Neovascular glaucoma retinal aspects....

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1. NEOVASCULAR
GLAUCOMA
PRESENTER: DR.HARSHA BHAMIDIPATI
MODERATORS: DR.DEEPAK ANTHWAL
DR. VENUGOPAL REDDY

2. CASE 1:
A 67 years female was referred from glaucoma department.
C/O Defective vision in LE since 1 week.
SYSTEMIC HISTORY: K/C/O DM since 4 years on treatment.
OCULAR HSTORY:BE K/C/O POAG on medication since 2 years but stopped
medication 6 months back , RE operated for TRAB.
O/E
RE LE
V/A 6/12 PL +
IOP 15 49
A/S LOW BLEB, PI
AT 12 O’CLOCK
360 DEGREE
NVI
GOINIOSCOPY

OPEN NVA +,
OCCLUDABLE
P/S CDR 0.8, IR
LOSS
CRVO, GOA

3. -
-
-
Diagnosis: LE NVG post CRVO.
LE IVB 1 dose was given and PRP was done
Patient was started on Dorsum e/d, Bidin T e/d and Cap. IOPAR-SR in LE
On next follow ups:




RE LE
1
ST
FOLLOWUPV/A 6/6P
IOP 17
V/A PL+,
REGRESSING
NVI
IOP 38
2
ND
FOLLOWUPV/A 6/6P
IOP 15
V/A PL+,
REGRESSING
NVI
IOP 39

5. CASE 2
A 66 years male was referred to retina. Patient was diagnosed as
RE ITBRVO 1.5 months elsewhere.
SYSTEMIC HISTORY : NIL
OCULAR HISTORY: NIL

O/E:


RE LE
V/A HM 6/18
IOP 49 18
A/S CONGESTION,
CORNEAL
EDEMA ,FLORID
NVI
IMC
GONIOSCOPYNVA, OPEN OPEN
P/S NO VIEW D/T
CORNEAL
EDEMA
CDR 0.5

6. -
-
-
-
Diagnosis: RE NVG post ITBRVO
LE ARC was done and 1 dose IVB given
Patient was started on BIDIN T,DORSUM e/d and IOPAR-SR in RE
On next follow up:







On this visit accessible PRP was done.
RE LE
V/A HM 6/12
IOP 28 19
A/S CONGESTION,
CORNEAL
EDEMA
REDUCING,
REGRESSING
NVI
IMC
P/S CDR 0.9,CRVOCDR 0.5

7. On further follow up


RE LE
V/A HM+
IOP 24
Regressing NVI at 10 &
6 o clock
V/A 6/12
IOP 20

8. CASE 3:
A 47 years male patient was referred from glaucoma department with C/O
defective vision BE and for evaluation of BE PDR with RE VH.
SYSTEMIC HISTORY: K/C/O DM since 11 years on treatment, HTN since 2
years on treatment.
OCULAR HISTORY: NIL
O/E:


RE LE
1. V/A 5/60 5/60
2. IOP 14 mmHG 44 mmHG
3. ANTERIOR
SEGMENT
No NVI NVI +,Ectropion
uvea+
4.
GONIOSCOPY
OPEN ANGLENVA + with PAS
5. POSTERIOR
SEGMENT
VH, no view PDR

9. -
-
-
-
Diagnosis: BE PDR, LE NVG

LE PRP was done and 1 dose of IVB given. And patient was started on BIDIN
T , DORSUM E/D and T. DIAMOX in LE

On follow-up, LE regression of NVI was seen but IOP was 48mmHG. Ripatec
E/D was added.

IOP was not in control even with maximum medical treatment, PRP and IVB.

So he was advised for AADI implantation with PPV in LE

10. -S/P AADI implantation on follow-up :

RE LE
1
ST
FOLLOWUPV/A 6/9
IOP 12
V/A 6/36
IOP 20
2
ND
FOLLOWUPV/A 6/9
IOP 18
V/A 6/36
IOP 20
3
RD
FOLLOWUPV/A 6/9
IOP 15
V/A 6/60
IOP 14

11. CASE 4:
A 60 year male was referred to retina OPD. He had C/O of defective vision
in RE since 3 years and LE since 1 week.
SYSTEMIC HISTORY: K/C/O DM since 8 years & hyperlipidemia since 3
years on treatment
OCULAR HISTORY: RE IV injection was given and LE PRP done elsewhere.
Details not available. one eyed since 4 years.
O/E
RE LE
V/A PL - 6/60
IOP 54 24
A/S CORNEAL EDEMA,
FLORID NVI,
NVI FROM 9 -11
O’CLOCK
GONIOSCOPY NVA NVA SUPERIORLY
AND OPEN ANGLE.
P/S HAZY, GOA PDR WITH VH.
INFERIOR LASER
MARKS SEEN

12. -
-
-
-
Diagnosis: BE NVG,RE Absolute glaucoma
Patient was started on Dorsum T e/d in LE

PRP completion was done and 1 dose IVB given.

