharitis is often associated with rosacea.

 Primary therapy is application of warm compresses to the lids, with
periodic meibomian gland expression.
 Further treatment is determined by the associated conjunctival and
corneal changes.
 Topical therapy with antibiotics is guided by results of bacterial
cultures from the lid margins.
 Frank inflammation of the lids calls for anti-inflammatory treatment,
including long-term therapy with topical Metrogel (metronidazole,
0.75% daily), oral doxycycline (50–100 mg twice daily), or oral
azithromycin (1 g weekly for 3 weeks).
 Short-term treatment with weak topical steroids (eg, prednisolone
acetate, 0.125% twice daily) can be considered.
 Tear film dysfunction may necessitate artificial tears with a preference
for preservative free formulations to avoid toxic reactions.
 Hordeola and chalazia should be treated appropriately.
 ANATOMIC DEFORMITIES OF THE LIDS

Entropion is an inward turning of the lid

margin.
Involutional entropion is the most common
and by definition occurs as a result of aging.
 ANATOMIC DEFORMITIES OF THE LIDS

Congenital entropion is rare.

 It causes corneal irritation and may result in

corneal ulceration.
 Ectropion

Ectropion is an outward turning of the lid

margin.
Symptoms of tearing and irritation resulting
in exposure keratitis may occur with any type.
CONJUNCTIVITIS
 CONJUNCTIVITIS

Inflammation of the conjunctiva

(conjunctivitis) is the most common eye
disease worldwide.
It varies in severity from a mild hyperemia
with tearing to a severe conjunctivitis with
copious purulent discharge.
The cause is usually exogenous, but rarely
may be endogenous.
 CONJUNCTIVITIS

Because of its location, the conjunctiva is exposed

to many microorganisms and other environmental
factors.
 Several mechanisms protect the surface of the
eye.
 In the tear film, the aqueous component dilutes
infectious material, mucus traps debris, and a
pumping action of the lids constantly flushes the
tears to the tear duct.
 In addition, the tears contain antimicrobial
substances, including lysozyme and antibodies
(immunoglobulin [Ig] G and IgA).
 CONJUNCTIVITIS

Common pathogens that can cause

conjunctivitis include Streptococcus
pneumoniae, Haemophilus influenzae,
Staphylococcus aureus, Neisseria
meningitidis, most human adenovirus strains,
herpes simplex virus type 1 and type 2, and
two picornaviruses. Two sexually transmitted
agents that cause conjunctivitis are
Chlamydia trachomatis and Neisseria
gonorrhoeae.
 Symptoms of Conjunctivitis
The important symptoms of conjunctivitis
include:
- foreign body sensation,
- scratching or burning sensation,
- sensation of fullness around the eyes,
- itching,
- photophobia.
Pain rather than discomfort commonly
indicates corneal involvement.
 Signs of Conjunctivitis

Hyperemia is the most conspicuous

clinical sign of acute conjunctivitis.
The redness is most marked in the fornix and
diminishes toward the limbus by virtue of the
dilation of the posterior conjunctival vessels.
(A perilimbal dilation or ciliary flush suggests
inflammation of the cornea or deeper
structures.)
 Signs of Conjunctivitis

Tearing (epiphora) is often prominent in

conjunctivitis, with the tears resulting
from the foreign body sensation, the burning
or scratching sensation, or the itching.
Mild transudation also arises from the
hyperemic vessels and adds to the tearing.
 An abnormally scant secretion of tears and
an increase in mucous filaments suggest dry
eye syndrome.
 Signs of Conjunctivitis
Exudation is a feature of all types of
acute conjunctivitis.
The exudate is flaky and amorphous in
bacterial conjunctivitis and stringy in allergic
conjunctivitis. “Mattering” of the eyelids
occurs upon awakening in almost all types of
conjunctivitis, and if the exudate is copious
and the lids are firmly stuck together, the
conjunctivitis is probably bacterial or
chlamydial.
 Signs of Conjunctivitis

Pseudoptosis is a drooping of the upper

lid secondary to infiltration and
inflammation of Müller’s muscle.
 The condition is seen in several types of
severe conjunctivitis, for example trachoma
and epidemic keratoconjunctivitis.
Papillary hypertrophy is a nonspecific
conjunctival reaction.
 Signs of Conjunctivitis

Chemosis of the conjunctiva strongly

suggests acute allergic conjunctivitis but
may also occur in acute gonococcal or
meningococcal conjunctivitis and especially
in adenoviral conjunctivitis.
 Signs of Conjunctivitis

Follicles are seen in most cases of viral

conjunctivitis, in all cases of chlamydial
conjunctivitis except neonatal inclusion
conjunctivitis.
 Follicles in the inferior fornix and at the
tarsal margins have limited diagnostic value,
but when they are located on the tarsi
(especially the upper tarsus), chlamydial,
viral, or toxic conjunctivitis (following topical
medication) should be suspected.
 Signs of Conjunctivitis

