Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

Corneal complications

Transient epithelial edema, massive deposition of precipitates on the endothelium that may itself lead to stromal and epithelial haze.

Myopia is induced due to irritative spasm of ciliary body, plasmoid aqueous and edema of cornea. This is transient and reversed by use of cycloplegic. Cycloplegic itself can cause iatrogenic loss of accommodation and unmasking of facultative hypermetropia. A school going child following bilateral use of atropine may require near correction for the period of treatment. Loss of accommodation persists for two weeks following stoppage of atropine.

Cystoid macular edema and papillitis are common feature of loss of vision, exact causes of these are not well understood most probably they are toxic in nature.

Hypopyon : Accumulation of pus in anterior chamber is common in many bacterial uveitis. It is most commonly seen in pneumococcal inflammation. It is sterile in nature. Presence of pus in anterior chamber is an emergency that may be ominous sign of ensuing endophthalmitis. It is also seen in ankylosing spondylitis and Behcet’s disease.

Hyphaema in acute uveitis is seen in cases of gonococcal uveitis and uveitis due to herpes simplex and zoster.

Complication of chronic anterior uveitis

These complications develop after days or months of unchecked uveal inflammation. They can be grouped in following categories :

1.Keratopathy.

2.Iris and pupillary changes.

3.Altered aqueous dynamics.

4.Lenticular changes.

5.Vitreous changes.

6.Fundus changes.

7.Amblyopia and squint in children.

Keratopathy in chronic anterior uveitis

Involvement of cornea in long standing anterior uveitis in inevitable due to direct continuation of corneal endothelium and iris endothelium. The commonest chronic form of keratopathy in anterior uveitis is band kerotopathy (See page 214) which develops on the cornea like a horizontal band in the inter palpebral area. It is due to the deposition of calcium carbonate and calcium phosphate in the Bowman’s membrane and anterior stroma. The calcium deposited in band keratopathy is extra cellular. The epithelium in the initial stage is normal with intact corneal sensation. On long run the epithelium may become irregular and stains with fluorescein giving a fake impression of inflammatory keratitis. The exact cause of band keratopathy is not known, especially why it should have predilection for central cornea in a horizontal fashion and its more frequent occurrence in children than in senile age group. It is generally seen in badly damaged eyes of long duration. Generally there is grave lose of vision however there may be sufficient salvageable vision. There seems to be an unanimity in the theory that it is a degenerative condition, other hypothesis put forward are that its deposition is influenced by actinic rays, resulting into a chemical change between cornea and air causing

a low CO2 and low pH in the cornea.27 The corneal hemidesmosome may act as a lattice over which calcium crystals are built.35 Children are more capable of mobilizing calcium than adults.

The condition starts as faint vertical line on each cornea 1 mm inside the limbus in the inter palpebral zone and gradually spreads towards the center. The progress is very slow, it may take one to two years for the two ends to meet in front of the pupil. May be slightly below the center of the cornea. The band is wider in the mid cornea. A rare type begins in the center and spreads towards the periphery. The band is white colour with a few deficiencies in between in circular fashion, these deficiencies represents the entry of the corneal nerves. In late stages the cracks appears in the band. The overlying epithelial is not invaded for a long time but ultimately the crystals protrode through the epithelium making it susceptible to infection. The calcium crystals can be scrapped off the Bowman’s membrane leaving a clear stroma.

Ocular causes of band keratopathy are : chronic anterior and pan uveitis in children, chronic uveitis in young adults phthis bulbae, trauma, absolute glaucoma, failed keratoplasty, anterior segment ischaemia.37

Symptoms

Band keratopathy is almost symptomless except gradual diminished vision. Diminished vision is commonest symptoms which the patient attributes to underlying ocular disease. Sometimes there may be recurrent redness, watering and photophobia.

Signs

Signs consists of horizontally placed sub-epithelial calcarious opacity with holes in between. There is always signs of primary disease i.e. chronic uveitis, glaucoma.

Management of band karatpathy is difficult. It is presumed that an early and satisfactory treatment of underlying ocular pathology wards-off band keratopathy. There are two possible modes of treatment, 1. Lamellar corneal graft and 2. Medical treatment.

