Transcript lec_4

Grodno State Medical University
KERATITIS. GLAUCOMA.
DIAGNOSIS AND TREATMENT.
Pavel Ch. Zavadski
Assistant lecturer
Of the Department of Ophthalmology
CORNEA (ANATOMY)
The average corneal diameter is
11.5 mm (vertical) and 12 mm (horizontal).
The cornea consists of the following layers:
Epithelium.
Bowman 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.
CORNEA (ANATOMY)
The epithelium is stratified
squamous and nonkeratinized.
CORNEA (ANATOMY)
Bowman
layer
is
the
acellular superficial layer of the
stroma.
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).
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 nonbanded zone, laid down throughout life by
the endothelium.
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.
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.
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).
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.
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.
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.
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.
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 blepharoconjunctivitis 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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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.
GLAUCOMA (INTRAOCULAR PRESSURE)
GLAUCOMA (OPTIC NERVE DAMAGE)
GLAUCOMA (CLASSIFICATION)
There are four major types of glaucoma:
•Open-angle (chronic) glaucoma
•Angle-closure (acute) glaucoma
•Congenital glaucoma
•Secondary glaucoma
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
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
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
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
GLAUCOMA (DIAGNOSIS, TONOMETRY)
GLAUCOMA (DIAGNOSIS, GONIOSCOPY)
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SHAFFER
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GRADING
GLAUCOMA (DIAGNOSIS, OPHTALMOSCOPY)
GLAUCOMA (DIAGNOSIS, PERIMETRY)
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.
Thank You
For Your Attention