Keratitis dan Konjungtivitis

Meika Meidina Yuanita – I4061191024

Pembimbing:
dr. Wirawan Adikusuma, Sp.M

KEPANITERAAN KLINIK STASE ILMU KESEHATAN MATA

RUMAH SAKIT UMUM DAERAH DOKTER SOEDARSO
FAKULTAS KEDOKTERAN UNIVERSITAS TANJUNGPURA
PONTIANAK
2021
 01
Conjunctivitis
 Conjunctiva
The conjunctiva is a transparent mucous membrane that lines the inner surface of the
eyelids and the anterior surface of the globe, terminating at the corneoscleral limbus. It is
richly vascular, supplied by the anterior ciliary and palpebral arteries.

Anatomically, it is divided into the following:

• The palpebral conjunctiva
• The forniceal conjunctiva
• The bulbar conjunctiva
 Conjunctivitis
Symptoms
Non-specific symptoms include lacrimation, grittiness, stinging and burning. Itching is the
hallmark of allergic disease. Significant pain, photophobia or a marked foreign body
sensation suggest corneal involvement.
 
Discharge
• Watery discharge is composed of a serous exudate and tears, and occurs in acute viral
or acute allergic conjunctivitis.
• Mucoid discharge is typical of chronic allergic conjunctivitis and dry eye.
• Mucopurulent discharge typically occurs in chlamydial or acute bacterial infection.
• Moderately purulent discharge occurs in acute bacterial conjunctivitis.
• Severe purulent discharge is suggestive of gonococcal infection.
 Conjunctivitis
Conjunctival reaction
• Hyperaemia that is diffuse, beefy-red and more
intense away from the limbus is usual in bacterial
infection (Fig. A).
• Haemorrhages may occur in viral conjunctivitis,
when they are often multiple, small and discrete
(‘petechial’ – Fig. B), and severe bacterial
conjunctivitis, when they are larger and diffuse.
• Chemosis (conjunctival oedema) is seen as a
translucent swelling (Fig. C)
• Acute chemosis usually indicates a hypersensitivity
response (e.g. pollen), but can also occur in severe
infective conjunctivitis.
 Conjunctivitis
• Membranes
 Pseudomembranes (Fig. D)
 True membranes
 Causes include severe adenoviral conjunctivitis,
gonococcal and some other bacterial
• Infiltration represents cellular recruitment to the
site of chronic inflammation and typically
accompanies a papillary response. It is recognized
by loss of detail of the normal tarsal conjunctival
vessels (Fig. E).
• Subconjunctival cicatrization (scarring) may
occur in trachoma and other severe conjunctivitides
(Fig. F).
 Conjunctivitis
• Follicles
Multiple, discrete, slightly elevated lesions resembling translucent grains of rice, most prominent in the
fornices (Fig. A). Causes include viral and chlamydial conjunctivitis.

• Papillae
In contrast to follicles, a vascular core is present. Micropapillae form a mosaic-like pattern of elevated
red dots as a result of the central vascular channel, macropapillae (<1 mm – Fig. C) and giant papillae
(>1 mm) develop with prolonged inflammation. Causes include bacterial conjunctivitis, allergic
conjunctivitis, chronic blepharitis, contact lens wear, superior limbic keratoconjunctivitis and floppy
eyelid syndrome.
Forms of Conjunctival Injection
 Bacterial Conjunctivitis
Acute bacterial conjunctivitis is a common and usually selflimiting condition caused by direct
contact with infected secretions. The most common isolates are Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilus influenzae and Moraxella catarrhalis.

Symptoms
 Acute onset of redness, grittiness, burning and discharge.
 Involvement is usually bilateral although one eye may become affected 1–2 days before the
other.
 On waking, the eyelids are frequently stuck together and may be difficult to open.
 Bacterial Conjunctivitis
Signs
 Eyelid oedema and erythema (Fig. A) may occur
in severe infection, particularly gonococcal.
 Conjunctival injection (Fig. B and Fig. A).
 The discharge can initially be watery, mimicking
viral conjunctivitis, but rapidly becomes
mucopurulent (Fig. C).
 Hyperacute purulent discharge (Fig. D) may
signify gonococcal or meningococcal
conjunctivitis.
 Bacterial Conjunctivitis
Treatment
• Topical antibiotics  Chloramphenicol, aminoglycosides (gentamicin, neomycin,
tobramycin), quinolones (ciprofloxacin, ofloxacin, levofloxacin, lomefloxacin,
gatifloxacin, moxifloxacin, besifloxacin), macrolides (erythromycin, azithromycin)
polymyxin B, fusidic acid and bacitracin. Gonococcal and meningococcal
conjunctivitis should be treated with a quinolone, gentamicin, chloramphenicol or
bacitracin 1–2 hourly as well as systemic therapy.

