RED EYE WITH 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.
Streptococcal
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
Gram-Negative Gram-Positive
Gentamicin. Cefazolin.
Tobramycin. Vancomycin.
Polimiksin. 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.
 Herpes Simplex Keratitis
Herpes simplex viral infection of the cornea.
Human herpes viruses have in common a state
called latency.
Keratitis caused by HSV is the most common
cause of cornea-derived blindness in
developed nations.
 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 and Symptom
Symptom
Same as keratitis
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
Hypopyon and endothelial plaque
 Pseudomonas Ulcer
Pseudomonas aeruginosa is the most common gram-
negative 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

Early Bacterial ulcer Late Bacterial ulcer

 Herpes Simplex Ulcer
Symptoms of an HSV infection are usually
irritation, photophobia, and tearing.
When the central cornea is affected, there is
also some reduction in vision.
Since corneal anesthesia usually occurs early
in the course of the infection, the symptoms
may be minimal and the patient may not seek
medical advice.
 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

Early Fungal ulcer Late 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.
(a) Local peripheral ulceration; (b) circumferential and central
spread; (c) advanced disease; (d) healed stage
VOGT-KOYANAGI-HARADA
SYNDROME
 Definition
Vogt-Koyanagi-Harada syndrome (V-K-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.
 Active Harada disease.
(a)Multifocal serous retinal
detachments
(b)FA venous shows multiple
hyperfluorescent spots
(c)late phase shows extensive
areas of hyperfluorescence due
to pooling of dye under the
serous detachments
 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.
 Multifocal choroidal infiltrates in the midperiphery
and sub-RPE infiltrates, corresponding to Dalen-
Fuchs nodules seen on histology.
Exudative retinal detachment may occur in severe
cases.
Residual chorioretinal scarring may cause for
visual loss when involving the macula.
'Sunset-glow' appearance, similar to Vogt-
Koyanagi-Harada syndrome (V-K-H)
(a) Penetrating injury with iris prolapse;(b)
lymphocytic infiltration and granuloma
formation in the choroid; (c) Dalen-Fuchs
nodule - a granuloma situated between Bruch
membrane and the retinal pigment epithelium;
(d) mutton fat keratic precipitates in
granulomatous anterior uveitis; (e) multifocal
choroiditis
 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 (1-1.5mg/kg)
is usually effective although occasionally
ciclosporin or azathioprine may be required.
 Acute closed angle glaucoma
In acute angle closure glaucoma, intraocular
pressure elevated. Humor aquosus behind the
iris cant flow because iris dilated and thickening
in the part near trabecula, and blocking the
flow.
 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
 Iritis, iridocyclitis, anterior uveitis,
and panuveitis
The iris, ciliary body, and choroid are similar
embryologically and are known as the uveal tract.
Inflammation of the iris (iritis) does not occur
without inflammation of the ciliary body (cyclitis)
and together these are referred to as iridocyclitis or
anterior uveitis
Divided by : acute-chronic granulomatous and acute-
chronic non-granulomatous
The cause of iritis cant be known from the
symptoms only. Iritis and iridocyclitis can manifest
from late immunologic reaction, from infection
before.
 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
If there is an underlying cause it must be treated, but in many cases no
cause is found.
Ensure there is no disease of the eye that is giving rise to signs
of an anterior uveitis, such as more posterior inflammation, a
retinal detachment, or an intraocular tumour.
Treatment :
a. topical steroids to reduce the inflammation and prevent
adhesions within the eye.
b. The intraocular pressure may also rise because inflammatory
cells block the trabecular meshwork, and antiglaucoma (ex.
Acetazolamid) treatment may be needed if this occurs.
c. Cyclophlegia to relief pain and to relax inflamed iris.
 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