Corneal ulcer

CORNEAL ULCER BY DNYANESHWAR BHAGWAN POTFODE

1. Corneal ulcer DNYANESHWAR B. POTFODE OPHTHALMIC OFFICER

2. Corneal anatomy

3. Corneal layer Epithelium Bowmens membrane Stroma Descement memebrane Endothelium

4. Corneal layer

5. Infective condition of cornea 1. Infective keratitis (a) Bacterial (b) Viral (c) Fungal (d) Chlamydia (e) Protozoa (f) Spirochete

6. Corneal ulcer Corneal ulcer may be defined as discontinuation in normal epithelial surface of cornea associated with necrosis of the surrounding corneal tissue. Pathologically it is characterised by oedema and cellular infiltration

7. INFECTIVE KERATITIS BACTERIAL CORNEAL ULCER the cornea is exposed to atmosphere and hence prone to get infected easily C ornea is protected from the minor infections by the normal defence mechanisms present in tears lysozyme , betalysin , and other protective proteins.

8. Corneal ulcer either the local ocular defence mechanism is jeopardized. there is some local ocular predisposing disease. H ost's immunity is compromised . The causative organism is very virulent.

9. Etiology Damage to corneal epithelium . Infection of the eroded area. Neisseria gonorrhoeae , Corynebacterium diphtheriae Neisseria meningitidis .

10. 1. Corneal epithelial damage Corneal abrasion due to small foreign body, misdirected cilia, concretions and trivial trauma in contact lens wearers or otherwise. Epithelial drying as in xerosis and exposure keratitis . Necrosis of epithelium as in keratomalacia . Desquamation of epithelial cells as a result of corneal oedema as in bullous keratopathy . Epithelial damage due to trophic changes as in neuroparalytic keratitis .

11. corneal abrasion A corneal abrasion (scratched cornea or scratched eye ) is one of the most common  eye injuries. A scratched  cornea often causes significant discomfort, red eyes and hypersensitivity to light. Corneal abrasions result from a disruption or loss of cells in the top layer of the cornea, called the corneal epithelium.

12. Corneal abrasion

13. 2. Source of infection include i . Exogenous infection . ii. From the ocular tissue . iii. Endogenous infection .

14. Exogenous infection. Most of the times corneal infection arises from Exogenous source like C onjunctival sac , L acrimal sac ( dacryocystitis ), Infected foreign bodies, I nfected vegetative Material W ater-borne A ir-borne infections.

15. Infected foreign bodies

16. D acryocystitis

17. From the ocular tissue. Anatomical continuity, diseases of the conjunctiva readily spread to corneal epithelium, those of sclera to stroma , and of the uveal tract to the endothelium of cornea.

18. Endogenous infection . Avascular nature of the cornea, endogenous infections are of rare occurrence.

19. 3. Causative organisms Common bacteria associated with corneal ulceration are : Staphylococcus aureus , Pseudomonas pyocyanea , S treptococcus Pneumoniae , E . coli, Proteus , Klebsiella , N. gonorrhoea , N . meningitidis C . diphtheriae .

20. Pathogenesis Once the damaged corneal epithelium is invaded by the offending agents the sequence of pathological changes which occur during development of corneal ulcer can be described under four stages - infiltration, active ulceration, regression and cicatrization . The terminal course of corneal ulcer depends upon the virulence of infecting agent, host defence mechanism and the treatment received

21. Pathogenesis

22. Clinical picture In bacterial infections the outcome depends upon the virulence of organism, its toxins and enzymes, and the response of host tissue. Broadly bacterial corneal ulcers may manifest as: i . Purulent corneal ulcer without hypopyon ; or ii. Hypopyon corneal ulcer.

23. Hypopyon corneal ulcer

24. Symptoms 1. Pain and foreign body sensation occurs due to mechanical effects of lids and chemical effects of toxins on the exposed nerve endings. 2. Watering from the eye occurs due to reflex hyperlacrimation . 3. Photophobia , i.e., intolerance to light results from stimulation of nerve endings. 4. Blurred vision results from corneal haze. 5. Redness of eyes occurs due to congestion of circumcorneal vessels.

25. Signs 1. Lids are swollen . 2. Marked blepharospasm 3. Conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion . 4. Corneal ulcer 5. Anterior chamber may or may not show pus ( hypopyon ). 6. Iris may be slightly muddy in colour 7. Pupil may be small due to associated toxin induced iritis . 8. Intraocular pressure may some times be raised

26. Hypopyon - pus in anterior chamber

27. Chemosis

28. Management Management of hypopyon corneal ulcer is same as for other bacterial corneal ulcer. Special points which need to be considered are : Secondary glaucoma should be anticipated and treated with 0.5% timolol maleate , B.I.D. eye drops and oral acetazolamide . Source of infection, i.e., chronic dacryocystitis if detected , should be treated by dacryocystectomy

29. Complications of corneal ulcer 1. Toxic iridocyclitis . 2. Secondary glaucoma . 3. Descemetocele . 4. Perforation of corneal ulcer 5. Corneal scarring.