 Pseudomembranes and membranes are the result of an

exudative process and differ only in degree.
 A pseudomembrane is a coagulum on the surface of the
epithelium, and when it is removed, the epithelium remains
intact.
 In contrast, a true membrane is a coagulum involving the entire
epithelium, and if it is removed, a raw, bleeding surface remains.
 Both pseudomembranes and membranes may accompany
epidemic keratoconjunctivitis, primary herpes simplex virus
conjunctivitis, streptococcal conjunctivitis, diphtheria, mucous
membrane pemphigoid, Stevens-Johnson syndrome, toxic
epidermal necrolysis, and erythema multiforme.
 They may also be an aftermath of chemical exposure, especially
alkali burns.
 Treatment

 Specific therapy of bacterial conjunctivitis depends on

identification of the microbiologic agent.
 While waiting for laboratory reports, the physician can start
topical therapy with a broad-spectrum antibacterial agent
(eg, polymyxintrimethoprim).
 In any purulent conjunctivitis in which the Gram stain shows
gram-negative diplococci suggestive of Neisseria, both
systemic and topical therapy should be started immediately.
 In purulent and mucopurulent conjunctivitis, the conjunctival
sac should be irrigated with saline solution as necessary to
remove the conjunctival secretions.
 To prevent spread of the disease, the patient and family
should be instructed to give special attention to personal
hygiene.
 CHLAMYDIAL CONJUNCTIVITIS

1. TRACHOMA
Worldwide the number of individuals with
profound vision loss from trachoma has
dropped from 6 million to 1.3 million, but it
remains one of the leading causes of
preventable blindness.
 It is endemic in regions with poor hygiene,
overcrowding, poverty, lack of clean water,
and poor sanitation.
 CHLAMYDIAL CONJUNCTIVITIS

Clinical Findings
A. Symptoms and Signs
Trachoma typically begins in childhood as a bilateral
chronic follicular conjunctivitis that due to recurrent
episodes progresses to conjunctival scarring.
In severe cases trichiasis develops in early adult life.
The constant abrasion by inturned lashes combined
with defective tear film leads, usually after age 30
years, to corneal scarring.
 CHLAMYDIAL CONJUNCTIVITIS

 Treatment
 Improvement is usually achieved with single-dose azithromycin, 1 g orally;
 doxycycline, 100 mg orally twice daily for 3 weeks; erythromycin, 1 g/d orally in
four divided doses for 3–4 weeks; or tetracycline, 1–1.5 g/d orally in four divided
doses for 3–4 weeks; but maximum effect is usually not achieved for 10–12
weeks, and several courses may be necessary for a cure. (Systemic tetracyclines
should not be given to a child under 7 years of age or to a pregnant woman
because tetracycline binds to calcium in developing teeth and in growing bone,
leading to discoloration of the teeth and skeletal abnormalities.)
 Azithromycin has become the first choice for mass treatment campaigns, but
repeated administrations may be necessary.
 Topical ointments or drops, including preparations of sulfonamides,
tetracyclines, erythromycin, and rifampin, used four times daily for 6 weeks,
also are effective.
 Surgical correction of trichiasis, which can be performed by nonspecialist
physicians or specially trained auxiliary personnel, is essential to prevent
scarring from late trachoma.
 Course & Prognosis
 Characteristically, trachoma is a chronic disease of long duration. Under good
hygienic conditions (specifically, face-washing of young children), the disease
resolves or becomes milder so that severe sequelae are avoided.
 VIRAL CONJUNCTIVITIS

Viral conjunctivitis is common and can be

caused by a wide variety of viruses.
Severity ranges from mild, rapidly self-limited
infection to severe, disabling disease.
 ACUTE VIRAL CONJUNCTIVITIS

 Pharyngoconjunctival Fever is characterized by fever of

38.3–40°C, sore throat, and a follicular conjunctivitis in one
or both eyes.
 The follicles are often very prominent on both the
conjunctiva and the pharyngeal mucosa.
 The disease can be either bilateral or unilateral.
 Injection and tearing often occur, and there may be
transient superficial epithelial keratitis and occasionally
some subepithelial opacities.
 Nontender preauricular lymphadenopathy is characteristic.
 Pharyngoconjunctival fever is most frequently caused by
adenovirus type 3 and occasionally by types 4 and 7.
 The condition is more common in children than in adults
and can be transmitted in poorly chlorinated swimming
pools.
 epidemic keratoconjunctivitis

 The onset of epidemic keratoconjunctivitis is often unilateral, with both eyes

subsequently being affected but the first eye usually being more severely affected. Initial
symptoms include conjunctival injection, moderate pain, and tearing.
 Usually by 5–14 days, photophobia, epithelial keratitis, and round subepithelial opacities
have also developed.
 Corneal sensation is normal. A tender preauricular node is characteristic.
 Edema of the eyelids, chemosis, and conjunctival hyperemia mark the acute phase, with
follicles and subconjunctival hemorrhages often appearing within 48 hours.
 Pseudomembranes (and occasionally true membranes) may occur and may be followed
by flat scars or symblepharon formation.
 The conjunctivitis usually resolves by 3–4 weeks at most. The subepithelial opacities are
concentrated in the central cornea, usually sparing the periphery, and may persist for
months but generally heal without scars.
 Herpes Simplex Virus Conjunctivitis

