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 First described in detail as a clinical entity by 
Mooren in 1867. 
 Mooren’s ulcer is a chronic, painful, peripheral 
...
 Wood and Kaufman classified the disease 
into 2 groups according to the age of onset. 
Unilateral 
older patients (fou...
Pathogenesis 
 Precise pathophysiological mechanism 
unknown 
 autoimmune process: with both cell-mediated 
and humoral ...
partially purified corneal 
antigen (Co-Ag). 
Ab & complement 
bound to conjunctival 
epithelium 
Neutrophils, 
lymphocyte...
PATHOLOGY 
 Mooren’s ulcer is characterized by a progressive, 
crescentic, peripheral corneal ulceration that is 
slightl...
 Characteristic extensive, 
undermined, “overhanging” 
edge 
 The histopathology of 
Mooren's ulcer suggests an 
immune ...
 The midstroma 
hyperactivity of fibroblasts 
disorganization of the collagen lamellae. 
 The deep stroma 
heavy macr...
 Leading edge of the ulcer 
Heavy neutrophil infiltration 
dissolution of the superficial stroma 
degranulated neutrop...
Clinical features 
 Patients with Mooren’s ulcer will 
present with redness, increased 
lacrimation and photophobia, but ...
 The disease may begin as several 
patchy peripheral stromal infiltrates 
that then coalesce, commonly in the 
region of ...
 The anterior 1/3 to 1/2 of the stroma is involved 
characteristically with a steep overlying central and leading 
edge. ...
 Adjacent conjunctiva may be 
inflamed and edematous 
 iritis is sometimes associated 
with Mooren’s ulcer. 
 Hypopyon ...
 Healing and vascularization 
occurs slowly with the disease 
running a chronic course over 4- 
18 months. 
 Portions of...
 The end stage is a typical scarred, vascularised 
thinned cornea with the patient experiencing sudden 
relief from the e...
DIFFERENTIAL DIAGNOSIS 
 Collagen Vascular Diseases 
Rheumatoid Arthritis 
Wegener's Granulomatosis 
Polyarteritis Nod...
DIAGNOSIS 
 It is a diagnosis of exclusion. 
 The differential diagnosis is that of peripheral 
ulcerative keratitis and...
 Investigation includes 
Total blood count 
differential count, 
erythrocyte sedimentation rate, 
rheumatoid factor, ...
TREATMENT 
 step-wise approach to the management of 
Mooren's ulcer, which is outlined as follows: 
1. Topical steroids 
...
1. Topical steroids 
 Initial therapy should include intensive topical steroids 
 Prednisolone 1%, hourly in association...
 Oral therapy (60 to 100 mg daily of oral 
prednisone) 
 Topical tetracycline or medroxyprogesterone 
may be used for an...
2. Conjunctival resection 
 Conjunctiva adjacent to the ulcer contains 
inflammatory cells that produce antibodies 
again...
 The overhanging lip of ulcerating cornea may also be 
removed. 
 Tissue adhesive and a therapeutic soft contact lens 
m...
3. Systemic immunosuppressives 
 The most commonly used agents are 
cyclophosphamide (2 mg/kg/day), 
methotrexate (7.5 ...
 Agents such as cyclophosphamide may be effective by 
suppressing B lymphocytes, which produce 
autoantibodies and promot...
 Adverse effects of these, such as anaemia, 
alopecia, nausea, nephrotoxicity and 
hepatotoxicity, 
 local or systemic s...
4. Additional Surgical 
Procedures 
 Superficial lamellar keratectomy, has been shown to 
arrest the inflammatory process...
 Small perforations may be treated with 
application of tissue adhesive and 
placement of a soft contact lens to provide ...
 When a perforation is too large for tissue 
adhesive to seal the leak, some type of 
patch graft will be necessary. 
 T...
 In case of larger peripheral perforations, a 
partial penetrating keratoplasty may be 
performed. 
 It should be emphas...
5. Rehabilitation 
 Rehabilitative surgical therapy in two stages, namely initial 
lamellar tectonic grafting followed by...
 It removes antigenic targets of the cornea, 
prevents immunological reactions, 
reconstructs the anatomical structure, 
...
 For an ulcer smaller than half 
circle of the limbus and the 
central 7-8 mm of the cornea 
uninvolved crescent shaped 
...
 Double lamellar grafts (a fresh thin inner graft with 
corneal endothelial cells is used to repair the 
perforation, on ...
Mooren’s ulcer
Mooren’s ulcer
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Mooren’s ulcer

