Download to read offline
Corneal Ulcer (bacterial, fungal, acanthamoeba).pptx
- 1. CORNEAL ULCER Moderator :Dr Rajesh R Nayak Presenter : Dr Sriraj Alapati
- 3.
- 4. SOURCE • Exogenous • Endogenous: immunological Phlyctenular - TB IK – Syphilis • Contiguous: Conjunctiva – trachoma, VKH Sclera – sclerosing scleritis Uveal – HSV endothelitis STAGES 1. Progressive : infiltrates 2. Active : ulceration 3. Regressive : resolution of infiltrates 4. Cicatrizing : scarring LOCATION • Superficial • Deep • Impending perforation • Perforation ETIOLOGY Infection, immune, degenerative, neoplastic, traumatic PATHOLOGY • Suppurative (purulent) – bacteria, fungi • Non Suppurative (non purulent) – virus, parasitic
- 5. Rapidly Progressive SuppurativeInfiltrate • Bacteria: S. aureus S. pneumoniae Pseudomonas N. Gonorrhoea • Viral • Mixed Infection Slowly Progressive Localized Infiltrate • Bacteria: S. epidermidis Alpha hemolytic Streptococci Actinomycetales Moraxella ATM • Fungi • Protozoa Clinical Evaluation
- 6.
- 7. Penetrate intact epithelium: oNeisseria o Corynebacterium diptheria o H. influenzae o Shigella o Listeria Etiology Gram positive cocci: • Staphylococci (MC) • Streptococci Gram negative cocci: • Neisseria Gram positive bacilli: • Actinomyces • Corynebacterium • Listeria Gram negative bacilli: • Pseudomonas • E.coli
- 8. •Trauma •Contact lens (PSEUDOMONAS) •Loosesutures •Steroids •Dry eye •Misdirected cilia •Lagophthalmos •Dacrocystitis •Recurrent epithelial erosions Predisposing Factors Disruption of integrity of corneal epithelium
- 9. Symptoms: • Pain • Redness •Photophobia • Blurred vision • Mucopurulent discharge Signs: • Eyelid swelling • Chemosis • Epithelial defect with infiltrate • Circumcorneal injection • Stromal oedema • DM folds • Hypopyon (STERILE & MOBILE) • Posterior synechiae Clinical features
- 10. Organism specific features Grampositive cocci: (staph, strepococci) Well defined margins Localized, deep penetration Gram negative bacilli: (pseudomonas) Ill defined margins due to more tissue destruction (Exotoxins)
- 11. ULCUS SERPANS S.Pneumococcus One edge - infiltration , other – cicatrization Healing at leading edge, progress at advancing edge
- 12. • Needle-like, crystalline opacities,arborizing without cellular infiltrate or ocular inflammation. • Corneal grafts, contact lens wear, topical anesthetic, steroids abuse. • Streptococci viridans Infectious crystalline keratopathy (ICK)
- 13. Gram negative cocci: (N.goncocci) Rapidly progressive Corneal melting <24 hrs STD Systemic treatment Moraxella: Steroids Mild reaction Well defind lesion
- 14. Nocardia: Beaded, branching, slender, AFB, filamentousbacteria. Multiple calcareous elevations Wreath ulcer (ring)/ cracked wind shield app. Rx : AG’s
- 15. NTM: (M. chelonae) Aerobic, nonmotile, AFB, non - sporing bacteria. Sx, trauma, keratoplasty Cracked wind shield app Persistent infiltrates On & off S/S Rx : Macrolides / AG’s
- 16. Corneal ulcer scrapingsto be taken before starting treatment Margins (More bacteria) & base of ulcer with 15 blade or kimura spatula • Sac syringing • RBS Investigations PCR FUNGI
- 18.
- 20.
