INTERSTITIAL KERATITIS & MOOREN’S ULCER GURJEET SINGH

VI TERM

INTERSTITIAL KERATITIS

DEFINITION

Interstitial keratitis denotes an inflammation of the corneal stroma without primary involvement of epithelium or endothelium.

CAUSES

Congenital syphilis Tuberculosis Cogan's syndrome Acquired syphilis Trypanosomiasis Malaria Leprosy Sarcoidosis

SYPHILITIC (LEUTIC) INTERSTITIAL KERATITIS

Syphilitic interstitial keratitis is associated more frequently (90%) with congenital syphilis.

Disease is generally bilateral in inherited syphilis & unilateral in acquired syphilis.

Congenital syphilis manifestation develops between 5-15 years of age.

CLINICAL FEATURES

The clinical features of interstitial keratitis can be divided into three stages:

INTIAL PROGRESSIVE STAGE

FLORID STAGE

STAGE OF REGRESSION

INTIAL PROGRESSIVE STAGE

The disease begins with oedema of endothelium & deeper stroma,secondary to anterior uveitis .

Associated with pain,photophobia,lacrimation blepharospasm,diffuse corneal gaze giving it ground glass appearance

This stage last for 2 weeks.

FLORID STAGE

Eye is acutely inflamed. Deep vascularization covered by hazy cornea appear dull

reddish pink- salmon patch appearance. Superficial vessels and conjunctiva heap at the limbus. This stage last for 2 months.

STAGE OF REGRESSION

Acute inflammation resolves. Clearing of cornea from periphery to centre. Resolution with some opacities and ghost vessels- non

perfused vessels

DIAGNOSIS

Diagnosis is confirmed with blood tests : FTA-ABS or MHA- treponema pallidum.

Follow up with VDRL.

Local treatment . Systemic treatment.

TREATMENT

LOCAL TREATMENT

It includes: Topical corticosteroids drops eg: dexamethasone. Atropine eye ointment 1% 2-3 times in a day. Dark goggles to be used in photophobia. Keratoplasty is required where dense corneal opacities are

left.

SYSTEMIC TREATMENT

Benzyl Penicillin for ten days in high doses should be started to prevent development of further syphilitic lesions.

Systemic steroids may be added in refractory cases of keratitis

TUBERCULOUS INTERSTITIAL KERATITIS

The features of tuberculous interstitial keratitis are similar to syphilitic interstitial keratitis except that is more frequently unilateral & sectorial.

(usually involving a lower sector of cornea )

TREATMENT

It consists of :

Systemic Antitubercular drugs

Topical steroids.

Cycloplegics.

COGAN’S SYNDROME

This syndrome compromise unknown etiology, acute tinnitus,vertigo, deafness

It typically occurs in middle aged adults & is often bilateral.

TREATMENT

It consists of: topical & systemic corticosteroids.

Early treatment usually prevents permanent deafness & blindness

MOOREN’S ULCER

DEFINITION

Mooren’s ulcer ( chronic serpiginious or rodent ulcer ) is a severe inflammatory peripheral ulcerative keratitis.

ETIOLOGY

The exact etiology of mooren’s ulcer is not known. Most probably it is an auto immune disease. ( antibodies against corneal epithelium have been

demonstrated in serum)

CLINICAL FEATURES

Two clinical varities of mooren’s ulcer have been recognised .

Benign or limited form which is usually unilateral affect the elderly Caucasians & is characterised by a relative slow progress.

Cont.

virulent type also called the progressive form is bilateral the ulcer is rapidly progressive risk of scleral involvement.

SYMPTOMS

It includes : Severe pain Photophobia Lacrimation Defective vision

SIGNS

It is a superficial ulcer which start at the corneal margin patches of grey infiltrates which coalesce to form a shallow furrow over the whole cornea.

Peripheral ulcer is associated with undermining of the epithelium & superficial stromal lamellae at the advancing border which forms a whitish overhanging edge .

Base of ulcer soon become vascularized . End stage cornea is thinned & conjuctivalised. Ulcer rarely perforates & the sclera remains uninvolved.

