Corneal ulcers

Corneal Ulcers, description & classification of almost all types of corneal ulcers, pathology of corneal ulcers & much more

1. CORNEAL ULCERS -SOLANKI RIDDHI 2 ND YEAR (B.OPTOM)

2. CLASSIFICATION INFECTIVE KERATITIS: I. BACTERIAL CORNEAL ULCERS Hypopyon corneal ulcer Marginal catarrhal ulcer Mycotic corneal ulcer II. VIRAL CORNEAL ULCERS Herpes simplex keratitis Herpes zoster ophthalmicus III. PROTOZOAL KERATITIS Acanthamoeba keratitis

3. ALLERGIC KERATITIS: I. PHLYCTENULAR KERATITIS II. VERNAL KERATITIS III. ATOPIC KERATITIS TROPHIC: I. NEUROPARALYTIC KERATITIS II. EXPOSURE KERATITIS KERATITIS ASSOCIATED WITH DISEASES OF SKIN & MUCOUS MEMBRANE: I. ROSACEA KERATITIS

4. KERATITIS ASSOCIATED WITH SYSTEMIC COLLAGEN VASCULAR DISEASES IDIOPATHIC KERATITIS: I. MOOREN’S ULCER

5. INFECTIVE KERATITIS: I. BACTERIAL CORNEAL ULCER: Being the most ant. part of eyeball, the cornea is exposed to atmosphere & hence prone to get infected easily. At the same time cornea is protected from the defence mechanisms present in tears in the form of lysozyme, betalysin , & other protective proteins. I nfective corneal ulcer may develop when: Either the local ocular defence mechanism is jeopardised , or The causative organism is very virulent.

6. ETIOLOGY: F ollowing 3 pathogens can invade the intact corneal epithelium & produce ulceration: Neisseria gonorrhoeae Corynebacterium diphtheriae Neisseria meningitidis . Corneal epithelial damage : It may occur in following conditions: Corneal abrasion Epithelial drying Necrosis of epithelium Desquamation of epithelial cells Epithelial damage due to trophic changes

7. Source of infection include: Exogenous infection From the ocular tissue Endogenous infection Causative organism: common bacterias associated with corneal ulceration are: Staphylococcus aureus Pseudomonas pyocyanea Streptococcus pneumoniae E. coli N. gonorrhoea N. meningitidis C. diphtheriae .

8. Bacterial corneal ulcer

9. [A] pathology of localised corneal ulcer Stage of progressive infiltration : It is characterised by the infiltration of polymorphonuclear &/or lymphocytes into the epithelium from the peripheral circulation supplemented by similar cells from the underlying stroma if this tissue is also affected. Subsequently necrosis of the involved tissue may occur.

10. Stage of active ulceration : Active ulceration results from necrosis & sloughing of the epithelium, bowman’s membrane & the involved stroma . During this stage, accumulation of purulent exudates on the cornea. There occurs vascular congestion of the iris & ciliary body & some degree of iritis due to absorption of toxins from the ulcer .

11. Stage of regression : Regression is induced by the natural host defence mechanisms. A line of demarcation develops around the ulcer. The digestion of necrotic material may result in initial enlargement of the ulcer. This process may be accompanied by superficial vascularization that increases the humoral & cellular immune response. The ulcer now begins to heal & epithelium starts growing over the edges.

12. Stage of cicatrization : In this stage, healing continues by progressive epithelization which forms a permanent covering. Beneath the epithelium, fibrous tissue is laid down partly by the corneal fibroblasts & partly by the endothelial cells of the new vessels. The degree of scarring from healing varies. If the ulcer is very superficial & involves the epithelium only, it heals without leaving any opacity behind. When ulcer involves bowman’s layer& few superficial stromal lamellae, the resultant scar is called a ‘nebula’.

13. Pathology of corneal ulcer

14. [b] pathology of perforated corneal ulcer Perforation of corneal ulcer occurs when the ulcerative process deepens & reaches up to descemet’s membrane. This membrane is tough & bulges out as Descemetocele. At this stage, any exertion on the part of patient, such as coughing, sneezing, straining for stool etc. will perforate the corneal ulcer. Immediately after perforation, the aqueous escapes, IOP falls & the iris-lens diaphragm moves forward. When the perforation is small & opp. to iris tissue, it is usually plugged & healing by cicatrization proceeds rapidly.

