Bacterial corneal ulcer DrBP

1. Bacterial Corneal Ulcer.. Dr. Bhushan Patil .

2. Defination A loss of epithelium with inflammation in the sorrounding cornea is called as corneal ulcer. Host cellular and immunologic responses to offending agent which may be bacterial,viral,fungal or protozoal organisms leads to formation of ulcer. Sight threatening condition and should be considered as ocular emergency.

3. Normal defence mechanism Corneal epithelium- mechanical barrier Conjunctiva- cellular & chemical components Tear film- biological protective system Major components of ocular defence system

4. Barriers of microbial infection

5. Predisposing factors Ocular 1. Trauma- -breach in corneal epithelium -inoculation of organism 2.Eyelid & adnexal diseases- - blepharitis , ectropion , entropion , trichiasis , lagophthalmos , chronic dacryocystitis Disturbed Tear film Recurrent epithelial erosions

6. 3. Ocular surface disorder- - Dry eye, Steven-Johnson syndrome, ocular burn, bullous keratopathy . 4. Contact lens use- -Increased risk of bacterial keratitis with use of Extended soft contact lens corneal hypoxia & decompensation . - Contamination of CL solution. 5 . Local immune suppression due to topical corticosteroids . 6.Ocular surgery- cataract , LASIK.

7. Systemic factors 1.Malnutrition 2.Diabetes 3.Immunosupression-Systemic steroids, AIDS 4.Chronic alcoholism

8. Aetiology of Bacterial ulcer Caused by organisms which produce toxins causing tissue death i.e. necrosis characterized by pus formation. Such purulent keratitis is usually exogenous due to infection by pyogenic bacteria such as pseudomonas, staphylococcus,streptococcus , N. gonorrhoeae and C. diphtheriae

9. Aetiology of Bacterial ulcer Most of the bacteria are capable of producing corneal ulcer only when the epithelium is damaged N Gonorrhoeae , C Diphtheriae , Hemophilus , Shigella and Listeria Monocytogenes – can penetrate intact corneal epithelium.

10. ORGANISM SPECIES BACTERIOLOGY Staphylococcus S.Aureus S.Epidermidis Gram positive cocci 1.Most common organism 2.Eyelid diseases 3.Dry eye, bullous keratopathy , atopic disease. Streptococcus S.Pneumoniae S. Viridans Gram positive cocci chronic Dacryocystitis . Corneal grafts . Pseudomonas P. Aeruginosa Gram negative bacilli 1.Contact Lens users 2.Comatose pt. 3.Pt on mechanical ventillator 4.HIV Moraxella M.Lacunata Gram negative diplobacilli Malnourished, alcoholics , diabetes Nocardia,Actinomycets Gram positive bacilli Ocular trauma contaminated by soil Atypical Mycobacteria M. Chelonae Acid fast bacilli Following LASIK

11. PATHOGENESIS Corneal abrasion  Microbes adhere to epithelium, release toxins & lytic enzymes Host response PMNs at the site of ulcer from tears & limbal vessels  release of cytokines & interleukins  progressive invasion of cornea & increase in size of ulcer Phagocytosis Release of free radicals,proteolytic enymes  Necrosis & sloughing of epithelium, Bowman’s membrane & stroma A saucer shaped defect with projecting walls above the normal surface due to swelling of tissue resulting from fluid imbibition by corneal stroma with grey zone of infiltration

12. Stage of progressive infiltration Entry and adherance of organism to breached epithelium  enters into stroma. PMNs and lymphocytes infiltrate into stroma and epithelium. Infective organism multiplies  release toxins and enzymes.

13. Stage of active ulceration Necrosis occurs due to toxins and enzymes released by infective organism. Sloughing of epithelium and stroma  ulcer. Ulcer Borders thickening due to infiltrates and edema. It is associated with iritis due to diffusion of toxins of infecting bacteria into AC.

14. Sometimes iridocyclitis is so severe that it is accompanied by outpouring of leucocytes from uveal blood vessels and these cells gravitate to bottom of the AC to form hypopyon (sterile).