• Systemic antibiotics are required in the following circumstances:

 Gonococcal infection is usually treated with a third generation cephalosporin such
as ceftriaxone
 H. influenzae infection, particularly in children, is treated with oral amoxicillin with
clavulanic acid
 Bacterial Conjunctivitis
• Topical steroids may reduce scarring in membranous and pseudomembranous
conjunctivitis, although evidence for their use is unclear.
• Irrigation to remove excessive discharge may be useful in hyperpurulent cases.
• Contact lens wear should be discontinued until at least 48 hours after complete
resolution of symptoms. Contact lenses should not be worn whilst topical antibiotic
treatment continues.
• Risk of transmission should be reduced by hand-washing and the avoidance of towel
sharing.
 Adult Chlamydial Conjunctivitis
• Chlamydia trachomatis is a species of Chlamydiae, a phylum of bacteria that cannot
replicate extracellularly and hence depends on host cells. Adult chlamydial (inclusion)
conjunctivitis is an oculogenital infection usually caused by serovars (serological
variants) D–K of C. trachomatis, and affects 5–20% of sexually active young adults in
Western countries.

• Transmission is by autoinoculation from genital secretions, although eye-to-eye spread

probably accounts for about 10%. The incubation period is about a week.
 Adult Chlamydial Conjunctivitis
• Symptoms consist of the subacute onset of unilateral
or bilateral redness, watering and discharge. It is
important to enquire about sexual exposure if
chlamydial conjunctivitis is suspected.

• Signs
 Watery or mucopurulent discharge.
 Tender preauricular lymphadenopathy.
 Large follicles are often most prominent in the
inferior fornix (Fig. A) and may also involve the
upper tarsal conjunctiva (Fig. B).
 Superficial punctate keratitis is common.
 Perilimbal subepithelial corneal infiltrates (Fig. C)
may appear after 2–3 weeks.
 Mild conjunctival scarring and superior corneal
pannus (Fig. D) are not uncommon.
 Adult Chlamydial Conjunctivitis
• Investigations  Tarsal conjunctival scrapings, PCR, Giemsa staining, Direct
immunofluorescence, Enzyme immunoassay for direct antigen detection, McCoy cell
culture

• Treatment
Systemic therapy involves one of the following:
 Azithromycin 1 g repeated after 1 week is generally the treatment of choice
 Doxycycline 100 mg twice daily for 10 days
 Erythromycin, amoxicillin and ciprofloxacin are alternatives.

Topical antibiotics such as erythromycin or tetracycline ointment are sometimes used to

achieve rapid relief of ocular symptoms, but are insufficient alone.
 Trachoma
Trachoma is the leading cause of preventable irreversible blindness in the world. It is
related to poverty, overcrowding and poor hygiene, the morbidity being a consequence of
the establishment of re-infection cycles within communities. The fly is an important vector,
but there may be direct transmission from eye or nasal discharge.
 Trachoma
Diagnosis
Features of trachoma are divided into an ‘active’
inflammatory stage and a ‘cicatricial’ chronic stage,
with considerable overlap.

• Active trachoma is most common in pre-school

children and is characterized by the following:
 Mixed follicular/papillary conjunctivitis (Fig. A)
associated with a mucopurulent discharge. In
children under the age of 2 years the papillary
component may predominate.
 Superior epithelial keratitis and pannus formation
(Fig. B).
 Trachoma
• Cicatricial trachoma is prevalent in middle age.
 Linear or stellate (Fig. C) conjunctival scars in
mild cases, or broad confluent scars (Fig. D) in
severe disease.
 Although the entire conjunctiva is involved, the
effects are most prominent on the upper tarsal
plate.
 Superior limbal follicles may resolve to leave a
row of shallow depressions (Herbert pits – Fig. E).
 Trichiasis, distichiasis, corneal vascularization and
cicatricial entropion (Fig. F).
 Severe corneal opacification.
 Trachoma
Management
The SAFE strategy for trachoma management supported by the WHO and other agencies
encompasses Surgery for trichiasis, Antibiotics for active disease, Facial hygiene and
Environmental improvement.