30. 1. Toxic iridocyclitis . It is usually associated with cases of purulent corneal ulcer due to absorption of toxins in the anterior chamber.

31. 2. Secondary glaucoma. It occurs due to fibrinous exudates blocking the angle of anterior chamber (inflammatory glaucoma).

32. 3. Descemetocele . Some ulcers caused by virulent organisms extend rapidly up to Descemet's membrane, which gives a great resistance, but due to the effect of intraocular pressure it herniates as a transparent vesicle called the descemetocele or keratocele .

33. 4. Perforation of corneal ulcer Sudden strain due to cough, sneeze or spasm of orbicularis muscle may convert impending perforation into actual perforation

34. 5. Corneal scarring. It is the usual end result of healed corneal ulcer. Corneal scarring leads to permanent visual impairment ranging from slight blurring to total blindness. Depending upon the clinical course of ulcer, corneal scar noted may be nebula , macula, leucoma , ectatic cicatrix or kerectasia , adherent leucoma or anterior staphyloma .

35. Management of a case of corneal ulcer [ A] Clinical evaluation [B] Laboratory investigations [C] Treatment

36. [A] Clinical evaluation 1. Thorough history taking to elicit mode of onset , 2. General physical examination N ourishment Anaemia I mmunocompromising disease . 3. Ocular examination i . Diffuse light examination ii. Regurgitation test and syringing iii. Biomicroscopic examination

37. [B] Laboratory investigations ( a) Routine laboratory investigations (b) Microbiological investigations.

38. Routine laboratory investigations hemoglobin, TLC , DLC , ESR, blood sugar, Complete urine and stool examination

39. Microbiological investigations. 1. Gram and Giemsa stained smears for possible identification of infecting organisms . ii. 10 per cent KOH wet preparation for identification of fungal hyphae . iii. Calcofluor white (CFW) stain preparation is viewed under fluorescence microscope for fungal filaments, the walls of which appear bright apple green . iv. Culture on blood agar medium for aerobic organisms . v. Culture on Sabouraud's dextrose agar medium for fungi.

40. [C] Treatment I. Treatment of uncomplicated corneal ulcer II . Treatment of non-healing corneal ulcer of uncomplicated corneal ulcer III. Treatment of impending perforation IV. Treatment of perforated corneal ulcer

41. I. Treatment of uncomplicated corneal ulcer 1 . Specific treatment for the cause . 2. Non-specific supportive therapy . 3. Physical and general measures.

42. 1. Specific treatment for the cause. Topical antibiotics . Initial therapy should be with combination therapy to cover both gram-negative and gram-positive organisms. Ciprofloxacin (0.3%) eye drops, or Ofloxacin (0.3%) eye drops, or Gatifloxacin (0.3%) eye drops . Systemic antibiotics are usually not required. However , a cephalosporine and an aminoglycoside or oral ciprofloxacin may be given in perforation and when sclera is involved .

43. Topical antibiotic

44. 2. Non-specific supportive therapy. (a) Cycloplegic drugs 1 percent atropine eye ointment or drops should be used to reduce pain from ciliary spasm and to prevent the formation of posterior synechiae from secondary iridocyclitis . (b) Systemic analgesics and anti-inflammatory drugs such as paracetamol and ibuprofen relieve the pain and decrease oedema (c) Vitamins (A, B-complex and C) help in early healing of ulcer.

45. 3. Physical and general measures. (a) Hot fomentation . Local application of heat (preferably dry) gives comfort, reduces pain and causes vasodilatation. (b) Dark goggles may be used to prevent photophobia . (c) Rest, good diet and fresh air may have a soothing effect.

46. Hot formentation

47. II. Treatment of non-healing corneal ulcerof uncomplicated corneal ulcer 1. Removal of any known cause of non-healing ulcer. i . Local causes . Ii . Systemic causes : 2. Mechanical debridement of ulcer 3. Cauterisation of the ulcer 4. Bandage soft contact lens 5. Peritomy

48. Peritomy of conjunctiva

49. III. Treatment of impending perforation 1. No strain . 2. Pressure bandage 3. Lowering of intraocular pressure 4. Tissue adhesive glue such as cynoacrylate 5. Conjunctival flap . 6. Bandage soft contact lens 7. Penetrating therapeutic keratoplasty

50. Bandage soft contact lens

51. Treatment of perforated corneal ulcer Best is to prevent perforation. However, if perforation has occurred, immediate measures should be taken to restore the integrity of perforated cornea. Depending upon the size of perforation and availability , measures like use of tissue adhesive glues, covering with conjunctival flap, use of bandage soft contact lens or therapeutic keratoplasty should be undertaken . Best is an urgent therapeutic keratoplasty .

52. keratoplasty

53. Fungal corneal ulcer

54. VIRAL CORNEAL ULCERS HERPES SIMPLEX KERATITIS Ocular infections with herpes simplex virus (HSV) are extremely common and constitute herpetic keratoconjunctivitis and iritis .

55. Herpes zoster ophthalmicus .