On follow- up, LE:V/A improved to 6/12 and IOP was 20

Later patient lost follow-up and came after 3 months, on this visit: RE LE
V/A PL - 5/60
IOP 50 40
A/S CORNEAL
EDEMA, FLORID
NVI
MICROCYSTIC
EDEMA, FLORID
NVI
P/S GOA HAZY VIEW

13. -
-
-
-
-
ARC was done and 1 dose IVB given. Was started on Bidin T,Dorsum,
Ripatec e/d and Tab. Diamox.

Further 2 more IVB doses were given.

IOP was not controlled with maximum medical treatment, PRP and ARC.

So PPV+AADI implantation was advised.
On follow - up:
RE LE
1
st
follow-up V/A PL –
IOP 38
V/A 6/12
IOP 18
2
nd
follow-upV/A PL-
IOP 40
V/A 6/18
IOP 20

15. INTRODUCTION



Neovascular glaucoma (NVG) is severe form of secondary glaucoma
characterized by the proliferation of brovascular tissue in the anterior
chamber, which subsequently causes elevation in intraocular pressure
(IOP).
In 1906, G.Coats rst demonstrated new blood vessels growth on iris
surface in prior CRVO cases
Also known as:
1.Hemorrhagic glaucoma
2.Congestive glaucoma
3.Thrombotic glaucoma

16. This is a case report in 43 year old female with Carotid Cavernous Fistula.
It is noted that IOP elevation was related to new vessels and associated connective
tissue growth and proposed the term NEOVASACULAR GLAUCOMA which was early
termed as hemorrhagic glaucoma.

17. 1.
2.
3.
4.
NVG has a high risk of causing severe vision impairment and can result in both unilateral
and bilateral blindness.
Retinal ischemia is the underlying etiology in more than 95%
of cases.
NVG makes approximately 3.9% of all glaucoma's.

RISK FACTORS FOR NVI:

RETINAL ISCHEMIA
SURGICAL CAUSES
TUMORS
OCULAR INFLAMATORY DISEASES

18. The most common causes of NVG
1.Proliferative diabetic retinopathy
(PDR)
2.Retinal vein occlusion (RVO)
3.Ocular ischemic syndrome (OIS).
CAUSES OF NEOVASCULAR
GLAUCOMA

19. PREVALENCE
A.








DIABETIC RETINOPATHY:
NVI incidence 65% in PDR.
5 % blindness in diabetics is
due to NVG.
Risk for NVI and NVG increases
in DR patients after vitrectomy,
cataract and posterior
capsulotomy.
Risk factors for development of
NVG post vitrectomy:
Pre op NVI/NVA
increased IOP
HbA1C levels
Retinal tamponade used in
retinal surgery.

20. DIABETIC RETINOPATHY
MOST COMMON CAUSE FOR NVGMOST COMMON CAUSE FOR NVG
Incidence of NVI in diabetics
Incidence of NVI in PDR
Risk of contralateral eye developing NVG in people with diabetes with
NVG in other eye
Incidence of NVG after PPV for PDR
Incidence of NVI after PPV for PDR
1-17%
65%
33%
4 - 5%
8 - 9%

21. 


B. CENTRAL RETINAL VIEN OCCLUSION:
90 DAY GLAUCOMA (develops in 3 months of onset)

incidence of NVG following CRVO - 16%

45% ischemic CRVO develop NVG due to retinal capillary non perfusion






Study done in 2019
Retrospective study done in 646 CRVO
patients
To determine risk factors for NVG
development
13% developed NVG
Risk factors for NVG : RAPD,Poor V/A and
H/O HTN
Rong AJ, Swaminathan SS, Vanner EA, Parrish RK 2nd. Predictors of Neovascular Glaucoma in Central Retinal Vein
Occlusion. Am J Ophthalmol. 2019 Aug;204:62-69. doi: 10.1016/j.ajo.2019.02.038. Epub 2019 Mar 9. PMID: 30862502;
PMCID: PMC6642681.