- 21. Treatment Topical antibiotics: • Eyedrops • Eye ointment ( To compensate night lag period ) Atropine (mydriatic – break PS & cycloplegic – reduce pain) NSAIDS AGM T. VIT C 500 MG ( Improves wound healing ) Collagen cross linking System antibiotics (no role) are indicated only in case of: • Endophthalmitis • Perforated corneal ulcer • Ulcer extended beyond limbus • Gonococci
- 22. Gram Positive- • Cephalosporins: Cefazolin 50 mg/ml – 5% Ceftazidime 50 mg/ml– 5% • Vancomycin 50 mg/ml– 5% • Chloramphenicol • 2nd gen fluroquinolones: Gatifloxacin / Moxifloxacin Gram Negative- • Aminoglycosides : Tobramicin 14 mg/ml – 1.4% Getamicin 14 mg/ml– 1.4% Amikacin 50 mg/ml – 5% • 1st gen fluroquinolones: Ciprofloxacin / ofloxacin Aminoglycosides for nocordia & NTM
- 23. MOXI : G+>G- GATI: G->G+ Topical : no vitreous penetration Oral GATI : vitreous penetration OFLOX : CORNEAL PERFORATION CIPLOX : CORNEAL DEPOSITS LEVO, NOR, BESIFLOXACIN 0.6% GENTA – nephro, oto, retinotoxic Sofra, neo, tobra, amikacin
- 24. Empirical Therapy: {Fluoroquinolone monotherapy/ fortified vancomycin + ceftazidime} • Initial treatment • Small non-severe ulcers • Close follow up • Perform microbiology if worsens All severe (> 3 mm) cases must be treated based on microbiology G+ COCCI G- RODS Q1H for 48 hours Q2H in morning, Q4H in night Q6H (healing)
- 25. Ceftazidime: 50mg/ml(5%) Method: Reconstituteparenteral Ceftazidime 500mg with 2ml sterile water/BSS available with the injection and add to 8ml of artificial tears. Storage: Refrigerate in 4 degrees C. Shelf Life: week under refrigeration at 4 degrees C and 3 days in room temperature. Vancomycin: 50mg/ml(5%) Method: Reconstitute 500mg of vancomycin powder for injection with 2 ml sterile water/BSS. Add to 8ml of artificial tears. Storage: Refrigerate at 4 Degrees C. Shelf Life: 28 days at 4 Degrees C. Preparation of Fortified antibiotic eye drops
- 26.
- 27. Classification of Fungi: •Yeasts (Candida) • Yeast like fungi • Filamentous • Dimorphic (Blastomyces) Etiology
- 29. Candida • Immunocompromised hosts (ICU,DM) • Alcoholics • Vitamin deficiency • Protracted epithelial ulceration Predisposing factors Filamentous fungi • Immunocompetent hosts • Trauma with vegetative matter • Agricultural & warehouse workers • June – September ( humid )
- 30. Pathogenesis ADHERANCE PENETRATION HOSTRESPONSE Disruption of integrity of corneal epithelium • Parallel growth of hyphae to stroma • Release of : Mycotoxins Proteolytic enzymes Soluble fungal antigen Release of lysosomal substances by PMN Destruction of corneal stroma
- 31. Clinical features SIGNS >SYMPTOMS ( large organisms, Inflammation process takes time ) •Dry, greyish, elevated, irregular margins •Feathery edges ( HALLMARK) •Satellite lesions ( multiple small ulcers ) •Hyphae •Hypopyon ( non sterile, non mobile ) •Non specific infiltrate •Pseudodendrite ( knobs absent ) •Endothelial plaques •Immune ring of wessely •Pigmentation
- 32. Flower pot -pseudodendrite on FS Feathery edges
- 33. Satellite lesions (multiple small ulcers ) Endothelial plaques
- 34. Immune ring Pigmentation( Aspergillus. Niger )
- 35. Investigations Corneal ulcer scrapingsfeels gritty Helps in debulking & improves drug penetration Staining Methods- A. Light Microscopy: 10% KOH ( dissolves the tissue so fungi are visualized ), Gram’s, Giemsa, Grocott- Gomori Methenamine Silver (GMS) Stains, PAS B. Fluorescent Microscopy: Calcofluor White (CCF) staining
- 36.