Medical treatment is an outdoor procedure where under local anaesthesia the epithelium is scrapped off the band. The calcarious deposits is rubbed with sodium EDTA 0.5% for about 10 minutes. This should remove all the deposits, if it fails strength of EDTA is increased to 1% and rubbed for 20 minutes, the eye is bandaged with antibiotic and cycloplegic till the cornea is reepithelised. Recently excimer photo keratotomy has given encouraging results.38

Iris changes in chronic anterior uveitis are generally associated with changes in pupil. Common iris changes are formation of nodules, posterior synechia, peripheral anterior synechia, iris atrophy, increased translucency of iris and neovascularisation.

Iris nodules : There are many types of nodules that develop on the iris which fade away with treatment, some take just few days to disappear, others may linger for longer duration. Common nodules are Keoppe nodule, Busacca’s nodule, tubercular, syphilitic, lepromatous nodules and nodules of sarcoid.27, 32, 39

Keoppe nodules are equivalent of mutton fat KPs. They are seen on the pupillary margin and may project in the pupil. They develop from ectodermal tissue, vary in number, not exceeding more than fifteen in each eye. They are accumulation of large epitheloid cells and lymphocytes. They were thought to be diagnostic feature of granulomatous uveitis, however, they are metwith in both types of uveitis. Generally posterior synechia develops at the site where this nodule comes in contact with the lens capsules.

Busacca’s nodules : These nodules are less common, fewer and smaller than Koeppe’s nodule. They develop from mesodermal tissue at the periphery of the iris, around the collarette. They take weeks to months to disappear. They may get hyalinised on long run, they are not diagnostic of any specific disease. However they may be allergic in nature.

Tubercular nodule : Prior to the advent of anti tubercular drugs tuberculosis was thought to be commonest cause of endogenous both anterior and posterior uveitis. With available effective anti tubucular chemotherapy incidence of tubercular uveitis have come down to a large extent still it remains an important cause of uveitis in developing countries in all ages.

The tubucular nodules are scattered throughout the iris and ciliary body mostly in the stroma. They are more common in the pupillary margin, they vary in size from 1 mm. to 1.5 mm. They are grayish yellow in colour some times new vessels develop round the base of the nodule. Incidence of nodules is greatly reduced by systemic chemotherapy. Large single nodule has predilection for iris root. They disappear with systematic chemotherapy and local steroids.

Syphilitic nodules40 : The syphilitic nodules are unilateral even in case of bilateral involvement, only one eye develops nodules and can be considered as papule. They are generally located near the pupillary margin, size and number vary. The nodules are generally hyperemic. Like other nodules the syphilitic nodules disappear with treatment, sometimes leaving a patch of atrophy behind. In rare instances one of the nodules may be converted in to a gumma. Hyperemia of iris in syphilitic iridocyclitis is known as roseola.

Sacroid nodule : Iritis is most frequent ocular manifestation of sarcoidosis. The nodules of sarcoid look similar to that of tubercular nodule. They may be seen on the pupillary margin or in the stroma of the iris. They are more hyperemic and vascularised than tubercular nodules. The vessels form a lattice like pattern over the nodule.

There are many conditions that may mimic iris nodule. Some of them may be benign not requiring any treatment.

Posterior synechia in chronic uveitis are generally broad and difficult to break when dilated with strong cycloplegic. These pupil take a festooned appearance. It is directly related to amount of fibrin present in the aqueous. They are generally initiated by Koeppe nodules. Long standing posterior synechia may start anterior capsular opacification. If the posterior synechia involves the whole periphery of the pupillary border it is called seclusio pupillae. In severe cases of whole of this posterior surface of iris can get plastered on the anterior lens capsule that does not separate with maximum permissible cycloplegic drugs. An annular posterior synechia prevents the posterior chamber from communicating with the anterior chamber via pupil, resulting in forward bowing of the iris causing the anterior chamber to be deep in the center and shallow at the maximum bulge, such condition is called iris bombe, the periphery of the iris may touch posterior surface of the cornea resulting into peripheral anterior synechia. Peripheral anterior synechia may result even in absence of iris bombe i.e. due to prolonged contact between edematous iris and corneal endothelium at the periphery. Prolonged dilatation of pupil and nodules on the periphery may obstruct an anatomically narrow angle causing rise of tension. The peripheral anterior synechia may obstruct the trabecular mesh work and form a barrier between the anterior chamber and the trabeculum such a condition is called pseudo angle formation.