 Herpes simplex virus (HSV) conjunctivitis, usually a disease of young children,

is an uncommon entity characterized by unilateral injection, irritation, mucoid
discharge, pain, and mild photophobia.
 It occurs during primary infection with HSV when commonly there is also lid
involvement or during recurrent episodes of ocular herpes.
 It is often associated with herpes simplex keratitis, in which the cornea shows
discrete epithelial lesions that usually coalesce to form single or multiple
branching epithelial (dendritic) ulcers .
 The conjunctivitis is follicular or, less often, pseudomembranous. (Patients on
topical antivirals may develop follicular conjunctivitis that can be differentiated
because the herpetic follicular conjunctivitis has an acute onset.)
 Herpetic vesicles may sometimes appear on the eyelids and lid margins,
associated with severe edema of the eyelids.
 Typically, there is a small tender preauricular node.
 Herpes Simplex Virus
Conjunctivitis

Complications consist of corneal involvement

(including dendrites) and vesicles on the skin.
 Although type 1 herpesvirus causes the
overwhelming majority of ocular cases, type 2
is the usual cause of herpetic conjunctivitis in
newborns and a rare cause in adults.
 Herpes Simplex Virus
Conjunctivitis
 In the newborn, there may be generalized disease with encephalitis,
chorioretinitis, hepatitis, etc.
 Any HSV infection in the newborn must be treated with systemic antiviral
therapy (acyclovir) and monitored in a hospital setting.
 If the conjunctivitis occurs in a child over 1 year of age or in an adult, it is
usually self-limited and may not require therapy.
 Topical or systemic antivirals should be given, however, to prevent corneal
involvement.
 For corneal ulcers, corneal debridement may be performed by gently wiping
the ulcer with a dry cotton swab, applying antiviral drops, and patching the
eye for 24 hours.
 Topical antivirals alone should be applied for 7–10 days (eg, trifluridine every
2 hours while awake or ganciclovir aqueous gel 0.15% five times daily until
the ulcer heals and then three times daily).
 Herpetic keratitis may also be treated with 3% acyclovir five times daily for
10 days, or with oral acyclovir, 400 mg five times daily for 7 days.
 Corticosteroid use is contraindicated since it may aggravate herpetic
infections, causing a prolonged and usually more severe course.
 Acute Hemorrhagic Conjunctivitis

Characteristically, the disease has a short incubation

period (8–48 hours) and course (5–7 days).
 The usual signs and symptoms are pain, photophobia,
foreign-body sensation, copious tearing, redness, lid
edema, and subconjunctival hemorrhages.
Chemosis sometimes also occurs.
The subconjunctival hemorrhages are usually diffuse but
may be punctate at onset, beginning in the upper bulbar
conjunctiva and spreading to the lower.
Most patients have preauricular lymphadenopathy,
conjunctival follicles, and epithelial keratitis.
CHRONIC VIRAL CONJUNCTIVITIS
 Molluscum Contagiosum Blepharoconjunctivitis
 A molluscum skin nodule is round, waxy, and pearly-white, with an
umbilicated center.
 A nodule on the lid margin or the skin of the lids or brow may produce
unilateral chronic follicular conjunctivitis, superior keratitis, and
superior pannus resembling trachoma.
 The inflammatory reaction is predominantly mononuclear (unlike the
reaction in trachoma).
 Excision or even incision of the nodule, thus allowing peripheral blood
to permeate it, or cryotherapy cures the conjunctivitis.
 On very rare occasions, molluscum nodules have occurred on the
conjunctiva. In these cases, excision of the nodule has also relieved the
conjunctivitis.
 Multiple lid or facial lesions of molluscum contagiosum occur in
patients with acquired immunodeficiency syndrome (AIDS).
 HAY FEVER CONJUNCTIVITIS

 A mild, nonspecific conjunctival inflammation is

commonly associated with hay fever (allergic
rhinitis).
 In most cases, there is a history of allergy to
pollens, grasses, animal danders, or other
allergens.
 The patient complains of itching, tearing, and
redness of the eyes and often states that the eyes
seem to be “sinking into the surrounding tissue.”
 There is mild injection of the palpebral and bulbar
conjunctiva and, during acute attacks, often a
severe chemosis, which no doubt accounts for the
“sinking” description.
 There may be a small amount of ropy discharge,
especially if the patient has been rubbing the eyes.
 Eosinophils are difficult to find in conjunctival
scrapings.
 A papillary conjunctivitis may occur if the allergen
persists.
 HAY FEVER CONJUNCTIVITIS

