Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

Commonly used cycloplegics are :

1.Atropine sulphate 1% ointment (drops should be avoided in children to eliminate over dosage).

2.Home atropine hydrobromide 5% drops two to three times a day.

3.Cyclopentolate HCL. One percent drops three times a day.

(ii) Cortico steroid. These are double edged medicament that areindicated in stromal involvement but contra indicated in epithelial ulcer. They should be used under umbrella of antiviral drug specially those that have stromal penetration, weakest possible solution in least but effective frequency should be used for shortest period.

(iii) Antibiotics. Broad spectrum antibiotic drops, ointments are used to prevent bacterial secondary infection especially in anaesthetic cornea, patients under steroid and abnormal tear film. The antibiotics do not have any antiviral effect.

(iv) Tear film substitute. Corneal scarring and corneal anaesthesia are associated with abnormality of tear film. A lubrication cum tear film substitute give relief to the patient.

(v) Imuno potentiating drugs. Levamesol, BCG, vitamin A, cematidine, antioxidants have been tried without constant result.

3.Non medical methods. Tissue adhesive cyanoacrylate is used in cases of stromal keratitis threatening to perforate or in a small perforation.

4.Debridement. Debridement is single most effective physical treatment for dendritic and geographical ulcer. It is still treatment of choice where antiviral drugs are not available. In the past debridement was always followed by chemical cautery either by iodine or carbolic acid. Chemical cautery has not been found to have any added advantage over simple debridement. On the contrary it is known to produce stromal damage, produce keratitis metaherpatica and predispose perforation.

Keratoplasty. Penetrating keratoplasty is the ultimate treatment for corneal scar. However it should be tried only when inflammation has been under control for at least six months, otherwise the graft itself can get infected by HSV.

Treatment of individual lesions :

1.Blepharitis and blepharo conjunctivitis. They are often missed as bacterial infection. Treatment consists of local use of idoxuridine 0.1% drop four to five times a day and 0.5% ointment at bed time for four to five days or vidarabine 3% ointment three times a day for four to five days. These drugs when used for more than five days are likely to produce corneal toxicity that may be confused as epithelial defect. Trifluridine and acyclovir should be used when above drugs do not seem to be effective.

2.Primary keratitis. Diagnosis of this condition requires high degree of suspicion on the part of treating physician. Once diagnosis has been established treatment is similar to treatment of dendritic ulcer.

3.Neonatal HSV57 infection is a life threatening disease, it requires management by neonatologist along with local treatment by antiviral drops.

4.Recurrent HSV keratitis. There is no effective method of preventing recurrence because primary infection does not provide any immunity. Latent period between primary

attack and subsequent recurrence is variable even gaps between attacks of two episodes of recurrence is not definite. Number of recurrence is also uncertain. It is claimed that if trigger mechanism like fever, stress, food allergen, ultra violet exposure can be avoided, recurrence is averted.

One of recommendation is to put patients above twelve years on oral 200 mg acyclovir every alternate day few months after patient has received a full course of oral acyclovir i.e. 200 to 400 mg five times a day for five to ten days.

5. Dendritic and Geographic ulcer.

(i) First antiviral drug of choice should be trifluridine locally whenever available or acyclovir locally supplemented by oral acyclovir.

Idoxuridine and vidarabine are effective against epithelial lesions only idoxuridine is most kerato toxic.

(ii) Debridement. Simple debridement is an effective treatment for epithelial keratitis, debridement may be followed by local instillation of trifluridine or acyclovir. Chemical cautery by 7% alchoholic solution of iodine and carbolic was standard treatment before advent of antiviral drugs. Now they have been given up. However when antiviral drugs are not available, they still hold the fort when done carefully.

(iii) Cycloplegic. Cycloplegics are neither antiviral nor anti inflammatory analgesic. Their main function is to treat associated anterior uveitis. Whenever there is associated lacrimation and photophobia, instillation of cycloplegic drugs relieve discomfort.

6.Stromal involvement. Stromal involvement both necrotising or non necrotising are most difficult to manage. Idoxuridine and vidarabine have no role in stromal involvement. Trifluridne and acyclovir are effective in stromal herpes. Stromal HSV infection is always associated with uveitis making use of cycloplegic almost mandatory. Use of steroid is one of the trickiest decisions. Whenever steroids are deemed necessary it should be under cover of effective antiviral drug, well supervised and with weakest strength, least frequently for shortest possible period.