The exudates may be deposited in front of the lens as a white membrane in the pupillary area. The membrane may be dusted by iris pigment obscuring the third Purkinge image making it difficult to evaluate transparency of the lens, this condition is known asocclusio pupillae.

Iris atrophy

In some types of anterior uveitis especially in herpes zoster and Fuch’s heterochromic iritis patches of atrophy develop. In herpes vesicles develops on iris which on healing leaves white areas on the iris. These are areas of hyalinised scars from where pigment is removed. These patches may have sectorial removal of pigment, this accentuates already distorted pupil. The pupil adjacent to the patches of iris atrophy does not react to light or reacts weakly. Fluorescein angiography of iris in healed herpes zoster show occuluded iris vessels at the site of atrophy. In Fuch’s heterochromic iridocyclitis patches of atrophy are most marked at the pupillary margin. This is a non-inflammatory process.

Areas of atrophic patch of full thickness transmit reflected light of retinoscope and retro illumination. Other condition that allows passage of reflected light through iris are- iridectomics, iridotomies, essential iris atrphy and polycoria.

Neovascularisation of iris is a rare phenomenon in iridocyclites, it is seen in some chronic anterior uveitis, generally at the site of previous nodule. It can be seen anywhere but is more common at the collarette. New vessels lead to formation of small patches of haemorrhage or may cause frank hyphaema.29, 32

Rubeosis of iris is due to chronic iridocyclitis. It should be differentiated from other causes of neo vascularisation of iris and ciliary body which in adults, are central vein thrombosis, diabetic retinopathy, sickle cell retinopathy, and Coats disease.

Altered aqueous dynamics in chronic uveitis:

Glaucoma. Formation and flow of aqueous may be normal, maintaining normal intra ocular pressure in majority of cases of chronic anterior uveitis. There is a rise of intra ocular pressure, which may prove to be the important missed cause of loss of vision. Glaucoma thus developed is generally chronic secondary open angle. Sometimes there may be acute rise of tension in eyes that are predisposed to angle closure due to crowding of iris at the periphery following use to long acting cycloplegic.

Causes of secondary glaucoma are multiple, which may act separately or in combination. They are—Inflammatory edema of trabecular meshwork that reduce the diameter of the pore, making it difficult for the plasmoid aqueous to pass through. The outflow is also hampered due to fibrosis and hyalin deposits in the mesh work. Peripheral anterior synechia may plaster the face of the meshwork to form a pseudo angle in front of the original angle. In case of anatomically narrow angle swollen peripheral iris may block the entrance to trabecular meshwork, this is worsened by the use of long acting cycloplegic in anterior uveitis of long duration. There may be neovascularisation of angle. A seclusio pupil may cause not only pupillary block but also angle block. Long term use of cortico steroid locally or systemically in genetically predisposed eyes is a common cause of rise of intra ocular tension, which generally comes down following stoppage of the steroid. Chronic swelling of ciliary body can cause forward rotation of lens iris resulting in angle closure glaucoma. Miotics are contra indicated in all

types of uveitis as they worsens acute iridocyclitis, reactivate chronic uveitis and results in to pupillary block glaucoma. Glaucoma should be suspected in all cases of anterior uveitis, hence it should be a practice to measure intra ocular pressure not only on first visit but also on subsequent visits also. A reduction of vision with normal macula and no evidence of papillitis should always warn about possibility of glaucoma, specially if the patient is on the steroid or cycloplegic. The tension should be brought down by the use of betablockers, alpha agonist, carbonic anhydrase inhibitors. Latanoprost which is an anti prostglandin drug that increases uveo scleral out flow is better avoided because it can reactivate uveitis. Short term systemic carbonic anhydrase inhibitors may be used to bring down the tension fast. Patients not responding to medical therapy are subject to standard glaucoma surgery.