22. •
•
Data was analyzed on 1108
patients
The study showed probability
of conversion of nonischemic
to ischemic CRVO at 6 months
and 18 months was 13.2% and
18.6 5 respectively

•
•
Study was done in 93 eyes with PDR
treated by argon laser
This study showed PRP was more
effective in controlling NVI in diabetics
than in CRVO

23. 
C. Ocular Ischemic Syndrome:

Develop NVG in 50% cases




Retrospective study in 25 OIS
patients
To determine risk factors for NVG
Risk factors: severity of carotid
artery stenosis and duration of
time from symptoms to diagnosis

24. CAROTID OCCLUSIVE DISEASE

25. A stenosis of
90% or more
of the common
or internal
carotid arteries
Reduces the perfusion
pressure within the
central retinal artery by
approximately 50% 
Poor collateral
circulation between the
internal and external
carotid arteries or
between the two
internal carotid arteries
Well-
developed
collateral
circulation 
OISOIS
May not
develop OIS
In most cases , well developed
collateral circulation is present –
hence NVG is less common

26. D. Chronic RD
•
•
•
•
Schulz reported RD as one of the common cause of NVI (23%)


Persistent RD in post-vitrectomy case often causes NVI.

RD due to Coats disease, x-linked Retinoschisis & Marfan’s syndrome are reported with
presenting feature of NVI.

Old settled RD must be considered when no obvious cause of NVI is found. These eyes
present with low IOP.

27. E. Ocular inamatory disease:
•
•
•
•
Low grade uveitis like Fuchs heterochromic iridocyclitis – frequently associated with NVA
and rarely NVI

NVG is hence not reported with this condition.

Gartner and Henkind mentioned endophthalmitis and sympathetic ophthalmitis as causes
of rubeosis

But no studies provide enough details regarding the pathogenesis of rubeosis iridis in
inammatory conditions

28. F. Tumors and Radiation:
A)


B)





RETINOBLASTOMA:
Howard & Ellsworth (1965) noted association of RB & NVI.
Signicant correlation was found between extent of tumor involvement & occurrence of NVI.





MALIGNANT MELANOMA:
0.5%-15%
NVG may occur due to RD, retinal hypoxia or tumor necrosis.
Irradiation doesn't seem to decrease the incidence of NVG in these cases.

29. THEORIES OF
NEOVASCULOGENESIS:
A. RETINAL HYPOXIA:
Diminished perfusion of retina
↓
Capillary non perfusion areas causing retinal ischemia
↓
New vessels formation on retina, optic disc, iris and anterior
chamber angle

30. 



B. Angiogenesis Factor:

Presence of angiogenic factors:- regulation of normal development of retinal blood
vessels

VEGF - Potent angiogenic stimulator, major role in normal and pathologic
angiogenesis. Major source: MULLER CELLS

FOUR isoforms: VEGF 121, VEGF 165, VEGF 189, VEGF 206

VEGF has ability to induce vascular permeability, also known as: Vascular Permeability
factor

31. 


Aim was to evaluate VEGF family in
aqeous humor of patients with NVG
Comparitive study between 22 NVG
cases and 20 contols
it concluded that high concentrations of
VEGF family except for VEGF B were
found in aqeous humor of patients with
NVG



Aim was to assess effectiveness
of intra ocular anti VEGF
medications alone or with other
types of conventional therapies
it concluded that Anti VEGF as an
adjunct to conventional treatment
could help reduce IOP in NVG in
short term
No evidence seen on its effect for
long term.

32. 


Aim: To determine timing of neovascular regression
after intra vitreal Avastin given as initial therapy for
eyes with high risk PDR with or without CSME
Done in 24 PDR eyes
It concluded that majority of new vessels
completely regressed within 48 hours after IVB.
The effect occured within 48 hours and was
mtained for atleast 2 weeks.
THIS STUDY SUPPORTED
ANGIOGENIC FACTOR THEORY
OF NEOVASCULARIZATION
THIS STUDY SUPPORTED
ANGIOGENIC FACTOR THEORY
OF NEOVASCULARIZATION

33. 


C. Vasoinhibitory Factors:

Ocular tissues produce substances inhibiting neovascularisation

Sources of vasoinhibitory substances: LENS and VITREOUS

RPE cells also release vaso inhibitory substances.


•Study showed lens may play an active
role in prevention of iris
neovascularisation.

35. PATHOPHYSIOLOGY:

36. STAGES OF NEOVASCULAR
GLAUCOMA
•Pre-glaucoma stage (i.e.,
rubeosis iridis), characterized
by new vessels on the
surface of the iris (a) and in
the anterior chamber angle
(b).
A
•Open- angle glaucoma stage,
characterized by an
increase in
neovascularization and a
brovascular membrane on
the iris (c) and in the anterior
chamber angle (d).
B
•Angle- closure glaucoma
stage, characterized by
contracture of the
brovascular membrane,
causing corectopia,
ectropion uvea (e), attening
of the iris (f), and peripheral
anterior synechiae (g).
C
Clinicopathologic stages of neovascular glauc

37. 


A. PRE RUBEOSIS:
Predisposing factor, such as diabetic retinopathy or CRVO have risk of
developing rubeosis iridis and chance for progression to neovascular
glaucoma.