Treatment consists of the instillation of topical

antihistamines;
mast cell stabilizers;
 combined antihistamines and mast cell stabilizers;
nonsteroidal antiinflammatory drugs .
Mast cell stabilization takes longer to act than
antihistamine and nonsteroidal anti-inflammatory
effects but is useful for prophylaxis.
Topical vasoconstrictors, alone or in combination with
antihistamines, but are of limited efficacy in allergic
eye disease and may produce rebound hyperemia and
follicular conjunctivitis.
 VERNAL KERATOCONJUNCTIVITIS
 Vernal keratoconjunctivitis, also known as
“spring catarrh,” “seasonal conjunctivitis,”
or “warm weather conjunctivitis,” is an
uncommon bilateral allergic disease that
usually begins in the prepubertal years
and lasts for 5–10 years.
“Cobblestone” papillae on  It occurs much more often in boys than in
the superior palpebral girls.
conjunctiva in  The specific allergen or allergens are
vernal difficult to identify, but patients with vernal
keratoconjunctivitis. keratoconjunctivitis usually show other
manifestations of allergy known to be
related to grass pollen sensitivity.
 The disease is less common in temperate
than in warm climates and is almost
nonexistent in cold climates.
 It is almost always more severe during the
spring, summer, and fall than in the winter.
 VERNAL
KERATOCONJUNCTIVITIS

The patient usually complains of extreme itching

and a ropy discharge.
There is often a family history of allergy (hay fever,
eczema, etc), and sometimes, there is a history of
allergy in the young patient as well.
The conjunctiva has a milky appearance with many
fine papillae in the lower palpebral conjunctiva.
The upper palpebral conjunctiva often has giant
papillae that give a cobblestone appearance.
Each giant papilla is polygonal, has a flat top, and
contains tufts of capillaries.
 VERNAL
KERATOCONJUNCTIVITIS

 A stringy conjunctival discharge and a fine, fibrinous

pseudomembrane (Maxwell-Lyons sign) may be noted,
especially on the upper tarsus on exposure to heat.
 In some cases, especially in persons of black African
ancestry, the most prominent lesions are located at the
limbus, where gelatinous swellings (papillae) are noted.
 A pseudogerontoxon (arcus-like haze) is often noted in the
cornea adjacent to the limbal papillae.
 Trantas’ dots are whitish dots seen at the limbus in some
patients with vernal keratoconjunctivitis during the active
phase of the disease.
 Treatment

 The disease may also be associated with keratoconus.

 Topical and systemic corticosteroids, which relieve the itching,
affect the corneal disease only minimally, and their side effects
(glaucoma, cataract, and other complications) can be severely
damaging.
 Newer mast cell stabilizer–antihistamine combinations are
useful prophylactic and therapeutic agents in moderate to
severe cases.
 Vasoconstrictors, cold compresses, and ice packs are helpful,
and sleeping (and, if possible, working) in cool, air-conditioned
rooms can keep the patient reasonably comfortable.
 The acute symptoms of an extremely photophobic patient who
is unable to function can often be relieved by a short course of
topical or systemic corticosteroids followed by
vasoconstrictors, cold packs, and regular use of histamine-
blocking eye drops.
MILD CONJUNCTIVITIS SECONDARY TO
CONTACT BLEPHARITIS

 Contact blepharitis caused by atropine, neomycin, broad-spectrum

antibiotics, and other topically applied medications, or the preservatives in
them, is often followed by a mild infiltrative conjunctivitis that produces
hyperemia, mild papillary hypertrophy, a mild mucoid discharge, and some
irritation.
 Treatment should be directed toward finding the offending agent and
eliminating it.
 The contact blepharitis may clear rapidly with topical corticosteroids, but
their use should be limited.
 Long-term use of corticosteroids on the lids may lead to steroid glaucoma
and to skin atrophy with disfiguring telangiectasis.
 CONJUNCTIVITIS DUE TO AUTOIMMUNE
DISEASE
SJÖGREN SYNDROME

 Sjögren syndrome is an autoimmune disease characterized by

dry eye syndrome (keratoconjunctivitis sicca and dry mouth
(xerostomia).
 When associated with a generalized autoimmune disease, usually
rheumatoid arthritis, it is known as secondary rather than primary
Sjögren syndrome.
 The syndrome is overwhelmingly more common in women at or
beyond menopause than in other groups, although men and
younger women may also be affected.
 The lacrimal gland is infiltrated with lymphocytes and occasionally
with plasma cells, leading to atrophy and destruction of the
glandular structures.
 SJÖGREN SYNDROME

 Dry eye syndrome is characterized by bulbar conjunctival

hyperemia (especially in the palpebral aperture) and symptoms
of irritation that are out of proportion to the mild inflammatory
sign, with pain increasing by the afternoon and evening but
being absent or only slight in the morning.
 It often begins as a mild conjunctivitis with a mucoid
discharge.
 Blotchy epithelial lesions appear on the cornea, more
prominently in its lower half, and filaments may be seen.
 Rose bengal or lissamine green staining of the cornea and
conjunctiva in the palpebral aperture is a helpful diagnostic
test.
 The tear film is diminished and often contains shreds of mucus.
 Results of the Schirmer test are abnormal.
 SJÖGREN SYNDROME

 Conjunctival scrapings may show increased numbers of

goblet cells.
 Lacrimal gland enlargement occurs uncommonly in patients
with Sjögren syndrome.
 The principal diagnostic investigations in Sjögren syndrome
are detection of antibodies and lymphocytic and plasma cell
infiltration of the accessory salivary glands in a labial biopsy
obtained by means of a simple surgical procedure.
 Treatment is directed toward preserving and improving the
quality of the tear film with artificial tears, obliteration of
the puncta.
 Topical corticosteroid or calcineurin inhibitor may be
required in some cases.
 CONJUNCTIVITIS ASSOCIATED WITH
SYSTEMIC DISEASE