Hypotony

Reduction in intra ocular tension is common in initial stages of acute anterior uveitis due to hypo secretion of aqueous. This is a self limiting condition, after a few days aqueous production is resumed and intra ocular tension returns to normal or may rise to cause secondary glaucoma, however some times, this hypotony persists for a long time or may develop after few weeks. It is common is patient with juvenile rheumatoid arthritis. Intra ocular tension as low as 6.5 mm is well tolerated by the eyes without any immediate deleterious effect. Prolonged hypotony leads to shallowing of anterior chamber that brings peripheral iris in contact with cornea resulting in formation of peripheral anterior synechia that may cause pseudo angle closure glaucoma. A narrow inter palpebral fissure with reduced corneal curvature and shallow anterior chamber should arouse suspicion of hypotony. There is no specific treatment cycloplegic and steroid are continued. If the patient is on oral carbonic anhydrase inhibitor or local anti glaucoma drops they are withdrawn. Prolonged hypotony over months may results in total ciliary shutdown and result in phthisis bulbae.

Lenticular changes in chronic anterior uveitis

Lenticular complications are common aftermath of chronic uveitis of all types, anterior, posterior, intermediate and pan uveitis.

Cause of cataract in uveitis is not well understood, it is mostly due to altered bio-chem- istry of aqueous, vitreous or lens in various proportion. Cataract formation is more common in cyclitis than in posterior uveitis. It takes months to years for lenticular opacity to develop. The opacity is mostly posterior subcapsular in the form of polychromatic lusture. The cortical fibre in front of this may also be involved, the nucleus becomes yellowish. The anterior capsule also develops sub capsular opacity later, ultimately whole of the lens is opacified. Broad posterior synechias that fail to break develop opacities under the synechia and just ahead of the synechia, these do not progress. Deposition of exudates in occulsio pupilli may be confused as opacity in the lens without a true cataract formation. In prolonged cyclitis the zonules may give way resulting in subluxation or complete dislocation either spontaneously or with minimal trauma. A common cause of posterior capsular opacity is prolonged use of steroid both local and systemic.

Vitreous changes in chronic anterior uveitis

Vitreous changes in chronic uveitis is less common. The vitreous may develop floaters and liquefaction. Chorioretinitis and vasculitis may result in formation of vitreous bands

leading to rhegmatogenous retinal detachment. Posterior vitreous detachment is more common than detachment from the base.

Fundus changes consists of : Macular edema, macular pigmentation papillitis, peripheral retinal degeneration, peripheral vaseulitis and chronic papillitis or post neuritic optic atrophy. Patches of chroiditis and chorioretinitis may be present.

Complications of posterior uveitis consists of loss of vision, scattered scotomas in the field, exudative retinal detachment, neovascularisation, traction detachement complicated cataract, vitreous detachment and liquefaction, optic neuritis and optic atrophy, glaucoma, hypotony, phthisis.

Pan uveitis

Involvement of all the parts of uvea in an inflammatory process24 is called pan uveitis. All the parts may not be equally involved. Generally pan uveitis is discussed under chronic uveitis, however, it can have both acute and chronic onset with or without recurrence depending upon the etiology. It is generally bilateral, one eye may be involved earlier than the other. Clinical presentation in the eye vary according to etiology, duration and treatment undertaken. The signs and symptoms of pan uveitis are a combination of both anterior and posterior uveitis. It can be bacterial or viral. Common bacteria are tuberculosis, syphilis, brucellosis and lyme disease. The viruses involved in pan uveitis are herpes zoster and simplex, rubella, rubeolla, Aids, Epistein-Barr virus. Commonest parasite causing pan uveitis is toxoplasmosis. Conditions that have uncertain etiology are—Sympathelic ophthalmia, parsplanitis, Vogt Koyanagi Harada syndrome, sarcoidosis and Behcet’s disease. The course tends to be chronic with fair prognosis.

