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HERPEX SIMPLEX KERATITIS (DISCIFORM KERATITIS) Viral antigen is detectable in stromal disease but viral replication is not thought to be an important component. – PowerPoint PPT presentation

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Title: KERATITIS. GLAUCOMA.


1
Grodno State Medical University
KERATITIS. GLAUCOMA. DIAGNOSIS AND TREATMENT.
Pavel Ch. Zavadski
Assistant lecturer Of the Department of
Ophthalmology
2
CORNEA (ANATOMY)
The average corneal diameter is 11.5 mm
(vertical) and 12 mm (horizontal). The cornea
consists of the following layers Epithelium. B
owman layer. Stroma. Descemet
membrane. Endothelium. The cornea is the most
densely innervated tissue in the body. The
sensory supply is via the first division of the
trigeminal nerve. There is a subepithelial and a
stromal plexus of nerves. In eyes with corneal
abrasions the direct stimulation of these nerve
endings causes pain, reflex lacrimation and
photophobia.
3
CORNEA (ANATOMY)
The epithelium is stratified squamous and
nonkeratinized.
4
CORNEA (ANATOMY)
Bowman layer is the acellular superficial layer
of the stroma.
5
CORNEA (ANATOMY)
The stroma makes up 90 of corneal thickness.
It is principally composed of regularly
orientated layers of collagen fibrils, whose
spacing is maintained by proteoglycan ground
substance (chondroitin sulphate and keratan
sulphate) with interspersed modified fibroblasts
(keratocytes).
6
CORNEA (ANATOMY)
Descemet membrane is composed of a line
latticework of collagen fibrils. It consists of
an anterior banded zone that is deposited
in-utero and a posterior non-banded zone, laid
down throughout life by the endothelium.
7
CORNEA (ANATOMY)
The endothelium consists of a single layer of
hexagonal cells that cannot regenerate. It plays
a vital role in maintaining corneal
deturgescence. The adult cell density is about
2500 cells/mm2. The number of cells decreases
at about 0.6, per year and neighboring cells
enlarge to fill the space as cells die.
8
BACTERIAL KERATITIS
Bacterial keratitis is very uncommon in a normal
eye and usually only develops when the ocular
defence have been compromised. Bacteria that
can penetrate an apparently normal corneal
epithelium are N. Gonorrhoeae, N. meningitides,
C. diphtheriae and H. influenzae. The
virulence of the organism and the anatomic site
of the infection determine the pattern of
disease. The most common pathogens are P.
aeruginosa, S. aureus, S. pyogenes, S. pneumoniae.
9
BACTERIAL KERATITIS (RISK FACTORS)
Contact lens wear. Trauma. Ocular surface
disease (such as herpetic keratitis, bullous
keratopathy, dry eye, chronic blepharitis,
trichiasis, exposure, severe allergic eye disease
and corneal anesthesia). Other factors (include
topical or systemic immunosuppression, diabetes,
vitamin A deficiency).
10
BACTERIAL KERATITIS (CLINICAL FEATURES)
Presenting symptoms include pain, photophobia,
blurred vision and discharge. Signs in
chronological order An epithelial defect
associated with an infiltrate around the margin
and base associated with circumcorneal injection.
Enlargement of the infiltrate associated with
stromal oedema and small hypopyon. Severe
infiltration with enlarging hypopyon.
Progressive ulceration may lead to corneal
perforation and endophthalmitis. Scleritis may
develop with infections at the limbus.
11
BACTERIAL KERATITIS (TREATMENT)
Bacterial keratitis has the potential to
progress rapidly to corneal perforation, Even
small axial lesions can cause surface
irregularity and scar that can lead to
significant loss of vision.   Decision to treat
is based on clinical grounds but the causative
organism cannot be guessed reliably from the
appearance or the ulcer. Treatment should be
initiated even if Gram stain is negative and
before the results of culture are available.
12
BACTERIAL KERATITIS (TREATMENT)
Topical antibiotics are initially instilled at
hourly intervals day and night for 24-48 hours.
Treatment is continued until the epithelium has
healed. Oral antibiotics (ciprofloxacin 750 mg
twice daily for 7-10 days) is not usually
necessary. Exceptions are threatened or actual
corneal perforation or a peripheral ulcer in
which there is scleral extension. Oral therapy is
also indicated for isolates for which there are
potential systemic complications. Mydriatics
(atropine 1 or cyclopentolate 1) are used to
prevent the formation of posterior synechiae and
to reduce pain from ciliary spasm. Topical
steroids.
13
BACTERIAL KERATITIS (TREATMENT)
Topical steroids therapy in established
bacterial infection is unproven and the following
guidelines apply They should not be
introduced until the sensitivity of the isolate
to antibiotics has been demonstrated and fungal
infection excluded. They can potentiate
coexisting fungal or herpes infection and may
make elimination of acanthamoeba infection more
difficult. They reduce inflammation and can
rapidly make the eye more comfortable. However,
their use probably does not affect the amount of
scar formation or the final visual outcome.
