Transcript 17-NEOVASCULAR-GLAUCOMA-hubli

NEOVASCULAR GLAUCOMA
Dr.Gowri J Murthy, DNB, FRCO, FRCS
Glaucoma Service
Vittala International Institute of Ophthalmology
Prabha Eye Clinic and Research Centre
Neovascular Glaucoma
• One of the most intractable types of
secondary glaucoma.
• If not recognised early– can lead to rapid and profound vision loss
quickly progressing to absolute stage.
• 66y,F, BCVA- HMCF, IOP- 52 mmhg
• 65y, F, BCVA- 6/9, IOP- 18 mmhg, PDR
Syn: Rubeotic Glaucoma, Hemorrhagic
glaucoma, Thrombotic glaucoma.
HISTORY:
• Coats described new vessels in a
case of CRVO.
• Weiss et al proposed the term:
Neovascular Glaucoma.
• Neovascularisation Iris ( NVI)
proposed by Walton and Grant.
Duke Elder (1969)
• A disastrous condition, severe, and painful, the
cornea is hazy and may become vascularised, the anterior
chamber is typically of normal depth, and may contain
blood, the pupil is small and the iris trabeculae show new
vessels on their surface. The vitreous is often clouded by
red cells precluding view of the fundus, the tension is
stony hard, all perception of light is lost. Any
attempt at operative reduction of the ocular tension makes
matters worse by inducing profuse and recurrent
hemorrhages, and the only practical treatment if
retrobulbar alcohol or cyclodiathermy fails to
relive pain, is enucleation.
Pathogenesis
• In 97% of cases, the causal factor is retinal
ischaemia.
• 3%- by inflammation without retinal ischaemia.
• Ischaemia- release of factors which both inhibit
and promote new vessel growth.
• Pre requisites: Viable retinal tissue, low oxygen
tension, and venous drainage that allows
accumulation of these factors.
Factors
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VEGF- Muller Cells
FGF
IGF.
PDGF
IL 6
Ischemia
Release of angiogenesis factors ( PRE RUBEOSIS STAGE)
( FGF, VEGF, angiogenin, TGF, interferon, tumor necrosis factor-a, and
platelet derived growth factor)
New blood vessels on the iris and angle ( RUBEOSIS IRIDIS/PRE
GLAUCOMA STAGE)
open angle but occlusion of aqueous outflow( NVG-OAG)
fibrosis with NV, closed angle, Ectropion uveae( NVG-ACG)
Raised IOP
• Fibrovascular tissue over the trabeculum
decreases trabecular outflow.
• Myofibroblasts.
• Corneal endothelial proliferation.
Underlying etiology:
1) Proliferative Diabetic Retinopathy
2) CRVO
3) Other conditions•
Most common among these- CAROTID OCCLUSIVE
DISEASE.
•
Others •
BRVO
- Severe uveitis.
•
CRAO
- Endophthalmitis.
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TUMOURS.
- Sickle cell retinopathy
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CHR RD.
- Radiation retinopathy
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ROP
- Eales disease, Ocular Ischaemic
Synd.
•Symptoms –
•Early- none
•Late- symptoms attributable to the raised IOP,
and its sequelae
•Signs•Early- NVI, NVA
•Late:
• Ectropion uveae , Pupillary reaction may
be sluggish ,RAPD may be seen , corneal
stromal, and epithelial edema.
•Visual acuity is grossly reduced.
•Anterior segment flare
Early diagnosis
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High index of suspicion.
Undilated pupil examination
Undilated Gonioscopy
IOP measurement
Dilated fundus exam
Gonioscopy
• Fine blood vessels which cross the TM
Investigations:
- Fundus Fluorescein Angiogram- to assess retinal
ischaemia
- Electroretinogram – to assess for retinal ischemia.
The electroretinogram measures a mass electrical
response of the retina, allowing for assessment of the
retinal periphery, which cannot be seen with
fluorescein angiography.
- Iris angiography- in cases of doubtful NVI, to
confirm the diagnosis
- B scan ultrasound- if view of retina not possible
due to media opacity/ corneal edema.