In PDR,rubeosis iridis is reported to occur in approximately one- half of the
cases.

Risk for rubeosis iridis and NVG in patients
with diabetic retinopathy is greatly increased when arteriolar or
capillary nonperfusion is present or after vitrectomy or lensectomy,

38. 



On iris FFA - peripupillary leakage correlates with the presence of abnormal iris
vessels.


Iris FFA can give idea of risk for rubeosis iridis after vitrectomy in DR


On S/L -pupillary margin of iris: First site for neovascularisation earliest
biomicroscopic evidence of anterior segment rubeosis.


Gonioscopy is also important - check for NVA

39. 


Incidence of NVI and NVG in eyes with CRVO is correlated with the extent
of retinal capillary nonperfusion.
FFA is the most direct method of evaluating CNP areas
RAPD also indicates an increased risk for NVI after CRVO, and infrared
pupillometry is an objective method of documenting this nding
- Prospective study in 20 CRVO cases and 20
controls
- It was noted that marked reduction in venous
velocity was seen in CRV in affected eyes
- Suggesting that colour doppler ow imaging
has role on CRVO diagnosing and also help in
differentiation of ischemic and non ischemic.
- Non invasive, easy to perform and well tolerated

40. FUNCTIONAL
TESTS
MORPHOLOGICA
L TESTS

41. FFA IN ISCHEMIC CRVOFFA IN ISCHEMIC CRVO
FFA IN NON ISCHEMIC CRVOFFA IN NON ISCHEMIC CRVO

42. •
•
•
45 cases of CRVO were taken and
ERG was done.
It was seen that cases with b/a ratio
0.84 developed NVG,no complications
were seen in b/a ratio >1 and b/a ratio
0.73 were treated with PRP and NVG
developed in none.
The study showed b/a amplitude ratio
reected degree of retinal ischemia
and had prognostic value in predicting
which cases NVG may develop

•
•
•
Aim was to evaluate usefulness of 30 Hz
icker ERG in predicting outcome in
patients with CRVO
76 CRVO cases underwent 30 Hz icker
ERG.
It concluded that 30 Hzicker ERG
provides useful information about CRVO
by computing the probability of NVI

43. Fluorescein angiographic
demonstrates uorescein leakage
along the pupillary margin. In
subsequent frames, the area of
uorescein leakage enlarges.
(From Reiss GR,Sipperley JO. Glaucoma associated with retinal disorders and retinal surgery. In:Tasman W, Jaeger EA, eds.
Duane’s Clinical Ophthalmology. Vol 3. Philadelphia,PA: Lippincott Williams & Wilkins:chap 54E.)

44. B. RUBEOSIS IRIDIS:
Normal IOP
NVI starts from the pupillary margin as tiny tufts or red
spots.
Can be easily missed so examine carefully on S/L with an undilated pupil
under high magnication .
Usually NVI is usually present before NVA.
However, in some cases, neovascularization can start at the angle rst.
Gonioscopy in an undilated pupil is essential in all high-risk
cases to diagnose early NVA.
MCC of NVI: DM ,CRVO

45. NVI
Thin , tortuous , arborising,
fenestrated, irregular size
and course
Randomly oriented on
the surface of iris
Arise near the
pupillary margin
NORMAL
IRIS
VESSELS
Thick, radial , non
fenestrated, Uniform size
Arise from the iris
root
Visible until mid periphery
and disappear into the
stroma
LEAKS ON FALEAKS ON FA DOES NOT LEAK ON FADOES NOT LEAK ON FA

46. Slitlamp view of the iris
showing
rubeosis with tortuous
vessels on the surface of the
iris.
The rubeosis iridis begins intrastromally and then develops on
the
surface of the iris

47. C. OPEN ANGLE GLAUCOMA:
New vessels from the pupillary margin grow radially on the surface of the iris.

These vessels grow toward the angle, cross the ciliary body band and scleral spur.

A brovascular membrane, invisible on gonioscopy, accompanies the new vessels,
blocks the trabecular meshwork, and raises the IOP.

Incidence of NVG in patients with diabetes and rubeosis iridis ranges from 13% to
41%.

However, incidence of NVI in CRVO is probably signicantly higher.

48. NVI is more orid in this stage.

S/L often reveals an inammatory reaction and sometimes a hyphema

On Gonioscopy: AC angle-open, NVA ++.

The IOP is elevated and may rise suddenly, causing the patient to present with acute-
onset glaucoma.

Hallmark- brovascular membrane that covers the anterior chamber angle

Chronic inammatory changes are also typically seen on histologic examination.

