Transcript Cornea pathology A lecture covering a range of corneal

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 coloniesGram + 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
hyphafilamentous
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
Scleritis
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 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
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 H3 / TGF-B1 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.