• Antibiotics  A single dose of azithromycin (20 mg/kg up to 1 g) is the treatment of

choice. Erythromycin 500 mg twice daily for 14 days or doxycycline 100 mg twice
daily for 10 days.
• Facial cleanliness is a critical preventative measure.
• Environmental improvement, such as access to adequate water and sanitation, as well
as control of flies, is important.
• Surgery is aimed at relieving entropion and trichiasis and maintaining complete lid
closure, principally with bilamellar tarsal rotation.
 Neonatal Conjunctivitis
Neonatal conjunctivitis (ophthalmia neonatorum) is defined as conjunctival inflammation
developing within the first month of life. It is the most common infection of any kind in
neonates, occurring in up to 10%. It is often the result of infection transmitted from mother
to infant during delivery.

Causes
• Organisms acquired during vaginal delivery:
C. trachomatis, N. gonorrhoeae and herpes simplex virus (HSV, typically HSV-2). C.
trachomatis is the most common cause in cases involving moderate to severe conjunctival
inflammation.
• Staphylococci are usually responsible for mild conjunctivitis; other bacterial causes
include streptococci,
H. influenzae and various Gram-negative organisms.
.
 Neonatal Conjunctivitis
Signs
 A mildly sticky eye may occur in staphylococcal
infection, or with delayed nasolacrimal duct
canalization (mucopurulent reflux on pressure over
the lacrimal sac).
 Discharge is characteristically watery in chemical and
HSV infection, mucopurulent in chlamydial
infection, purulent (Fig. 5.8) in bacterial infection,
and hyperpurulent in gonococcal conjunctivitis.
 Severe eyelid oedema occurs in gonococcal infection
 Eyelid and periocular vesicles may occur in HSV
infection, and can critically aid early diagnosis and
treatment.
 Neonatal Conjunctivitis
Investigations:
 The results of any parental prenatal testing for STI should be obtained
 Conjunctival scrapings are taken for nucleic acid amplification (PCR)
 Gram and Giemsa staining
 Papanicolaou smear (HSV)
 Conjunctival scrapings or fluid from skin vesicles can be sent for viral culture for HSV.
 Neonatal Conjunctivitis
Treatment
• Prophylaxis is routinely performed but there is no standard protocol.
 A single instillation of povidone-iodine 2.5% solution is effective against common pathogens.
 Erythromycin 0.5% or tetracycline 1% ointment.
 Silver nitrate 1% solution

• Mild conjunctivitis  A broad-spectrum topical antibiotic such as chloramphenicol, erythromycin

or fusidic acid ointment is adequate in most cases. Further investigation and treatment can be instituted
if the condition fails to settle.

• Moderate to severe  If bacteria are evident on Gram stain, a broad-spectrum topical antibiotic (e.g.
chloramphenicol, erythromycin or bacitracin for Gram-positive organisms, neomycin, ofloxacin or
gentamicin for Gram-negatives) should be used until sensitivities are available.

• Severe conjunctivitis  A broad-spectrum topical antibiotic, such as erythromycin, commenced. The

ocular risk is usually most acute from gonococcal infection, so empirical topical treatment should cover
this, and in most cases consideration given to systemic treatment such as parenteral ceftriaxone.
 Neonatal Conjunctivitis
• Chlamydial infection is treated with oral erythromycin for 2 weeks
• Gonococcal conjunctivitis is treated systemically with a third-generation
cephalosporin and often with supplementary topical treatment. Saline irrigation to
remove excessive discharge should be considered
• Herpes simplex infection should always be regarded as a systemic condition and is
treated with high-dose intravenous aciclovir under paediatric specialist care.
 Viral Conjunctivitis
Viral conjunctivitis is a common external ocular infection, adenovirus (a non-enveloped
double-stranded DNA virus) being the most frequent (90%) causative agent. It may be
sporadic, or occur in epidemics in environments such as workplaces (including hospitals),
schools and swimming pools. Transmission is generally by contact with respiratory or
ocular secretions, including via fomites such as contaminated towels.
 Viral Conjunctivitis
Signs
• Eyelid oedema ranges from negligible to
severe.
• Lymphadenopathy is common: tender
pre-auricular.
• Conjunctival hyperaemia and follicles
(Fig. A) are typically prominent; papillae
may also be seen, particularly in the
superior tarsal conjunctiva.
• Severe inflammation may be associated
with conjunctival haemorrhages (usually
petechial in adenoviral infection – see Fig.
B), chemosis, membranes (rare) and
pseudomembranes (Fig. B), sometimes
with conjunctival scarring after resolution
(Fig. C).
 Viral Conjunctivitis
• Spontaneous resolution of adenoviral infection usually occurs within 2–3 weeks, so
specific treatment is typically unnecessary.
• Reduction of transmission risk by meticulous hand hygiene, avoiding eye rubbing and
towel sharing.
• Topical steroids such as prednisolone 0.5% four times daily may be required for severe
membranous or pseudomembranous adenoviral conjunctivitis.
 Allergic Conjunctivitis
Allergic conjunctivitis is a Type I (immediate) hypersensitivity reaction,
mediated by degranulation of mast cells in response to the action of IgE;
there is evidence of an element of Type IV hypersensitivity in at least
some forms.