49. brovascular
membrane,
inammation
and
hemorrhage
neovascular
tissue found
in the
trabecular
spaces
obstruction
of the
trabecular
meshwork
IOP elevation
in eyes with
neovascular
glaucoma.
Results in
glaucoma in
this stage
This stage is often responsive to medical IOP-lowering therapy
since the trabecular meshwork may still be partially functional

50. Hyphema in neovascular glaucoma from CRVO.
A: hyphema is present,with rubeosis. B: Fundus
in the same eye shows diffuse intraretinal
hemorrhages along the vascular arcades and
macula.
From Scruggs BA, Quist TS, Syed NA, Alward WLM. Neovascular
Glaucoma. EyeRounds.org. Posted May 22, 2018.
NEOVASCULARIZATION OF
ANGLE

51. D. CLOSED ANGLE GLAUCOMA
Myobroblasts in the brovascular membrane proliferate and contract to form PAS

Contracture of these brovascular membrane causes alterations of iris and anterior
chamber angle causing angle closure.

This leads to angle-closure glaucoma.

Glaucoma in this stage is typically severe and usually requires surgical
intervention.

52. The clinical features of advanced stage of NVG are as
follows:
• Severe decrease in visual acuity
• Eye pain
• Conjunctival and episcleral congestion
• Corneal edema
• Aqueous are
• Very high IOP
• Florid NVI and angle
• Ectropion Uveae
• Synechial angle closure on gonioscopy

53. Ectropion uvea in neovascular glaucoma. Slit lamp view
shows numerous new vessels on the iris, with pupillary
dilatation and ectropion uvea due to contracture of the
brovascular membrane.

54. THE TIME SEQUENCE OF PROGRESSION
FROM RUBEOSIS IRIDIS - ANGLE
CLOSURE IS VARIABLE
PROGRESSION
Rubeosis to angle closure within
days
Rubeosis to angle involvement –
may take years
Rubeosis – ANGLE
INVOLVEMENT (MAY TAKE
YEARS ) – AND ANGLE CLOSURE
CAN OCCUR WITHIN DAYS
CRVO – FULMINANT COURSECRVO – FULMINANT COURSE DIABETIC RETINOPATHY – SLOW COURSEDIABETIC RETINOPATHY – SLOW COURSE
WHY ? IN DIABETIC RETINOPATHY , PERHAPS IT TAKES A LONGER
TIME FOR ENOUGH RETINA TO BECOME ISCHEMIC

55. DIFFERENTIAL DIAGNOSIS:
Condition Differentiating Features
Uveitis* Radial, engorged iris vessels, are,
keratic precipitates
Acute Angle Closure Pupillary block; convex iris contour,
lack of neovascularization or
retinal pathology
Chronic Angle Closure Lack of neovascularization or
retinal pathology
Retinal Detachment* Fundus pathology
Intraocular Tumors* Fundus pathology
Postretinal Detachment Repair*Angle closure

56. EVALUATION IN NVG:
1. Clinical history:
Systemic risk factors and its assessment.
Systemic condition Recommended tests
Hypertension Blood pressure
Diabetes Blood sugar and HbA1c
Ocular ischemic syndromereCarotid Doppler (retrobulbar vessels, intra, and extracranial)
Magnetic resonance and computed tomographic angiography Carotid
intra-arterial digital subtraction angiography (selectively and with
extreme caution)
Carotid cavernous stula/tumor
metastasis Uveitis, retinal
vasculitis, blood dyscrasis
CT scan/magnetic resonance imaging/MR venogram/PET scan HLA B
27 Hemogram+ESR, CRP, ANA, VDRL, serum protein electrophoresis,
and immunoelectrophoresis (rules out hyperviscosity syndromes
Ancillary investigations to exclude tubeculosis, sarcoidosis, blood
dyscrasias, etc.

57. Past ocular history for possible conditions that can lead to the development of NVG,
including PDR or CRVO.

 Assess what previous treatments the patient has had for underlying retinal ischemic
disorders (PRP or anti VEGF)

Whether the patient has ever been diagnosed with high IOP or glaucoma in the past.

Assess the onset and duration of disease.

Based on symptoms: Early-asymptomatic, late stages- pain, decreased vision,
headache.

58. 1.
1.
2.
3.
2. Examination:
VISUAL ACUITY: most cases poor D/T corneal edema or underlying retinal disease

PUPIL EXAMINATION: for RAPD, studies showed CRVO cases with RAPD are at more risk of
NVI formation

IOP: initially normal, as angle starts to close, IOP rises.