7.Metaherpatic keratitis. Besides antiviral drops, lubricants, pad and bandage, bandage contact lens help to epithelise the effected cornea.

Varicella Zoster Viral Keratitis

Herpes zoster ophthalmicus54. This is an acute multi systemic disease with chronic sequel caused by a DNA virus that produces two distinct type of systemic disease i.e. vericella (chicken pox) and herpes zoster (shingles). The herpes zoster virus is similar to herpes simplex virus in structure but different antigenically and clinically. Both viruses have primary infection followed by a period of latency and a recurrence. In herpes zoster there is a single recurrence that may have a prolonged course while more than one recurrences are common in HSV infection. In both conditions the virus lies dormant in posterior root ganglion only to be activated after an indefinite latent period when the virus travels down the nerve to produce mucocutaneous and ocular lesion. Herpes zoster virus involves single dermatome HSV has irregular distribution. Herpes zoster infection does not cross the midline. Herpes zoster gives life long immunity.

Herpes zoster virus infection differs from vericella in following ways. Vericella is very common, self limiting disease with predominant skin involvement and less pronounced ocular involvement in children. It is rare in adults, while herpes zoster infection is more common in adults, however children are not immune. Ocular involvement in herpes zoster is known as herpes zoster opthalmicus that has severe vision threatening ocular involvement with neurological defect, which may involve other cranial nerves as well. In rare cases it may produce contra lateral hemiplegia. In severe viremia encephalitis is possible. Involvement of cranial nerves other than ophthalmic is mostly immunological rather than infectious in nature. (See Chapter 22 as well)

Though involvement of first division of trigeminal is commonest manifestation. The second and third divisions may also be involved. Involvement of maxillary division produces vesicular eruption in the lower lid, which is otherwise rare. Any of the branches of ophthalmic division may be involved but common involvements are supra orbital, supra trochlear, nasociliary and lacrimal. Involvement of nasociliary nerve that supply the lateral part of the skin of nose and tip of the nose is invariably associated with corneal involvement (Hutchinson’s sign). However there may be corneal involvement without involvement of nasociliary nerve, reverse is also possible. There may be localised involvement of any of the branches of ophthalmic division without ocular involvement. Only ocular involvement without cutaneous manifestation has not been observed.

Ocular involvement in herpes zoster ophthalmicus can be divided under following heads :

1. Cutaneous. Skin of the lids, forehead and scalp are most commonly involved. There is generally mild pain in the distribution of dermatome where vescicles develop in due course. Initially the lesions are maculo papular which become pustular within few days, that rupture to form crust. The crusts gradually fall off leaving depressed marks similar to chicken pox. The crusts are loaded with live viruses, which are infective to others and can cause chicken pox in children. The papulo macular stage is associated with intense edema that may spill over the mid line but not the rashes.

Edema of the lids may obliterate the interpalpebral fissure due to mechanical pseudo ptosis. As the scabs fall of the edema subsides with punched out scar marks that can either be hyperpigmented or hypopigmented. Vescicles on the lid margin may heal by producing notch in the lid margin. It can produce madarosis, trichiasis, ectropion or entropion.

There may be ptosis due to various factors i.e. :

1.Pseudo ptosis is generally due to inflammatory edema.

2.True ptosis is due to involvement of upper division of third nerve.

Some degree of loss of sensation is always present, may last for years associated with post herpetic neuralgia.

Generally orbiculosis is not involved in herpes zoster ophthalmicus. Commonest cause of paralysis of orbicularis is Ramsay Hunt syndrome where vescicles develops in the external auditory canal. However rarely orbicularis palsy may develop independent of Ramsay Hunt

syndrome. Involvement of nasociliary nerve produces development of vescicle on the lateral side of nose and tip of nose. This is invariably accompanied with corneal involvement.

2.Kerato conjunctival involvement :

1.Conjunctival involvement become obvious within first few days as mucopurulent conjunctivitis. This is always associated with vescicles of the lid. Mucopurulent conjunctivitis becomes worse with obliteration of I.P.A. Rarely there may be vescicles on the conjunctiva itself. Conjunctival sensation is either lost or diminished.

2.Corneal involvement. Corneal involvement is one of the most serious complications of herpes zoster ophthalmicus, effect of which could last for years and may cause permanent damage.