Acute allergic conjunctivitis

Acute allergic conjunctivitis is a common condition caused by an acute
conjunctival reaction to an environmental allergen, usually pollen.
Acute itching and watering are common, but the hallmark is chemosis
(Figs A and B).

Treatment is not usually required and the conjunctival swelling settles

within hours as the acute increase in vascular permeability resolves.
Cool compresses can be used and a single drop of adrenaline 0.1% may
reduce extreme chemosis.
 Allergic Conjunctivitis
• Symptoms  transient acute or subacute attacks of redness, watering and itching, associated with
sneezing and nasal discharge.
• Signs  conjunctival hyperaemia with a relatively mild papillary reaction, variable chemosis and
lid oedema.
• Investigations  are generally not performed although conjunctival scraping in more active cases
may demonstrate the presence of eosinophils. Skin testing for particular allergens is rarely required.
 Allergic Conjunctivitis
Treatment
• Artificial tears for mild symptoms.
• Mast cell stabilizers (e.g. sodium cromoglicate, nedocromil sodium, lodoxamide)
• Antihistamines (e.g. emedastine, epinastine, levocabastine, bepotastine) can be used for
symptomatic exacerbations and are as effective as mast cell stabilizers.
• Non-steroidal anti-inflammatory preparations (e.g. diclofenac) can provide symptomatic
relief but are rarely used.
• Topical steroids are effective but rarely necessary.
• Oral antihistamines may be indicated for severe symptoms. Some, such as
diphenhydramine, cause significant drowsiness and may be useful in aiding sleep; others,
such as loratadine, have a far less marked sedative action.
 Vernal Keratoconjunctivitis
Vernal keratoconjunctivitis (VKC) is a recurrent bilateral disorder in which both IgE- and cell-
mediated immune mechanisms play important roles. It primarily affects boys and onset is generally
from about the age of 5 years onwards. There is remission by the late teens in 95% of cases.

Classification
• Palpebral VKC primarily involves the upper tarsal conjunctiva. It may be associated with
significant corneal disease as a result of the close apposition between the inflamed conjunctiva and
the corneal epithelium.
• Limbal disease typically affects black and Asian patients.
• Mixed VKC has features of both palpebral and limbal disease.