Systemic:
FBS and PPBS- to r/o Diabetes Mellitus.
- Carotid Doppler in case OIS is suspected- NVG in
absence of either PDR, or CRVO.
CRVO:
• More common in ischaemic CRVO.
•The overall incidence of NVI in all CRVO cases is 12% to 30%
• Conventionally termed 100 day glaucoma
•can occur 2weeks to 2 years after initial occlusion.
• FFA important to categorize.
•In case of indeterminate FFA, consider ischaemic
and follow up.
•Non ischaemic variety can convert to ischaemic.
•ERG findings.Quantitative measurement of RAPD.
•Consider preexisting POAG/ ACG. Examine other eye
carefully especially gonioscopy.
DIABETIC RETINOPATHY:
• Retinal capillary non perfusion on FFA.
• ERG changes.( oscillatory potential of the b-wave)
• NVG in one eye of a diabetic patient, invariably other eye also
develops.
• Cataract extraction/ vitrectomy- increases risk of NVG.
•PC/ Anterior hyaloid is a relative barrier.
•Preop extent and severity
of retinopathy more predictive.
CAROTID ARTERY OCCLUSIVE DISEASE:
• Accounts for 13% of cases.
• May not be associated with elevated IOP sometimes.
• Consider CAOD if markedly asymmetric Diabetic
retinopathy, with no apparent cause for NVG.
•Asymmetric/ absent carotid pulse.
•Doppler studies.
• Carotid endarterectomy- ocular benefits unclear.
Differential Diagnosis:
1)
Fuchs Heterochromic Cyclitis.
2)
Acute Angle closure Glaucoma.
Other Inflammatory Glaucomas.
Treatment
• Treatment of the underlying process
• Treatment of the raised Intraocular pressure.
Treatment of the underlying
process
• Panretinal Photocoagulation.
– Slit lamp, LIO, Endolaser
• Retinal cryoablation.
• Trans scleral retinal ablation.
– Diode TSCPC.
– ( regression of NV in 68%, and normalisation
of IOP in 42% of patients)
– OhnishiY etal, Fluorescein Gonioangiography
in Diabetic Neovascularisation.Graefes arch
clin exp ophthalmol 1994;232:199-204
Treatment of the raised IOP
• Medical
– Aqueous suppressants- beta blockers, carbonic
annhydrase inhibitors, alpha agonists.
– Avoid: Pilocarpine, dipivefrine, prostaglandin
analogues.
– Topical Atropine 1% .
– Topical Steroids.
Treatment of Raised IOPSurgical
• Trabeculectomy- with Antimetabolites
– 61-68% success.( Mandal AK etal, IJO)
• Aqueous shunt devices.- 21-90% success
• Cyclodestruction:
– Cyclocryotherapy.
– TSCPC, other contact and non contact trans
scleral cyclodestructive procedures.
– Endoscopic cyclophotocoagulation.
• High rate of failure in all methods.
• Cyclodestruction associated with incidence
of hypotony, phthisis,post op pain,
intraocular hemorrhage, and loss of BCVA.
Adjuvant treatments
• ANTI VEGF agents– Bevacizumab
– Pegaptanib
– Ranibizumab
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Intravitreal Triamcinolone
Provide a window for definitive treatment
Make surgery easier
NOT sufficient alone for management of this
condition
55 y, M, Rapid DoV Right eye
• Vision(BCVA)
RE CF 2M
LE 6/18
• PUPIL
• IOP
RE - RAPD
LE - normal
RE 12, LE 8mmhg
Fundus Photo RE
Fundus Photo LE
•
GENERAL
EXAMINATION
PULSE 78 / MIN
PERIPHERAL
PULSE
RIGHT
LEFT
Carotid
+
+++
Brachial
+
+++
Radial
+
+++
Popliteal
+++
+++
Dorsalis Pedis
+++
+++
MR ANGIOGRAM
TAKE home message
•High index of suspicion
•Prompt management
•Use newer adjuncts like anti VEGF
•Definitive surgery must follow .
•Endoscopic surgery and CPC can play a
role