Keratitis-Conjungtivitis

SUCI PURNAMASARI (I11109023)

ANATOMY

Conjunctiva is a thin, protective mucous membrane

composed of nonkeratinized stratified colummnar
epithelium.
Palpebral conjunctiva: lines the inner aspect of the eyelids.
Bulbar conjunctiva: passes from the eyelids into the
surface of the eyeball, where it covers the sclera but not
the cornea.

Conjunctiva

A healthy cornea, together with the overlying tear film, is

necessary to provide a proper anterior refractive surface
(2/3) and to protect the eye against infection and
structural damage to the deeper components of the eye.
Horizontal diameter (adult): 11.5-12 mm, 1.0 mm larger
than the vertical diameter.
Anterior refractive power: 4343.50 diopters.
Shape: prolate, being flatter in the periphery and steeper
centrally creates an aspheric optical system.
Layer of cornea: epithelium, Bowman membrane, stroma,
descement membrane, endothelial.
Inervates by N.V.

Cornea

Anatomy

Keratitis

Many pain fibers superficial or deep lesion cause pain

and photophobia.
The pain is worsened by movement of the lids.
Refracts light rays usually blur vision, especially if
centrally located, minimal in herpetic keratitis.
Tearing

Physiology of Symptoms

Classification

Corneal disease caused by bacterial organisms.

Leading causes of blindness in the world, especially
monocular blindness.
Preventable or treatable ophthalmic disease.
Cellular infiltration of the corneal epithelium or stroma
corneal inflammation and necrosis.

Bacterial Keratitis

30000 cases in United States.

The increasing popularity of contact lens rising
incidence, 1030 per 100000 who wear contact lenses
develop ulcerative keratitis annually in the United States.
Specific organisms varies by region local epidemiological
patterns

Bacterial Keratitis (Epidemiology)

The clinical signs and symptoms of bacterial keratitis

depend greatly on the virulence of the organism and the
duration of infection.
Other influential factors the previous status of the
cornea and the use of corticosteroids.
Patients may describe decreased vision, pain, and
photophobia.
The cardinal corneal sign a localized or diffuse infiltration
of the epithelium or stroma (with or without epithelial
absence).

Clinical Features

Other ocular structures inflammation lid erythema

and edema, conjunctival injection and chemosis, tearing,
and discharge, conjunctival papillary response might be
seen, anterior chamber inflammation, hypopyon, aqueous
might become dense and fibrinoid, and fibrinous
endothelial plaques might develop.

Clinical Features

Principal Types of Epithelial Keratitis

Principal Types of Epithelial Keratitis

Staphylococcus

Opportunistic pathogens in
compromised corneas.
a well-defined, cream-colored
or gray-white stromal infiltrate
with an overlying epithelial
defect, multiple foci of abscesses,
resemble fungal satellite lesions.
More severe infiltration and
necrosis than S. Epidermidis
extend deep into the stroma, and
necrosis of this abscess can lead
to perforation. A hypopyon and
endothelial plaque can be seen.

Streptococcus
Corneal infection follow trauma.
Infiltration that begins at the site
of injury can readily spread
producing a deep stromal
abscess, fibrin deposition,
plaque formation, severe
anterior chamber reaction,
hypopyon, and iris synechiae

Infection Agents (Gram positive

cocci)

Bacillus after penetrating injury (soil contamination), develops within 24

hours of injury, chemosis, profound lid edema, and proptosis, microcystic
edema, circumferential corneal abscess. Extremely virulent organism,
perforation of the cornea can develop within hours.
Corynebacteria , infrequently cause corneal disease, associated with
pseudomembranous conjunctivitis and preauricular lymphadenopathy.
Listeria, occurs in animal handlers, lead to a necrotizing keratitis (Typically, a
ring ulcer and an exuberant anterior chamber reaction with fibrinous exudate
and a hypopyon).
Pseudomonas aeruginosa, the most common gram-negative organism isolated
from corneal ulcers, frequent cause of contact lens-associated keratitis,
produces destructive enzymes such as protease, lipase, elastase, and
exotoxin, which results in necrotic, soupy ulceration. The ulcer often extends
peripherally and deeply within hours and can rapidly involve the entire cornea.
The corneal stroma appears to dissolve into a greenish yellow mucous
discharge. Extensive keratitis can extend to the limbus and produce an
infectious scleritis.

