corneal neovascularaization

1. Corneal
vascularization
DHRITIMAN DEB
INTERNEE
DEPT. OF OPHTHALMOLOGY

2. definition
• Corneal vascularization - in-growth of
new blood vessels from the pericorneal plexus
into avascular corneal tissue as a result of
hypoxia i.e. oxygen deprivation.
• Maintaining avascularity of the corneal
stroma - An important aspect of corneal
pathophysiology as it is required for
corneal transparency and optimal vision.

4. Types
• Superficial:-
 It involve the epithelium & anterior to
Bowman’s layer with an arborizing pattern.
• Deep:-
 It involve the stromal layer with radially
oriented parallel channels.

5. Etiology:-
• Contact lens
• Infection like herpes simplex
• Injury
• Inflammation
• Dystrophy
• Degeneration or cancerous conditions

6. Pathogenesis:
• Chemical theory
There may be presence of vasostimulatory
factor (VSF) or the breakdown (destruction) of
previously existing vasoinhibitory factor (VIF).
• Mechanical theory
Blood vessels cannot invade normal cornea
because of its compactness and loosening of the
compactness of corneal tissue due to oedema
was mandatory for neovascularization.

7. Symptoms:-
• Decreased vision
• Lacrimation
• Redness
• Photophobia
• ‘Foreign body’ sensation
• Pain
• Visible ‘whiteness’ of the cornea

8. Signs:-
• Loss of transparency & decrease in vision.
• Circumcorneal congestion.
• Loss of smoothness of the surface
• Epithelial defect
• Vascularization
• Change in shape,thickness or curvature
• Appearance of nodules or growth on the
surface.

9. Treatment:-
• Medical Options
• Surgical Options

10. •Medical Options
• If contact lens–related hypoxia is suspected, it
is important to cease contact lens use while
the NV is addressed.
• Anti-inflammatory drugs. Topical
administration of steroids and/or nonsteroidal
anti-inflammatory drugs (NSAIDs) should be
first-line treatment for corneal NV. These
drugs are best administered within 24 hours
following the initial corneal insult, before
leukocyte infiltration and recruitment occurs.

11. • Anti-VEGF agents. Recent studies involving
monoclonal anti-VEGF antibodies have shown
promising results for the reduction of corneal NV.
Topical and/or subconjunctival administration of
bevacizumab or ranibizumab has demonstrated
good short-term safety and efficacy.
• MMP inhibitors. Under inflammatory conditions,
suppression of enzymes that compromise corneal
structural integrity may block corneal NV. The
combination of orally administered doxycycline (a
nonselective MMP inhibitor) plus topical
corticosteroids has been shown to suppress
neovascularization.

12. oSurgical Options:-
• Laser ablation. Argon and Nd:YAG lasers may
be used to occlude invading blood vessels by
coagulating blood vessels and ablating tissue.
Careful attention must be paid to avoid
excessive irradiation and damage to adjacent
tissues, as complications such as corneal
hemorrhage and corneal thinning may
develop. Failure due to vessel lumen
reopening is common, and new shunt vessels
may form.

13. • Photodynamic therapy. Irradiation of a previously
injected photosensitive dye causes a reaction that
produces reactive oxygen species in the vessel lumen,
inducing apoptosis and necrosis of the endothelium
and basement membrane. The highly specific tissue
damage, combined with the resulting thrombogenic
response, seals off the vessel. Although it is effective,
photodynamic therapy has limited clinical acceptance
due to high costs and potential complications related
to laser irradiation and generation of reactive oxygen
species.

14. • Diathermy and cautery. A fine needle may be
inserted into feeder vessels at the limbus.
Vessels are occluded either by application of a
coagulating current through a unipolar
diathermy unit or by thermal cautery using an
electrolysis needle. Although initial studies
found these techniques to be safe and
effective

15. Thank you