 CONJUNCTIVITIS IN GRAVES OPHTHALMOPATHY

 In Graves ophthalmopathy, the conjunctiva may be red and chemotic,
and the patient may complain of copious tearing.
 As the disease progresses, the chemosis increases, and in advanced
cases, the chemotic conjunctiva may extrude between the lids, leading
to corneal exposure that is exacerbated by any proptosis.
 Treatment is directed toward control of the thyroid disease, and every
effort must be made to protect the conjunctiva and cornea by bland
ointment, surgical lid adhesions (tarsorrhaphy) if necessary, or even
orbital decompression if the lids do not close enough to cover the
cornea and conjunctiva.
 DEGENERATIVE DISEASES OF THE
CONJUNCTIVA

 PINGUECULA
 Pingueculae are extremely common in adults.
 They appear as yellow nodules on both sides of the cornea (more
commonly on the nasal side) in the area of the palpebral aperture.
 The nodules, consisting of hyaline and yellow elastic tissue, rarely
increase in size, but inflammation is common.
 In general, no treatment is required, but in certain cases of
pingueculitis, weak topical steroids (eg, prednisolone 0.12%) or
topical nonsteroidal anti-inflammatory agents may be given.
 DEGENERATIVE DISEASES OF THE
CONJUNCTIVA

 PTERYGIUM
 A pterygium is a fleshy, triangular encroachment of a pinguecula onto the cornea,
usually on the nasal side bilaterally.
 It is thought to be an irritative phenomenon due to ultraviolet light, drying, and windy
environments, since it is common in persons who spend much of their lives out of
doors in sunny, dusty, or sandy, windblown surroundings.
 The pathologic findings in the conjunctiva are the same as those of pinguecula.
 In the cornea, there is replacement of Bowman’s layer by hyaline and elastic tissue.
 If the pterygium is enlarging and encroaches on the pupillary area, it should be
removed surgically along with a small portion of superficial clear cornea beyond the
area of encroachment.
 Conjunctival autograft at the time of surgical excision has been shown to reduce the
risk of recurrent disease.
 SUBCONJUNCTIVAL HEMORRHAGE

 This common disorder may occur spontaneously, usually in only one

eye, in any age group.
 Its sudden onset and bright-red appearance usually alarm the patient.
 The hemorrhage is caused by rupture of a small conjunctival vessel,
sometimes preceded by a bout of severe coughing or sneezing.
 The best treatment is reassurance.
 The hemorrhage usually absorbs in 2–3 weeks.
 In rare instances, if the hemorrhages are bilateral or recurrent, the
possibility of blood dyscrasias should then be ruled out.
 THE TEAR FILM

 LAYERS OF THE TEAR FILM

 The tear film is composed of three primary layers.
 The three primary layers of the tear film covering the superficial
epithelial layer of the cornea.
 1. The superficial lipid layer is a monomolecular film derived from
meibomian glands. It is thought to retard evaporation and form a watertight
seal when the lids are closed.
 2. The middle aqueous layer is elaborated by the major and minor lacrimal
glands and contains water-soluble substances (salts and proteins).
 3. The deep mucinous layer is composed of glycoprotein and overlies the
corneal and conjunctival epithelial cells.

 DRY EYE SYNDROME
(KERATOCONJUNCTIVITIS SICCA)

Dryness of the eye may result from any disease

ssociated with deficiency of the tear film components
(aqueous, mucin, or lipid), lid surface abnormalities, or
epithelial abnormalities.
Hence, there are many causes of dry eye syndrome
(keratoconjunctivitis sicca).
 Primary Sjögren syndrome, an immune mediated
disorder of the lacrimal and salivary glands,
characteristically manifesting as dry mouth as well as
dry eyes, is the most important specific disease entity.
 Clinical Findings

 Patients with dry eyes complain most frequently of a scratchy or sandy

(foreignbody) sensation.
 Other common symptoms are itching, excessive mucus secretion, inability to
produce tears, a burning sensation, photosensitivity, redness, pain, and difficulty
in moving the lids.
 On gross examination, the eyes may appear normal, but on careful slitlamp
examination, subtle indications of the presence of chronic dryness and irritation
are found.
 The most characteristic feature is interruption or absence of the tear meniscus at
the lower lid margin.
 Tenacious yellowish mucus strands are sometimes seen in the lower conjunctival
fornix.
 The bulbar conjunctiva loses its normal luster and may be thickened, edematous,
and hyperemic.
 Clinical Findings

 The corneal epithelium shows varying degrees of fine punctate stippling

in the interpalpebral fissure.
 The damaged corneal and conjunctival epithelial cells stain with 1% rose
bengal, and defects in the corneal epithelium stain with fluorescein.
 In the late stages of keratoconjunctivitis sicca, filaments may be seen—
one end of each filament attached to the corneal epithelium and the other
end moving freely.
 Accurate diagnosis and grading of dry eye syndrome can be achieved
using various diagnostic tests.
 A. Schirmer Test

