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 (rubeosis iridis). The
common aetiological
factor is severe, diffuse and chronic retinal
ischemia. It is postulated
that hypoxic retinal tissue produces
angiogenic factors 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 synechial angle-
closure glaucoma

4. Causes
 Ischaemic central retinal vein occlusion
third of cases, 50% of eyes develop NVG following
ischaemic CRVO , 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 appropriate PRP,
increased by cataract extraction, Pars plana
vitrectomy
Arterial retinal vascular disease CRAO
Miscellaneousintraocular tumours,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
hypotony may supervene.
 AC Flare,cells and posterior synechiae may be
present, depending on severity and stage
sometimes with AC hemorrhage
 Pupillary margin vessels at the pupillary margin
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 neovascularization may
commonly occur without other signs, particularly
after CRVO, careful non-mydriatic gonioscopy in
eyes at risk, obstructing fibrovascular membrane
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 ischaemia is
established
 • Posterior segment. Signs correspond to
aetiology.Glaucomatous optic neuropathy may be
present.
• Investigations.
 FA may be helpful in confirming aetiology and
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 ischaemic CRVO,
and the first few weeks following diabetic vitrectomy.
 Medical treatment of elevated IOP as for POAG but
miotics should 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 synechiae and 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 apraclonidine and oral acetazolamide may be
useful temporizing measures; acetazolamide can be
associated with renal dysfunction in diabetes, especially
type1, and should be used with caution in these patients.

9. Panretinal photocoagulation
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
Ciliary body ablative procedures. Cyclodiode or
cyclocryotherapy should be considered if medical
IOP control is not possible.
Filtration surgery if VA is HM or better, glaucoma
drainage device and trabeculectomy
Pars plana vitrectomy
Retrobulbar alcohol 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 chronicity and severity
of disease. Secondary glaucoma is particularly common in
Fuchs uveitis syndrome and chronic anterior uveitis
associated with juvenile idiopathic arthritis.
 Posterior uveitis is less likely to affect the aqueous outflow
pathway and consequently less likely to lead to IOP
elevation.
 Diagnostic dilemmas (IOP fluctuation , Ciliary body
shutdown ,uncertain Pathogenesis , Assessment of
glaucomatous damage , Iris vessels

11.  Angle-closure glaucoma with pupillary
block : Secondary angle closure is caused by posterior
synechiae extending 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 shallowing of the anterior chamber and apposition of the
iris to the trabeculum and peripheral cornea .
Such an inflamed iris easily sticks to the trabeculum and the
iridocorneal contact 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 uveitis causes 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 gonioscopy shows
extensive angle closure by PAS.

13. Open-angle glaucoma
In acute anterior uveitis :IOP is usually normal or
subnormal due to concomitant ciliary shutdown. secondary
OAG develops due to obstruction of aqueous outflow, most
commonly as acute inflammation is subsiding and ciliary body
function returning. This effect, which is often transient and
innocuous, may be steroid-induced or caused by combination
of the following mechanisms:
• Trabecular obstruction inflammatory cells and debris,
which may be associated with increased aqueous viscosity
due to leakage of protein from inflamed iris blood vessels.
• Acute trabeculitis inflammation and oedema of
the trabecular meshwork with secondary diminution of
intertrabecular porosity may result in a reduction in outflow
facility (herpes zoster, herpe simplex, other viral anterior
uveitides and toxoplasma retinitis.

14.  In chronic anterior uveitis
main mechanism for reduced outflow facility is
thought to be trabecular scarring 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
trabecular damage is difficult. In some eyes, a
gelatinous exudate is 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 hypotensive drugs 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
 Miotics are contraindicated as they increase vascular
permeability, formation of posterior synechiae.

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

17. Posner–Schlossman syndrome
(PSS)
 PSS (glaucomatocyclitic crisis) 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 uveitis can present in an almost identical
manner
Presentation mild discomfort, haloes around lights
and slight blurring of vision in one eye, and sometimes
redness.
 Slit lamp biomicroscopy few AC cells and one to several
fine white central keratic precipitates ,Injection are absent
Mild corneal epithelial oedema.
 Mydriasis is common; posterior synechiae are not a
feature.
 Gonioscopy shows 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)