This document discusses retinal vascular occlusions, including their classification, presentation, investigations, and management. It begins by introducing retinal arterial and venous occlusions as significant causes of blindness. It then covers the anatomy of retinal blood supply and classifies occlusions by anatomical site. The remainder of the document details the characteristics, risk factors, clinical features, investigations, and treatment approaches for various types of retinal arterial occlusions (central retinal artery occlusion, branch retinal artery occlusion, cilioretinal artery occlusion) and venous occlusions (central retinal vein occlusion, branch retinal vein occlusion, hemiretinal vein occlusion).

1. RETINAL VASCULAR
OCCLUSIONS
M O D E R A T O R : D R M A D H U R I M A N A Y A K
P R E S E N T E R : D R P O O J A

2.  INTRODUCTION
 ANATOMY
 CLASSIFICATION
 ARTERIAL
OCCLUSIONS
 VENOUS OCCLUSIONS
 REFERENCES

3. INTRODUCTION
 Retinal vascular occlusions are serious
diseases and significant causes of blindness
that include arterial and venous obstructions
 The clinical presentation aids in distinguishing
the type of the occlusion, which may be
classified according to the anatomical site of
the occlusion

4. Blood supply of RETINA
 Outer 4 layers of RETINA: Choriocapillaries.
 Inner 6 layers of RETINA: Central retinal artery
 The fovea is avascular and is mainly supplied
by Choriocapillaries.
 Cilio retinal artery is present in 20% of eyes
 The veins of the RETINA unite to form Central
retinal vein at the disc , which follows the
corresponding artery

6. CLASSIFICATION
 CENTRAL RETINAL
ARTERIAL
OCCLUSION
 BRANCH RETINAL
ARTERIAL
OCCLUSION
 CILIORETINAL
ARTERIAL
OCCLUSION
 CENTRAL RETINAL
VEIN OCCLUSION
 BRANCH RETINAL
VEIN OCCLUSION
 HEMI RETINAL
VEIN OCCLUSION
ARTERIAL OCCLUSION VENOUS OCCLUSION
COMBINED CENTRAL RETINAL ARTERY
AND
VENOUS OBSTRUCTION

7. RETINAL ARTERIAL
OCCLUSIONS
 Visual loss from retinal arterial occlusion
(RAO) occurs from the loss of blood supply to
the inner layers of the retina
 CAUSES:
ATHEROSCLEROSIS
EMBOLISM

8. Hollenhorst plaques(Cholesterol) Fibrin platelet
Calcific emboli

9.  Systemic cardiovascular disease
 Coagulopathies
 Systemic vasculitis
 Oncologic
 Infective diseases
 Trauma
 Ocular conditions
 Oral contraceptives, Pregnancy, Drug abuse,
Migraine

10. CENTRAL RETINAL ARTERY
OCCLUSION
 Incidence and demographics:
 Frequency -1 per 10,000 outpatients visits
 CRAO accounts for (57%), BRAO(38%), CRAO(5%)
 Mean age at the time of presentation is in the early 60’s
 Men affected more then women
 1-2 % of cases have B/L involvement, for which the
DD : should include cardiac valvular disease , GCA and
other vascular inflammations.

11. CLINICAL FEATURES
 Sudden and profound LOSS of vision,
painless except in GCA.
 VA is severely reduced
 RAPD present
 RUBEOSIS IRIDIS(1/5 eyes)

12. FUNDUS
 Superficial retina
YELLOW WHITE APPEARANCE
 CHERRY RED SPOT
 Cattle trucking/box caring
 Retinal/Disc NV(2%)
 LATE signs:
Optic atrophy
Narrowing of vessels
Vessel sheathing
RPE changes

13. CRAO with patent cilioretinal .
A
Old CRAO

14. INVESTIGATIONS
 FA: Delay in retinal arterial filling (highest
SPECIFICITY).
Delay in Retinal A-V transit time (Most common and
highest SENSITIVITY)

15. OCT: shows highly reflective emboli plaque within
superficial nerve head
ERG: Diminution of amplitude of “b” wave,
with normal “a” wave

16. BRANCH RETINAL ARTERIAL
OCCLUSION
 BRAO occurs when the embolus lodges in a
more distal branch of the retinal artery.
 Typically involves the TEMPORAL retinal
vessels
 Clinical features
 Sudden and painless SECTORAL visual field loss
 VA is variable.
 RAPD is often present.

