neovascular glaucoma dr.gowri j murthy, dnb, frco, frcs glaucoma service vittala international...

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

• 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.

• TUMOURS. - Sickle cell retinopathy

• CHR RD. - Radiation retinopathy

• 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

• 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 IOP- Surgical

• 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

• 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 RE - RAPD

LE - normal

• IOP 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

•High index of suspicion

•Prompt management

•Use newer adjuncts like anti VEGF

•Definitive surgery must follow .

•Endoscopic surgery and CPC can play a role

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