Infection Agents (Gram-Positive

Bacilli)

Neisseria gonorrhoeae and N. Meningitidis:

In a newborn with ophthalmia neonatorum, gonorrheal conjunctivitis is a
significant concern. Corneal infection is often peripheral and can progress
to perforation and endophthalmitis.
In adults, ocular gonorrhea is accompanied by a copious weeping,
hyperpurulent discharge. Keratitis most commonly occurs after prolonged
conjunctivitis.
Keratitis is characterized by diffuse edema or a ring ulcer with hypopyon,
and there is a significant risk of corneal necrosis and perforation.

Infection Agents (Gram negative

cocci)

The presumptive diagnosis clinical history and physical examination

Confirmation examining stained smears of corneal scrapings, laboratory
cultures of the scrapings.
Stains Gram's and Giemsa (most common)
Suspected filamentous bacterial or nontuberculous mycobacterial
Ziehl-Neelsen

Diagnosis

Diagnosis

Treatment

Corneal disease caused by fungal organisms.

Relatively infrequent in the developed, larger proportion of keratitis cases
in developing world; agrarian; tropical countries; corneal disease and local
immunosuppression caused by chronic corticosteroid use; systemic
disease
In the United States 1500 cases per year
Fusarium, Aspergillus, Candida most common
Filamentous: Fusarium, Cephalosporium, Aspergillus, Curvularia,
Alternaria, Mucor, Rhizopus
Yeast: Candida and Cryptococcus
Diphasic formsare: Histoplasma, Coccidioides, Blastomyces

Fungal Keratitis

Common in traumatized (vegetable matter), diseased, and

immunocompromised corneas.
Slowly progressive and insidious, but a fairly rapid infiltrate development
does not rule out fungal infection.
Epithelium might heal over an intrastromal infiltrate produces little
inflammation and minimal discomfort.
Inflammation might be so severe as to result in hypopyon formation. The
ulcer and infiltrate might be indistinguishable from a bacterial ulcer.
Certain features suggest a fungal infection feathery edges or a dry,
gray, elevated infiltrate and satellite lesions.
Symptoms: Pain, photophobia, red eye,
tearing, discharge, foreign body
sensation.

Clinical Features

Important historical elements pre-existing corneal

disease, chronic corticosteroid use, or trauma, with
attention to the possibility of vegetable matter
contamination.
Definite diagnosis requires laboratory confirmation.
Stain: Gram's, Giemsa, inkpotassium hydroxide, Gomori's
methenamine silver.
Culture media: blood agar, Sabouraud, BHI.

Diagnosis

Treatment

Corneal disease caused by protozoal organisms.

Significant cause of ocular morbidity.
Onchocerca in developing world.
Acanthamoeba in developed world as a potentially
disastrous complication of contact lens wear requires
early aggressive treatment.

Parasitic Keratitis

Opportunistic infection in humans. Since 1973

increasing frequency to cause a severe, blinding keratitis.
Species: A. castellani, Vahlkampfia and Hartmannella.
Thrives in soil and water: ponds, swimming pools, hot
tubs, and contact lens saline solutions/ exposure to
contaminated water (93%).
Almost all cases history of exposure to contaminated
water or corneal trauma (+), exposure to contaminated
water (93%).

Parasitic Keratitis
(Acanthamoeba)

Early infection irregularity and infiltration,

pseudodendrites, or elevated epithelial ridges.
Infiltrates around corneal nerves.
Satellite lesions, corneal neovascularization is uncommon
- fluctuating, nongranulomatous anterior chamber
inflammation may contribute.
Severe cases hypopyon, diffuse or nodular anterior
scleritis, or posterior scleritis can occur.

Parasitic Keratitis
(Acanthamoeba)

Herpes simplex viral infection of the cornea.

Human herpesviruses have in common a state called
latency where the virus remains dormant in cells and
periodically reactivates.
Keratitis caused by HSV is the most common cause of
cornea-derived blindness in developed nations.
The incidence 20 000 per year and the total number of
cases per year is estimated to be 48 000 in the United
States with a prevalence of 400 000. [4] [5]

Herpes Simplex Keratitis

Herpes Simplex Keratitis

Blepharoconjunctivitis
Lid vesicles and conjunctival dendrites (rare).
Kaposis varicelliform eruption extensive vesicular
eruptions, malaise and lymphadenopathy.
Usually occurs in atopic or immunocompromised patients.