They may help to prevent rejection following
infection of a corneal graft.
14
VIRAL KERATITIS (HERPES SIMPLEX KERATITIS)
Herpetic eye disease is the major cause of
unilateral corneal scarring worldwide, and is the
most common infectious cause of corneal
blindness in developed countries. As many as 60
of corneal ulcers in developing countries may be
the result of herpes simplex virus (HSV) and 10
million people worldwide may have herpetic eye
disease.   Primary infection (no previous viral
exposure) usually occurs by droplet transmission,
or less frequently by direct inoculation. Due to
protection bestowed by maternal antibodies. it is
uncommon during the first 6 months of life. Most
cases are probably subclinical or only cause mild
fever, malaise and upper respiratory tract
symptoms. Children may develop blepharoconjunctivi
tis which is usually benign and self-limited
although corneal microdendrites develop in a
minority of cases.   Recurrent disease
(reactivation in presence of cellular and humoral
immunity occurs as follows after primary
infection and subclinical reactivation.
15
HERPEX SIMPLEX KERATITIS (EPITHELIAL FORM)
Epithelial (dendritic, geographic) keratitis is
the result of virus replication and is the most
common presentation. 1. Presentation may be at
any age with mild discomfort, watering and
blurred vision. 2. Signs in chronological order
Opaque epithelial cells arranged in a coarse
punctate or stellate pattern. Central
desquamation results in a linear-branching
(dendritic) ulcer, most frequently located
centrally. The ends of the ulcer have
characteristic terminal buds and the bed of the
ulcer stains well with fluorescein.
16
HERPEX SIMPLEX KERATITIS (DISCIFORM KERATITIS)
The exact etiology of DISCIFORM KERATITIS
(endotheliitis) is controversial. It may be an
HSV infection of keratocytes or endothelium, or
hypersensitivity reaction to viral antigen in the
cornea. A past history of dendritic ulceration is
not always present. A central zone of stromal
oedema often with overlying epithelial oedema
occasionally the lesion is eccentric. Healed
lesions often have a faint ring of stromal
opacification and thinning.
17
HERPEX SIMPLEX KERATITIS (STROMAL NECROTIC
KERATITIS)
Viral antigen is detectable in stromal disease
but viral replication is not thought to be an
important component. Lymphocytes, antigen
presenting cells and polymorphonuclear
neutrophils are critical for viral clearance but
they also mediate tissue destruction. Stromal
necrosis and melting often with profound
interstitial opacification. Associated anterior
uveitis with keratic precipitates underlying the
area of active stromal infiltration. If
inappropriately treated, scarring,
vascularization and lipid deposition may result.
18
HERPEX SIMPLEX KERATITIS (METAHERPETIC ULCERATION)
METAHERPETIC ULCERATION is caused by failure of
reepithelialization resulting from devitalization
of the stroma and epithelial toxicity rather than
viral replication. A non-healing epithelial
defect after prolonged topical treatment. There
may be stromal ulceration although necrosis is
not a major feature. The stroma beneath the
defect is grey and opaque.
19
HERPEX SIMPLEX KERATITIS (TREATMENT)
TREATMENT OF HSV disease is with purine or
pyrimidine analogues that are incorporated to
form abnormal viral DNA. Idoxuridine and
vidarabine (Ara-A) are poorly soluble and
relatively toxic, but are still used in regions
where low cost is essential. Trifluridine
(TFT) and aciclovir (Zovirax) have low toxicity
and the latter can be used systemically. Both are
active against HSV1 and HSV2.
20
FUNGAL KERATITIS
Fungal keratitis is rare in temperate countries
but is a major cause of visual loss in tropical
and developing countries. In some hot and humid
regions it accounts for 50 of cases. The
primary risk factors for infection are trauma 65
of cases in tropical areas, particularly with
vegetable matter chronic ocular surface disease
and epithelial defects, diabetes, systemic
immunosuppression and hydrophilic contact lenses.
Fungal infection and a severe inflammatory
response that can cause stromal necrosis and
melting. Filamentous fungi can penetrate the
intact Descemet membrane and corneal perforation
is common. Once in the anterior chamber the
infection is very difficult to eradicate and
aggressive surgery is usually required.
21
FUNGAL KERATITIS (CLINICAL FEATURES)
The diagnosis is often delayed unless there is a
high index of suspicion. I. Presenting symptoms
are a gradual onset of foreign body sensation,
photophobia, blurred vision and discharge.
Patients often have a history of trauma or
chronic ocular surface disease. 2. Signs vary
with the infectious agent. In early disease there
tends to be less redness and lid swelling than
with bacterial infection. - A grey-yellow
stromal infiltrate with indistinct margins or
dense suppuration. - Progressive infiltration,
often surrounded by satellite lesions and
hypopyon.
22
FUNGAL KERATITIS (TREATMENT)
1. Removal of the epithelium over the lesion
enhances penetration of antifungal agents.
