Katarzyna Pikulska
Inflammation of the ocular globe and adnexa
GLOBE
Episcleritis
Etiology
Exact etiology is not known. It is found in association with gout, rosacea and
psoriasis. It has also been considered a hypersensitivity reaction to endogenous tubercular or streptococcal toxins.
Characteristical signs
Episcleritis is characterised by redness, mild ocular discomfort described as gritty, burning or foreign body sensation. Many a time it may not be accompanied by any discomfort at all. Rarely, mild photophobia and lacrimation may occur.
On examination two clinical types of episcleritis, diffuse (simple) and nodular may be
recognized. Episclera is seen acutely inflamed in the involved area.
In diffuse episcleritis, although whole eye may be involved to some extent, the maximum inflammation is confined to one or two quadrants
In nodular episcleritis, a pink or purple flat nodule surrounded by injection is seen, usually situated 2-3 mm away from the limbus. The nodule is firm, tender and the overlying conjunctiva moves freely.
Work-up
Differential diagnose
Episcleritis may be confused with inflamed pinguecula, swelling and congestion due to foreign body lodged in bulbar conjunctiva and very rarely with scleritis.
Treatment
Topical corticosteroid eyedrops instilled 2-3 hourly, render the eye more comfortable and resolve the episcleritis within a few days.
Cold compresses applied to the closed lids may offer symptomatic relief from ocular discomfort.
Systemic non-steroidal anti-inflammatory drugs (NSAIDs) such as flurbiprofen (300 mg OD), indomethacin (25 mg three times a day), or oxyphenbutazone may be required in recurrent cases.
Follow up
Rarely, a fleeting type of disease - episcleritis periodica - may occur.
Scleritis
It is found in association with multiple conditions which are as follows:
Autoimmune collagen disorders, especially rheumatoid arthritis, is the most common association. Overall about 5% cases of scleritis are associated with some connective tissue disease. About 0.5 percent of patients (1 in 200) suffering from seropositive rheumatoid arthritis develop scleritis. Other associated collagen disorders are Wegener's granulomatosis, polyarteritis nodosa (PAN), systemic lupus erythematosus (SLE) and ankylosing spondylitis.
Metabolic disorders like gout and thyrotoxicosis have also been reported to be associated with scleritis.
Some infections, particularly herpes zoster ophthalmicus, chronic staphylococcal and streptococcal infection have also been known to cause scleritis.
Granulomatous diseases like tuberculosis, syphilis, sarcoidosis, leprosy can also cause scleritis.
Miscellaneous conditions like irradiation, chemical burns, Vogt-Koyanagi-Harada syndrome, Behcet's disease and rosacea are also implicated in the
etiology.
Surgically induced scleritis follows ocular surgery. It occurs within 6 month postoperatively. Exact mechanism not known, may be precipitation
of underlying systemic cause.
Idiopathic. In many cases cause of scleritis is unknown.
Patients complain of moderate to severe pain which is deep and boring in character and often wakes the patient early in the morning . Ocular pain radiates to the jaw and temple. It is associated with localised or diffuse redness, mild to severe photophobia and lacrimation. Occasionally there occurs diminution of vision.
Clinical types:
1. Non-necrotizing anterior diffuse scleritis. It is the commonest variety, characterised by widespread inflammation involving a quadrant or more of the anterior sclera. The involved area is raised and salmon pink to purple in colour
2. Non-necrotizing anterior nodular scleritis. It is characterised by one or two hard, purplish elevated scleral nodules, usually situated near the limbus. Sometimes, the nodules are arranged in a ring around the limbus (annular scleritis).
3. Anterior necrotizing scleritis with inflammation. It is an acute severe form of scleritis characterised by intense localised inflammation associated with areas of infarction due to vasculitis . The affected necrosed area is thinned out and sclera becomes transparent and ectatic with uveal tissue shining through it.
4. Anterior necrotizing scleritis without inflammation It is characterised by development of yellowish patch of melting sclera; which often together with the overlying episclera and conjunctiva completely separates from the surrounding normal sclera. This sequestrum of sclera becomes dead white in colour, which eventually absorbs leaving behind it a large punched out area of thin sclera through which the uveal tissue shines.
5. Posterior scleritis.. It is characterised by features of associated inflammation of adjacent structures, which include: exudative retinal detachment, macular oedema, proptosis and limitation of ocular movements.
Following laboratory studies may be helpful in identifying associated systemic diseases or in establishing the nature of immunologic reaction:
- TLC, DLC and ESR
- Serum levels of complement (C3), immune
complexes, rheumatoid factor, antinuclear
antibodies and L.E cells for an immunological
survey.
- FTA - ABS, VDRL for syphilis.
- Serum uric acid for gout.
- Urine analysis.
- Mantoux test.
- X-rays of chest, paranasal sinuses, sacroiliac joint and orbit to rule out foreign body especially in patients with nodular scleritis.
Scleritis may be confused with conjunctivitis, episcleritis, myositis, orbital pseudotumor. Rarely masquerade syndrome with malignant melanoma of the choroid, lymphoma, and multiple myeloma (posterior scleritis) or invasive squamous cell carcinoma of the conjunctiva (necrotizing anterior scleritis).
Non-necrotising scleritis. It is treated by topical steroid eyedrops and systemic indomethacin 100 mg daily for a day and then 75 mg daily until inflammation resolves.