On Slit Lamp Biomicroscopy:
Conjunctiva and Cornea: - Conjunctival hyperamia
- Corneal edema: in acute IOP rise
- Cornea can be clear in cases with longstanding high IOP

Anterior Chamber: - hyphema due to NVI,
- mild AC reaction
-advancestagesshallowACduetoPAS

59. 4.
5.
Iris: - Examination of the iris prior to dilation and under high magnication to assess NVI
- Neovascularization is usually rst noted at the pupillary border
- Corectopia and ectropion uveae in advanced stages
- Fibrovascular membrane formed in advance stages
- posterior synechiae or an infammatory membrane at the pupil margin

Gonioscopy: - Undilated for NVA
- Early stages: NVA + but angle open
- Late stages: NVA +,PAS +,angle closure

Dilated Fundus: Thorough dilated fundus examination for underlying etiologies for NVG
a. PDR (NVD or NVE),
b. Old CRVO (optociliary shunt vessels, vessel sheathing)
c. Ocular ischemic syndrome (mid-peripheral retinal hemorrhage )
d. Presence of tractional retinal detachment in PDR or other
disease requiring silicone oil for repair may impact surgical planning, such

60. 3. Ancillary Testing:
While NVG is primarily a clinical diagnosis, ancillary testing can help assess the degree of
glaucoma damage and identify underlying etiologies.

Fundus Fluorescein Angiography (FFA) of the retina and iris: FFA is an invasive test to
detect NVD,NVE, and areas of CNP. In early stages, the NVI may be unnoticeable, so it can
be detected by iris uorescein angiography.

Optical coherence tomography angiography (OCTA) of the retina: OCTA of the retina is a
rapid, non-invasive modality for diagnosing NVD, NVE, and CNP areas. Retinal ischemia can
also be assessed OCTA. OCTA can also be used to monitor disease status over
subsequent visits.

OCTA of iris: Neovascularization of the iris can also be detected using OCTA.

61. B-scan: Detection of lesions of the posterior segment of the eyes. B scan can
detect the presence of vitreous hemorrhage and additional brous proliferation,
tractional or rhegmatogenous retinal detachment. Mass lesions like choroidal
melanoma, ciliary body melanoma, and retinoblastoma can be detected. Detect
retinal detachment in the advanced stages of ROP with NVG

62. 


Recent Tests:

Electroretinogram also can help in diagnosing retinal ichemia

Anterior segment optical coherence tomography

ultrasound biomicroscopy.


ASOCT AND UBM - diagnosis and staging
of the disease as they illustrate anterior chamber structures
in greater detail.

63. PROPHYLACTIC THERAPY IN NVG:


Panretinal photocoagulation effective prophylaxis against the development
of NVG.
Indications:
- In CRVO, on follow up if early signs of NVI seen
- In DR, Vitrectomy, Lensectomy and peripupillary orescein leak.

64. •
•
•
•
Randomized controlled trial in
eyes with ischemic central vein
occlusion
Aim was to see if PRP in ischemic
CVO prevents development of NVI
or NVA.
It concluded that prophylactic
PRP does not totally prevent NVI or
NVA
It was recommended to have
frequent follow up in such cases
and prompt PRP on NVI formation

65. TREATMENT:
Management of NVG can be divided into two types:
1. Treatment of underlying disease process responsible for
rubeosis

2. Treatment of elevated IOP.

Anti-neovascular therapies and aggressive management of the retinal
disease are of utmost importance in any stage of NVG to target the
primary etiology.

66. TREATMENT PRINCIPLES
PRINCIPLE
S
Treat Retinal
Ischemia
Control IOP
Control
Inammation
Treat
underlying
systemic
disease
PRPPRP ANTI VEGFANTI VEGF

67. 1. TREATMENT OF UNDERLYING
DISEASE:
A. Panretinal Photocoagulation:
- mainstay in controlling the neovascular drive
- should be considered in all cases of NVG if retinal ischemia is present.
- done in clear media


MECHANISM →

68. - Signicantly reduce anterior segment neovascularization and reduce NVI.

- Performed in 1–3 sittings.

- Additional laser treatment needs to be done until complete regression of new vessels.

- In CRVO, PRP is indicated in the ischemic form and also in anterior segment
neovascularization.

- In OIS, uveal ischemia can be responsible for neovascularization and PRP should be
performed only if FFA shows retinal ischemia

69. • Aim of the study was to assess
efficacy of laser therapy for ischemic
CRVO. It was noted that laser photo
coagulation prevents severe vascular
complications of CRVO. It was also
seen laser photo coagulation was able
to increase retinal blood ow in eyes
with ischemic CRVO.