Endophthalmitis

Endophthalmitis is a severe form of pan uveitis with involvement of vitreous, retina and optic nerve. The inflammation is always intra ocular. The organism may reach the eye via the blood stream, may spread from sloughing corneal ulcer. Commonest source of infection is penetrating injury either accidental or surgical. Endophthalmitis can be acute or chronic, it may be infective or sterile. Among infective organism, bacteria are the commonest causative factors, which invariably produces acute endophthalmitis while fungal endophthalmitis develops late and progresses slowly. Viral endophthalmitis is unknown.

Panophthalmitis

Panophthalmitis is an acute superative inflammation of eye as well as periocular structures basically it is an endophthalmitis that crosses the scleral barrier. It is generally unilateral. With profound loss of vision, pain, copious discharge, edema of lids, proptosis, changes of conjunctivitis or sloughed hazy cornea, massive hypopyon and restricted movement.

Management of uveitis

Management of uveitis may be very simple with recovery without recurrence or complications. Otherwise it may be frustrating, long drawn with complications. Treatment depends upon its onset, severity, part of the uvea involved, probable cause of uveitis, associated complication, tolerance of the patient towards therapy and compliance.

Aim of the treatment for acute anterior uveitis is to 1. Reduce discomfort i.e. pain, lacrimation, photophobia. 2. Bring inflammation under control. 3. Eliminate infective process, when detected. 4. Prevent and treat complication as and when they arise.

Treatment of acute uveitis is divided into non-specific and specific treatment.

Non specific can be

1. Physical : Hot fomentation. This gives some relief from pain in the eye. Dry fomentation is better as it is convenient to apply. The eye is fomented for three to five minutes at a time for two to three times a day.

Dark glasses : In initial stages it helps in reducing photophobia, once the pupil is dilated it reduces glare.

2. Medical treatment of acute anterior uveitis consists of

Cycloplegic, cortico steroid, non steroidal anti inflammatory drug, immuno suppressive

drugs.

Specific antibiotic for tuberculosis, syphilis, toxoplasmosis etc.

Cycloplegics : Purpose of cycloplegic is to relieve spasm of ciliary body which is a major cause of pain in and around the eye. All cycloplegics are mydriatics. Instillation of cycloplegic also causes much needed mydriasis that keeps the pupil dilated, prevents post synechia, breaks posterior synechia. Mydriatics themselves do not have any therapeutic value in treatment of uveitis, they may be added to cycloplegics to enchance mydiratic effect of the later.

Cycloplegics are parasympatholytic agents they are of two types :

1.Long acting—Atropine.

2.Short acting—Home atropine, cyclopentolate and tropicamide.

Action of these drugs are not neutralized by miotics in therapeutic dose. The cyloplegics have local as well as systemic action especially with long acting drug i.e. atropine. Cycloplegics are used as drops, ointment and subconjunctival injections. As drops they may be used singly or in combination of two cycloplegics or a cycloplegic with mydriatic. Commonest combination is that of tropicamide, cyclopentolate with phenyle pherine. Out of all cycloplegics only atropine is available in ointment and injectable form. Cycloplegics are metabolized faster in inflamed uvea, hence their action passes off faster in uveitis and require more frequent instillation. Atropine is strongest of all cycloplegic, it is an alkaloid. Its action starts within one hour and lasts ten to fifteen days in normal eye. In inflamed eye the action starts late and for shorter period, requiring frequent use for long period. Some times increase in concentration may be required to produce desired therapeutic results. Atropine is used as sulphate either as ointment or drops. Commonly used concentration is half to one percent as ointment and one to two percent as drops. Concentration of more than two percent is hazardous in children. Drops should be avoided because each moderate sized drop contains 0.6 mg. of atropine, which is within therapeutic limit, this means that two drops contain 1.2 mg that is more than upper limit of safety. Similarly each drop of two percent will contain 1.2 mg and such two drops when absorbed through conjunctiva and nasolacrimal duct will produce toxicity. Absorption through

nasolacrimal duct can be minimized if the punctum is obliterated by finger for one minute just following instillation.