Herpes Simplex Keratitis

Herpes Simplex Keratitis

Herpes Simplex Keratitis

Herpes Simplex Keratitis

Corneal inflammation with no known infectious cause.

Characterized by persistent corneal epithelial defects,
stromal inflammation, and enzymatic degradation of the
corneal collagen.
Visual loss may result from an irregular surface, corneal
opacity, or altered topography from corneal thinning.
General therapeutic principles include determination of the
specific cause; promotion of epithelial healing; limitation of
ulceration and stromal loss; and support of repair. Both
local and systemic routes of therapy may be necessary for
effective management.

Non Infectious

Moorens ulcer is a rare, chronic, painful, peripheral ulcerative

keratitis.
Two clinical types :
The limited type is typically unilateral, occurs in older patients (fourth
decade and older), and is more responsive to local surgical and
medical therapy.
The second type, which is more resistant to systemic
immunosuppression, involves a bilateral, painful, relentless,
progressive destruction of the cornea, usually in younger individuals
(third decade), many of whom are of African descent.
The pathogenesis is unknown, but appears to involve an autoimmune
reaction.
Moorens ulcer is characterized by a progressive, crescentic,
peripheral corneal ulceration that is slightly central to the
corneoscleral limbus.

Non Infectious Keratitis (Moorens

Ulcer)

Non Infectious Keratitis (Moorens

Ulcer)

Moorens ulcer is by definition, not associated with any

systemic abnormality, except for the occasional association
with hepatitis C.
A secondary Moorens ulcer-like PUK may occur following
other types of corneal inflammation, including trauma,
cataract surgery, herpes simplex keratitis, alkali injury, and
herpes zoster.
Patients complain of severe ocular pain, photophobia, and
tearing.

Non Infectious Keratitis (Moorens

Ulcer)

CONJUNCTIVITIS

Inflammation of the conjunctiva, may be infectious or

noninfectious.

Conjunctivitis

Pathogenesis of Conjunctivitis

Bacterial conjunctivitis can be classified into three clinical

types: acute, hyperacute, and chronic.
The most common conjunctival pathogens include
Staphylococcus, Streptococcus pneumoniae, Haemophilus
species, Moraxella, Corynebacterium diphtheriae, Neisseria
species, and enteric gram-negative rods.[1]

Bacterial Conjunctivitis

Bacterial conjunctivitis is characterized by a rapid onset of

unilateral conjunctival hyperemia, lid edema, and
mucopurulent discharge.
The second eye typically becomes involved 12days later.
Symptoms: a foreign body sensation, a scratching or
burning sensation, a sensation of fullness around the eyes,
itching, and photophobia.
Signs: hyperemia, tearing, exudation, pseudoptosis,
papillary hypertrophy, chemosis, follicles,
pseudomembranes and membranes, granulomas, and
preauricular adenopathy.

Bacterial Conjunctivitis

Conjunctival membranes and pseudomembranes are the

findings associated with bacterial conjunctivitis, produced
in association with Neisseria gonorrhoeae, -hemolytic
streptococci, and C. diphtheriae.

Bacterial Conjunctivitis

Hyperacute Conjunctivitis

The most common cause N. gonorrhoeae.

Seen primarily in neonates and sexually active young adults.
Development of symptoms occurs within 24hours and signs
include profuse, thick, yellow-green purulent discharge, painful
hyperemia, chemosis of the conjunctiva, and tender preauricular
nodes.
Untreated cases may lead to peripheral corneal ulceration and
eventual perforation with possible endophthalmitis.
Milder Meningococcal conjunctivitis caused by Neisseria
meningitidis.

