Lecture on Corneal Ulcers For 4th Year MBBS Undergraduate Students By Prof. Dr. Hussain Ahmad Khaqan

1. Prof. Dr. Hussain Ahmad Khaqan
 MD
 FRCS(Glasgow)
 FCPS(Ophth.)
 FCPS(Vitreo Retina)
 MHPE (KMU)
 CICO(UK)
 CMT(UOL)
 Fellowship in Medical Retina (LMU, Munich)
 Fellowship in Vitreo Retinal Surgery (LMU, Munich)
 Consultant Ophthalmologist & Retinal Surgeon
Professor of Ophthalmology
Lahore General Hospital, Lahore
Ameer Ud Din Medical College, Lahore
Post Graduate Medical Institute, Lahore
Shaukat Khanum Memorial Cancer Hospital & Research Centre ,Lahore
Corneal Ulcers

2. CORNEAL ULCER

3. • Corneal ulcer is an inflammatory or infective
condition of cornea involving disruption of its
epithelium layer with involvement of corneal stroma.
DEFINITION

4. RISK FACTORS

5. Risk Factors for Microbial Keratitis
Ocular Trauma Corneal abrasion
Contact Lens Extended wear > soft> disposable rigid gas permeable
Iatrogenic Corneal surgery
Loose suture
Long term topical steroids
Ocular surface
disease
Dry Eye
Chronic Keratitis
Bullous keratopathy
Immune mediated ocular surface disease
Lid disease Entropion
Trichiasis
Lagophthalmos
Nasolacrimal
disease
Chronic dacryocystitis
Systemic Immunosuppres
sion
Drugs
Diabetes
Rheumatoid Arthritis
Immunodeficiency syndromes
Nutritional Vitamin A deficiency
RISK FACTORS

6. TYPES CONTINUE
1. Bacterial keratitis
2. Fungal keratitis
3. Herpes simplex keratitis
4. Herpes zoster ophthalmicus

7. TYPES
5. Interstitial keratitis
6. Protozoan keratitis
7. Helminthic keratitis

8. 1- BACTERIAL KERATITIS

9. ORGANISMS
1. Pseudomonas aeruginosa
2. Staphylococcus aureus
3. Streptococci

10. SYMPTOMS
1. Pain,
2. Photophobia,
3. Blurred vision
4. Mucopurulent
5. Purulent discharge.

11. SIGNS CONTINUE
1. An epithelial defect with infiltrate involving a larger
area and significant circumcorneal injection
2. Scleritis
3. Endophthalmitis
4. Reduced corneal sensation

12. 5. Stromal oedema, folds in Descemet membrane and
anterior uveitis, commonly with a hypopyon and
posterior synechiae in moderate–severe keratitis.
Plaque like keratic precipitates can form on the
endothelium contiguous with the affected stroma.
SIGNS CONTINUE

13. 6. Chemosis and eyelid swelling in moderate–severe
cases.
7. Severe ulceration may lead to descemetocoele
formation and perforation, particularly in
Pseudomonas infection
SIGNS

14. Fig. 1 Bacterial keratitis. (A) Early ulcer; (B) large ulcer; (C) ulcer
with hypopyon (arrow); (D) perforation associated with
Pseudomonas infection

15. WORK UP
1. Corneal scraping.
2. Conjunctival swabs
3. Contact lens cases
4. Gram staining
5. Culture and sensitivity

16. TREATMENT CONTINUE
1. Hospital admission
2. Discontinuation of contact lens wear
3. Clear plastic eye shield
4. Topical antibiotics

17. 5. Subconjunctival antibiotics
6. Mydriatics (cyclopentolate 1%, homatropine 2% or
atropine 1%)
7. Steroids
8. Systemic antibiotics
TREATMENT