17. FUNDUS
 Cattletrucking/boxcarrin
g.
 Cloudy white
oedematous retina
corresponding to the
area of ischaemia.
 Artery to artery
collateral may develop
in retina

18. INVESTIGATIONS
 FA shows delay in arterial filling and hypo
fluorescence of the involved segment due to blockage
of background fluorescence by retinal swelling

19. CILIO RETINAL ARTERIAL
OCCLUSION
 Cilioretinal arteries-Temporal aspect of the
optic disc , separate from the CRA
 20% of eyes
 Provides second arterial supply to the
MACULA from posterior ciliary circulation.
 On FFA fill concomitantly with choroidal
circulation 1-2 seconds before retinal arteries

20. THREE VARIANTS
ISOLATED :
• >40%
• Young patients
with systemic
vasculitis
• Good visual
prognosis
• No ocular
treatment required

21. WITH CRVO:
 >40%
 Reduced pressure in the
CilioRA as compared to CRA
 Better visual prognosis
 No ocular treatment required

22. WITH AION :
 15%
 Both appear to be
manifestations of
posterior ciliary
insufficiency
 Poor prognosis
 GCA as a cause
should be
investigated.

23. TREATMENT OF ACUTE ARTERIAL
OCCLUSION:
OCULAR
 Retinal artery occlusion is an emergency
because it causes irreversible visual loss unless
the retinal circulation is re-established prior to
the development of retinal infarction
 The following treatments may be tried in
patients with occlusions of less than 24 hours
duration at presentation.
.

24.  Adoption of a supine posture
 Ocular massage
 Anterior chamber paracentesis
 Sublingual isosorbide dinitrate to induce vasodilation.

25.  ‘Rebreathing’ into a paper bag OR Breathing
‘CARBOGEN’.
 Topical apraclonidine 1%, timolol 0.5% and intravenous
acetazolamide 500 mg to achieve sustained lowering
of intraocular pressure
 Hyperosmotic agents. Mannitol or glycerol
 Transluminal Nd: YAG laser embolysis.

26. SYSTEMIC
 General risk factors like smoking to be discontinued.
 Anti- Platelet therapy to be started , if not CI.
 Oral anticoagulants treatment (e.g.Warfarin) in
patients with AF
 Carotid endarterectomy in symptomatic stenosis
greater than 70%
 Asymptomatic retinal embolus if identified ,indicates
increased risk of stroke and IHD, evaluation and
treatment of risk factors is required.

27. FOLLOW UP
 CRAO: After 3-4 weeks and a minimum of twice
subsequently at monthly intervals to detect
neovascularization of Anterior segment
 BRAO: After 3 months

28. RETINAL VENOUS
OCCLUSIONS

29. RISK FACTORS:
1. AGE: 50% of cases occur in >65 years .
2. HYPERTENSION :73% in >50 years ,25% in younger
patients
3. HYPERLIPIDAEMIA (total cholesterol >6.5 mmol /l) is
present in 35% of patients
4. DIABETES MELLITUS 10% of cases over the age of 50
years
5.OCULAR: OAG, Ischemic optic neuropathy , Optic
nerve head drusen

30. CENTRAL RETINAL VEIN
OCCLUSION
 Incidence and demographics :
 Prevalence of CVO - 0.1-0.4%.
 Age at the time of presentation is above
60’s
 Men and women equally affected
 U/L ,with 1% risk of development in the
fellow eye by the end of 1 year, 7% risk by
the end of 7 years.

