Professional Documents
Culture Documents
DECREASED VISION
FAWAID AKBAR
I11112029
Subjects
Keratitis
Corneal ulcer
Vogt Koyanagi-Harada Syndrome
Symphatetic Ophthalmiitis
Acute congestive glaucoma
Uveitis anterior
Endophthalmitis, panophthalmitis
Keratitis
Introduction
Keratitis is a condition which the
eyes cornea become inflamed and
clouded.
Bacterial Keratitis
Corneal disease caused by bacterial
organisms.
Bacterial keratitis is considered a
leading cause of monocular blindness
in the developing world.
Clinical Features
The clinical signs and symptoms of
bacterial keratitis depend greatly on the
virulence of the organism and the duration
of infection.
Key features : Cellular infiltration of the
corneal epithelium or stroma, corneal
inflammation, and necrosis.
Associated features : lid edema,
conjunctival inflammation, discharge,
anterior chamber reaction, hypopyon.
Etiology
Many bacteria can cause bacterial keratitis.
Gram-Positive bacteria that infect cornea :
staphylococci, streptococci, Bacillus cereus,
corynebacteria, Listeria monocytogenes,
clostridium, and Propionibacterium acnes.
Gram-Negative bacteria that infect cornea :
pseudomonas, serratia, escherichia,
klebsiella, proteus, moraxella, haemophilus,
neisseria, and Branhamella catarrhalis.
Mycobacterium.
Streptococc
al bacterial
keratitis
with
infiltration
of the
central
cornea.
Intraepithelial
infiltration of
the cornea by
Pseudomonas
organisms in a
hydrophilic
contact lens
wearer.
Diagnosis
The presumptive diagnosis of
infectious keratitis is based primarily
on the clinical history and physical
examination, but confirmation of
infectious infiltration and definitive
identification of the offending
organism can be achieved only by
examining stained smears of corneal
scrapings and laboratory cultures of
these scrapings.
Treatment
GramNegative
Gram-Positive
Gentamicin.
Tobramycin.
Polimiksin.
Cefazolin.
Vancomycin.
Basitracin.
Fungal Keratitis
Corneal disease caused by fungal
organisms.
Fungal infections of the cornea are
relatively infrequent in the developed
world but constitute a larger
proportion of keratitis cases in many
parts of the developing world.
Clinical Features
Fungal infection tends to arise in traumatized,
diseased, and immunocompromised corneas.
Key features : Cellular infiltration of the corneal
epithelium or stroma, corneal inflammation, and
necrosis.
Associated features : long-term steroid use,
trauma involving vegetative matter, corneal
infiltrate with feathery borders or satellite
lesions.
Definite diagnosis : laboratory confirmation, by
scraping for stains and cultures.
Treatment
1. Polyenes : amphotericin B,
natamycin.
2. Imidazoles : ketoconazole,
miconazole.
3. Triazoles : fluconazole.
4. Pyrimidines : flucytosine.
Classification
1. Epithelial keratitis,
2. Stromal/endothelial keratitis,
Caused by actively
replicating virus on
the corneal surface.
Initial episodes
present with foreign
body sensation but
subsequent
episodes are
usually painless.
Dendritic ulcer
classic feature of
epithelial disease.
This is usually an
immune-mediated
response to
nonreplicating viral
particles, but more
severe forms may
be caused by live
virus.
Focal endotheliitis
(disciform
keratitis) classic
feature of stromal
disease.
Diagnosis
Diagnostic testing is seldom needed
in epithelial Herpes Simplex Virus
Keratitis (HSVK) because of its classic
clinical features and is not useful in
stromal keratitis as there is usually
no live virus present.
Diagnostic testing that can be used :
culture, DNA testing, fluorescent
antibody testing, Tzanck smear,and
serum antibody testing.
Treatment
Treatment of HSV is diametrically
different from epithelial and stromal
keratitis.
Antiviral : acyclovir, valacyclovir,
famciclovir.
Noninfectious Keratitis
Noninfectious keratitis is typically
characterized by persistent corneal
epithelial defects, stromal
inflammation, and enzymatic
degradation of the corneal collagen.
Keratoconjunctivitis
Sicca
Happened due to dryness on the
corneal surface.
Patient may complain itch, foreign
body sensation, and blurred vision.
Treatment
Artificial tears,
Contact lens,
Lacrimal puncta block.
CORNEAL ULCER
Definition
A corneal ulcer is an
area of the cornea
that has lost its
epithelium and a
variable amount of
stroma.