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”Mooren's ulcers. (a) Peripheral corneal ulceration in a study patient; there is no involvement of the sclera (arrow). (b) A clear corneal ulcer with a prowling edge in another study patient, showing the ulcer beginning at the conjunction of the cornea and the sclera (arrow). (c) A rheumatoid arthritis-associated peripheral corneal ulcer. The corneal ulceration is close to the central corneal area (arrow). There is a clear corneal area between the peripheral corneal ulceration and corneal limbus. (d) Peripheral ulceration in a patient with Wegener's granuloma involving the peripheral cornea and the sclera (arrow).

TREATMENT step-wise approach to the management of Mooren's ulcer, which is outlined as

follows:

1. Topical steroids

2. Conjunctival resection

3. Systemic immunosuppressives`

4. Additional surgical procedure

5. Rehabilitation

The overall goals of therapy are to arrest the destructive process and to promote healing and reepithelialization of the corneal surface

TOPICAL STEROIDS

Initial therapy should include intensive topical steroids

Prednisolone 1%, hourly in association with topical cycloplegics and prophylactic antibiotics.

If epithelial healing does not occur within 2 to 3 days, the frequency of topical steroid application can be increased to every half hour.

Once healing occurs, the frequency can be reduced, and tapered slowly over a period of several months.

Such management, especially in unilateral, benign form gives good results.

Cont.

Topical Oral therapy (60 to 100 mg daily of oral prednisone)

tetracycline or medroxyprogesterone may be used for anticollagenolytic properties of each.

A therapeutic soft contact lens or patching

CONJUCTIVAL RESECTION

Conjunctiva adjacent to the ulcer contains inflammatory cells that produce antibodies against the cornea and cytokines which amplify the inflammation and recruit additional inflammatory cell.

conjunctival excision to bare sclera extending at least 2 clock hours to either side of the peripheral ulcer, and approximately 4 mm posterior to the corneoscleral limbus and parallel to the ulcer.

CONT.

The overhanging lip of ulcerating cornea may also be removed.

Tissue adhesive and a therapeutic soft contact lens may be beneficial.

Cryotherapy of limbal conjunctiva may have a similar effect.

Systemic immunosuppressives

The most commonly used agents are cyclophosphamide (2 mg/kg/day),

methotrexate (7.5 to 15 mg once weekly) and

azathioprine (2 mg/kg body weight/day).

The degree of fall in white blood cell count is considered as the most reliable indicator of immunosuppression produced by cyclophosphamide.

CONT.

Agents such as cyclophosphamide may be effective by suppressing B lymphocytes, which produce autoantibodies and promote immune complex disease.

oral cyclosporin A (10 mg/kg/day) has been successfully used to treat a case of unresponsive bilateral Mooren's ulcer.

It work by suppression of the helper T cell population and stimulation of the depressed population of suppressor and cytotoxic T cells present in patients with Mooren's ulcer.

CONT.

Adverse effects of these, such as anaemia, alopecia, nausea, nephrotoxicity and hepatotoxicity.

SURGICAL PROCEDURES

Superficial lamellar keratectomy, has been shown to arrest the inflammatory process and allow healing.

Application of isobutyl cyanoacrylate, a tissue adhesive, forms a biological barrier between host cornea and the reepithelializing conjunctiva and the immune components it may carry.

CONT.

When a perforation is too large for tissue adhesive to seal the leak, some type of patch graft will be necessary.

This may range from a small tapered plug of corneal tissue to a penetrating keratoplasty

Rehabilitation

Rehabilitative surgical therapy in two stages, namely initial lamellar tectonic grafting followed by central penetrating keratoplasty may be required in advanced cases.

LKP is the most widely practiced surgery at present

CONT.

For an ulcer smaller than half circle of the limbus and the central 7-8 mm of the cornea uninvolved crescent shaped lamellar graft can be used.

For an ulcer larger than 2/3 of a circle of the limbus where the central 7-8 mm of cornea is intact, a doughnut shaped lamellar graft is recommended.

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