NORMAL CORNEA HISTOLOGY 1 2 3 1 4
- Slides: 123
NORMAL CORNEA HISTOLOGY
1 2 3 1 4 5
epithelium 5 cells Stratified Non-keratinising Bowmans-12 microns thick Non-secretory
STROMA keratocytes ARTEFACTUAL CLEFTS
Endothelial cells Descemet’s
CORNEAL REACTION PATTERNS
Atrophy and Oedema
Epithelial hyperplasia
Bullous lifting
Excessive intraepithelial basement membrane
Band keratopathy Dystrophic calcification Epithelial hyperplasia
Breaks in Bowman’s
Stromal thinning
Neutrophils in stroma. Acute keratitis
Chronic inflammationchronic keratitis Blood vessels Plasma cells
Foamy macrophages lipid keratopathy
Infective agent-bacteria
protozoa
Dystrophic deposits
Dystrophic deposits
Dystrophic deposits
GUTTAE
Endothelial Cell Loss
Ruptured Descemet’s
Host-donor interface scar
Corneal pathology
Case 1
Acute inflammation
Bacterial colonies. Gram + cocci
Diagnosis ?
Bacterial acute keratitis Predisposing factors: adnexal infection, entropion, exposure, dry eyes, contact lens, bullous keratopathy, trauma etc G + cocci-s aureus, S. epidermidis, S pneumoniae, S pyogenes, S viridans G – cocci-N gonorrhoeae, M meningitidis G + bacilli-C Diphtheriae, diphtheroids G- bacilli- Moraxella, Acinebacter, E-coli, K pneumoniae, proteus, psuedomanas G+ filamentous bacteria
Case 2
History Topical steroids after PK. Drop in vision……………….
Gram + cocci without inflammation
INFECTIOUS CRYSTALLINE KERATOPATHY Elaboration of biofilm by bacteria-protects them from immune system-therefore no inflammation, but also means poor response to antibiotics. Commonest bugs-strep viridans and staph epidermidis Aso can be caused by fungi and protozoa.
CASE 3
Fungal hypha -filamentous branching septate spores Fungal keratitis Penetrate Descemet’s without any problem
Common causes of fungal keratitis Trauma with organic material Humid warm conditions Exogenous or endogenous(immunocompromised) Aspergillus Candida Fusarium Sabaraud’s or equivalent medium for culturing Immunocompromised, steroids
CASE 4
cyst Trophozoite
DIAGNOSIS ?
AMOEBIC KERATITIS Amoebic keratitis-cysts and trophozoites-little inflammation Loss of keratocytes PERIODIC ACID SCHIFF (PAS) + GIEMSA + Can use immunohistochemistry Differential: Acanthamoeba, Hartmannella Vahlkampfia, Naegleria
Amoeba 10 -50 microns Replicate by binary fission Exist as trophozoites and cysts Trophozoites are active, infectious and feed by phagocytosing. Cysts from under hostile conditions and have a double layer.
Corneal epithelial trauma predisposes to infection Trophizoites attach to damaged epithelium, multiply and cause cytolysis. Migrate to stroma-elicit inflammation. Trigger keratoneuritis (inflammation follows corneal nerves).
Diagnosis Culture-corneal scrapes, biopsies, keratoplasty specimens. Contact lens, cases and solutions. Non-nutrient agar inoculated and seeded with Ecoli-food source for the amoeba. Wet-mount examination of contact lens solution. Can use PAS, calcofluor white, silver stains, immunohistochemistry, EM
CASE 5
Stromal thinning
chronic Inflammation With giant cells. Bowman’s loss due to ulceration
Chronic inflammation Scarring vascularisation
Secondary lipid keratopathy Cholesterol clefts=leaky vessels
DIAGNOSIS ?
Herpes simplex chronic DISCIFORM keratitis
HSV DNA VIRUS Type 1 usually, occasionally type 2 Diagnosis-Electron microscopy of affected cells, aspirate from blister, viral cultures, staining paraffin sections with monoclonal antibodies to HSV, PCR on corneal biopsy.
HSV Primary infection-self-limiting periocular vesicles and crusting, follicular and papillary blepharconjunctivitis, punctate epithelial keratopathy. Virus lives in trigeminal ganglionreactivation Dendritic ulcer
HSV Geographic ulcer Trophic keratitis Stromal infiltrative keratitis Disciform keratitis-type 4 hypersensitivity reaction-immune response to parasitized corneal stromal keratocytes-sets up vicious circle of inflammation-scarringinflammation.
Complications Uveitis Glaucoma Episcleritis Secondary bacteria infection Perforation Recurrence in corneal graft.