- 37. Culture : SDA,PDA,BHI, cooked meat broth
- 38. Confocal microscopy Only fungi& acanthamoeba are visualized
- 39. Treatment Filamentous fungi –NATAMYCIN Yeast - NYSTATIN + AMP.B
- 40. Intrastromal / intracameralinjections: • Voriconazole : 50 microgram in 0.1ml • Amphotericin B: 5-10 microgram in 0.1ml Oral antifungal therapy: • Indication: Scleritis, Endophthalmitis • Drugs : Ketoconazole 200-600mg Voriconazole 200-400mg Fluconozole 200-400mg Itraconazole 200mg • Duration of treatment : 14-21 days. • LFT & Hallucinations
- 41. TST Protocol ( Topical,Systemic, Targeted therapy ) • First line of Rx: Topical Natamycin 5%. • Addition of Oral Ketoconazole / Voriconazole in severe ulcers. • Second Line of Rx: Addition of topical Voriconazole 1%. • Third line of Rx: Intrastromal + Intracameral antifungals. • Fourth Line of Rx: TPK.
- 42. BACTERIAL FUNGAL Diffusion ofbacterial toxins Invasion of fungal hyphae Sterile Non sterile Fluid Fibrinous network Mobile (gravity, head position) Non mobile Easily absorbed Not absorbed HYPOPYON (PMN’S) • Virulence of organism • Resistance of tissues
- 43.
- 44. Free living amoeba 2forms : trophozoite ( active ) cyst ( dormant ) Risk factors: • Contact lens users ( pseudomonas > acanthamoeba ) • Swimming pool • Trauma with soiled matter
- 45. Clinical features • Severepain, watering and photophobia • Ring infiltrate / ulcer • Radial Perineuritis / Perineural Infiltrate • Punctate Epitheliopathy • Pseudodendrite • Limbitis • Hypopyon • Anterior Scleritis
- 46. Investigations Giemsa, GMS, CCF,PAS Stains Non nutrient agar with E.COLI
- 47. Confocal microscopy • Brightspots (89 %) • Double walled cysts (83%) • Signet rings (17%) Bacteria cant be visualized
- 48. Biguanides: •Poly Hexa MethyleneBiguanide (PHMB) 0.02% - 0.06 % •Chlorhexidine 0.02% - 0.2% Diamidines: •Propamidine Isethionate 0.1% •Hexamidine 0.1% MOA : Highly charged cationic molecules bind to negatively charged phospholipid membrane of amoeba causing denaturation of proteins. Aminoglycosides: •Neomycin MOA : inhibition of protein synthesis Treatment Duration : 6- 9 months
- 49. MICROSPORIDIA • Epithelial keratitis •Typical stuck on appearance of SPK • Treatment : 0.3% fluconazole
- 50. Complications A. Small perforation B.Large perforation Pseudocornea Anterior staphyloma Adherent leucoma
- 51. • Keratectasia • Keratocoele/ descemetocoele (DM herniates through ulcer) • Perforation Coughing, sneezing, straining, spasm of orbicularis Rise in BP Rise in IOP Perforation Prolapse of iris <2mm : tissue adhesive (cyanoacrylate) 2-4mm : patch graft/tenoplasty >4mm : tectonic keratoplasty
- 52. • Secondary glaucoma(iris & cicatricial tissue are too weak to support the restored IOP) • Anterior staphyloma • ASCC (contact with ulcer) • Corneal fistula • Pseudocornea • Spontaneous expulsion of lens and vitreous • Expulsive hemorrhage (sudden reduction in IOP) • Endophthalmitis • Panophthalmitis • Scarring (irregular astigmatism)
- 53. Non healing ulceralways check for: Diabetes mellitus (immunocompromised) Chronic dacryocystitis Contamination of medications Drug resistance Atypical microorganisms Incomplete treatment Improper diagnosis
- 54. Non infectious causes: •Chronic epithelial defect • Autoimmune disease • Rheumatoid arthritis • Mooren's ulcer • Terrien's marginal degeneration • Staphylococcal marginal disease • Phlyctenulosis • Contact lens-related infiltration • Vernal keratoconjunctivitis (shield ulcer) • Smokable drug-induced • Anesthetic abuse • Xerophthalmia, keratomalacia
- 56.
- 58.
- 59.