 Schirmer strips (Whatman filter paper No. 41) are inserted into the lower
conjunctival cul-de-sac at the junction of the mid and temporal thirds of the
lower lid.
 The moistened exposed portion is measured 5 minutes after insertion.
 When performed without anesthesia, the test measures the function of the main
lacrimal gland, whose secretory activity is stimulated by the irritating nature of
the filter paper.
 Less than 10 mm of wetting without anesthesia is considered abnormal.
 Schirmer tests can be performed after topical anesthesia (0.5% tetracaine) to
measure the function of the accessory lacrimal glands, but the test is considered
unreliable.
 Less than 5 mm in 5 minutes is abnormal.
 The Schirmer test is a screening test for assessment of tear production.
 Falsepositive and false-negative results occur. Low readings are sporadically
found in normal eyes, and normal tests may occur in dry eyes—especially those
secondary to mucin deficiency.
 A. Schirmer Test

 Measurement of the tear film break-up time may sometimes be useful

to estimate the mucin content of tear fluid.
 Deficiency in mucin may not affect the Schirmer test, which quantifies
tear production, but may lead to instability of the tear film, resulting
in its rapid break-up. “Dry spots” are formed in the tear film, followed
by exposure of the corneal or conjunctival epithelium.
 This process ultimately damages the epithelial cells, which can then
be stained with rose bengal.
 Damaged epithelial cells may be shed from the cornea, leaving areas
susceptible to punctate staining when the corneal surface is flooded
with fluorescein.
 B. Tear Film Break-Up Time

 The tear film break-up time is measured by applying a slightly

moistened fluorescein strip to the bulbar conjunctiva and asking the
patient to blink.
 The tear film is then scanned with the aid of the cobalt filter on the
slitlamp while the patient refrains from blinking.
 The time that elapses before the first dry spot appears in the corneal
fluorescein layer is the tear film break-up time.
 Normally it is over 15 seconds, but it will be reduced appreciably by
the use of local anesthetics, by manipulating the eye, or by holding the
lids open.
 Tear film break-up time is reduced in eyes with aqueous tear deficiency
and is always shorter than normal in eyes with mucin deficiency.
 E. Fluorescein Staining

Touching the conjunctiva with a dry strip of

fluorescein is a good indicator of wetness,
and the tear meniscus can be seen easily.
Fluorescein will stain the eroded and
denuded areas as well as microscopic defects
of the corneal epithelium.
 F. Rose Bengal and Lissamine Green Staining

Rose bengal and lissamine green are equally

sensitive for staining the conjunctiva.
Both dyes will stain all desiccated nonvital
epithelial cells of the conjunctiva and to a
lesser extent the cornea.
 Unlike rose bengal, lissamine green does not
cause significant irritation.
 G. Tear Lysozyme Assay
Reduction in tear lysozyme concentration
usually occurs early in the course of Sjögren
syndrome and is helpful in diagnosis.
Tears can be collected on Schirmer strips and
assayed, usually by spectrophotometric
methods.
 Complications

 Early in the course of dry eye syndrome, vision is slightly

impaired.
 As the condition worsens, discomfort can become disabling.
 In advanced cases, corneal ulceration, corneal thinning, and
perforation may develop.
 Secondary bacterial infection occasionally occurs, and corneal
scarring and vascularization may result in marked reduction in
vision.
 Early treatment may prevent these complications.
 Treatment

The patient should understand that dry eye

syndrome is a chronic condition and complete
relief is unlikely except in mild cases when
the corneal and conjunctival epithelial
changes are reversible.
 Artificial tears, particularly preservative-free
tears in more advanced cases, are the
mainstay of symptomatic treatment.
 Treatment

Disease modification can be achieved with topical

anti-inflammatory agents such as corticosteroids.
Patients with excessive tear lipids may require
specific instructions for removal of lipid strands from
the eyelid margin.
Antibiotics topically or systemically may be
necessary.
Dietary supplementation with omega-3 fatty acids or
flax seed oil has been advocated to modulate
favorably meibomian gland secretion.
Topical vitamin A may be useful in reversing ocular
surface metaplasia.
 Surgical treatment for dry eyes

Surgical treatment for dry eyes includes

insertion of temporary (collagen) or extended
(silicone) punctal plugs to retain lacrimal
secretions.
Permanent closure of the puncta and canaliculi
can be achieved by thermal, electrocautery, or
laser treatment.
 Injection of botulinum toxin into the medial
lower eyelid is reported to improve discomfort
by reducing tear drainage.
Cornea
 MICROBIAL KERATITIS

Microbial keratitis is a major cause of visual

loss throughout the world.
 BACTERIAL KERATITIS

Staphylococcus aureus,
Staphylococcus epidermidis, &
Alpha-Hemolytic Streptococcus
Keratitis
Central corneal ulcers caused by
these organisms have become
more common, many of them in
corneas compromised by topical
corticosteroid use.
 The ulcers are often indolent but
may be associated with hypopyon
and some surrounding corneal
 VIRAL KERATITIS

Herpes Simplex Virus Keratitis

Herpes simplex virus (HSV) keratitis occurs in two
forms: primary and recurrent.
 It is a common cause of corneal scarring and loss of
vision.
The epithelial form is the ocular counterpart of labial
herpes, with which it shares immunologic and
pathologic features as well as having a similar time
course.
The only difference is that the clinical course of the
keratitis may be prolonged because of the avascularity
of the corneal stroma, which retards the migration of
lymphocytes and macrophages to the lesion.
 VIRAL KERATITIS

HSV keratitis is classified clinically as epithelial, stromal, or endothelial.