(i) Hypoethesia of cornea. First and foremost sign is diminished corneal sensation that may range between reversible hypoethesia to irreversible anaesthesia that on long run may lead to trophic ulcer.

(ii) Keratitis. Earliest infective manifestation is punctate lesions in epithelium. They are generally multiple, mostly on the periphery, stain with rose bengal and contain live viruses, which may respond to local antiviral drugs. They appear within forty-eight hours of onset of skin lesion. They are transient in nature, however, some of them may coalesce to form lesions similar to dendrites. Dendrites of herpes zoster are smaller than dendrites of herpes simplex. They stain with rose bengal, they are transient, are seen between fourth to sixth day. By tenth day there is infiltration of superficial stroma in the form of nummular keratitis that may last for months and cause vascularisation of cornea.

Disciform keratitis is late feature, by this time the rashes have crusted and may have fallen i.e. three weeks after appearance of rashes. Disciform keratitis are associated with thickening of stroma and anterior uveitis. It may be vascularised and cause lipid degeneration.

Loss of sensation leads to formation of trophic ulcer. Due to loss of sensation patient does not complain of pain that may lead to secondary bacterial infection resulting in perforation. Mucous plaque formation is an unique feature of herpes zoster ophthalmicus that develops between third and sixth month in the form of deposit of mucus on swollen epithelium. The plaque can be removed with ease. It is associated with anterior uveitis and stromal infiltration.

3.Scleral. Episcleritis and scleritis are very common in herpes zoster ophthalmicus in first week following onset of rashes, may be missed due to swollen lid and inflamed conjunctiva. Scleritis may cause sclerokeratitis and sclero uveitis

4.Uveitis. Uveitis in herpes zoster ophthalmicus is limited to anterior uvea causing acute iridocyclitis within fortnight.

Iridocyclitis in herpes zoster is a non granulomatous in nature. To begin with iridocyclitis is mild with fine KP and few cells and flare. In severe cases hypopyon may develop due to ischemic necrosis of iris which in turn leads to iris atrophy and formation of holes in iris.

5. A common complication of herpes zoster uveitis is secondary glaucoma that may be overshadowed by keratitis and missed altogether unless sought specifically. It is caused due to associated trabeculitis, the swollon trabecular meshwork and inflammatory debris may cause obstruction of the drainage.

Neurological involvement in herpes zoster ophthalmicus :

(i) Commonest neurological sign of herpes zoster ophthalmicus is loss of sensation. On the distribution of the dermatome involved leading to anaesthesia of cornea, conjunctiva and skin resulting in delayed healing and may lead to trophic ulcer. Anaesthesia masks pain of corneal and uveal involvement.

(ii) The next bothersome symptom is post herpetic neuralgia that may persist for months to years. Fortunately it is rare and milder in children. It is very severe in old age. Exact cause of post herpetic neuralgia in absence of sensation is not well understood. It is called anaesthesia dolorosa.

(iii) Other neurological involvement’s are—optic neuritis, cranial nerve palsy and contra lateral hemiplegia that may take few months to develop. Encephalitis is a rare manifestation of herpes zoster ophthalmicus.

Management of herpes zoster ophthalmicus58. Management of herpes zoster ophthalmicus in children does not differ from management in adults. Children have advantage of less frequent post herpetic neuralgia which is very mild.

1.Skin lesions are best treated with oral acyclovir in dose of 50-60 mg/kg/day divided in five doses. Children can get as much as 400 mg acyclovir five times a day for 7 days. This reduces viremia and enhances healing, resulting in scar formation. Acyclovir does not have much effect on corneal lesions or postherpeticneuralgia but is known to diminish uveal involvement. Acyclovir should be started within 48 hours of onset of rashes. Local skin ointment of acyclovir is applied in the vesicular stage. In the vesicular stage combination of calamine with talcum powder or starch should be avoided as it masks the changes in the vescicles, cause secondary infection and deep scar formation. Combination of antibiotic and steroid is recommended at the crusting stage.

Systemic corticosteroid under the umbrella of systemic antiviral drugs reduces lid edema, and deep scar. Steroids also helps in reducing post herpetic neuralgia. They help to treat stromal involvement and uveitis.

As pain is not a very prominent feature of herpes zoster ophthalmicus in children, mild analgesic given orally is sufficient.