15. Perforated corneal ulcer

16. i . Bacterial corneal ulcer HYPOPYON CORNEAL ULCER Causative Organisms: Staphylococci Streptococci Gonococci Moraxella Pseudomonas pyocyanea Pneumococcus. Source Of Infection: For pneumococcal infection is usually the chronic dacryocystitis .

17. Clinical features: Symptoms: Pain Foreign body sensation Watering Photophobia Blurred vision Redness of eye. Signs: Lids are swollen Blepharospasm Conjunctiva is chemosed Hyperaemia & ciliary congestion.

18. hypopyon

19. Complications Of Corneal Ulcer: 1. Toxic iridocyclitis : usually associated with cases of purulent corneal ulcer. 2. Secondary glaucoma: occurs due to fibrinous exudates blocking the angle of ant. chamber (inflammatory glaucoma) 3. Descemetocele: occurs when virulent organisms extends upto descemet’s memb . 4. Perforation Of Corneal Ulcer: occurs due to s udden strain due to cough, sneeze or spasm of orbicularis muscle. 5. Corneal Scarring: It is the usual end result of healed corneal ulcer.

20. descemetocele

21. TREATMENT: Topical antibiotics: Ciprofloxacin or Ofloxacin or Gatifloxacin (0.3%) eye drops, Cycloplegic drugs Systemic analgesics Anti-inflammatory drugs such as paracetamol & ibuprofen Vitamins ( A, B-complex & C) Hot fomentation Removal of any known cause of non-healing ulcer Peritomy

22. MARGINAL CATARRHAL ULCER These superficial ulcers situated near limbus are frequently seen especially in old people. ETIOLOGY: Marginal catarrhal ulcer is thought to be caused by a hypersensitivity rxn to staphylococcal toxins. It occurs in association with chronic staphylococcal blepharoconjunctivitis . Moraxella & Haemophilus are also known to cause such ulcers.

23. Clinical Features: Patient usually presents with mild ocular irritation, pain, photophobia & watering. The ulcer is shallow, slightly infiltrated & often multiple, usually associated with staphylococcal conjunctivitis. Recurrences are very common. Treatment: T opical corticosteroid Antibiotic therapy Treatment of associated blepharitis & chronic

24. Marginal catarrhal ulcer

25. MYCOTIC CORNEAL ULCER T he incidence of suppurative corneal ulcers caused by fungi has increased in the recent years due to injudicious use of antibiotics & steroids. ETIOLOGY: Causative fungi: Aspergillus Fusarium Alternaria Penicillium . Candida & Cryptococcus.

26. CLINICAL FEATURES: Symptoms: Pain Foreign body sensation Watering Photophobia Blurred vision Redness of eye . Signs: Dry-looking Greyish white Delicate feathery finger-like extensions A sterile immune ring may be present Multiple, small satellite lesions may be present

27. TREATMENT: A ntifungal drugs Natamycin , Fluconazol , Nystatin Therapeutic penetrating keratoplasty

28. Mycotic corneal ulcer

29. ii. Viral corneal ulcers HERPES SIMPLEX KERATITIS Ocular infections with herpes simplex virus (HSV) are extremely common & constitute herpetic keratoconjunctivitis & iritis. ETIOLOGY: Herpes simplex virus (HSV): It is a DNA virus. Its only natural host is man. According to different clinical & immunological properties, HSV is of two types: HSV type I typically causes infection above the waist & HSV type II below the waist (herpes genitalis ).