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Mooren’s ulcer

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Mooren’s ulcer

  1. 1.  First described in detail as a clinical entity by Mooren in 1867.  Mooren’s ulcer is a chronic, painful, peripheral ulcerative keratitis.  More common in males. (M:F = 1.6:1)
  2. 2.  Wood and Kaufman classified the disease into 2 groups according to the age of onset. Unilateral older patients (fourth decade and older)  limited More responsive to local surgical and medical therapy. Bilateral younger individuals (third decade) Progressive resistant to systemic immunosuppression
  3. 3. Pathogenesis  Precise pathophysiological mechanism unknown  autoimmune process: with both cell-mediated and humoral components.  A type III hypersensitivity mechanism has been implicated in the etiopathogenesis of Mooren’s ulcer.
  4. 4. partially purified corneal antigen (Co-Ag). Ab & complement bound to conjunctival epithelium Neutrophils, lymphocytes & macropages
  5. 5. PATHOLOGY  Mooren’s ulcer is characterized by a progressive, crescentic, peripheral corneal ulceration that is slightly central to the corneoscleral limbus.
  6. 6.  Characteristic extensive, undermined, “overhanging” edge  The histopathology of Mooren's ulcer suggests an immune process.  Involved limbal cornea consisted of three zones.  The superficial stroma vascularized and infiltrated with plasma cells and lymphocytes. destruction of the collagen matrix. Epithelium and Bowman's layer are absent.
  7. 7.  The midstroma hyperactivity of fibroblasts disorganization of the collagen lamellae.  The deep stroma heavy macrophage infiltrate Descemet's membrane and the endothelium were spared
  8. 8.  Leading edge of the ulcer Heavy neutrophil infiltration dissolution of the superficial stroma degranulated neutrophils  The adjacent conjunctiva epithelial hyperplasia and a subconjunctival lymphocytic and plasma cell infiltration.
  9. 9. Clinical features  Patients with Mooren’s ulcer will present with redness, increased lacrimation and photophobia, but pain is typically the outstanding feature.  The pain is excruciating and may seem well out of proportion to the corneal inflammation.  Decreased visual acuity may be secondary to associated iritis, irregular astigmatism due to the peripheral corneal thinning.
  10. 10.  The disease may begin as several patchy peripheral stromal infiltrates that then coalesce, commonly in the region of the palpebral fissure.  Generally there is involvement upto the limbus.  The ulcerative process spreads circumferentially and then centrally to involve the entire cornea eventually.
  11. 11.  The anterior 1/3 to 1/2 of the stroma is involved characteristically with a steep overlying central and leading edge.  It is difficult to judge the depth of the involvement unless the lesion is gently probed at the overlying edges.
  12. 12.  Adjacent conjunctiva may be inflamed and edematous  iritis is sometimes associated with Mooren’s ulcer.  Hypopyon is rare unless secondary infection is present.  Glaucoma and cataract may complicate the process.  Perforation can occur, especially following minor trauma.
  13. 13.  Healing and vascularization occurs slowly with the disease running a chronic course over 4- 18 months.  Portions of the ulcer may be quiescent while the remaining may be active.  Topography demonstrates severe irregular astigmatism and peripheral steepening.
  14. 14.  The end stage is a typical scarred, vascularised thinned cornea with the patient experiencing sudden relief from the excruciating pain  Chronic Mooren’s ulcer ultimately results in a central island of hazy stromal tissue with severe peripheral thinning.
  15. 15. DIFFERENTIAL DIAGNOSIS  Collagen Vascular Diseases Rheumatoid Arthritis Wegener's Granulomatosis Polyarteritis Nodosa Systemic lupus erythematosus  Corneal degenerations Terrien's Degeneration Pellucid Degeneration  Other Staphylococcal Marginal Keratitis Ocular Rosacea
  16. 16. DIAGNOSIS  It is a diagnosis of exclusion.  The differential diagnosis is that of peripheral ulcerative keratitis and is extensive.  Infectious aetiologies should be excluded.  Mooren's ulcer is easily distinguished from the non-inflammatory corneal degenerations, in which the epithelium remains intact and pain is absent.  The presence of Mooren's-like ulcer requires an extensive search for occult and potentially lethal systemic diseases.
  17. 17.  Investigation includes Total blood count differential count, erythrocyte sedimentation rate, rheumatoid factor, complement fixation, antinuclear antibodies (ANA), antineutrophil cytoplasmic antibody (ANCA), circulating immune complexes, liver function tests, blood urea nitrogen and creatinine, Serum protein electrophoresis, urinalysis, and a chest roentgenogram.
  18. 18. 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
  19. 19. 1. 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.
  20. 20.  Oral therapy (60 to 100 mg daily of oral prednisone)  Topical tetracycline or medroxyprogesterone may be used for anticollagenolytic properties of each.  A therapeutic soft contact lens or patching
  21. 21. 2. Conjunctival 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.
  22. 22.  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.
  23. 23. 3. 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.
  24. 24.  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.
  25. 25.  Adverse effects of these, such as anaemia, alopecia, nausea, nephrotoxicity and hepatotoxicity,  local or systemic side effects attributable to topical cyclosporin A were not observed.
  26. 26. 4. Additional 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.
  27. 27.  Small perforations may be treated with application of tissue adhesive and placement of a soft contact lens to provide comfort and to prevent dislodging of the glue.
  28. 28.  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.
  29. 29.  In case of larger peripheral perforations, a partial penetrating keratoplasty may be performed.  It should be emphasized that the prognosis of corneal graft in the setting of acute inflammation in patients with Mooren's ulcer is very poor.
  30. 30. 5. 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.
  31. 31.  It removes antigenic targets of the cornea, prevents immunological reactions, reconstructs the anatomical structure, prevents perforation and improves vision.  The principle of lamellar keratoplasty surgery in Mooren’s ulcer is to remove necrotic ulcerative cornea and to reconstruct the anatomical structure of the cornea.
  32. 32.  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.
  33. 33.  Double lamellar grafts (a fresh thin inner graft with corneal endothelial cells is used to repair the perforation, on which another lamellar graft shaped in accordance with the shape of the ulcer is placed) can be used for perforations of the peripheral cornea.  Postoperative use of topical steroids and 1% cyclosporine
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Mooren’s ulcer

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