15. Stage of regression Natural host defence & antimicrobial treatment Line of demarcation forms around ulcer which contains leucocytes which phagocytose the organism & necrotic debris Necrotic material fall off- ulcer becomes larger -> infiltration and swelling reduce and disappears -> margin & floor becomes smooth. Vascularization develops from limbus to corneal ulcer to restore lost tissue and to supply antibodies.

16. Stage of Healing Vascularization is followed by cicatrization due to regeneration of collagen and formation of fibrous tissue Newly formed fibers are laid down irregularly, not conforming to normal pattern of stromal fibers. Therefore this fibrous tissue refracts light irregularly and forms opacity.

17. Clinical features Clinical signs and symptoms are variable depends on the virulence of the organism duration of infection, pre-existing corneal conditions immune status of host previous use of local steroids

18. Presentation 1. Diminution of vision, depending on location of corneal ulcer 2. Watering due to reflex lacrimation 3. Photophobia 4. Pain due to exposed nerve endings 5. Mucopurulent / purulent discharge

19. Work-up Evaluation of predisposing and aggravating Factors A detailed history. Prior ocular history Review of related medical problems, current ocular medications and history of systemic steroids.

20. Ocular examination 1.Visual acuity-reduced 2.Slit lamp Biomicroscope Lids - edema Conjunctiva – Ciliary congestion

21. Cornea -Location of the ulcer- central, paracentral , peripheral,total . -Size , shape, depth, margins & floor- depends on stage of ulcer. -Density and extent of stromal infiltration. Anterior chamber - Cells/flare, mobile Hypopyon .

22. Iris- muddy Toxin induced iritis Pupil – miotic Other: -Sac syringing -corneal sensation -Fluorescein staining

23. Grading of corneal ulcer Features Mild Moderate Severe Size <2mm 2-5mm >5mm Depth of ulcer <20% 20-50% >50% Stromal infiltrate 1.Density 2.Extent Dense Superficial Dense Upto mid- stroma Dense Deep stromal Scleral involvement present Harrison SM. Grading corneal ulcers. Ann Ophthalmol 1975;7:537-9, 541-2.

24. Special features 1.Staphylococcal Central,oval , opaque Distinct margins. Mild oedema of remaining cornea. Stromal abscess in longstanding cases. Mild to moderate AC reaction. Affects compromised corneas e.g. Bullous keratopathy , dry eyes , atopic diseases.

25. 2.Pneumococcal Ulcer serpens is greyish white or yellowish disc shaped ulcer occuring near center of cornea. starts at periphery & spreads towards centre Tendency to creep over the cornea in serpiginous fashion- Ulcus Serpen . Violent iridocyclitis is often associated with it. Hypopyon – always present It has great tendency for PERFORATION.

26. BACTERIAL ULCER WITH HYPOPYON HYPOPYON.

27. 3. Pseudomonas Rapidly spreading. Extends periphery & deep within 24 hrs. Stromal necrosis with shaggy surface Spreads concentrically and symmetrically to involve whole depth of cornea-Ring ulcer. Greenish-yellow discharge. Hypopyon is present. Untreated  corneal melting.

28. 4. Streptococcus viridans Infectious crystalline keratopathy type of stromal keratitis . Crystalline arborifoem (needle like) white opacities in stroma , not associated with infiltration & ocular inflammation Due to proliferation of bacteria between the stromal lamellae. Seen in following corneal grafts , prolonged use of topical steroid.

29. Complications of corneal ulcer Spread of ulcer horizontally and depth-wise, leading to thinning of cornea 2. Descemetocele – This appears as transparent vesicle surrounded by grayish zone of infiltration. It represents condition of impending perforation of cornea

30. 3. Perforation of ulcer – sudden exertion such as coughing, sneezing, straining at stool or firm closure of eyes  increase in intra-ocular pressure (IOP)  perforation a) Peripheral perforation - iris prolapse through opening. Exudation takes place on prolapsed tissue -> an adherent leucoma .

31. b) Central perforation  anterior chamber collapse  lens comes in contact with corneal endothelial surface  anterior capsular cataract  repeated healing and perforation leading to corneal fistula formation c) Sloughing of whole cornea: prolapse of iris  pupillary block and exudation on iris  pseudocornea  anterior synechiae  angle of anterior chamber is occluded leading to secondary glaucoma  anterior staphyloma .