30. Mode Of Infection: HSV-I infection: It is acquired by kissing or coming in close contact with a patient suffering from herpes labialis . HSV-II infection: It is transmitted to eyes of neonates through infected genitalia of the mother. Ocular Lesions Of Herpes Simplex: [A] Primary herpes: Skin lesions Conjunctiva-acute follicular conjunctivitis Cornea

31. [B] Recurrent herpes: E pithelial keratitis: Punctuate epithelial keratitis Dendritic ulcer Geographical ulcer Stromal keratitis Disciform keratitis Diffuse stromal necrotic keratitis Metaherpetic keratitis

32. [A] Primary Ocular Herpes Primary infection (first attack) involves a nonimmune person. It typically occurs in children betn 6 months & 5 yrs & in teenagers. Clinical Features: Skin lesions : Vesicular lesions may occur involving skin of lids, periorbital region & the lid margin. Acute follicular conjunctivitis with regional lymphadenitis is the usual. Keratitis : Cornea is involved in about 50% of the cases. The keratitis can occur as a coarse punctuate or diffuse branching epithelial.

33. [B] Recurrent Ocular Herpes The virus which lies dormant in the trigeminal ganglion, periodically reactivates & causes recurrent infection. Epithelial keratitis: Punctuate epithelial keratitis: The initial epithelial lesions of recurrent herpes resemble those seen in primary herpes & may be either in the form of fine or coarse superficial punctuate lesions. Dendritic ulcer: Dendritic ulcer is a typical lesion of recurrent epithelial keratitis. The ulcer is of an irregular, zigzag linear branching shape.

34. Geographical ulcer : Sometimes, the branches of dendritic ulcer enlarge & coalesce to form a large epithelial ulcer with a ‘geographical’ or ‘amoeboid’ configuration, hence the name. Symptoms Photophobia Lacrimation Pain. Treatment same as of epithelial keratitis.

35. Stromal Keratitis: Disciform keratitis: Endothelium damage results in corneal oedema due to imbibation of aqueous humour . Signs: Focal disc-shaped patch of stromal oedema w/o necrosis Folds in descemet’s memb Keratic precipitates Ring of stromal infiltrate Corneal sensations are diminished IOP may be raised. Treatment: consists of diluted steroid eye drops (acyclovir 3%).

36. Diffuse Stromal Necrotic Keratitis: It is a type of interstitial keratitis caused by active viral invasion & tissue destruction. Symptoms: Pain Photophobia Redness Signs: Necrotic Blotchy Cheesy white infiltrates Treatment: Keratoplasty .

37. Metaherpetic Keratitis: It is not an active viral disease, but is a mechanical healing problem which occurs at the site of a previous herpetic ulcer. Clinically it represents as an indolent linear or ovoid epithelial defect. Treatment Lubricants (artificial tears) Bandage soft contact lens Lid closure ( tarsorrhaphy ).

38. Lesions of recurrent herpes simplex keratitis

39. HERPES ZOSTER OPHTHALMICUS Herpes zoster ophthalmicus is an acute infection of Gasserian ganglion of the Vth cranial nerve by the varicella-zoster virus (VZV). It constitutes approx 10% of all cases of herpes zoster. ETIOLOGY Varicella-zoster virus: It is a DNA virus & produces acidophilic intranuclear inclusion bodies. It is neurotropic in nature.

40. Clinical Features F rontal nerve is more frequently affected than the lacrimal & nasociliary nerves. About 50% cases of herpes zoster ophthalmicus get ocular complications. The Hutchinson’s rule, which implies that ocular involvement is frequent if the side or tip of nose presents vesicles, is useful but not infallible. Lesions of herpes zoster are strictly limited to one side of the midline of head.

41. C linical Phases of H. zoster ophthalmicus are: Acute, which may totally resolve. Chronic, which may persist for years. Relapsing, where the acute or chronic lesions reappear sometimes years later. Treatment: Oral antiviral drugs Cimetidine Amitriptyline Antibiotic-corticosteroid skin ointment or lotions Keratoplasty

42. Herpes zoster ophthalmicus keratitis

43. III. PROTOZOAL KERATITIS ACANTHAMOEBA KERATITIS Acanthamoeba keratitis has recently gained importance because of its increasing incidence, difficulty in diagnosis & unsatisfactory treatment. ETIOLOGY Acanthamoeba is a free lying amoeba found in soil, fresh water, well water, sea water, sewage & air. It exists in trophozoite & encysted forms.