70. Hamanaka T, Omata T, Akabane N, Yajima T, Ishida N(2012) Retinal
Photocoagulation Density in the Treatment of Neovascular Glaucoma due to
Diabetic Retinopathy. J Clinic Experiment Ophthalmol S4:007. doi:10.4172/2155-
9570.S4-007

71. Study was done in 80 vitrectomy eyes with
previtrectomy PRP and compared with 402
eyes without PRP. Study showed that PRP
before vitrectomy for diabetic retinopathy
did not prevent postoperative rubeosis
iridis.In these cases, intraocular PRP at the
time of vitrectomy may be the procedure of
choice.
Retrospective cross sectional study was done in
11 eyes with new on-set neovascular glaucoma
cases without PRP and with UWFA completed.
Aim was to study patterns of non perfusion in
neovascular glaucoma cases. Ischemic index was
found to be 91% in far periphery 77% in mid
periphery and 42% at the posterior pole. There
was a statistically signicant difference between
the ischemic index in far periphery, posterior Pole
and mid periphery. The study concluded that this
knowledge can be used for further guide
treatment and understand risk of NVG.

72. B. Panretinal Cryotherapy
- Done in cloudy media where PRP not possible.

- In these cases transscleral panretinal cryotherapy can be combined with cyclocryotherapy.

- It controls the IOP and reduce or abolish the neovascularization.

74. Anterior Retinal Cryotherapy



8 cryo application in each quadrant – anterior to the equator in two rows

Each application for 8 seconds

75. •
•
•
•
•
•
Prospective study, the effect of anterior
retinal cryoablation (ARC) in the management
of neovascular glaucoma (NVG)
74 eyes were studied.
Following ARC, pain relief with regression of
anterior chamber inammatory reaction was
observed in 95% of the patients.
Regression of neovascularization of the iris
was documented in 93.5%.
Intraocular pressure control was achieved in
82.3%
ARC is strongly recommended in NVG,
especially in eyes with media opacities and as
a preliminary procedure for ltering surgery
or drainage implant surgery.

77. C. Anti VEGF Agents
- Anti-VEGF injection leads to regression of anterior and posterior segment
neovascularization and reduction of IOP.
- Anti-VEGF agents used: bevacizumab (Avastin), ranibizumab, and aibercept
- IV Bevacizumab causes regression of NVI and NVA within 24–48 h compared to PRP,
which takes 2–3 weeks.
- Avastin effective in reducing intraocular inammation and pain, and IOP lowering has
been noted in the open-angle stage.
- anti-VEGFs are used only as an adjunct to PRP, medical therapy, and surgery

78. - The most frequent recommendation is the combination of IV anti VEGF and PRP.

- PRP with adjunctive use of intravitreal anti-VEGF agent along with antiglaucoma
medications may be sufficient to control IOP in the open-angle stage of NVG.

- Surgical intervention for IOP lowering is often required in advanced stage with
synechial angle closure.

- repeated intravitreal anti-VEGF injections may cause both transient as well as
sustained elevation of IOP

79. •
•
•
•
Retrospective study done in 34
NVG eyes.
Aim was to assess long term
effects of IVB in NVG
Study concluded IVB has
favorable effect in controlling IOP
and pain in as it decreases
angiogenesis.
It can be used as an adjunctive
treatment
•
•
•
Prospective study done in newly
diagnosed NVG.
Aim was to investigate initial results
regarding treatment of NVG with IV
aibercept.
Study concluded that IV aibercept
may be an effective treatment for
stage 1 and 2 NVG. Results in rapid
regression of NVI and NVA as well as
IOP control.

80. •
•
•
Purpose was to summarize reports of both
transient and sustained IOP elevation due to
anti VEGF injections
Repeated IV anti‑VEGF injections may
cause both transient as well as sustained
elevation of IOP.
Regular monitoring needed

81. 1.
2.
3.
D. Gene Therapy : Future Therapeutic strategies
Various pharmacological agents that modulate the angiogenesis cascade now
offer great potential as therapeutic agents for NVG.
Pigment epithelium derived factor (PEDF) overexpression inhibits retinal
inammation and neovascularization in mouse models.
VEGF trap (EYLEA, Bayer), a modied soluble VEGF receptor analog binds VEGF
more tightly than all other anti-VEGF therapies.
Small interfering RNA (siRNA) targeting VEGF expression has been
downregulated in vitro and in vivo, leading to .inhibition of retinal
neovascularization.

82. 2. CONTROL OF IOP
A.
-
-
Medical management
- Sufficient to control the pressure in the OAG stage if treatment is
initiated early
AGM of rst choice: Beta blockers, topical carbonic anhydrase inhibitors,
alpha‑2 adrenergic agonists.
PG analouges are not of much use in closed angles and have risk to
increase inammation.

83. -
-
-
-
Pilocar is C/I as they may increases inammation and worsen synechial angle
closure due to miosis .

Atropine: cycloplegia.

