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:

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 % 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 RIGHTLEFT 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 TAKE home message