Active immunisation against vericella has been recommended to prevent herpes zoster but its efficacy has not been proved beyond doubt.

2.Conjunctival lesions are treated by local broad spectrum antibiotics instilled in the conjunctiva. Role of local antiviral drugs to combat conjunctivitis is not established.

3.Corneal involvement in herpes zoster is a clinical riddle. Local antiviral drugs are of doubtful value. Local steroids must be given under strict medical supervision. Steroid in weakest possible strength is recommended. The patient must be put on steroid for months. Loss of corneal sensation is a perpetual problem that requires frequent instillation of broad spectrum antibiotic, long acting cycloplegic. If

necessary, tarsoraphy must be performed. Loss of corneal sensation is a contra indication for keratoplasty and contact lens.

4.Optic neuritis, cranial nerve palsy are self limiting. Systemic steroid helps in shortening the course.

Adeno virus keratitis in children62

Almost all adeno viruses that cause conjunctivitis in children involve cornea to some degree. Corneal involvement is seen five to seven days after onset of conjunctivitis which has various degree of follicular reaction and sometimes pseudo membrane formation. Adeno viral keratitis is associated with systemic symptom and pre auricular lymphadenopathy. Corneal involvement in adeno viral infection is less common and less troublesome than seen in herpes simplex. Corneal involvement are less marked in children than in adults. They are generally epithelial in nature and present as fine superficial keratitis that stain brightly with fluorescein. Sub-epithelial involvement is less frequent, transient and leave no scar.

Fungal keratitis42, 63, 64

Fungal infection of cornea is less frequent than bacterial or viral keratitis. It is generally unilateral and central following history of injury. The injury is caused by foreign body of vegetable origin. It is more common in hot and humid climate than in cold and dry climate. Besides trauma, other conditions that predispose fungal keratitis are situations where corneal defence mechanism is compromised i.e. loss of sensation, stromal herpetic keratitis, prolonged local or systemic steroid therapy, paralysis of orbicularis, dry eye, vitamin A deficiency. Fungal keratitis is a suppurative, indolent corneal ulcer with severe anterior chamber reaction, hypopyon and conjunctival congestion. It takes more than ten to fifteen days for a fungal corneal ulcer to develop following trauma by vegetable material. There is an initial corneal abrasion that either heals spontaneously or is treated as bacterial corneal ulcer generally with antibiotic drops. Use of steroid in such situation makes the condition worse. Severity of infection depends upon size of inoculum and immuno competence of the cornea.

Fungi that cause corneal ulcer can be divided into two main groups i.e.

1. Filamentous and 2. Non filamentous. Common fillamentous fungi that cause corneal ulcer are aspergillus, fusarium, cephalosporium. (See Chapter 22 also)

Following trauma with vegetable matter, the initial breach in epithelium heals as simple corneal ulcer. After a gap of ten to fifteen days acute fungal keratitis becomes manifest causing lacrimation, photophobia, blurring of vision and pain. The appearance is characteristic; first a sub epithelial gray white lesion develops at the site of trauma. The epithelium is raised over this and a dirty white, raised dry rough lesion with raised margin develops. Sub epithelial and stromal feathery extension may develop. At the end of the feathery extension multiple satellite lesions may develop which vary in number, shape and size. Their appearance is similar to original central ulcer. The satellite ulcer may join to form a ring called Wessely ring. There may be a epithelial plaque formation. The conjunctiva is severely inflamed.

There is intense anterior chamber reaction with thick yellowish white hypopyon and severe anterior uveitis. The ulcer may extend in to surrounding sclera.

It is not always possible to differentiate non filamentous fungal ulcer from filamentous ulcer. Unlike bacterial ulcers there are no characteristic features that can help clinically to differentiate various filamentous ulcers.

Management and complication of all fungal corneal ulcers is almost the same. If a fungal ulcer is not treated in time, it invariably perforates and the eye is lost. Even if the ulcer does not perforate, it leaves a dense central opacity that compromises vision to great extend. Other common complications are secondary glaucoma, complicated cataract, and phthisis.

Diagnosis :

Diagnosis of fungal keratitis depends on :

History of injury by organic matter specially of vegetable origin about a fort night ago with development of ulcer should alert the physician for possible fungal ulcer that have typical features described above and not responding to usual antibiotic and cycloplegic drops.