Hyperacute Bacterial Infection

Signs include profuse, thick, yellow-green purulent

discharge, painful hyperemia, chemosis of the conjunctiva

Hyperacute Bacterial Infection

By specific pathogen.
Examination: Conjunctival scraping for Gram stain and culture on blood and
chocolate agar.
Gonococcal conjunctivitis 1g of intramuscular ceftriaxone followed by a
2- to 3-week course of oral tetracycline or erythromycin. Topical
medications may include penicillin (333000units/mL) or bacitracin or
erythromycin ointment every 2hours.
Meningococcal conjunctivitis systemic treatment includes intravenous
penicillin, or for penicillin resistant infections, cefotaxime i.v. /ceftriaxone.
In penicillin-allergic patients, consider an oral fluoroquinolone (e.g.,
ciprofloxacin 500 mg p.o., for 5 days)
Frequent irrigation of the ocular surface.
Patients need to be seen daily.
Treat sexual partners with oral antibiotics for both gonorrhea and
chlamydia. Treat for possible chlamydial coinfection (azithromycin 1 g p.o.
single dose or doxycycline 100 mg p.o., for 7 days).

Acute Conjunctivitis

Begins unilaterally with hyperemia, irritation, tearing,

mucopurulent discharge, and mattering of the lids.
Other manifestation: blepharitis, keratitis, marginal ulcers, and
phlyctenulosis.
These infections are normally self-limited, lasting 710days.
H. influenzae, S. pneumoniae, and Moraxella catarrhalis young
children, institutional epidemics.
H. influenzae systemic infection e.g. upper respiratory infection
and fever.

Acute Bacterial Conjunctivitis

The treatment of acute bacterial conjunctivitis consists of

topical antibiotic drops or ointments.
Antibiotic speeds the resolution and lessens the severity.
DOC A broad-spectrum antibiotic with good grampositive coverage such as a third- or fourth-generation
fluoroquinolone, 10% sodium sulfacetamide, or
trimethoprim-polymyxin may be used for 710days.

Acute Bacterial Conjunctivitis

Most commonly adenovirus.

Acute hemorrhagic conjunctivitis: Associated with a large
subconjunctival hemorrhage, coxsackie and enterovirus, 1
to 2 weeks duration. Tends to occur in tropical regions.

Acute Viral Conjunctivitis

Symptoms: Itching, burning, foreign body sensation; history of

recent upper respiratory tract infection or sick contact.
Sign: Inferior palpebral conjunctival follicles, tender palpable
preauricular lymph node.
Other sign: Watery discharge, red and edematous eyelids,
pinpoint subconjunctival hemorrhages, punctate keratopathy,
membrane/pseudomembrane.
Often starts in one eye and involves the fellow eye a few days
later.

Acute Viral Conjunctivitis

Cool compresses several times per day.

Antihistamine if itching is severe.
If a membrane/pseudomembrane present, it may be gently peeled or left.
If a membrane/pseudomembrane is acutely present or if SEIs reduce vision
later, use topical steroids. For membranes/ pseudomembranes, use a more
frequent steroid dose or stronger steroid (e.g., loteprednol 0.5% q.i.d.) and
consider a steroid ointment (e.g., fluorometholone 0.1% ointment q.i.d. or
dexamethasone/ tobramycin 0.1%/0.3% ointment q.i.d.) in the presence of
significant tearing to maintain longer medication exposure. For SEIs, a
weaker steroid with less frequent dosing is usually sufficient (e.g.,
loteprednol 0.2% b.i.d.). Given the possible side effects (see
Pharmacopoeia), prescription of topical steroids is cautionary in the
emergency room setting or in patients with questionable follow-up. Steroids
may hasten resolution of the symptoms but prolong the infectious period.
Steroid treatment is maintained for 1 week and then slowly tapered. SEIs
can recur during or after tapering.

Acute Viral Conjunctivitis

Counsel the patient that viral conjunctivitis is a self-limited

condition that typically gets worse for the first 4 to 7 days after
onset and may not resolve for 2 to 3 weeks or longer with corneal
involvement.
Viral conjunctivitis is highly contagious, usually for 10 to 12 days
from onset as long as the eyes are red. Patients should avoid
touching their eyes, shaking hands, sharing towels, etc. Restrict
work and school for patients with significant exposure to others
while the eyes are weeping.
Frequent handwashing.
Preservative-free artificial tears (e.g., Refresh Plus) four to eight
times per day for 1 to 3 weeks. Use single-use vials to limit tip
contamination and spread of the condition.

Acute Viral Conjunctivitis

Known as Apollo disease.

