NORMAL CORNEA HISTOLOGY

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NORMAL CORNEA HISTOLOGY
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epithelium
5 cells
Stratified Non-keratinising Non-secretory
Bowmans-12 microns thick
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STROMA
keratocytes
ARTEFACTUAL CLEFTS
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Descemets
Endothelial cells
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CORNEAL REACTION PATTERNS
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Atrophy and Oedema
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Epithelial hyperplasia
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Bullous lifting
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Excessive intraepithelial basement membrane
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Band keratopathy Dystrophic calcification
Epithelial hyperplasia
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Breaks in Bowmans
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Stromal thinning
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MELT
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Neutrophils in stroma. Acute keratitis
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Chronic inflammation-chronic keratitis
Blood vessels
Plasma cells
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Foamy macrophages lipid keratopathy
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Infective agent-bacteria
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protozoa
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Dystrophic deposits
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Dystrophic deposits
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Dystrophic deposits
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GUTTAE
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Endothelial Cell Loss
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Ruptured Descemets
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Host-donor interface scar
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Corneal pathology
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Case 1
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Acute inflammation
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Bacterial colonies-Gram cocci
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Diagnosis ?
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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

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Case 2
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History

• Topical steroids after PK.
• Drop in vision.

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Gram cocci without inflammation
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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.

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CASE 3
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Fungal hypha-filamentous branching
septate spores Fungal keratitis Penetrate
Descemets without any problem
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Common causes of fungal keratitis

• Trauma with organic material
• Humid warm conditions
• Exogenous or endogenous(immunocompromised)
• Aspergillus
• Candida
• Fusarium
• Sabarauds or equivalent medium for culturing
• Immunocompromised, steroids

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CASE 4
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cyst
Trophozoite
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DIAGNOSIS ?
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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

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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.

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• 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).

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Diagnosis

• Culture-corneal scrapes, biopsies, keratoplasty
  specimens. Contact lens, cases and solutions.
• Non-nutrient agar inoculated and seeded with
  E-coli-food source for the amoeba.
• Wet-mount examination of contact lens solution.
• Can use PAS, calcofluor white, silver stains,
  immunohistochemistry, EM

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CASE 5
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Stromal thinning
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chronic Inflammation With giant cells.
Bowmans loss due to ulceration
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Chronic inflammation Scarring vascularisation
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Secondary lipid keratopathy Cholesterol
cleftsleaky vessels
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DIAGNOSIS ?
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Herpes simplex chronicDISCIFORM keratitis
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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.

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HSV

• Primary infection-self-limiting periocular
  vesicles and crusting, follicular and papillary
  blepharconjunctivitis, punctate epithelial
  keratopathy.
• Virus lives in trigeminal ganglion-reactivation
• Dendritic ulcer

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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-scarring-inflammation.

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Complications

• Uveitis
• Glaucoma
• Episcleritis
• Scleritis
• Secondary bacteria infection
• Perforation
• Recurrence in corneal graft.

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CASE 6
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Angulated Bowmans breaks
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Perls stain shows intraepithelial iron
deposits-Fleischers ring
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DIAGNOSIS ?
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KERATOCONUS

• Associations
• Atopy
• Downs syndrome
• Turners syndrome
• Marfans syndrome
• Ehlors-Danlos syndrome
• Aniridia
• Retinitis pigmentosa
• Ectopia Lentis
• Microcornea
• Non-specific systemic collagen abnormalities
• Chronic eye rubbing.
• Cause of prominent corneal nerves.

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Ruptured Descemets-KC Hydrops-PAS stain
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CASE 7
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Massons trichrome stain-deep pink, non-birefringe
nt hyaline bodies in anterior stroma
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DIAGNOSIS ?
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GRANULAR DYSTROPHY

• Massons trichrome positive hyaline deposits.
• Mutations in BIG H3 /TGF-B1 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

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CASE 8
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DIAGNOSIS ?
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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 H3 / TGF-B1 gene
• Exclude Avellino by doing Massons 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 stroma-elaboration of
  amyloid in donor graft.

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CASE 9
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DIAGNOSIS?
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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

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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 Massons
  trichrome
• Avellino dystrophy-use both Congo Red and
  Massons trichrome
• Macular dystrophy-mucopolysaccharide-use Alcian
  Blue or Hales colloidal iron stains or PAS
• Iron-use Perls / Prussian Blue stain- BLUE
  colour
• Calcium in band keratopathy- Alizarin Red- Red
  colour
• Basemant membranes, Descemets, Fungi- PAS stain-
  great for guttata.
• Bugs-Gram (bacteria), PAS (Fungi and Amoeba),
  Grocott silver stains for fungi.

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CASE 10
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Epithelial bullous lifting. Thinned epithelium
over bulla Epithelium loses polarity
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Excessive intraepithelial basement
membrane-indication of chronic corneal oedema
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Endothelial cell loss Thickened
Descemets-implies chronic endothelial cell
loss No obvious guttata
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• Patient had a cataract operation 1 year ago

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DIAGNOSIS ?
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Pseudoaphakic Bullous Keratopathy
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CASE 11
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HISTORY

• 65 YEAR OLD MALE
• Recent cataract operation
• Early corneal decompensation.
• No better
• PK

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Fuchs Endothelial Dystrophy

• Axial diffuse guttae or excrescences
• Endothelial cell loss
• Thickened-multilayered
• Descemets
• Burried guttata
• Can get non-guttate forms, with just very
  thickened Descemets.
• With chronicity, fibrous degenerative pannus
  formation under epithelium.

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CASE 12
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Multilayered cells-retrocorneal surface No
previous surgery or trauma
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Cytokeratin positive Multilayered cells
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DIAGNOSIS ?
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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)

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CASE 13
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Ruptured and recoiled Descemets
Shelved / sloping stroma Pauciinflammatory perfora
tion
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DIAGNOSIS ?
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Rheumatoid Corneal melt

• Rheumatoid arthritis
• Systemic lupus erythematosis
• Scleroderma
• Churg-Strauss.
• Wegeners 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, Moorens Terriens.
• Imbalance between matrix metalloproteinases and
  tissue inhibitors of metalloproteinases
• Enzymes released by keratocytes and epithelial
  cells to cause dissolution of stromal collagen.