Laboratory finding consists of :

1.Examination of corneal scrapping :

1.In KOH solution65

2.Staining — Grams stain

Giemsa stain

Gomori methamine silver stain

Lactophenol cotton blue66

Caleoflour white67

Culture68 — Sabouraud’s medium

Blood agar

Brain heart infusion

1.10% KOH solution is used most frequently to visualise septed fungal hyphae directly under microscope. It is a reliable test.

2.Gram stain is useful to visualise candida, it fails to stain filamentous fungi.

3.Giemsa stain is more useful to define filamentous fungus.

4.Gomori stain provide better fungal cytology.

Culture is done at room temperature, it may take as long as fifteen to twenty days to show positive result.

Management of fungal keratitis :

Management of fungal corneal ulcer is one of the most frustrating forms of treatment due to :

1.Failure to diagnose.

2.Non availability of broad spectrum antifungal antibiotic.

3.Frequent serious complications.

Antifungal drugs69 :

Three groups of antifungal drops are available. They are :

1. Polyenes, 2. Imidazoles, 3. Pyrimidines

1.Polyenes. Amphotericin B, nystatin, natamycin

2.Imidazoles. Clotrimazole, miconazole, ketoconazole, econazole

3.Pyrimidine. Flucytocine

In all cases of suspected fungal keratitis, initial treatment is instillation of natamycin 5% drop every hourly by day. If stain confirms presence of yeast (candida) nystatin 50,000 IU, flucytosine 1% and amphotericin B 0.1% to 0.2% should be given every hourly.

In case of confirmed filamentous fungal ulcer, miconazole, ketaconazole or clotrimazole may be given hourly.

Antifungal treatment should be continued for at least ten days before any improvement occurs.

All cases should get 1% atropine sulphate as ointment two times a day. In children atropine should be administered under supervision to avoid serious systemic complication.

Local betablockers and oral acetazolamide keeps IOP low and lowers incidence of perforation.

Local broad spectrum antibiotic drops are given to prevent secondary bacterial infec-

tion.

Cortico steroids have no role in management of fungal keratitis

Surgical treatment. Good debridement if necessary under general anaesthesia helps to remove infected material. Debridement may be followed by chemical cautery. Too enthusiastic cauterisation may enhance perforation hence it should be done carefully under magnification.

Lamellar keratoplasty fails to eliminate the infection. Penetrating keratoplasty shows better results. However the donor cornea itself may get infected in course of time.

Peripheral keratitis70

Peripheral keratitis may result due to many local and systemic condition both infective as well as non infective. Non infective causes outnumber infective causes. They are generally bilateral, in spite of a benign course they are more painful than infective keratitis. They are caused by allergy, or auto immune disorders. Peripheral ulcers by themselves do not perforate. Perforation is due to secondary bacterial invasion. The keratitis may be self limiting. Most of them respond to local steroid. Anterior chamber reaction is either absent or minimal. Out of many marginal keratitis only phlyctenulosis of cornea is commonly seen in older children. Some times marginal (catarrhal) ulcer may be seen in older children who may also be effected by autoimmune diseases like rheumatoid arthritis.

Phlyctenulosis of cornea. Phlyctenular kerato conjunctivitis is very common in developing countries. It may be limited to conjunctiva only, may involve limbus effecting both cornea and conjunctiva or may primarily develop in the cornea.

Other causes of peripheral keratitis are - Vernal kerato conjunctivitis and rheumatoid arthtitis, Moorens ulcer, which is an important marginal keratitis is not seen in children.

Parenchymatous (Interstitial) Keratitis in Children71, 72, 73, 74. Interstitial keratitis is a chronic disease of cornea with acute onset and protracted course. It can be diffuse or central. In children interstitial keratitis is generally diffuse and bilateral. The other eye getting involved few days after the first. It is due to an antigen antibody reaction to spirochete trapenoma pallidum, tuberculosis and leprosy. Other causes are - Lymphogranuloma venereum, herpes simplex, malaria, onchocerciasis.

In children commonest type of interstitial keratitis is due to syphilis in the form of congenital syphilis or hereditary syphilis. The child is infected in utro between first and second trimester, interstitial keratitis manifesting between 5 to 15 years of age.

Primarily interstitial keratitis is a disease of stroma. The epithelium and endothelium getting involved later. In late stages all the layers of cornea get effected. Anterior uveitis is early and prominent feature.

