Grodno State Medical University DIAGNOSIS AND TREATMENT. 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.

The epithelium is stratified squamous and nonkeratinized. CORNEA (ANATOMY) The epithelium is stratified squamous and nonkeratinized.

Bowman layer is the acellular superficial layer of the stroma. CORNEA (ANATOMY) Bowman layer is the acellular superficial layer of the stroma.

The stroma makes up 90% of corneal thickness. 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 non-banded zone, laid down throughout life by the endothelium.

The adult cell density is about 2500 cells/mm2. 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. 1 2 3 4 5 6

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)

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.

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