18. 2- FUNGAL KERATITIS

19. ORGANISMS
1. Yeasts(e.g. genus Candida),
2. Filamentous fungi(e.g. genera Fusariumand
Aspergillus),

20. SYMPTOMS
1. Gradual onset of pain,
2. Grittiness,
3. Photophobia,
4. Blurred vision
5. Watery or mucopurulent discharge

21. • Candida keratitis
1. Yellow–white densely suppurative infiltrate is
typical.
• Filamentous keratitis
1. Grey or yellow–white stromal infiltrate with
indistinct fluffy margins
2. Progressive infiltration, often with satellite
lesions
SIGNS CONTINUE

22. 3. Feathery branch-like extensions or a ring-shaped
infiltrate may develop. (Fig. 2C)
4. Rapid progression with necrosis and thinning can
occur.
5. Penetration of an intact Descemet membrane may
occur and lead to endophthalmitis without evident
perforation
SIGNS CONTINUE

23. • An epithelial defect is not invariable and is sometimes
small when present.
• Other features include anterior uveitis, hypopyon,
endothelial plaque, raised IOP, scleritis and sterile or
infective endophthalmitis
SIGNS

24. Fig. 2 Fungal keratitis. (A) Filamentous keratitis with fluffy edges
(arrow). There is a large epithelial defect, and folds in Descemet
membrane; (B) satellite lesions; (C) ring infiltrate, with hypopyon; (D)
candida mycology stained with calcofluor white

25. WORK UP CONTINUE
1. Staining:
• Potassium hydroxide (KOH
• Gram and Giemsa staining
• Other stains include periodic acid–Schiff, Calcoflour
white and methenamine silver

26. 2. Culture
• Sabouraud dextrose agar
• Blood agar
• Enrichment media
WORK UP CONTINUE

27. 3. Polymerase chain reaction (PCR) analysis
4. Corneal biopsy
5. Anterior chamber tap
6. Confocal microscopy
WORK UP

28. 1. General measures are as for bacterial keratitis
2. Topical antifungals
3. Broad-spectrum antibiotic
4. Cycloplegia
TREATMENT CONTINUE

29. 5. Subconjunctival antifungals
6. Systemic antifungals
7. Tetracycline
TREATMENT

30. 3- HERPES SIMPLEX KERATITIS

31. ORGANISM
• Herpes simplex virus (HSV)

32. SYMPTOMS
1. Mild–moderate discomfort,
2. Redness,
3. Photophobia,
4. Watering
5. Blurred vision.

33. 1. Reduced visual acuity.
2. Swollen opaque epithelial cells arranged in a coarse
punctate or stellate pattern.
3. The virus-laden cells at the margin of the ulcer stain
with rose Bengal
SIGNS CONTINUE

34. 4. Central desquamation results in a linear-branching
(dendritic) ulcer most frequent located centrally.
The branches of the ulcer have characteristic
terminal buds and its bed stains well with
fluorescein.
SIGNS CONTINUE

35. 5. Inadvertent topical steroid treatment may promote
progressive enlargement of the ulcer to a
geographical or ‘amoeboid’ configuration
6. Corneal sensation is reduced.
7. Mild anterior chamber activity
8. Follicular conjunctivitis
SIGNS

36. Fig. 3 Epithelial herpes simplex keratitis. (A) Stellate lesions; (B) bed
of a dendritic ulcer stained with fluorescein; (C) margins of a dendritic
ulcer stained with rose Bengal; (D) geographic ulcer corneal graft

37. WORK UP
1. Corneal scrapings can be sent in viral transport
medium for culture.
2. PCR and immunocytochemistry
3. Giemsa staining
4. HSV serological titres

38. TREATMENT CONTINUE
1. Topical antivirals
2. Debridement of corneal surface
3. Oral antiviral therapy
4. Interferon mono therapy