Symptoms consist of intense itching, which may be associated with lacrimation, photophobia, a
foreign body sensation, burning and thick mucoid discharge. Increased blinking is common.
 Vernal Keratoconjunctivitis
Palpebral disease
 Early-mild disease is characterized by conjunctival
hyperaemia and diffuse velvety papillary
hypertrophy on the superior tarsal plate (Fig. A).
 Macropapillae (<1 mm) have a flat-topped
polygonal appearance reminiscent of cobblestones;
focal (Fig. B) or diffuse (Fig. C) whitish
inflammatory infiltrates may be seen in intense
disease.
 Progression to giant papillae (>1 mm) can occur, as
adjacent smaller lesions amalgamate when dividing
septa rupture (Fig. D).
 Mucus deposition between giant papillae (Fig. E).
 Decreased disease activity is characterized by
milder conjunctival injection and decreased mucus
production (Fig. F).
 Vernal Keratoconjunctivitis
Limbal disease
 Gelatinous limbal conjunctival papillae that may be associated with transient apically
located white cellular collections (Horner–Trantas dots – Fig. A–C).
 In tropical regions, limbal disease may be severe (Fig. D).
 Vernal Keratoconjunctivitis
General measures
 Allergen avoidance, if possible. An allergy specialist opinion may be requested;
allergen (e.g. patch) testing is sometimes useful, but often gives non-specific results
 Cool compresses may be helpful
 Lid hygiene should be used for associated staphylococcal blepharitis
 Bandage contact lens wear to aid healing of persistent epithelial defects
 Vernal Keratoconjunctivitis
• Mast cell stabilizers (e.g. sodium cromoglicate, nedocromil sodium, lodoxamide)
reduce the frequency of acute exacerbations
• Topical antihistamines (e.g. emedastine, epinastine, levocabastine, bepotastine)
• Combined antihistamine and vasoconstrictor (e.g. antazoline with xylometazoline)
may offer relief in some cases.
• Combined action antihistamine/mast cell stabilizers (e.g. azelastine, ketotifen,
olopatadine) are helpful in many patients and have a relatively rapid onset of action.
• Non-steroidal anti-inflammatory preparations (e.g. ketorolac, diclofenac) may
improve comfort by blocking non-histamine mediators. Combining one of these with a
mast cell stabilizer is an effective regimen in some patients.
• Topical steroids (e.g. fluorometholone 0.1%, rimexolone 1%, prednisolone 0.5%,
loteprednol etabonate 0.2% or 0.5%) are used for severe exacerbations of conjunctivitis
 Vernal Keratoconjunctivitis
Systemic treatment
• Oral antihistamines help itching, promote sleep and reduce nocturnal eye rubbing.
Because other inflammatory mediators are involved besides histamines, effectiveness is not
assured. Some antihistamines (e.g. loratadine) cause relatively little drowsiness.
• Immunosuppressive agents (e.g. steroids, ciclosporin, tacrolimus, azathioprine)
02
Keratitis
 Cornea
The cornea is a complex structure which, as well as having a protective role, is responsible
for about three-quarters of the optical power of the eye. The normal cornea is free of blood
vessels; nutrients are supplied and metabolic products removed mainly via the aqueous
humour posteriorly and the tears anteriorly.
 Bacterial Keratitis
Bacterial keratitis usually develops only when ocular defences have been compromised.
However, some bacteria, including Neisseria gonorrhoeae, Neisseria meningitidis,
Corynebacterium diphtheriae and Haemophilus influenzae are able to penetrate a healthy
corneal epithelium, usually in association with severe conjunctivitis. It is important to
remember that infections may be polymicrobial, including bacterial and fungal co-
infection. Common pathogens include: Pseudomonas aeruginosa, Staphylococcus aureus,
Streptococci. (S. pyogenes, S. pneumoniae)
 Bacterial Keratitis
Risk factors
• Contact lens wear
• Trauma
• Ocular surface disease
• Other factors (include local or systemic immunosuppression, diabetes and vitamin A
deficiency)
 Bacterial Keratitis
Clinical features
• Presentation is with pain, photophobia, blurred
vision and mucopurulent or purulent discharge.
• Signs
 An epithelial defect with infiltrate involving a
larger area, and significant circumcorneal
injection (Fig. A and B).
 Stromal oedema, folds in Descemet membrane
and anterior uveitis, commonly with a
hypopyon (Fig. C) and posterior synechiae in
moderate–severe keratitis.
 Severe ulceration may lead to descemetocoele
formation and perforation, particularly in
Pseudomonas infection (Fig. D).
 Bacterial Keratitis
Local therapy
Topical therapy (Table 6.4) can achieve high tissue concentration
and initially should consist of broad-spectrum antibiotics that cover
most common pathogens.