Similarly, a superficial keratectomy may help
de-bulk the lesion. 2. Topical treatment should
be given intensively. As most antifungals are
only fungistatic topical treatment should be
continued fix several weeks (natamycin 5 or
econazole 1). Amphotericin B 0.15 and
miconazole 1 are alternatives. 3. Systemic
anti-fungals may be required for severe keratitis
or endophthalmitis. Preferred treatment options
are itraconazole 100 mg daily or voriconazole 100
mg with a loading dose of 200mg. 4. Excisional
penetrating keratoplasty may be required in
unresponsivy cases.
23
GLAUCOMA
In the world, glaucoma is the third leading
cause of blindness-an estimated 13.5 million
people may have glaucoma and 5.2 million of those
may be blind. Glaucoma has been nicknamed the
"silent thief of sight" because the loss of
vision normally occurs gradually over a long
period of time, and is often recognized only when
the disease is quite advanced. Once lost, this
damaged visual field cannot be recovered. If the
condition is detected early enough, it is
possible to arrest the development or slow the
progression with medical and surgical means.
1
2
3
4
6
5
24
GLAUCOMA (INTRAOCULAR PRESSURE)
Glaucoma refers to a group of eye conditions
that lead to damage to the optic nerve. This
nerve carries visual information from the eye to
the brain. In most cases, damage to the optic
nerve is due to increased pressure in the eye,
also known as intraocular pressure (IOP). The
front part of the eye is filled with a clear
fluid called aqueous humor. This fluid is always
being made behind the colored part of the eye
(the iris). It leaves the eye through channels in
the front of the eye in an area called the
anterior chamber angle, or simply the
angle. Anything that slows or blocks the flow
of this fluid out of the eye will cause pressure
to build up in the eye.
25
GLAUCOMA (INTRAOCULAR PRESSURE)
26
GLAUCOMA (OPTIC NERVE DAMAGE)
27
GLAUCOMA (CLASSIFICATION)
There are four major types of glaucoma Open-angl
e (chronic) glaucoma Angle-closure (acute)
glaucoma Congenital glaucoma Secondary glaucoma
28
PRIMARY OPEN-ANGLE GLAUCOMA
The cause is unknown. An increase in eye pressure
occurs slowly over time. The pressure pushes on
the optic nerve.
Most people have no symptoms Once vision loss
occurs, the damage is already severe There is a
slow loss of side (peripheral) vision (also
called tunnel vision) Advanced glaucoma can lead
to blindness
29
PRIMARY ANGLE-CLOSURE GLAUCOMA
ANGLE-CLOSURE GLAUCOMA occurs when the exit of
the aqueous humor fluid is suddenly blocked. This
causes a quick, severe, and painful rise in the
pressure in the eye. Angle-closure glaucoma is
an emergency. This is very different from
open-angle glaucoma, which painlessly and slowly
damages vision. Dilating eye drops and certain
medications may trigger an acute glaucoma attack.
Symptoms may come and go at first, or steadily
become worse Sudden, severe pain in one
eye Decreased or cloudy vision, often called
"steamy" vision Nausea and vomiting Rainbow-like
halos around lights Red eye Eye feels swollen
30
CONGENITAL GLAUCOMA
It is present at birth. It is caused by
abnormal eye development.
Symptoms are usually noticed when the child is a
few months old Cloudiness of the front of the
eye Enlargement of one eye or both eyes Red
eye Sensitivity to light Tearing
31
GLAUCOMA (DIAGNOSIS)
A complete eye exam is needed to diagnose
glaucoma. A test called (tonometry) is done to
check eye pressure. However, eye pressure always
changes. Eye pressure can be normal in some
people with glaucoma. This is called
normal-tension glaucoma. Doctor will need to
run other tests to confirm glaucoma. Using a
special lens to look at the eye
(gonioscopy) Photographs or laser scanning
images of the inside of the eye (optic nerve
imaging) Examination of the retina in the back
of the eye Slit lamp examination Visual
acuity Visual field measurement
32
GLAUCOMA (DIAGNOSIS, TONOMETRY)
33
GLAUCOMA (DIAGNOSIS, GONIOSCOPY)
34
GLAUCOMA (DIAGNOSIS, OPHTALMOSCOPY)
35
GLAUCOMA (DIAGNOSIS, PERIMETRY)
36
GLAUCOMA (TREATMENT)
The goal of treatment is to reduce eye pressure.
Treatment depends on the type of glaucoma.   Most
people can be treated successfully with eye
drops. Most of the eye drops used today have
fewer side effects than those used in the past.
Other treatments may involve Laser therapy
called an iridotomy Eye surgery if other
treatments do not work   Acute angle-closure
attack is a medical emergency. Blindness will
occur in a few days if it is not treated. Patient
receive Eye drops Medicines to lower eye
pressure, given by mouth and through a vein (by
IV)   Some people also need an emergency
operation, called an iridotomy. This procedure
uses a laser to open a new pathway in the colored
part of the eye. This relieves pressure and
prevents another attack.   Congenital glaucoma is
almost always treated with surgery. This is done
using general anesthesia. This means the patient
is asleep and feels no pain.
37
Thank You For Your Attention
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