Etiology: toxic
reaction, alergy,
autoimun and
infection.
Risk Factor
Usually trigerred by some factor that
can cause damage to corneal
epithelial, such as:
Eye lash and lacrimal system
abnormality
Trauma
Infection
Systemic
Vitamin A deficiency
Drugs
Etiology
Infection
Bacteria
Virus
Fungal
Non-Infection
Hypersensitivity
Sign
Ciliar injection
Lost of corneal layer
Infiltrate
In severe case there may be hypopion
Streptococcus Ulcer
Caused by : Streptococcus pneumonia,
Streptococcus viridans (Alpha hemolytic),
Streptococcus pyogenes (Beta hemolytic),
Streptococcus faecalis (non-hemolytic)
Exotoxin plays an important role
Ulcer extend from peripheral to the center
Yellow or grey ulcer disc with peripheral
elevation
Can rapidly spread to the deeper layer of
corneal and cause corneal perforation
Staphylococcus Ulcer
Caused by : Staphylococcus epidermidis,
Staphylococcus aureus (the most severity
from other Staphylococcus)
Usually have predisposition factor and
considered as opportunistic pathogens
Cream-colored or gray-white stromal infiltrate
with an overlying epithelial defect
Multiple foci of abscesses can develop that
resemble fungal satellite lesions
Over time, the former can extend deep into
the stroma, and necrosis of this abscess can
lead to perforation
Pseudomonas Ulcer
Pseudomonas aeruginosa is the most common gramnegative organism isolated from corneal ulcers
An aerob obligate bacil
Organism produces destructive enzymes such as
protease, lipase, elastase, and exotoxin, which
results in necrotic, soupy ulceration
Stromal invasion is rapid
Found in moist environments and frequently
contaminate inadequately chlorinated swimming
pools and hot tubs, ventilators, nebulizer and
vaporizer solutions, and ophthalmic solution bottles
Clinical Feature
The ulcer often extends peripherally and deeply within
hours and can rapidly involve the entire cornea
Ring ulcers can develop, and the corneal epithelium
peripheral to the primary ulcer typically develops a
diffuse gray, ground-glass appearance.
The corneal stroma appears to dissolve into a greenish
yellow mucous discharge that fluoresces under ultraviolet
(but not under cobalt blue) light.
The suppurative ulcer frequently thins to a
descemetocele that perforates. The ulcer is often
associated with a marked anterior chamber reaction and
hypopyon formation. Extensive keratitis can extend to
the limbus and produce an infectious scleritis.
Bacterial Ulcer
Clinical Feature
Dendritic ulcer.
It occurs in the corneal epithelium
Fluorescein staining makes the dendrite easy to
identify,
Herpetic keratitis can also simulate many corneal
infections and must be considered in the differential
diagnosis of many corneal lesions
Geographic ulceration is a form of chronic dendritic
disease in which the delicate dendritic lesion takes a
broader form.
Corneal sensation, as with dendritic disease, is
diminished.
Dendritic Ulcer
Fungal Ulcer
Most commonly in agricultural workers
Become more common in the urban population
Caused by opportunists such as candida, fusarium,
aspergillus, penicillium, cephalosporium, and others
Scrapings from fungal corneal ulcers, except those
caused by candida, contain hyphal elements
Fungal ulcers are indolent and have a gray infiltrate
with irregular edges, often a hypopyon, marked
inflammation of the globe, superficial ulceration,
and satellite lesions
Corneal abscesses frequently occur
Fungal Ulcer
Moorens Ulcer
Moorens ulcer is a rare, chronic,
painful, peripheral ulcerative
keratitis.
The pathogenesis of Moorens ulcer
is unknown but appears to involve an
autoimmune reaction against a
specific target molecule in the
corneal stroma, which may occur in
genetically susceptible individuals.
VOGT-KOYANAGI-HARADA
SYNDROME
Definition
Vogt-Koyanagi-Harada syndrome (VK-H) is an idiopathic, multisystem,
autoimmune disease against
melanocytes causing inflammation of
melanocyte-containing tissues such
as the uvea, ears, skin and
meninges.
Sign
Anterior uveitis
Posterior uveitis is frequently bilateral. In
chronological order the findings are as follows:
Diffuse choroidal infiltration.
Multifocal detachments of the sensory retina and
disc oedema.
Exudative retinal detachment.