Uveal involvement is so pronounced that it is thought that basic pathology starts in the uvea and cornea gets involved secondarily. Exact pathology of interstitial keratitis is not well understood. Trapenoma has been isolated from syphilitic foetus and new born without evidence of interstitial keratitis. Conversely trapenoma has not been demonstrated in cornea in interstitial keratitis. The disease is self limiting, it responds well to steroids but not to pure anti syphiletic treatment. Interstitial keratitis has a long latent period of five to ten years following intrauterine infection.

The clinical picture has been divided into :

1. Progressive ; 2. Florid and ; 3. Regressive stages.

1.Progressive stage lasts for two to three weeks following clinical symptom of lacrimation, photophobia, blepharospasm. On examination there is well developed circumcorneal congestion and haziness of cornea that starts from periphery extending towards centre followed by sprouting of new vessels in the stroma. This is the time when uveitis develops mostly in the form of acute iridocyclitis. There may be anterior choroiditis as well. Changes in iris are masked by corneal haze. There may be involvement of retina and choroid that result in to salt pepper appearance.

2.Florid stage—Progressive stage is followed by florid stage that lasts for two to three months. This is the stage when the symptoms are in peak. The cornea develops heavy deep vascularisation that gives a red hue to the cornea. Vascularisation spread from all sides.

It is expected that vessels in cornea should have bright red colour, due to corneal haze the redness is toned down to a peculiar pink colour known as Salmon red colour.

Causes of haziness are due to changes in all the layers of cornea i.e. from epithelium to endothelium with keratic precipitates. These changes when added result into a hazy cornea (ground glass appearance). Other change seen in cornea on biomicroscopy are; bedewing of epithelium, cellular infiltration round the newly formed vessels in front of the Descemet’s membrane, which is wrinkled. The Bowman’s membrane is wavy while deep vascularisation is

developing in the stroma. Superficial vascularisation may be superimposed in the epithelium on the periphery resulting into a crecentic pile of blood vessels known as epaulet.

3.Regressive stage—After four to five weeks, stage of regression starts which lasts for two to three years. Process of regression starts as the advancing vessel meet in the centre. Once the cornea is fully vascularised, inflammation suddenly subsides with clearing of the cornea, improvement in vision, reduction of lacrimation, pain and photophobia. Corneal clearing starts from periphery and slowly regains its transparency leaving only obliterated vessels as white streaks that are visible on slit lamp for years called ghost vessels. Besides ghost vessels late sequele are band keratopathy and overall thinning of cornea.

Systemic involvement in congenital syphilis :

1.Dental changes—Hutchinson’s teeth

The permanent upper central incisors are peg shaped reduced in length and breadth. They have a notch on the cutting edge.

2.Changes in ear—permanent deafness.

Interstitialkeratitis, Hutchinson’s teeth and deafness constituteHutchinson’s triade.

3.Forehead—shows frontal eminence.

4.Nose—Saddle shaped depression.

5.Rhagades at angle of mouth.

6.Other changes are—Retarded physical and mental growth, anterior bowing of shin, Clutton’s joint, cardio vascular disorders.

Differential diagnosis consists of—All causes of hazy cornea i.e. buphthalmos, trachoma and congenital corneal haze.

Diagnosis. Diagnosis is clinically simple, if possibility of interstitial keratitis is kept in mind especially in a child borne to known syphilitic mother. Otherwise stigmata of congenital syphilis i.e. saddle nose, frontal bossing, Hutchinson’s teeth, deafness with severely vascularised cornea leads to diagnosis.

Laboratory investigations72 include

1.Positive serological test in mother and child.

2.Reactive CSF-VDRL.

3.Elevated cell or protein in CSF without any other cause.

Treatment—72. Though systemic anti syphilitic treatment does not influence the ocular condition it is mandatory to treat the child with appropriate dose of penicillin to prevent future cardiovascular and maningovascular complication.

Interstitial keratitis is self limiting disease which starts improving within two to three months. The condition is very troublesome to the child who has intense lacrimation, photophobia and diminished vision. Local steroids reduce this period of ocular morbidity to few weeks. Cortico steroids are instilled at a rate of one drop every hour during day for first two days then gradually reduced in frequency over months. Once acute phase has subsided subconjunctival depot steroid can be given at an interval of 15 days. To treat associated uveitis that is always