44. CLINICAL FEATURES Symptoms : V ery severe pain Watering Photophobia Blepharospasm Blurred vision. Signs : Initial lesions in the form of Limbitis , Coarse, Opaque S treaks, Fine E pithelial & Sub-Epithelial Opacities & R adial Kerato -neuritis. Advanced cases shows a central or paracentral ring-shaped lesion with stromal.Hypopyon may also be present.

45. Treatment : It is usually unsatisfactory: Non-specific treatment is on the general lines for corneal ulcer. Specific medical treatment includes: propamidine isethionate(0.1%), neomycin drops, polyhexamethylene biguanide (0.01-0.02%). Penetrating keratoplasty is frequently required in non-responsive cases.

46. acanthamoeba

47. Allergic keratitis PHLYCTENULAR KERATITIS Corneal involvement may occur secondarily from extension of conjunctival phlycten ; or rarely as a primary disease. It may present in 2 forms: U lcerative phlyctenular keratitis Diffuse infiltrative keratitis

48. Ulcerative Phlyctenular Keratitis May occur in the following 3 forms: Sacrofulous ulcer : Is a shallow marginal ulcer formed due to breakdown of small limbal phlycten . Such an ulcer usually clears up without leaving any opacity. Fascicular ulcer : It has a prominent parallel leash of blood vessels. This ulcer usually remains superficial but leaves behind a band-shaped superficial opacity after healing. Miliary ulcer : In this form multiple small ulcers are scattered over a portion of or whole of the cornea.

49. Ulcerative phlyctenular keratitis

50. Diffuse Infiltrative Phlyctenular Keratitis It may appear in the form of central infiltration of cornea with characteristic rich vascularization from the periphery, all around the limbus. It may be superficial or deep. Recurrences are very common. Treatment Topical steroids Antibiotic drops & ointments Atropine (1%) eye ointment.

51. Diffuse infiltrative phlyctenular keratitis

52. VERNAL KERATITIS Corneal involvement in VKC may be primary or secondary due to extension of limbal lesions. Vernal keratitis includes following 5 types of lesions: Punctuate epithelial keratitis Ulcerative vernal keratitis (shield ulcertaion ) Vernal corneal plaques Subepithelial scarring Pseudogerontoxon

53. Punctuate epithelial keratitis Involving upper cornea is usually associated with palpebral form of disease. Ulcerative vernal keratitis Presents as a shallow transverse ulcer in upper part of cornea. The ulceration results due to epithelial macroerosions . Vernal corneal plaques Result due to coating of bare areas of epithelial macroerosions with a layer of altered exudates. Subepithelial scarring Occurs in the form of a ring scar. Pseudogerontoxon Is characterised by a classical ‘cupid’s bow’ outline .

54. Treatment Topical steroids Mast cell stabilizers Topical antihistaminics Acetyl cysteine Topical cyclosporine Supratarsal injection Cryo application Surgical excision

55. Vernal keratitis

56. ATOPIC KERATITIS It is an adult equivalent of vernal keratitis & is often associated with atopic dermatitis. Most of the patients are young atopic adults, with male predominance. Symptoms include: Itching, soreness, dry sensation Mucoid discharge P hotophobia or blurred vision Signs Lid margins are chronically inflammed with rounded posterior borders. Tarsal conjunctiva has milky appearance. Cornea may show punctuate epithelial keratitis.

57. Treatment is often frustrating Treat facial eczema & lid margin disease. Sodium cromoglycate drops, steroids & tear supplements may be helpful for conjunctival lesions.

58. Atopic keratitis

59. Trophic corneal ulcers Trophic corneal ulcers develop due to disturbance in metabolic activity of epithelial cells. This group includes: Neuroparalytic Keratitis Exposure Keratitis

60. NEUROPARALYTIC KERATITIS Neuroparalytic keratitis occurs due to paralysis of the sensory nerve supply of the cornea. Causes Congenital Familial dysautonomia (Riley-Day syndrome) Congenital insensitivity to pain. Anhidrotic ectodermal dysplasia. Acquired Following alcohol-block or electrocoagulation of Gasserian ganglion or section of the sensory root of trigeminal nerve for trigeminal neuralgia.