39. 5. Cycloplegics
6. Topical antibiotic prophylaxis
TREATMENT

40. 4- Herpes zoster ophthalmicus

41. ORGANISM
• Varicella-zoster virus (VZV)

42. SYMPTOMS
1. Mild–moderate discomfort,
2. Redness,
3. Photophobia,
4. Watering
5. Blurred vision.

43. 1. Reduced visual acuity.
2. Dendritic lesions that are smaller and finer than
herpes simplex dendrites and have tapered ends
without terminal bulbs. The lesions stain better
with rose Bengal than with fluorescein.
SIGNS CONTINUE

44. 3. Conjunctivitis(follicular and/or papillary)
4. Episcleritis
5. Scleritis
6. Anterior uveitis
7. Posterior uveitis
SIGNS

45. (Fig. ) Acute lesions in herpes zoster ophthalmicus. (A)Dendritic epithelial
lesions with tapered ends stained with fluorescein; (B) dendritic epithelial
lesions stained with rose Bengal;

46. WORK UP
1. Vesicular fluid can be sent for PCR, or
immunomicroscopy.
2. PCR of plasma for VZV DNA
3. IgM antibodies to VZV

47. TREATMENT
1. Oral antivirals
2. Intravenous antivirals
3. Systemic steroids-avoid in immunodeficiency

48. 5- INTERSTITIAL KERATITIS

49. DEFINITION
• Interstitial keratitis is an inflammation of the corneal
stroma without primary involvement of the
epithelium or endothelium.
• In most cases, the inflammation is thought to be an
immunemediated process triggered by an
appropriate antigen.
• Syphilitic interstitial keratitis is the archetype

50. CAUSES CONTINUE
1. Herpes simplex, varicella zoster and other viral
infections,
2. Tuberculosis,
3. Lyme disease
4. Parasitic diseases

51. 6. Sarcoidosis,
7. Cogan syndrome and non-infectious inflammatory
conditions
CAUSES

52. SYMPTOMS
1. Severe blurring of vision
2. Redness
3. Photophobia
4. Pain
5. Watering

53. 1. Profoundly decreased visual acuity is typical in the
active stage.
2. Limbitis associated with deep stromal
vascularization, with cellular infiltration and
clouding that may obscure the still-perfused vessels
to give the characteristic pinkish ‘salmon patch’
appearance.
SIGNS CONTINUE

54. 3. After several months the cornea begins to clear and
the vessels become non-perfused (‘ghost vessels’ –)
4. If the cornea later becomes inflamed, the vessels
may re-fill with blood and may rarely bleed into the
stroma.
SIGNS CONTINUE

55. 5. Granulomatous anterior uveitis.
6. The healed stage is characterized by ghost vessels,
feathery deep stromal scarring and sometimes
thinning, astigmatism and band keratopathy.
SIGNS

56. (Fig. ) Syphilitic interstitial keratitis. (A) Salmon patch showing deep
stromal vascularization with clouding (arrow); (B) ghost vessels; (C)
Intrastromal corneal haemorrhage from reperfused vessels; (D) typical
feathery scarring – the tracks of ghost vessels are clearly seen

57. WORK UP
1. White cell count
2. Erythrocyte sedimentation rate (ESR)
3. C-reactive protein (CRP)

58. TREATMENT
1. Topical steroids
2. Cycloplegics,
3. Systemic steroids

59. 6- PROTOZOAN KERATITIS

60. ORGANISM
1. Acanthamoeba spp.
• The cystic form (Figure) is highly resilient.

61. SYMPTOMS
1. Blurred vision
2. Discomfort
3. Pain is often severe and characteristically
disproportionate to the clinical signs.