 1. Epithelial HSV Keratitis—The most characteristic lesion is the dendritic
ulcer, which occurs in the corneal epithelium, has a branching, linear pattern
with feathery edges, and has terminal bulbs at its ends.
 Fluorescein staining makes the dendrite easy to identify. HSV keratitis can also
resemble many corneal diseases and must be considered in the differential diagnosis.
 A typical feature of HSV keratitis is reduced corneal sensation.
 Geographic ulceration is a form of chronic dendritic disease in which the
delicate dendritic lesion takes a broader form and the edges of the ulcer lose their
feathery quality. HSV also may cause a blotchy epithelial keratitis and stellate
epithelial keratitis, but these are usually transitory and often become typical
dendrites within 1–2 days.
 Subepithelial opacities can be caused by HSV infection.
 A ghost-like image, corresponding in shape to the original epithelial defect but
slightly larger, can be seen in the area immediately underlying the epithelial lesion. As
a rule, these subepithelial lesions do not persist for more than a few months.
 VIRAL KERATITIS

 2. Stromal HSV Keratitis—Focal areas of stromal infiltration and edema,

often accompanied by vascularization, are likely to be predominantly due to
viral replication.
 Corneal thinning, necrosis, and perforation may develop rapidly, particularly if
topical corticosteroids are being used without antiviral cover.
 If there is stromal disease in the presence of epithelial ulceration, it may be
difficult to differentiate bacterial or fungal superinfection from herpetic disease.
 The features of the epithelial disease need to be carefully scrutinized for
herpetic characteristics, but a bacterial or fungal component may be present,
and the patient must be managed accordingly.
 Stromal necrosis also may be caused by an acute immune reaction, again
complicating the diagnosis with regard to active viral disease.
 Hypopyon may be seen with necrosis as well as secondary bacterial or fungal
infection.
 VIRAL KERATITIS

 Disciform keratitis is the most common form of HSV

stromal keratitis.
 The stroma is edematous in a central, disk-shaped area, without
significant infiltration and usually without vascularization.
 The edema may be sufficient to produce folds in Descemet
membrane.
 Keratic precipitates may lie directly under the disciform lesion
but may also involve the entire endothelium because of the
frequently associated anterior uveitis.
 Like most herpetic lesions in immunocompetent individuals,
disciform keratitis is normally selflimited, lasting weeks to
months.
 Edema is the most prominent sign, and healing can occur with
minimal scarring and vascularization.
 VIRAL KERATITIS

3. Endothelial HSV Keratitis—A similar clinical

appearance to disciform
keratitis is seen with primary endothelial HSV
keratitis (endotheliitis), which can be associated
with anterior uveitis, raised intraocular pressure,
and focal inflammation of the iris.
Viral replication within the various anterior chamber
structures is thought to be responsible.
 Adenovirus Keratitis

 Keratitis usually accompanies all types of adenovirus

conjunctivitis, reaching its peak 5–7 days after onset of the
conjunctivitis.
 It is a fine epithelial keratitis best seen with the slitlamp after
instillation of fluorescein.
 The minute lesions may group together to make up larger ones.
 The epithelial keratitis is often followed by subepithelial
opacities.
 In epidemic keratoconjunctivitis (EKC), which is due to
adenovirus types 8 and 19, the subepithelial lesions are round
and grossly visible.
 They appear 8–15 days after onset of the conjunctivitis and may
persist for months or even (rarely) for several years.
 Acanthamoeba Keratitis

Acanthamoeba is a free-living protozoan that thrives in

polluted water containing bacteria and organic material.
Corneal infection with Acanthamoeba is usually
associated with soft contact lens wear, including silicone
hydrogel lenses, or overnight wear of rigid (gas-
permeable) contact lenses to correct refractive errors
(orthokeratology).
There have been cases associated with a particular
contact lens solution, probably related to insufficient
anti-Acanthamoeba efficacy.
 It may also occur in non–contact lens wearers after
exposure to contaminated water or soil.
The initial symptoms are pain out of proportion to the
clinical findings, redness, and photophobia.