32. d) Intra-ocular purulent infection: due to perforation bacteria enter in the eye and causes endophthalmitis / panophthalmitis

33. Investigations Routine – Hemogram BSL HIV Specific – Corneal scraping Gram stain, Culture & Antibiotic sensitivity Culture of contact lens & solution

34. Treatment of uncomplicated ulcer Hospitalization Treat the underlying cause/predisposing factor LOCAL TREATMENT Control of infection with appropriate antibiotic(s) a. based on clinical judgment b. based on finding of smear examination c. based on culture and sensitivity report

35. Combination therapy with fortified broad spectrum antibiotics 1. Cephalosporin – gram positive cocci & some gram negative rods Cefazolin 50mg/ml OR Ceftazidime 50mg/ml 2. Aminoglycoside - gram negative bacilli Tobramycin 14mg/ml OR Fluoroquinolone – broad spectrum-gram negative + gram positive Moxiflox 5mg/ml Topically every 30-60 min initially In severe cases- every 5 min for 30 min as a loading dose.

36. Vancomycin - reserved for very severe or recalcitrant infections (50mg/ml) Amikacin (10-20mg/ml) for AF-bacilli Fluoroquinolone monotherapy – 4 th generation < 3mm in diameter, peripheral & not associated with thinning

37. Systemic Antibiotics-Fluoroquinolone Indications Severe keratitis Scleral involvement hypopyon Impending perforation Frank perforation with risk of intraocular spread Infection in children P.aeruginosa infection

38. Adjuvant therapy 1.Cycloplegic : Atropine 1% or cyclopentolate 1% or Homatropine 2%- prevents ciliary spasm, relieves pain, breaks adhesions and prevent synechia formation. 2.Analgesic anti-inflammatory 3. Oral vitamin C 4. Acetazolamide Tab - impending perforation or perforated corneal ulcer and in cases where there is raised intra-ocular tension .

39. Straining should be avoided. Pressure bandage Lowering of IOP Tissue adhesive glue ( cynoacrylate ) Conjunctival flap Soft contact lens Bandage Penetrating keratoplasty Treatment of impending perforation

40. Treatment of non healing ulcer Removal of any known cause. ->LOCAL ->SYSTEMIC Mechanical debridement of ulcer. Cauterisation of ulcer. Bandage soft contact lens.

41. Treatment of perforated corneal ulcer Tissue adhesives Conjunctival flap Soft bandage Keratoplasty

42. Modification of initial antimicrobial therapy: -Should be based on clinical response not on culture sensitivity If pt is responding  no change in initial treatment If pt is not responding/ worsening drugs are changed according to antimicrobial sensitivity

43. Signs of healing : -resolution of lid edema , congestion -decreased density of stromal infiltrate -reduction of corneal oedema -reduction in AC reaction/ hypopyon -re- epithelization -corneal vascularization Antibiotic frequency-tapered to 4hrly after 72 hrs

44. Signs of non-response Increase in infiltration, epithelial defect, height of hypopyon , Corneal thinning, perforation Treatment Re-evaluate for Drug toxicity Non-infectious causes or Unusual organisms Modification of anti-microbial therapy according to antimicrobial sensitivity Scraping of ulcer floor followed by cauterization with pure (100%) carbolic acid or 10-20% trichloracetic acid. Therapeutic keratoplasty

45. Topical corticosteroids Controversial in bacterial keratitis The rationale for using steroids - to decrease tissue destruction. Criteria for topical steroids in ulcer -- 1.Must not be used in presence of active infected corneal ulcer 2.If bacteria shows in-vitro sensitivity to the antibiotic being used 3.Patients compliance for follow-up 4. No other virulent organism is found Monitor pt at 24 & 48 hrs after initiation

46. Surgical treatment 1.Tissue adhesives Cyanoacrylate glue- small perforations< 3mm - descemetocele

47. 2. P atch graft -perforation – 5mm in diameter 3 . Therapeutic keratoplasty -large areas of perforation, necrosis -Non-healing ulcer

48. Thank you..