Common side effect of atropine are—Glare, loss of accommodation, unmasking of facultative hypermetropia, dryness of mouth, flushing of face, thirst, rise of body temperature, constipation, in eyes with anatomically narrow angle atropine can precipitate angle closure glaucoma, which is not responsive to local miotics. Fortunately angle closure glaucoma following mydriasis is rare in children. In case there is rise of tension it should be brought down by systemic acetazolamide, local beta blockers or alpha agonist. Atropine is one of the local drugs that is frequent cause of dermatitis medicamentosa. Fortunately this passes off within a few days after stopping the drug. The patient may require local steroid ointment to treat allergic blepharitis and dermatitis of the lids.

If pupil does not dilate with BD dose, it is better to add five percent phenyl pherine, rather than increasing strength and frequency of drops in children.

In case of allergy to atropine, the drug should be withdrawn and replaced by home atropine hydrobromide 2% drops or cyclopentolate one percent. However many of the patients allergic to atropine are also allergic to home atropine. Similarly cyclo pentolate is known to aggravate iritis.

To summarise

Avoid atropine drops in children.

Inform parents about possible side effect of atropine.

Once synechia are broken maintain mydriasis with other cycloplegic or combination of cycloplegic and mydriatic drugs.

Sympathomimetic drugs have no role in uveitis except as adjuvant to cycloplegics. They may release uveal pigment in aqueous that may be mistaken as flare.

In case of glaucoma control tension by acetozolamide, beta blockers and alpha agonist. Latanoprost and cyclopentolate may aggravate uveitis.

Miotics are contra indicated in uveitis and do not counteract cycloplegic action. They also do not counteract drug induced mydriatic in therapeutic dose.

If pupil does not dilate with atropine BD or combination of tropicamide / cyclopentolate / home atropine with phenylpherine, every half an hour for four to five instillation, the pupil will most probably not dilate with subconjunctival injection of mydricane that is a combination of atropine, epinephrine and procaine/xylocaine.

Cortico steroids

Most commonly used drugs in uveitis is steroid. Steroids are effective in all types of uveitis, are easy to be administered, evaluate and adjust their dose. Steroid are very cost effective provided they are administered as per norms otherwise they can be potentially dangerous both locally and or systemic. Exact mode of action of steroid is not well understood, most widely accepted theory is that they act as potent anti inflammatory agent. They do not change the basic pathology. The steroids protect the tissue from the onslaught of inflammation till the immune system is capable enough to overcome inflammation by reducing phagocytes,

fibrosis and neovascularisation24. As steroid has no effect on micro organism they should be used under umbrella of anti microbial drugs other wise the condition may worsen. Steroids can be divided into two groups i.e. long acting and short acting. Both groups are available as local drops andointments, tablets and injectable forms. The drops can beclear solution or suspension. The clear solution have better corneal penetration hence are preferred over suspension. Injectable solutions are also available in soluble state or suspension form. The solution are generally short acting i.e. dexamethasone or betamethasone, which are absorbed quickly requiring repeated injection every day or alternate day till the inflammation has been brought under control. The suspensions are absorbed slowly from the site, they form depot from which the drug is released. The depot may remain visible under the conjunctiva as long as 20 to 25 days but its therapeutic efficacy is considerably reduced by seven to ten days. The injection may be repeated every fortnight. If the condition requires prolonged use of steroid they may be given every month. Depot injections are suitable for chronic cases. They are not to be used in acute states.

Injectable steroids can be given as sub conjunctival, anterior and posterior subTenon and retrobulbar. They may be give intra muscular or IV as well. Commonly used IV steroid are methylprednisone and ACTH.

Subconjunctival and subtenon injections are absorbed by conjunctiva which passes it over the aqueous or via sclera. A part of subconjunctival injection is bound to absorbed by systemic circulation. SubTenon and retrobulbar injections are given for lesions behind the lens and suspensory ligament. Retrobulbar injection is given less frequently mostly for optic nerve involvement and causes less rise of IOP, cataract is also less frequent following retrobulbar injection.

