corneal ulcer (ulcerative keratitis).pptx

corneal ulcer (ulcerative keratitis) reasearch and awarness ppt opthalomology morden mbbs

1. ULCERATIVE KERATITIS

2. 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.

3. INFECTIVE KERATITIS BACTERIAL CORNEAL ULCER Being the most anterior part of eyeball, the cornea is exposed to atmosphere and hence prone to get infected easily. At the same time cornea is protected from the day-to-day minor infections by the normal defence mechanisms present in tears in the form of lysozyme , betalysin , and other protective proteins.

4. Therefore, infective corneal ulcer may develop when: either the local ocular defence mechanism is jeopardised, or there is some local ocular predisposing disease, or host's immunity is compromised, or the causative organism is very virulent.

5. Etiology There are two main factors in the production of purulent corneal ulcer: - Damage to corneal epithelium; and - Infection of the eroded area.

6. following three pathogens below three Invade the intact corneal epithelium and produce ulceration: Neisseria gonorrhoeae , Corynebacterium diphtheriae and Neisseria meningitidis .

7. 1. Corneal epithelial damage. It is a prerequisite for most of the infecting organisms to produce corneal ulceration. It may occur in following conditions: i . Corneal abrasion- small foreign body, misdirected cilia ii. Epithelial drying as in xerosis

8. 2. Source of infection include: i . Exogenous infection. Most of the times corneal infection arises from exogenous source like conjunctival sac, lacrimal sac ( dacryocystitis ), infected foreign bodies etc.

9. 2. Source of infection include: ii. From the ocular tissue- Owing to direct 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.

10. Pathogenesis and pathology of corneal ulcer 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, viz., infiltration, active ulceration, regression and cicatrization .

11. The terminal course of corneal ulcer depends upon the virulence of infecting agent, Host defence mechanism and the treatment received.

12. Depending upon the prevalent circumstances the course of corneal ulcer may take one of the three forms: (A) Ulcer may become localised and heal; (B) Penetrate deep leading to corneal perforation; or (C) Spread fast in the whole cornea as sloughing corneal ulcer.

13. Pathology 1. Stage of progressive infiltration 2. Stage of active ulceration 3. Stage of regression 4. Stage of cicatrization

14. 1. Stage of progressive infiltration necrosis of the involved tissue may occur, depending upon the virulence of offending agent and the strength of host defence mechanism.

15. 2. Stage of active ulceration Active ulceration results from necrosis and sloughing of the epithelium, Bowman's membrane and the stroma .

16. 3. Stage of regression Regression is induced by the natural host defence mechanisms ( humoral antibody production and cellular immune defences) and the treatment. A line of demarcation develops around the ulcer.

17. 4. Stage of cicatrization In this stage healing continues by progressive epithelization which forms a permanent covering. The degree of scarring from healing varies. If the ulcer is very superficial and involves the epithelium only, it heals without leaving any opacity behind. When ulcer involves Bowman's membrane and few superficial stromal lamellae- resulting in scar

18. Stage of cicatrization

19. Clinical picture In bacterial infections the outcome depends upon the virulence of organism, its toxins and enzymes, and the response of host tissue.

20. Broadly bacterial corneal ulcers may manifest as: i . Purulent corneal ulcer without hypopyon ; or ii. Hypopyon corneal ulcer.

21. 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 .

22. Symptoms 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.

23. Signs 1. Lids are swollen. 2. Marked blepharospasm may be there. 3. Conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion.

24. Signs 4. Corneal ulcer usually starts as an epithelial defect associated with greyish -white circumscribed infiltrate (seen in early stage). Soon the epithelial defect and infiltrate enlarges and stromal oedema develops. A well established bacterial ulcer is characterized by

25. Yellowish-white area of ulcer which may be oval or irregular in shape. Margins of the ulcer are swollen and over hanging. Floor of the ulcer is covered by necrotic material. Stromal oedema is present surrounding the ulcer area.

26. Bacterial corneal ulcer without hypopyon

27. Characteristic features Characteristic features produced by some of the causative bacteria are as follows: Staphylococal aureus and streptococcus pneumoniae usually produce an oval, yellowish white densely opaque ulcer which is surrounded by relatively clear cornea.

28. Pseudomonas species usually produce an irregular sharp ulcer with thick greenish mucopurulent exudate , diffuse liquefactive necrosis and semiopaque (ground glass) surrounding cornea. Such ulcers spread very rapidly and may even perforate within 48 to 72 hours.