CASE 6
Angulated Bowman’s breaks
Perl’s stain shows intraepithelial iron deposits-Fleischer’s ring
DIAGNOSIS ?
KERATOCONUS Associations: Atopy Down’s syndrome Turner’s syndrome Marfan’s syndrome Ehlors-Danlos syndrome Aniridia Retinitis pigmentosa Ectopia Lentis Microcornea Non-specific systemic collagen abnormalities Chronic eye rubbing. Cause of prominent corneal nerves.
Ruptured Descemet’s-KC Hydrops-PAS stain
CASE 7
Masson’s trichrome stain-deep pink, non-birefringent hyaline bodies in anterior stroma
DIAGNOSIS ?
GRANULAR DYSTROPHY Masson’s trichrome positive hyaline deposits. Mutations in BIG H 3 /TGF-B 1 gene-encodes keratoepithelin protein. Exclude Avellino dystrophy (combined Lattice and Granular dystrophy)-by doing a Congo Red. Can recur in corneal graft-due to migration of host keratocytes into donor stroma, with elaboration of abnormal keratoepithelin
CASE 8
3
DIAGNOSIS ?
LATTICE DYSTROPHY Multiple, discrete, spindle shaped amyloid deposits in superficial, mid and deep stroma. Apple green birefringence of Congo red positive amyloid deposits when cross polarised Type 1, 2 and 3 Mutations in BIG H 3 / TGF-B 1 gene Exclude Avellino by doing Masson’s trichrome stain Other amyloid stains: Thioflavine T, Immunohistochemisty using antibodies to amyloid, Sirius Red. Recurs in graft because of migration of host keratocytes into donor stromaelaboration of amyloid in donor graft.
CASE 9
DIAGNOSIS?
MACULAR DYSTROPHY Alcian blue positive, deposits. Present in all layers except epithelium. Deposits in keratocytes and between collagen lamellae Material is mucopolysaccharide. Can recur in graft
Summary of corneal stains Lattice dystrophy-amyloid-use Congo Red / Sirius red and view under cross polarised light-apple green birefringence Granular dystrophy-hyaline material-use Masson’s trichrome Avellino dystrophy-use both Congo Red and Masson’s trichrome Macular dystrophy-mucopolysaccharide-use Alcian Blue or Hale’s colloidal iron stains or PAS Iron-use Perl’s / Prussian Blue stain- BLUE colour Calcium in band keratopathy- Alizarin Red- Red colour Basemant membranes, Descemet’s, Fungi- PAS stain- great for guttata. Bugs-Gram (bacteria), PAS (Fungi and Amoeba), Grocott silver stains for fungi.
CASE 10
Epithelial bullous lifting. Thinned epithelium over bulla Epithelium loses polarity
Excessive intraepithelial basement membrane-indication of chronic corneal oedema
Endothelial cell loss Thickened Descemet’s -implies chronic endothelial cell loss No obvious guttata
Patient had a cataract operation 1 year ago
DIAGNOSIS ?
Pseudoaphakic Bullous Keratopathy
CASE 11
HISTORY 65 YEAR OLD MALE Recent cataract operation Early corneal decompensation. No better PK
Fuch’s Endothelial Dystrophy Axial diffuse guttae or excrescences Endothelial cell loss Thickened-multilayered Descemet’s Burried guttata Can get non-guttate forms, with just very thickened Descemet’s. With chronicity, fibrous degenerative pannus formation under epithelium.
CASE 12
Multilayered cellsretrocorneal surface No previous surgery or trauma
Cytokeratin positive Multilayered cells
DIAGNOSIS ?
POSTERIOR POLYMORPHOUS DYSTROPHY Autosomal dominant, but can be recessive Circumscribed or total opacities in childhood Cells assume epithelial characteristics (stain for cytokeratin 7) Histological differential diagnosis-epithelial downgrowth, ICE syndrome, CHED (these conditions express cytokeratins)
CASE 13
Ruptured and recoiled Descemet’s Shelved / sloping stroma Pauciinflammatory perforation
DIAGNOSIS ?
Rheumatoid Corneal melt Rheumatoid arthritis Systemic lupus erythematosis Scleroderma Churg-Strauss. Wegener’s granulomatosis Polyarteritis nodosa Giant cell arteritis Relapsing polychondritis Rosacea Dysentery Leukaemias Above are associated with peripheral corneal ulcers and melt Other causes of peripheral corneal ulceration: Marginal, Mooren’s Terrien’s. Imbalance between matrix metalloproteinases and tissue inhibitors of metalloproteinases Enzymes released by keratocytes and epithelial cells to cause dissolution of stromal collagen.
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