61. A neoplasm pressing on Gasserian ganglion. Gasserian ganglion destruction due to acute infection in herpes zoster ophthalmicus . Acute infection of Gasserian ganglion by herpes simplex virus. Syphilitic ( luetic ) neuropathy. Involvement of corneal nerves in leprosy. Injury to Gasserian ganglion.

62. Clinical Features Characteristics features are no pain, no lacrimation, & complete loss of corneal sensations. Ciliary congestion is marked. Corneal sheen is dull. Initial corneal changes are in the form of punctuate epithelial erosions in the inter-palpebral area followed by ulceration due to exofoliation of corneal epithelium. Relapses are very common, even the healed scar quickly breaks down again.

63. Treatment Initial treatment with antibiotic & atropine eye ointment. T opical nerve growth factor drops & amniotic membrane transplantation. If, however, relapses occur, it is best to perform lateral tarsorrhaphy which should be kept for at least one year. Along with it prolonged use of artificial tears is also recommended.

64. Neuroparalytic keratitis

65. EXPOSURE KERATITIS Normally cornea is covered by eyelids during sleep & is constantly kept moist by blinking movements during awaking. When eyes are covered insufficiently by the lids & there is loss of protective mechanism of blinking the condition of exposure keratopathy develops. Causes Extreme proptosis due to any cause will allow inadequate closure of lids. Bell’s palsy or any other cause of facial palsy. Ectropion of severe degree. Symblepharon causing lagophthalmos .

66. Clinical Features Initial dessication occurs in the interpalpebral area leading to fine punctuate epithelial. Bacterial superinfection may cause deep suppurative ulceration which may even perforate. Treatment Topical antibiotics Cycloplegic drugs Systemic analgesics Vitamins (A,B-complex & C ) Hot fomentation.

67. Exposure keratitis

68. Keratitis associated with diseases of skin & mucous membrane ROSACEA KERATITIS Clinical Features The condition typically occurs in elderly women in the form of facial eruptions presenting as butterfly configuration . Ocular lesions include chronic blepharoconjunctivitis & keratitis. Rosacea keratitis occurs as yellowish white marginal infiltrates & small ulcers. Treatment Topical steroids Long course of systemic tetracycline.

69. Rosacea keratitis

70. Keratitis associated with systemic collagen vascular diseases Peripheral corneal ulceration &/or melting of corneal tissue is not infrequent occurrence in patients suffering from systemic diseases such as rheumatoid arthritis, systemic lupus rythematosus , polyarteritis nodosa & Wegener’s granulomatosis. Such corneal ulcers are usually indolent & difficult to treat. Systemic treatment of the primary disease may be beneficial.

71. Peripheral corneal ulcer

72. Idiopathic corneal ulcers MOOREN’S ULCER The M ooren’s ulcer (chronic serpiginous or rodent ulcer) is a severe inflammatory peripheral ulcerative keratitis. ETIOLOGY Exact etiology is not known. Different views are: It is an idiopathic degenerative condition. It may be due to an ischaemic necrosis resulting from vasculitis of limbal vessels. It may be due to the effects of enzyme collagenase & proteoglyconase from conjunctiva.

73. Clinical Features Two clinical varieties of Mooren ’ ulcer have been recognised . Benign form which is usually unilateral, affects the elderly people & is characterised by a relative slow progress. Virulent type also called the proressive form is bilateral, more often occurs in younger patients. The ulcer is rapidly progressive with a high incidence of scleral involvement.

74. Symptoms S evere pain Photophobia Lacrimation Defective vision. Signs P atches of grey infiltrates which coalesce to form a shallow furrow over the whole cornea. Whitish overhanging edge. The ulcer rarely perforates & the sclera remains uninvolved.

75. Treatment Topical corticosteroids Immunosuppressive therapy Soft contact lenses Lamellar or full thickness corneal grafts.

76. Mooren’s ulcer

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