Topical corticosteroids: reduce inammation and pain

Hyperosmotic agents and oral carbonic anhydrase inhibitors: for temporary
control high IOP and help clear corneal edema

84. MEDICAL THERAPY
ANTIGLAUCOMA MEDICATIONS -
B
BLOCKERS
ALPHA 2
AGONISTS
PILOCARPINE
PROSTAGLANDI
N ANALOGUES
CARBONIC
ANHYDRASE
INHIBITORSX
•
•
TOPICAL
STEROIDS – TO
REDUCE
INFLAMMATION
ATROPINE 1 % -
TO REDUCE
OCULAR
CONGESTION

85. B. Surgical management

Glaucoma surgery indications:
1. Open‑angle stage of NVG to control IOP until PRP takes effect
2. Synechial angle‑closure stage for long‑term IOP control.

Surgical interventions for NVG:
1. trabeculectomy with antimetabolites
2. Glaucoma Drainage Devices
3. Cyclodestructive procedures.

86. 1.
-
-
-
TRABECULECTOMY

- In NVG success of trabeculectomy alone is limited due inammation, high risk for
intraoperative bleeding and postoperative progression of the brovascular
membrane.
PRP with anti- VEGF, reduces NVI and inammation, increasing success rate of
trabeculectomy with 5-FU/MMC.
Prognostic factors for surgical failure: young age and vitrectomized eyes.
Surgical intervention should be planned within a week of injection of anti‑VEGF.

87. •
•
•
•
Prospective case series.
NVG cases not responding to PRP or
could not receive PRP were taken
Aim was to asses efficacy of preop IVB
with ltration surgery and MMC in NG
It concluded preop IVB with ltration
surgery with MMC is safe and effective
method to control IOP

•
•
•
•
Retrospective study done in 52 NVG eyes.
Aim was to study effects of preop IVB on
outcomes in trabeculectomy for NVG.
Study concluded that IVB reduces postop
hyphaema and increase surgical success
rates.
IVB is effective adjuunct to TRAB in NVG

88. -
-
-
2. Glaucoma drainage devices
Indications:
1. Trabeculectomy fails/Refractory glaucoma
2. High risk of failure because of excessive conjunctival scarring.
- implantation of drainage tubes or valves in:
1. Anterior chamber
2. Pars plana (with PPV)
Use of anti‑VEGFs is recommended at least 24 h before surgery.
GDD’s used: 1. Aurolab Aqueous Drainage Implant(AADI)
2. Baerveldt implant
3. Ahmed glaucoma valve

89. -
-
GDD tube in AC reported complications like endothelial cell loss ,tube corneal touch and
foreign body reaction.
Pars Plana insertion of GDD in vitreous cavity is preferred route in:
1. corneal edothelial compromise
2. corneal vascularization.
3. small eyes/inadequate AC depth

90. Kader MA, Dabke SB, Shukla AG, Reddy V, Abdul Khadar SM, Maheshwari D, Ramakrishnan R. Pars plana Aurolab
aqueous drainage implantation for refractory glaucoma: Outcome of a new modied technique. Indian J Ophthalmol. 2022
Mar;70(3):839-845. doi: 10.4103/ijo.IJO_1791_21. PMID: 35225526; PMCID: PMC9114538.

93. •
•
•
•
This study was done in 18
eyes with pp AGV and 18 eyes
with ac AGV
purpose of study was to
compare changes in corneal
endothelium cells after pars
plana AGV and anterior
chamber AGV
It concluded that endothelial
cell damage in ppAGV was less
than acAGV.
ppAGV can be preferred as it
has less endothelial cellloss

94. -
-
-
-
-
3. Cyclodestructive procedures:
Effective option in eyes with refractory NVG having poor visual prognosis.
Procedure destroys the ciliary body to reduce aqueous humor production.
Effective option to control IOP in poor visual prognosis
Transscleral cyclophotocoagulation or endocyclophotocoagulation (Limbal
or Pars Plana approach) may have a lower complication rate than
cyclocryotherapy.
painful blind eyes: retrobulbar alcohol injection

95. 



TRANSCLERAL CYCLOPHOTOCOAGULATION:
Most widely used method of ciliary ablation

DIODE LASER: 810 wavelength used

1250 mW for 3 seconds with 18-24 spots

40-80% success rates

96. FUTURE THERAPEUTIC OPTIONS




Several treatment options for NVG are under investigation

1. SURGICAL RETINECTOMY :

to reroute the aqueous through the choroidal circulation
done at the time of pars plana vitrectomy
complications : retinal detachment , proliferative vitreo retinopathy and
pthisis bulbi

97. 

2. PHOTODYNAMIC THERAPY :
VERTEPORFIN - To occlude new iris vessels without damaging the surrounding
healthy tissue or normal iris vessels
No results on the progression of rubeosis or nvg have been reported yet



3. INTRAVITREAL INJECTION OF CRYSTALLINE TRIAMCINOLONE : Being studied as
a potential treatment to regress iris vasculature

99. THANK YOU
THANK YOU