Neovascular glaucoma

Done by huda alhashimy - ophthalmology resident doctor
source of information - kaniski clinical ophthalmology

1. NEOVASCULAR GLAUCOMA
INFLAMMATORY GLAUCOMA

2. (NVG) occurs as a result of aggressive iris
neovascularization(rubeosisiridis). The
common aetiological
factor is severe, diffuse and chronic retinal
ischemia. It is postulated
that hypoxic retinal tissue produces
angiogenicfactors in an
attempt to revascularize hypoxic areas; the
most important of
these is probably vascular endothelial growth
factor (VEGF).
Pathogenesis

3. mediators induce both retinal and anterior segment
neovascularization, the latter initially impairing aqueous outflow
in the presence of an open angle, with subsequent progression
to typically severe and relentless secondary synechialangle-
closure glaucoma

4. Causes
Ischaemiccentral retinal vein occlusion
third of cases, 50% of eyes develop NVG following
ischaemicCRVO , Glaucoma typically
occurs 3 months after the occlusive event (‘100-day
glaucoma’) but intervals from 4 weeks to 2 years
have been documented.
Diabetes mellitus smaller proportion, The risk of
glaucoma is decreased by appropriatePRP,
increased by cataract extraction, Pars plana
vitrectomy
Arterial retinal vascular disease CRAO
Miscellaneousintraoculartumours,longstanding
retinal detachment (RD), chronic IO inflammation.

5. Clinical features
Symptoms none to severe pain, decreased
vision, redness and photophobia.
Cornea. Elevated IOP leads to corneal oedema.
IOP normal early but extremely high later on ,
anterior segment congestion, In advanced disease
hypotonymay supervene.
AC Flare,cellsand posterior synechiaemay be
present, depending on severity and stage
sometimes with AC hemorrhage
Pupillarymargin vessels at the pupillarymargin
are early sign, Diagnosis at this stage improve the
prognosis.

6. Iris surface New vessels grow radially, At
this stage the IOP normal, but elevation
can occur fairly acutely
Gonioscopy Angle neovascularizationmay
commonly occur without other signs, particularly
after CRVO, careful non-mydriaticgonioscopyin
eyes at risk, obstructing fibrovascularmembrane
that contracts to close the angle, leading to very
high IOP, severe visual impairment, congestion of
the globe and pain; the visual prognosis generally
poor by this stage, but aggressive management
can achieve comfort and retain sight in some
cases.

7. Cataract is common once ischaemiais
established
• Posterior segment. Signs correspond to
aetiology.Glaucomatousoptic neuropathy may be
present.
• Investigations.
FA may be helpful in confirming aetiologyand
delineating ischaemia.
B-scan ultrasonography will help to exclude
potential causes such as RD when the posterior
segment view is impaired.
Anterior segment OCT has been proposed as a
useful tool for angle assessment.

8. Treatment
Review first few months following an ischaemicCRVO,
and the first few weeks following diabetic vitrectomy.
Medical treatment of elevated IOP as for POAG but
mioticsshould be avoided, and prostaglandin
derivatives used with relative caution due to their
inflammation promoting potential. Topical atropine 1%
once or twice daily will resist posterior synechiaeand PAS
formation, and topical steroids should be given if
significant inflammation is present, watching for secondary
raised IOP.
Steroids and atropine alone may be adequate if there is
no visual potential
Topical apraclonidineand oral acetazolamidemay be
useful temporizing measures; acetazolamidecan be
associated with renal dysfunction in diabetes, especially
type1, and should be used with caution in these patients.

9. Panretinalphotocoagulation
Goniophotocoagulation
Intraocular VEGF inhibitors, e.g. bevacizumab
(Avastin®) at a dose of 1.25 mg in 0.05 ml, can
be an effective adjunctive measure whilst waiting
for PRP to take effect
Retinal detachment repair
Ciliarybody ablative procedures. Cyclodiodeor
cyclocryotherapyshould be considered if medical
IOP control is not possible.
Filtration surgery if VA is HM or better, glaucoma
drainage device and trabeculectomy
Pars planavitrectomy
Retrobulbaralcohol injection
Enucleation

10. INFLAMMATORY GLAUCOMA
Elevation of IOP secondary to intraocular inflammation
frequently presents a diagnostic and therapeutic challenge.
The elevation of IOP may be transient and innocuous, or
persistent and severely damaging. The prevalence of
secondary glaucoma increases with chronicityand severity
of disease. Secondary glaucoma is particularly common in
Fuchs uveitissyndrome and chronic anterior uveitis
associated with juvenile idiopathic arthritis.
Posterior uveitisis less likely to affect the aqueous outflow
pathway and consequently less likely to lead to IOP
elevation.
Diagnostic dilemmas (IOP fluctuation, Ciliarybody
shutdown ,uncertain Pathogenesis , Assessment of
glaucomatous damage , Iris vessels