Necrotising scleritis. It is treated by topical steroids and heavy doses of oral steroids tapered slowly. In non-responsive cases, immuno-suppressive agents like methotrexate or cyclophos-phamide may be required. Subconjunctival steroids are contraindicated because they may lead to scleral thinning and perforation.
It may cause visual impairment and even loss of the eye if treated inadequately. Spontaneous perforation is extremely rare.
Complications are quite common with necrotizing scleritis and include sclerosing keratitis, keratolysis, complicated cataract and secondary glaucoma.
Keratitis
It is difficult to classify and assign a group to each and every case of keratitis. Main classification is:
- Ulcerative keratitis (corneal ulcer)
- Non-ulcerative keratitis
Etiological classification:
1. Infective keratitis - bacterial, viral, fungal, chlamydial, protozoal, spirochaetal
2. Allergic keratitis - phlyctenular keratitis, vernal keratitis, atopic keratitis
3. Trophic keratitis - exposure keratitis, neuroparalytic keratitis, keratomalacia, atheromatous ulcer
4. Keratitis associated with diseases of skin and mucous membrane.
5. Keratitis associated with systemic collagen vascular disorders.
6. Traumatic keratitis, which may be due to mechanical trauma, chemical trauma, thermal burns, radiations
7. Idiopathic keratitis - Mooren's corneal ulcer, superior limbic keratoconjunctivitis, superficial punctate keratitis of Thygeson
In bacterial infections the outcome depends upon the virulence of organism, its toxins and enzymes, and the response of host tissue. Broadly bacterial corneal ulcers may manifest as purulent corneal ulcer without hypopyon or hypopyon corneal ulcer. In general, following symptoms and signs may be present.
Symptoms:
- pain and foreign body sensation occurs due to mechanical effects of lids and chemical effects of toxins on the exposed nerve endings.
- watering from the eye occurs due to reflex hyperlacrimation.
- photophobia, i.e., intolerance to light results from stimulation of nerve endings.
- blurred vision results from corneal haze.
- redness of eyes occurs due to congestion of circumcorneal vessels.
Signs:
- lids are swollen.
- marked blepharospasm may be there.
- conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion.
- corneal ulcer usually starts as an epithelial defect associated with greyish-white circumscribed infiltrate (seen in early stage). Soon the epithelial defect and infiltrate enlarges and stromal oedema develops. A well established bacterial ulcer is characterized by:yellowish-white area of ulcer which may be oval or irregular in shape, margins of the ulcer are swollen and over hanging, floor of the ulcer is covered by necrotic material, stromal oedema is present surrounding the ulcer area.
1. Thorough history taking to elicit mode of onset, duration of disease and severity of symptoms.
2. General physical examination, especially for built, nourishment, anaemia and any immunocompromising disease.
3. Ocular examination should include:
- diffuse light examination for gross lesions of the lids, conjunctiva and cornea including testing for sensations.
- regurgitation test and syringing to rule out lacrimal sac infection.
- biomicroscopic examination after staining of corneal ulcer with 2 per cent freshlyprepared aqueous solution of fluorescein dye or sterilized fluorescein impregnated filter paper strip to note site, size, shape, depth, margin, floor and vascularization of corneal ulcer. On biomicroscopy also note presence of keratic precipitates at the back of cornea, depth and contents of anterior chamber, colour and pattern of iris and condition of crystalline lens.
Laboratory investigations:
- routine laboratory investigations such as haemoglobin, TLC, DLC, ESR, blood sugar, complete urine and stool examination should be carried out in each case.
- microbiological investigations. These studies are essential to identify causative organism, confirm the diagnosis and guide the treatment to be instituted. Material for such investigations is obtained by scraping the base and margins of the corneal ulcer (under local anaesthesia, using 2 percent xylocaine) with the help of a modified Kimura spatula or by simply using the bent tip of a 20 gauge hypodermic needle. T
The most important thing is to diagnose witch of many reasons coused keratitis – classification is above. Keratitis may be confused with acute glaucoma, anterior uveitis or conjunctivitis.
Treatment of uncomplicated corneal ulcer
Bacterial corneal ulcer is a vision threatening condition and demands urgent treatment by identification and eradication of causative bacteria. Treatment of corneal ulcer can be discussed under three headings:
1. The specific treatment
Topical antibiotics. Initial therapy (before results of culture and sensitivity are available) should be with combination therapy to cover both gram-negative and gram-positive organisms. It is preferable to start fortified gentamycin (14mg/ml) or fortified tobramycin (14mg/ml) eyedrops along with fortified cephazoline (50mg/ml), every ½ to one hour for first few days and then reduced to 2 hourly.
Once the favourable response is obtained, the fortified drops can be substituted by more diluted commercially available eye-drops, e.g. : Ciprofloxacin (0.3%) eye drops or Ofloxacin (0.3%) eye drops or Gatifloxacin (0.3%) eye drops.
Systemic antibiotics are usually not required. However, a cephalosporine and an aminoglycoside or oral ciprofloxacin (750 mg twice daily) may be given in fulminating cases with perforation and when sclera is also involved.
2. Non-specific treatment
- Cycloplegic drugs. Preferably 1 percent atropine eye ointment or drops should be used to reduce pain from ciliary spasm and to prevent the formation of posterior synechiae from secondary iridocyclitis. Atropine also increases the blood supply to anterior uvea by relieving pressure on the anterior ciliary arteries and so brings more antibodies in the aqueous humour. It also reduces exudation by decreasing hyperaemia and vascular permeability. Other cycloplegic which can be used is 2 per cent homatropine eye drops.
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