62. 1. In early disease the epithelial surface is irregular
and greyish
2. Epithelial pseudodendrites resembling herpetic
lesions may form.
3. Limbitis with diffuse or focal anterior stromal
infiltrates
SIGNS CONTINUE

63. 4. Characteristic perineural infiltrates (radial
keratoneuritis) are seen during the first few weeks
and are virtually pathognomonic
5. Gradual enlargement and coalescence of infiltrates
to form a ring abscess is typical.
SIGNS CONTINUE

64. 6. Scleritis
7. Slowly progressive stromal opacification and
vascularization.
8. Corneal melting
SIGNS

65. Fig. . Initial signs of acanthamoeba keratitis. (A) Cysts in a corneal biopsy;
(B) greyish early epithelial involvement; (C) focal anterior stromal
infiltrates; (D) radial perineuritis (arrows)

66. Fig. Advanced acanthamoeba keratitis. (A)
Progression of infiltration, with incipient formation
of a ring abscess and early melting; (B) ring abscess;
(C) melting

67. 1. Staining of corneal scrapings: periodic acid–Schiff,
calcofluor white, Gram and Giemsa stains
2. Culture: Non-nutrient agar seeded with dead E. coli
WORK UP Continue

68. 3. Other investigations: Immunohistochemistry, PCR
and in vivo confocal microscopy. Corneal biopsy
may be necessary for diagnosis.
WORK UP

69. TREATMENT
1. Debridement of involved epithelium
2. Topical amoebicides.
3. Topical steroids-should be delayed for atleast two
weeks after starting antiamoebic treatment.

70. 7- HELMINTHIC KERATITIS

71. ORGANISM
• Onchocerca volvulus

72. SYMPTOMS
1. Blurring of vision
2. Redness
3. Photophobia
4. Pain
5. Watering

73. 1. Reduced visual acuity
2. Punctate keratitis (snowflake opacities): infiltrates
surrounding dead microfilariae
3. Slowly progressing sclerosing keratitis may
eventually involve the entire cornea.
SIGNS CONTINUE

74. 4. Anterior uveitis
5. Chorioretinitis
6. Optic neuritis
SIGNS

75. Fig. Ocular onchocerciasis. (A) Advanced corneal scarring;
(B) Intraretinal pigment clumping and RPE atrophy;
(C) Choroidal pigment clumping and chorioretinal atrophy

76. WORK UP
1. Skin-snip biopsy
2. Serology
3. Tear or urine antigen detection (oncho-dipstick)
4. PCR of lesion fluid.

77. TREATMENT
1. Ivermectin
2. Moxidectin
3. Doxycycline
4. Suramin
5. Steroids

78. COMPLICATIONS continue
1. Persistent epithelial defect: If persists for >2wk,
then consider switching to non preserved
preparations of topical medication (if not already
pres-free), reducing frequency of topical
medication, adding ocular lubrication, and assisting
lid closure (medical or surgical tarsorrhaphy).

79. 2. Resistant or progressive keratitis: Seek
specialist advice. In threatened scleral
extension, consider oral ciprofloxacin which
has high bioavailability at the limbus.
COMPLICATIONS continue

80. 3. In threatened corneal perforation: Consider
oral ciprofloxacin, therapeutic contact lens
(cyanoacrylate glue), or emergency
penetrating keratoplasty(PK)- after a
minimum of 2d intensive treatment.
COMPLICATIONS continue

81. 4. Scleritis: consider immunosuppression with
systemic steroids and a steroid-sparing agent such
as ciclosporin.
5. Endophthalmitis: Perform diagnostic vitrectomy,
and administer intravitreal antibiotics.
COMPLICATIONS continue

82. 6. Cataract secondary to inflammation or prolonged
steroid use.
7. Glaucoma secondary to inflammation or chronic
steroid use.
COMPLICATIONS continue

83. 8. Secondary infection. Herpetic eye disease is a
major predisposing factor for microbial keratitis.
9. Corneal scarring: consider PK once treatment is
completed and cornea is sterile.
COMPLICATIONS continue

84. 10. Extensive necrosis: consider emergency PK. Note
high risk of persistent or recurrent disease in
grafted tissue.
11. Intractable pain: patients may occasionally require
enucleation for severe pain.
12. Iris atrophy secondary to kerato-uveitis
COMPLICATIONS

85. THANK YOU