• Antibiotic monotherapy has the major advantage over

duotherapy of lower surface toxicity, as well as greater
convenience.
 A commercially available fluoroquinolone is the usual choice
for empirical monotherapy.
 Ciprofloxacin or ofloxacin
 Bacterial Keratitis
• Subconjunctival antibiotics are usually only indicated if there is poor compliance
with topical treatment.
• Mydriatics (cyclopentolate 1%, homatropine 2% or atropine 1%) are used to prevent
the formation of posterior synechiae and to reduce pain.
• Steroids reduce host inflammation, improve comfort, and minimize corneal scarring.
 Candidal and Filamentous Keratitis
• Symptoms. Gradual onset of pain, grittiness, photophobia,
blurred vision and watery or mucopurulent discharge.
• Candidal keratitis Yellow–white densely suppurative
infiltrate is typical (Fig. A).
• Filamentous keratitis
 Grey or yellow–white stromal infiltrate with indistinct
fluffy margins (Fig. B).
 Progressive infiltration, often with satellite lesions
(Fig. C and D).
 Feathery branch-like extensions or a ring-shaped
infiltrate (Fig. E) may develop.
 Candidal and Filamentous Keratitis
Treatment
• Removal of the epithelium over the lesion may enhance penetration of antifungal agents. It
may also be helpful to regularly remove mucus and necrotic tissue with a spatula.
• Topical antifungals should initially be given hourly for 48 hours and then reduced as signs
permit. Because most antifungals are only fungistatic, treatment should be continued for at
least 12 weeks. (amphotericin B 0.15% or econazole 1%; alternatives include natamycin 5%,
fluconazole 2%, clotrimazole 1% and voriconazole 1 or 2%.)
• Systemic antifungals may be given in severe cases. Options include voriconazole 400 mg
twice daily for one day then 200 mg twice daily, itraconazole 200 mg once daily, reduced to
100 mg once daily, or fluconazole 200 mg twice daily.
• Tetracycline (e.g. doxycycline 100 mg twice daily) may be given for its anticollagenase
effect when there is significant thinning.
 Epithelial Keratitis
Epithelial (dendritic or geographic) keratitis is associated with
active virus replication.
• Symptoms. Mild–moderate discomfort, redness,
photophobia, watering and blurred vision.
• Signs
 Swollen opaque epithelial cells arranged in a coarse
punctate or stellate (Fig. A) pattern.
 Central desquamation results in a linear-branching
(dendritic) ulcer (Fig. B), most frequent located
centrally; the branches of the ulcer have characteristic
terminal buds and its bed stains well with fluorescein.
 The virus-laden cells at the margin of the ulcer stain with
rose Bengal (Fig. C), and this may help distinction from
alternative diagnoses, particularly an atypical recurrent
corneal abrasion.
 Epithelial Keratitis
 Inadvertent topical steroid treatment may promote
progressive enlargement of the ulcer to a
geographical or ‘amoeboid’ configuration (Fig. D).
 Following healing, there may be persistent punctate
epithelial erosions and irregular epithelium (Fig. E)
which settle spontaneously and should not be
mistaken for persistent active infection.
 Mild subepithelial haze (Fig. F) may persist for
weeks after the epithelium heals.
 Protozoan Keratitis (Achantamoeba)
Acanthamoeba spp. are ubiquitous free-living protozoa commonly found in soil, fresh or
brackish water and the upper respiratory tract. The cystic form (Fig. A) is highly resilient.
Under appropriate environmental conditions, the cysts turn into trophozoites, with tissue
penetration and destruction. In developed countries acanthamoeba keratitis is most
frequently associated with contact lens wear, especially if tap water is used for rinsing.
 Protozoan Keratitis (Achantamoeba)
• Symptoms. Blurred vision and discomfort; pain is often
severe and characteristically disproportionate to the
clinical signs.
• Signs
 In early disease the epithelial surface is irregular and
greyish (Fig. B).
 Epithelial pseudodendrites resembling herpetic lesions
may form.
 Limbitis with diffuse or focal anterior stromal infiltrates
(Fig. C).
 Characteristic perineural infiltrates (radial
keratoneuritis) (Fig. D).
 Gradual enlargement and coalescence of infiltrates to
form a ring abscess (Figs A and B) is typical.
 Corneal melting may occur at any stage when there is
stromal disease. The melt often develops at the
periphery of the area of infiltrate (Fig. C).
 Marginal Keratitis
Marginal keratitis is believed to be caused by a hypersensitivity
reaction against staphylococcal exotoxins and cell wall proteins with
deposition of antigen-antibody complexes in the peripheral cornea
(antigen diffusing from the tear film, antibody from the blood vessels)
with a secondary lymphocytic infiltration.