The tablets can be given daily or alternate day or in pulse form. The daily dose can be given in divided dose of TDS or QID or as a single dose in the morning just before breakfast. The divided dose is more effective but produce more side effects. Both short and long acting drug can be used. Daily single dose or alternative dose reduces adrenalin suppression, hence they cause less side effects. Short acting steroids like dexamethasone or betamethasone are not suitable for alternate day schedule as steroid in therapeutic dose is not available on the skipped day. The commonest drug used for daily and alternate day regime is prednisolone in a dose of 1 mg to 1.5 mg per kg. In an adult this may be as high as 60 mg to 120 mg. per day. Children are put on steroid in consultation with pediatrician. The steroid should never be stopped abruptly. They are generally tapered over weeks or months.

General principles of use of steroid are : Use enough, soon enough, often enough and long enough. The above dictum is true for systemic and local steroids.

Local steroids

Local steroids are available as ointment as well as drops. Ointments are poorly absorbed, they form an oily layer over cornea that reduces vision and interferes with examination by slit lamp or opthalmoscope. The advantage of ointment is that it has prolonged effect hence can be used during sleep.

The drops are available as clear solution or suspension. The frequency of instillation depend upon severity of uveitis. In acute iridocyclitis they may be used initially every hour for first 6 hours followed by seven to eight times a day and gradually tapered to twice or once a

day. The steroids can be tapered not only in frequency but also in strength. They can be diluted as much as one tenth, not loosing much effectiveness when used for long time. Patients on systemic steroids require less local steroid. It is better to use a broad spectrum antibiotic drop along with local or systematic steroid to ward off possible secondary infection. Such prophylactic use of antiviral and antifungal drugs have doubtful role. It has been observed that eye under steroid therapy requires less cycloplegic to dilate the pupil.

Side effect of steroids:

Steroids are most potent anti inflammatory agents with a very wide spectrum utility, as expected such potent drugs have far reaching side effects both local as well as systemic. Local and periocular use of steroids produce less side effects but are not altogether free from them. Local steroids are capable of producing corneal complication and rise of intraocular tension like systemic used steroid, they may even produce systemic side effect to less extent when used for a long time. Local complication include delayed healing of both post traumatic and infective process. Reactivation of dormant infective process, corneal staining, rise of intra ocular pressure, moderate mydriasis, posterior subcapsular opacity and ptosis.

Systemic use produce all above side effects along with following in various combination : Precipitate latent diabetes in steroid responders, worsens existing diabetes, salt retention leading to weight gain, edema, hypertension. There is potassium loss, generilsed weakness, ptosis, personality change, sleep disturbance, Cushing syndrome, acne and poor healing.

Non steroidal anti inflammatory drugs:

These drugs are mostly prostaglandin inhibitors. They block the synthesis of enzyme prostaglandinsynthatase and cycloxygenase. They also block polypeptide of kinin system, lysosmal enzyme, lymphokinase. They are available as local drops, ointments, oral tablets and injection. They include age-old analgesic like salicylate, aspirin, indomethacine and recent drugs like ibuprofen, diclofenac sodium ad potassium, nimesulide, ketarolac etc. Newer drugs are being added frequently claming to be more effective and less toxic. Local drops are usually used twice a day. Their use is restricted to mild to moderate anterior uveitis, their simultaneous use with steroid results in lowering requirement of steroid. They do not replace steroid altogether. They can be used to prevent recurrence for long time. They hardly produce any ocular side effect. They antagonise prostaglandin induced miosis which may otherwise be atropine resistant. They also antagonise vasodilatation, and reduce aqueous flare. They are used to enhance preoperative mydriasis and maintain intraoperative mydriasis. They are also used in cystoid macular edema.

All NASID are potent analgesic and moderate antipyretic. Systematic side effects produce by NSAID are—hyper acidity and peptic ulceration. Systemic allergy has been reported.

Anti metabolites

These potentially dangerous drugs are used in following conditions: Bilateral vision threatening condition not responding to permissible dose of steroid or where steroids are not tolerated. The patient should follow the instructions and agree for adequate follow-up and have a knowledge of side effects of antimetabolites. There should be no contra indication of their use like tuberculosis, toxoplasmosis, fungal infecton, herpetic disease, cytomegalo virus infection.