 Acanthamoeba Keratitis

 The characteristic clinical signs are indolent

corneal ulceration, stromal ring, and
perineural infiltrates, but patients often
present with changes confined to the corneal
epithelium.
 The diagnosis is established by culturing on
nonnutrient agar with an overlay of
Escherichia coli.
 Better results are obtained by corneal biopsy
than corneal scraping, since histopathologic
examination for amebic forms (trophozoites
or cysts) can also be undertaken.
 In the early stages of the disease, epithelial
debridement
may be beneficial.
 CORNEAL ECTASIA

Keratoconus
Keratoconus is a stromal shape disorder that
is relatively prevalent in all ethnic groups.
It is usually bilateral and asymmetric but may
be unilateral. Symptoms caused by the
refractive consequences typically commence
in the second decade of life.
Pathologically, there are disruptive changes
in Bowman layer, stromal thinning, and
ruptures in Descemet membrane.
 Keratoconus

 Blurred vision is the only symptom. Many patients present

with rapidly increasing myopic astigmatism.
 Signs include cone-shaped cornea;
 linear narrow folds centrally in Descemet membrane
(Vogt’s lines), which are pathognomonic;
 An iron ring around the base of the cone (Fleischer’s ring);
 In extreme cases, indentation of the lower lid by the
cornea when the patient looks down (Munson’s sign).
 Keratoconus

There is an irregular or scissor reflex on retinoscopy and

a distorted corneal reflection with Placido disk or
keratoscope even early in the disease.
Color-coded topography provides earliest and more
qualitative information on the degree of corneal
distortion and irregular steepening.
Early topographic signs of keratoconus (forme fruste)
suggest possible progressive stromal thinning and
refractive change and an unsuitable candidate for laser
refractive surgery.
 Keratoconus

Acute hydrops of the cornea may occur,

manifested by sudden diminution of vision
associated with central corneal edema.
 This arises as a consequence of rupture of
Descemet membrane.
Usually it clears gradually without treatment
but often leaves apical and Descemet
membrane scarring.
 CORNEAL ECTASIA

Keratoconus is often slowly progressive and usually

stabilizes in the fourth decade of life.
Corneal collagen cross-linking has been shown to be
effective in arresting the progression of keratoconus.
 It is therefore essential that newly diagnosed patients
are reviewed every 6–12 months with serial corneal
topography scans to monitor progression.
 Corneal collagen cross-linking involves diffusing
riboflavin into the corneal stroma then shining
ultraviolet A light to trigger a chemical reaction, which
is thought to strengthen intercollagen bonds in the
corneal stroma.
Rigid contact lenses will markedly improve
vision in the early stages by correcting
irregular astigmatism.
Keratoconus is one of the most common
indications for corneal transplantation, either
anterior lamellar or penetrating.
Insertion of corneal intrastromal ring
segments may improve best corrected vision
and contact lens tolerance.
 Episcleritis

 Sometimes the eye becomes red due to inflammation of the

connective tissue underlying the conjunctiva, that is, the
episclera.
 The condition may be localized or diffuse.
 There is no discharge and the eye is uncomfortable although not
usually painful.
 Treatment - local steroids or non-steroid anti-inflammatory
agents. The underlying cause is often never discovered.
 Episcleritis tends to recur and may persist for several weeks
producing a worrying cosmetic blemish in a young person.
 Red Painful Eye Which May See
Normally

 Scleritis
 Inflammation of the sclera rather than the episclera is a less
common cause of red eye. There is no discharge but the eye is
painful. Vision is usually normal, unless the inflammation involves
the posterior sclera.
 It is most often seen in association with rheumatoid arthritis and
other collagen diseases and sometimes may become severe and
progressive to the extent of causing perforation of the globe. For
this reason steroids must be administered with extreme care.
 Treatment normally is with
systemically administered
non-steroidal anti-inflammatory
agents
 Acute Iritis

The eye is painful, but the pain is

never so severe as to cause
vomiting.
 The cornea remains bright and the
pupil tends to go into spasm and is
smaller than on the normal side.
Acute iritis is seen from time to time
mainly in the 20–40 age group,
whereas acute glaucoma is extremely
rare at these ages.
Unless severe and bilateral, acute
iritis is treated on an outpatient basis
with local steroids and mydriatic
drops.
 Acute Glaucoma

 The important feature here is that acute glaucoma

occurs in long-sighted people and there is usually a
previous history of headaches and seeing haloes
round lights in the evenings.
 The raised intraocular pressure damages the iris
sphincter and for this reason the pupil is semi
dilated.
 Edema of the cornea causes the eye to lose its
lustre and gives the iris a hazy appearance.
 The eye is extremely tender and painful and the
patient may be nauseated and vomiting.
 Immediate admission to hospital is essential where
the intraocular pressure is first controlled medically
and then bilateral laser iridotomies or surgical
peripheral iridectomies performed to relieve pupil
block.
 Mydriatics should not be given to patients with
suspected narrow angle glaucoma, without
consultation with an ophthalmologist.
 Neovascular Glaucoma

 The elderly patient who presents

with a blind and painful eye and who
may also be diabetic should be
suspected of having neovascular
glaucoma.
 Once the intraocular pressure rises,
the eye tends to become painful and
eventually degenerates in the
absence of treatment, and sometimes
even in spite of treatment.
 This form of secondary glaucoma
remains as one of the few indications
for surgical removal of the eye, if
measures to control intraocular
pressure are unsuccessful.