• Symptoms. Mild discomfort, redness and lacrimation; may be

bilateral.
• Signs
 Chronic blepharitis is typical.
 Inferior punctate epitheliopathy is an early manifestation.
 Subepithelial marginal infiltrates separated from the limbus by
a clear zone, often associated with an adjacent area of
conjunctival hyperaemia (Fig. A).
 Characteristically, any epithelial defect will be considerably
smaller than the area of infiltrate (Fig. B).
 Coalescence and circumferential spread (Fig. C).
 Marginal Keratitis
 Usually little or no anterior chamber reaction, even with large
infiltrates.
 Without treatment, resolution generally occurs in 1–4 weeks,
depending on severity. Occasionally there is residual superficial
scarring and slight thinning with mild pannus (Fig. D). Iris new
vessels may develop in the presence of persistent large lesions, but
resolve when inflammation settles.

Treatment
A weak topical steroid such as fluorometholone or prednisolone 0.5%
is instilled four times daily for 1–2 weeks, sometimes combined with a
topical antibiotic.
 Neurotrophic Keratopathy
Neurotrophic keratopathy is caused by failure of re-epithelialization
resulting from corneal anaesthesia, often exacerbated by other factors
such as drug toxicity.
• Signs
 A non-healing epithelial defect, sometimes after prolonged
topical treatment, is an early sign.
 The stroma beneath the defect is grey and opaque and may
become thin.
 Secondary bacterial or fungal infection may occur.
• Treatment is that of persistent epithelial defects; topical steroids
to control any inflammatory component should be kept to a
minimum.
 Mooren Ulcer
Mooren ulcer is a rare autoimmune disease characterized by
progressive circumferential peripheral stromal ulceration with later
central spread.

• Symptoms. Pain is prominent and may be severe. There is

photophobia and blurred vision.
• Signs
 Peripheral ulceration involving the superficial one-third of
the stroma (Fig. A), with variable epithelial loss.
 An undermined and infiltrated leading edge is
characteristic (Fig. B).
 Progressive circumferential and central stromal thinning
(Fig. C).
 The healing stage is characterized by thinning,
vascularization and scarring (Fig. D).
 Mooren Ulcer
Treatment
• Topical steroids as frequently as hourly are combined with a low-frequency prophylactic
topical antibiotic.
• Topical ciclosporin
• Adjunctive topical therapy includes artificial tears and collagenase inhibitors such as
acetylcysteine 10–20%.
• Conjunctival resection, which may be combined with excision of necrotic tissue, is
performed if there is no response to topical steroids.
• Systemic immunosuppression
• Systemic collagenase inhibitors
• Lamellar keratectomy involving dissection of the residual central island in advanced
disease may remove the stimulus for further inflammation.
 Episcleritis and Scleritis
The scleral stroma is composed of collagen bundles of varying size and shape that
are not uniformly orientated as in the cornea, and so are not transparent. The inner
layer of the sclera (lamina fusca) blends with the uveal tract. Anteriorly the
episclera consists of a connective tissue layer between the superficial scleral
stroma and Tenon capsule. There are three pre-equatorial vascular layers:

• Conjunctival vessels are the most superficial; arteries are tortuous and veins
straight.
• Superficial episcleral plexus vessels are straight with a radial configuration.
In episcleritis, maximal congestion occurs at this level (Fig. A). Topical
phenylephrine 2.5% will also constrict the conjunctival and 10% also the
superficial episcleral vessels.
• Deep vascular plexus lies in the superficial part of the sclera and shows
maximal congestion in scleritis (Fig. B); a purplish hue, best seen in daylight,
is characteristic.
 Episcleritis and Scleritis
• Episcleritis is a common, usually idiopathic and benign, recurrent and frequently bilateral
condition. Females may be affected more commonly than males, except possibly in children, in
whom episcleritis is rare; the average patient is middle-aged. It is typically self-limiting and tends
to last from a few days up to 3 weeks, but rarely longer. Associated disease, either ocular (e.g. dry
eye, rosacea, contact lens wear) or systemic (e.g. collagen vascular disorders such as rheumatoid
arthritis, herpes zoster ophthalmicus, gout and others) has been identified in up to a third of patients
seen at tertiary centres, with ocular disease the most common.

• Scleritis is an uncommon condition characterized by oedema and cellular infiltration of the entire
thickness of the sclera. Immunemediated (non-infectious) scleritis is the most common type, and is
frequently associated with an underlying systemic inflammatory condition, of which it may be the
first manifestation. Scleritis is much less common than episcleritis and comprises a spectrum from
trivial and self-limiting disease to a necrotizing process that can involve adjacent tissues and
threaten vision.
Terimakasih