29. Enterobacteriae (E. coli, Proteus sp., and Klebsiella sp.) usually produce a shallow ulcer with greyish white pleomorphic suppuration and diffuse stromal opalescence. The endotoxins produced by these Gram – ve bacilli may produce ring-shaped corneal infilterate .

30. 5. Anterior chamber may or may not show pus ( hypopyon ). In bacterial corneal ulcers the hypopyon remains sterile so long as the Descemet's membrane is intact. 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 (inflammatory glaucoma).

31. Hypopyon corneal ulcer Etiopathogenesis Causative organisms . Many pyogenic organisms (staphylococci, streptococci, gonococci, Moraxella ) may produce hypopyon , but by far the most dangerous are pseudomonas pyocyanea and pneumococcus .

32. Source of infection Source of infection for pneumococcal infection is usually the chronic dacryocystitis .

33. Factors predisposing to development of hypopyon Two main factors which predispose to development of hypopyon in a paitent with corneal ulcer are, The virulence of the infecting organism and The resistance of the tissues .

34. Mechanism of development of hypopyon . Corneal ulcer is often associated with some iritis owing to diffusion of bacterial toxins. When the iritis is severe the outpouring of leucocytes from the vessels is so great that these cells gravitate to the bottom of the anterior chamber to form a hypopyon .

35. Mechanism of development of hypopyon . Thus, it is important to note that the hypopyon is sterile since the outpouring of polymorphonuclear cells is due to the toxins and not due to actual invasion by bacteria. Once the ulcerative process is controlled, the hypopyon is absorbed.

36. Clinical features Symptoms are the same as described above for bacterial corneal ulcer. However , it is important to note that during initial stage of ulcus serpens there is remarkably little pain.

37. Signs. In general the signs are same as described above for the bacterial ulcer. Typical features of ulcus serpens are: Ulcus serpens is a greyish white or yellowish disc shaped ulcer occuring near the centre of cornea).

38. Violent iridocyclitis is commonly associated with a definite hypopyon . Hypopyon increases in size very rapidly and often results in secondary glaucoma. Ulcer spreads rapidly and has a great tendency for early perforation.

39. Hypopyon corneal ulcer : A, Diagrammatic

40. Hypopyon corneal ulcer : B, Clinical photograph

41. Management Management of hypopyon corneal ulcer is same as for other bacterial corneal ulcer.

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

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

44. [A] Clinical evaluation 1. Thorough history taking 2. General physical examination, 3. Ocular examination

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

46. [A] Clinical evaluation 1. Thorough history taking to elicit mode of onset, duration of disease and severity of symptoms. 2. General physical examination, especially for built, nourishment, anaemia and an immunocompromising disease.

47. Biomicroscopic examination after staining corneal ulcer with 2 per cent freshly prepared aqueous solution of fluorescein dye or sterilised fluorescein strip to note site, size, shape, depth, margin, floor and vascularization of corneal ulcer.

48. [B] Laboratory investigations (a) Routine laboratory investigations such as haemoglobin , TLC, DLC, ESR, blood sugar, complete urine and stool examination should be carried out in each case.

49. (b) Microbiological investigations. These studies are essential to identify causative organism, confirm the diagnosis and guide the treatment to be instituted. Material for such investigations is obtained by scraping the base and margins of the corneal ulcer (under local anaesthesia , using 2 percent xylocaine ) with the help of a modified Kimura spatula

50. [C] Treatment I. Treatment of uncomplicated corneal ulcer Bacterial corneal ulcer is a vision threatening condition and demands urgent treatment by identification and eradication of causative bacteria.

51. [C] Treatment Treatment of corneal ulcer can be discussed under three headings: 1. Specific treatment for the cause. 2. Non-specific supportive therapy. 3. Physical and general measures.

52. 1. The specific treatment (a) Topical antibiotics. Initial therapy (before results of culture and sensitivity are available) should be with combination therapy to cover both gram-negative and gram-positive organisms.

53. It is preferable to start fortified gentamycin (14 mg/ml) or tobramycin (14mg/ml) eyedrops along with cephazoline (50mg/ ml), every ½ to one hour for first few days and then reduced to 2 hourly. Once the favourable response is obtained, the drops can be substituted by more diluted commercially available eye-drops, e.g. : Ciprofloxacin (0.3%) eye drops, or Ofloxacin (0.3%) eye drops, or Gatifloxacin (0.3%) eye drops.

54. (b) Systaemic antibiotics are usually not required.

55. 2. Non-specific treatment (a) Cycloplegic drugs. Preferably 1 percent atropine eye ointment or drops should be used to reduce pain from ciliary spasm

56. (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.

57. 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.