5. 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.
6. CLINICAL FEATURES
The clinical features of interstitial keratitis can be divided into
three stages:
INTIAL PROGRESSIVE STAGE
FLORID STAGE
STAGE OF REGRESSION
7. 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.
9. 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.
11. STAGE OF REGRESSION
Acute inflammation resolves.
Clearing of cornea from periphery to centre.
Resolution with some opacities and ghost vessels- non
perfused vessels
13. DIAGNOSIS
Diagnosis is confirmed with blood tests : FTA-ABS
or MHA- treponema pallidum.
Follow up with VDRL.
15. 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.
16. 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
17. 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 )
19. COGAN’S SYNDROME
This syndrome compromise unknown etiology, acute
tinnitus,vertigo, deafness
It typically occurs in middle aged adults & is often bilateral.
20. TREATMENT
It consists of: topical & systemic corticosteroids.
Early treatment usually prevents permanent deafness &
blindness
23. DEFINITION
Mooren’s ulcer ( chronic serpiginious or rodent ulcer ) is a
severe inflammatory peripheral ulcerative keratitis.
24. 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)
25. 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.
26. Cont.
virulent type also called the progressive form is bilateral the
ulcer is rapidly progressive risk of scleral involvement.
28. 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.
29. “
”
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).
30. 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
31. 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.
32. 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
33. 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.
34. 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.
35. 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.
36. 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.
37. CONT.
Adverse effects of these, such as anaemia, alopecia, nausea, nephrotoxicity and
hepatotoxicity.
38. 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.
39. 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
40. 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
41. 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.