The chronic phase is characterized by diffuse RPE
atrophy (sunset-glow fundus) which may be
associated with small, peripheral, discrete atrophic
spots, often labeled Dalen-Fuchs nodules.
CNV and sub-retinal fibrosis may be responsible for
significant visual loss.
Investigations
CSF analysis shows pleocytosis with
predominant small lymphocytes.
FA shows multifocal hyperfluorescent dots
at the level of the RPE and the
accumulation of dye in the subretinal
space.
US may be helpful in cases of poor
visualization of the fundus, and may show
diffuse thickening of the posterior choroid,
serous retinal detachment and vitreous
opacities.
Sequelae of Harada
disease.
(a)'Sunset-glow' fundus
with scattered
depigmented spots
(b)subretinal fibrosis
Treatment
Posterior segment involvement is
treated with intravenous or high-dose
oral steroids. Steroid-resistant
patients may require ciclosporin.
Eyes with subfoveal CNV may benefit
from surgical excision or PDT.
SYMPHATETIC
OPHTHALMITIS
Definition
Sympathetic ophthalmitis is a
bilateral granulomatous panuveitis
occurring after penetrating trauma,
often associated with uveal prolapse
or, less frequently, following
intraocular surgery, usually multiple
vitreoretinal procedures.
Diagnosis
Presentation in 65% of cases is between 2
weeks and 3 months after initial injury and 90%
of all cases occur within the first year.
Signs in chronological order:
The exciting eye shows evidence of the initial trauma
and is frequently very red and irritable.
The sympathizing eye then becomes photophobic
and irritable.
Both eyes develop anterior uveitis which may be
mild or severe and granulomatous. Because the
severity of may be asymmetrical, mild involvement
in one eye may be missed.
Treatment
Enucleation within first 10 days following
trauma should be considered only in eyes
with a hopeless visual prognosis because
the exciting eye may eventually have
better vision than the sympathizing eye.
Topical treatment of anterior uveitis is with
steroids and cycloplegics.
Systemic treatment with steroids (11.5mg/kg) is usually effective although
occasionally ciclosporin or azathioprine
may be required.
History
There is pain in one eye, which can be extremely
severe and may be accompanied by vomiting.
a. The patient complains of impaired vision
and haloes around lights due to oedema of
the cornea.
b. Before get acute attack, The patient had
shown this prodroma symptoms: blurry eyes,
little headache, see the rainbow colors
around lamp. The symptoms are self limited
for several hours.
Examination
The eye is inflamed and tender.
The cornea is hazy and the pupil is semidilated
and fixed.
Vision is impaired according to the state of the
cornea.
On gentle palpation the eye feels harder than the
other eye.
The anterior chamber seems shallower than
usual, with the iris being close to the cornea.
Funduscopy is difficult to do because refraction
media is turbid
Management
Urgent Referral to Hospital with eye
management facilities.
Decreaser of intraocular pressure, like
pilocarpin drops 2-4%, one drop every
minute in 5 minute, then one drop every
hour in 6 hours.
Laser iridectomy. Surgery still need to do.
Give education to patient for planning
the surgery because it important
Symptoms
Pain
Photopobia
Red eye
Excessive tearing
Decreased vision
Sign
Ciliary injection
Pupillary miosis (common but not always present)
Marked cell and flare reaction in the anterior chamber
Keratic precipitates on corneal endothelium
Hypopyon
Various degrees of posterior synechiae
Iris Nodules
Ciliary Injection
Miosis Pupil
Aqueous Flare
Keratic Precipitates
(Cont..)
In panuveitis, both the anterior and
posterior segments of the eyes are
inflamed and patients may have
evidence of an associated systemic
disease (for example, sarcoidosis,
systemic lupus erythematosus,
polyarteritis nodosa, Wegeners
granulomatosis, or toxoplasmosis).
Management
Endophtalmitis
Great inflammaton inside eye ball, because infection
after trauma & surgery, or sepsis.
Most-caused bacteria : staphylococcus,
streptococcus, pneumococcus, pseudomonas
Most-caused fungi : actinomyses, aspergillus
History :
a. Pain
b. Red lid that difficult to open
c. Chemotic and red conjunctiva
d. Hazy cornea
e. Chamber oculi anterior usually filled with hypopion
Management
Antibiotic periocular or
subconjunctiva, if the cause is fungi :
Amphoterisin B150 mcg
subconjunctiva.
Cyclophlegia drops 3 times a day
Enucleation will be hold if eyes
become calm
Thank you