Caused by enterovirus 70 and coxsakievirus A24.
Pain, photophobia, foreign-body sensation, copious tearing,
redness, lid edema, chemosis and subconjunctival
hemorrhages.
The hemorrhages are petechial at first and then coalesce,
appearing post-traumatic.
The cornea may be involved
Resolves within 4-6 days

Acute Hemorrhagic Conjunctivitis

Adenoviruses produce the most common viral conjunctivitis

with varying degrees of severity.
Spread via respiratory droplets or direct contact from
fingers to the lids and conjunctival surface.
The incubation period: 5-12 days
Clinical illness is present for 515days.
The spectrum consists of follicular conjunctivitis,
pharyngoconjunctival fever, and epidemic
keratoconjunctivitis.

Adenovirus Conjunctivitis

Mildest form of adenoviral conjunctivitis.

Adenovirus serotypes 1 through 11 and 19.
acute onset and is initially unilateral with

possible involvement of the second eye

within 1week.
watery discharge, conjunctival hyperemia,
usually accompanied by follicular and
papillary conjunctival changes and
preauricular lymphadenopathy.
Resolve spontaneously, without sequelae,
within days to weeks.

Follicular Conjunctivitis

Adenovirus serotypes 3,4, and 7.

Characterized: combination of pharyngitis, fever, and
conjunctivitis.
Predominantly follicular with a scant watery discharge,
hyperemia, and mild chemosis.
Resolves spontaneously within 2 weeks.
Treatment: cold compresses, artificial tears and
vasoconstrictor eye drops.

Pharyngoconjunctival Fever

Usually occurs in children under 5 years old.

Most ocular herpetic infections result from herpes simplex
virus type 1.
Typical signs: ocular irritation, watery discharge, mixed
papillary and follicular conjunctivitis, hemorrhagic
conjunctivitis and preauricular lymphadenopathy.
Herpetic vesicles may sometimes appear on the eyelids
and lid margins, associated with severe edema of the
eyelids.

Herpes Simplex Virus

Conjunctivitis

May persist for 2-3 weeks

Complications consist of corneal involvement (including
dendrites) and vesicles on the skin.
Any HSV infection in the newborn must be treated with
systemic antiviral therapy (acyclovir) and monitored in a
hospital setting.
Conjunctivitis occurs in a child over 1 year of age or in an
adult, it is usually self-limited.
Topical or systemic antiviral should be given to prevent
corneal involvement.

Herpes Simplex Virus

Conjunctivitis

Herpes Simplex Virus

Conjunctivitis

Symptoms: itching, watery discharge, and a history of

allergies are typical.
Signs: chemosis, red and edematous eyelids, conjunctival
papillae, no preauricular node.

Acute Alergic Conjunctivitis

Eliminate the inciting agent.

Cool compresses several times per day.
Topical drops, depending on the severity.
Mild: Artificial tears four to eight times per day.
Moderate: Use olopatadine 0.1% (e.g., Patanol), epinastine
0.05% (e.g., Elestat), nedocromil 2% (e.g., Alocril), or ketotifen
0.025% (e.g., Zaditor) to help relieve itching. Ketorolac 0.5%
(e.g., Acular), pemirolast 0.1% (e.g., Alamast), and lodoxamide
0.1% (e.g., Alomast) q.i.d. can also reduce symptoms.
Severe: Mild topical steroid (e.g., loteprednol 0.2% or
fluorometholone 0.1%, for 1 to 2 weeks) in addition to the
preceding medications.
Oral antihistamine (e.g., diphenhydramine 25 mg p.o. or loratadine
10 mg p.o.) in moderate to severe cases can be very helpful.

Acute Alergic Conjunctivitis

Symptoms: itching, thick, ropy discharge, seasonal

(spring/ summer) recurrences, history of atopy.
Usually seen in young patients, especially boys.
Signs: large conjunctival papillae seen under the upper
eyelid or along the limbus (limbal vernal).
Other. Superior corneal shield ulcer (a well-delineated,
sterile, graywhite infiltrate), limbal raised white dots
(HornerTrantas dots) of degenerated eosinophils.

Vernal Conjunctivitis

Treat as for allergic except prophylactically use a mast cell

stabilizer (e.g., lodoxamide 0.1% or pemirolast 0.1%), or a mast
cell stabilizer and/or antihistamine (e.g., nedocromil 2%,
olopatadine 0.1% etc.) for 2 to 3 weeks before the season starts.
If a shield ulcer is present, add:
Topical steroid (e.g., loteprednol 0.5% or prednisolone 1%
drops, dexamethasone 0.1% ointment) four to six times per
day.
Topical antibiotic (e.g., erythromycin ointment q.i.d., bacitracin
ointment q.i.d., polymixin/bacitracin q.i.d.).
Cycloplegic agent (e.g., scopolamine 0.25% t.i.d.).
Add antiallergy drops as for allergic conjunctivitis if not already
using.
Cool compresses.