11. Angle-closure glaucoma with pupillary
block : Secondary angle closure is caused by posterior
synechiaeextending for 360, which obstruct aqueous flow
from the posterior to the anterior chamber. The resultant
increased pressure in the posterior chamber produces
anterior bowing of the peripheral iris (iris bombé)resulting
in shallowingof the anterior chamber and apposition of the
iris to the trabeculumand peripheral cornea .
Such an inflamed iris easily sticks to the trabeculumand the
iridocornealcontact may become permanent, with the
development of peripheral anterior synechiae(PAS).
Diagnosis
• Slit lamp biomicroscopy(posterior synechiae, iris bombé
and a shallow anterior chamber).
• Gonioscopy(angle closure from IT contact , Indentation )

12. Angle-closure glaucoma without pupillary
block:
Chronic anterior uveitiscauses the deposition of
inflammatory cells and debris in the angle Subsequent
organization and contraction pulls the peripheral iris over
the trabeculum, causing gradual and progressive synechial
angle closure eventual elevation of IOP. The eye with a pre-
existing narrow angle may be at higher risk.
• Diagnosis
The anterior chamber is deep but gonioscopyshows
extensive angle closure by PAS.

13. Open-angle glaucoma
In acute anterior uveitis:IOP is usually normal or
subnormal due to concomitant ciliaryshutdown. secondary
OAG develops due to obstruction of aqueous outflow, most
commonly as acute inflammation is subsiding and ciliarybody
function returning. This effect, which is often transient and
innocuous, may be steroid-induced or caused by combination
of the following mechanisms:
• Trabecularobstructioninflammatory cells and debris,
which may be associated with increased aqueous viscosity
due to leakage of protein from inflamed iris blood vessels.
• Acute trabeculitisinflammation and oedemaof
the trabecularmeshwork with secondary diminution of
intertrabecularporosity may result in a reduction in outflow
facility (herpes zoster, herpesimplex, other viral anterior
uveitidesand toxoplasmaretinitis.

14. In chronic anterior uveitis
main mechanism for reduced outflow facility is
thought to be trabecularscarring and/or sclerosis
secondary to chronic trabeculitis. The importance of
this mechanismis, however, difficult to determine as
most eyes also have some degree of synechial
angle closure. Because of the variable appearance
of the angle on gonioscopy, definitive diagnosis of
trabeculardamage is difficult. In some eyes, a
gelatinous exudateis seen on the trabeculum.

15. Medical Treatment
control of IOP achieved if the angle is completely open.
The target IOP is lower in eyes with advanced glaucomatous
optic neuropathy.
Long-acting depot steroid preparations should be used with
caution, and minimized in known or suspected steroid-
responders.
The effect of ocular hypotensivedrugs is less predictable in
uveitis
beta-blocker is usually the drug of first choice.
Prostaglandin derivatives should be avoided if possible as
they may promote inflammation and macular oedema.
choice of additional agents often depends on the IOP level
Mioticsare contraindicated as they increase vascular
permeability, formation of posterior synechiae.

16. Laser iridotomy
Laser iridotomyis performed to re-establish communication
between the PC and AC in eyes with pupillary-block angle-
closure glaucoma.Aniridotomyis likely to become occluded
in the presence of active uveitis, and intensive topical steroid
should be used following the laser.
Surgical iridectomyis the definitive method of preventing
further pupil block, and may be required if laser fails to
maintain a viable iridotomy.
Surgery
Trabeculectomywith mitomycinC enhancement or glaucoma
drainage device implantation
Cyclodestructiveprocedures
Control of chronic uveitisfor a minimum of 3 months before
surgery , Preoperative topical steroids should be used .
( prophylaxis against recurrent inflammation , reduce the
conjunctivalinflammatory cell population)

17. Posner–Schlossman syndrome
(PSS)
PSS (glaucomatocycliticcrisis) is a rare condition
characterized by recurrent attacks of unilateral acute raised
IOP associated with mild anterior uveitis. The mechanism is
speculated to be acute trabeculitis, and there is evidence
that infection, possibly cytomegalovirus (CMV) or H. pylori,
may play a role; anterior chamber sampling for viral PCR is
sometimes employed.
PSS typically affects young to middle-aged adults. Males are
affected more frequently than females. Episodes are
unilateral, although 50% of patients have involvement of the
other eye at different times.
The intervals between attacks vary, but usually become
longer with time.
significant proportion will develop chronic IOP elevation, with
the fellow eye also at risk so, pt. should be followed.

18. Diagnosis
An acute IOP rise in PDS and demonstrable CMV or other
viral anterior uveitiscan present in an almost identical
manner
Presentationmild discomfort, haloes around lights
and slight blurring of vision in one eye, and sometimes
redness.
Slit lamp biomicroscopyfew AC cells and one to several
fine white central keraticprecipitates ,Injection are absent
Mild corneal epithelial oedema.
Mydriasisis common;posterior synechiaeare not a
feature.
Gonioscopyshows an open angle; PAS do not form.
Glaucomatous optic neuropathy is relatively uncommon
in most cases. Reversible cupping has been described.
Treatment (Topical steroids, aqueous suppressants,
Topical or oral non-steroidal anti inflammatory agents)