Vernal Conjunctivitis

Chronic Conjunctivitis

Chronic bacterial conjunctivitis, which is defined by a duration of

longer than 3weeks, may result from S. aureus and Moraxella
lacunata; Proteus mirabilis, Escherichia coli; Klebsiella
pneumoniae, Serratia marcescens and Branhamella catarrhalis.
The clinical signs of chronic staphylococcal conjunctivitis include
diffuse conjunctival hyperemia with papillae or follicles, minimal
mucopurulent discharge, and conjunctival thickening. Eyelid
involvement may comprise redness, telangiectasis, lash loss,
collarettes, recurrent hordeolae, and ulcerations at the base of
the cilia.
Chronic staphylococcal blepharoconjunctivitis may lead to
marginal corneal ulcers.

Chronic Bacterial Konjunctivitis

The treatment proper antimicrobial therapy and good lid

hygiene, which includes hot compresses and eyelid scrubs.
Antibiotics: Erythromycin and bacitracin ointments.
Severe inflammation antibiotic and corticosteroid
combination drops or ointments can be rubbed into the lid
margins after the eye scrubs.
Oral therapy with tetracycline 250mg four times a day or
doxycycline 100mg twice a day or minocycline 50mg twice
a day may be needed for more severe infections.

Chronic Bacterial Konjunctivitis

Defined

by a duration of longer than

3weeks, may result from a number of
organisms.
The most common causative agent in
chronic bacterial conjunctivitis is S.
aureus, which colonizes the eyelid margin,
from which it causes direct infection of the
conjunctiva or conjunctival inflammation
through its elaboration of exotoxins.

Chronic Conjunctivitis

The

clinical signs of chronic staphylococcal

conjunctivitis include diffuse conjunctival
hyperemia with papillae or follicles, minimal
mucopurulent discharge, and conjunctival
thickening. Eyelid involvement may comprise
redness, telangiectasis, lash loss, collarettes,
recurrent hordeolae, and ulcerations at the
base of the cilia. Chronic staphylococcal
blepharoconjunctivitis may lead to marginal
corneal ulcers.

Chronic Conjunctivitis

 Combines

proper antimicrobial therapy and good

lid hygiene, which includes hot compresses and
eyelid scrubs.
Erythromycin and bacitracin ointments are
effective adjunct topical antibiotics.
When severe inflammation exists, antibiotic and
corticosteroid combination drops or ointments
can be rubbed into the lid margins after the eye
scrubs.
Oral therapy with tetracycline 250mg four times
a day or doxycycline 100mg twice a day or
minocycline 50mg twice a day may be needed for
more severe infections.

Chronic Bacterial Conjunctivitis

Adenovirus serotypes 8, 19 and 37.

More severe and typically last for 7-21 days.
Mixed papillary and follicular response of the conjunctival
stroma.
Watery discharge, hyperemia, chemosis, and preauricular
lymphadenopathy , subconjunctival hemmorhages,
conjunctival membrane formation and lid edema.
Membranes are common with severe infection.
Conjunctival scarring and symblepharon formation.

Epidemic Keratoconjunctivitis

Epidemic Keratoconjunctivitis

Corneal involvement.
Most patients have a diffuse, fine, superficial keratitis: first
week.
Focal, elevated, punctate epithelial lesions develop by day
6-13 -> foreign body sensation.
Subepithelial opacities by day 14.

Epidemic Keratoconjunctivitis

Epidemic Keratoconjunctivitis

Patients may be infectious for up 14 days after onset.

Transmission usually occurs from eye to fingers to eye, but
tonometers, contact lenses, and eye drops are other routes
of transmission.
Stage of acute conjunctivitis ->cold compresses and
decongestant eye drops.
Patients have decreased visual acuity or disabling
photophobia -> topical corticosteroid
1% prednisolone acetate three to four times a day, can
help eliminate subepithelial infitrates.

Epidemic Keratoconjunctivitis