31. NON-ISCHAEMIC CRVO
 Non-ischaemic CRVO is the most common
type, accounting for about 75%.
 CLINICAL FEATURES:
1.Sudden painless unilateral loss of vision.
2.VA is impaired to a moderate-severe degree.
3.RAPD is absent or mild (in contrast to ischaemic
CRVO)

32. FUNDUS
 Tortuosity and dilatation of all the branches
 Dot/blot and flame-shaped haemorrhages,
throughout ALL quadrants
 Cotton wool spots, Disc and macular oedema
are common.
 Most acute signs resolve over 6–12 months.
 OPTOCILIARY shunts/RETINOCHOROIDAL
shunts
Conversion to ischaemic CRVO occurs in 15%

33. Investigations
o FA shows delayed A-V transit time, blockage
by haemorrhages, good retinal capillary perfusion(<10 disc
areas of non perfusion) and late leakage.
o OCT is useful in the assessment of CMO(mild
in NI-CRVO)
Follow up:
Initial follow-up should take place after
3months.
Subsequent review is usually at 18-24

34. Recent non-ischaemic CRVO

35. Old non-ischaemic CRVO

36. ISCHAEMIC CRVO
 Clinical features:
1. Sudden and severe painless unilateral loss of
vision, occasionally can present with pain,
redness or photophobia
2. VA is CF or worse
3. RAPD is present
4. Anterior segment findings : NVI , ANV,
NVG(100 day glaucoma).CVOS STUDY

37. RUBEOSIS IRIDIS

38. FUNDUS
 Tortuosity of all branches
 Extensive deep dot/blot and
flame-shaped
haemorrhages,
 Cotton wool spots are
prominent, optic disc
swelling usually present.
 Most acute signs resolve
over 9–12 months.

39. INVESTIGATIONS
 FA shows delayed arteriovenous transit time,
masking by haemorrhages, extensive areas of
retinal capillary non- perfusion(10 or > disc areas in
diameter)
 OCT is useful in quantification of CMO
 Electroretinogram (ERG).

40. Recent ischemic CRVO

41. MANAGEMENT

42. SYSTEMIC ASSESSMENT
 ALL PATIENTS
 BP
 ESR,CBC
 RBS
 HDL . Cholesterol
 OTHERS:
 Urea Creatinine Electrolytes (renal
disease @ with HTN)
 Thyroid function tests
 ECG(LVH is associated with HTN)
 SELECTED
PATIENTS
(<50 yrs, B/L, Common inv-negative, family h/o
thrombophilia)
 Chest X ray: TB, Sarcoidosis
 CRP: sensitive indicator for
inflammation
 Plasma homocysteine level
 “Thrombophilia screen”
 Plasma Protein electrophoresis
 Autoantibodies: RF, ANA, ANCA,
anti-DNA antibody
 ACE: Sarcoidosis
 Treponemal serology
 Carotid duplex imaging

43.  Medical therapy
 Treatment of MACULAR OEDEMA:
a) VA worse than 6/9 and significant central macular
thickening on OCT
b) Intravitreal anti-VEGF agents: Ranibizumab showed
a significant visual benefit when used for CMO
c) Intravitreal Dexamethasone implant
d) Intravitreal Triamcinolone:
The SCORE study showed an improvement in the vision of 3 or more
lines at one year in over 25% of patients treated with an average of 2
injections of 1 mg triamcinolone versus 7% of controls.

44.  e) Laser photocoagulation
CVOS study: Grid pattern argon laser photocoagulation did
reduce macular oedema by 1 year (31%), BUT it did not result
in an improvement in visual acuity.
OTHER treatments include
Chorioretinal anastomosis
Pars plana vitrectomy
Radial optic neurotomy
Recombinant tissue plasminogen
activator(r-tPA)

45.  Treatment of NEOVASCULARIZATION
a) PRP in eyes with NVI or NVA:application of
1500–3000 burns (0.5–0.1 second, spaced one burn
width apart).
CVOS study: PRP should be given after the development of INV/ANV
and not prophylactically, to be considered in patients with RF of
developing INV/ANV or follow up not possible
b) Intravitreal anti-VEGF agents

47. BRANCH RETINAL VEIN
OCCLUSION
 Macular BRVO involving only a macular branch
 Peripheral BRVO not involving the macular circulation
 Clinical features:
1. Sudden painless onset of blurred vision
Peripheral occlusion may be asymptomatic
2.VA is variable
3. NVI and NVG are much less common than CRVO
(2-3% at 3 years )

48. FUNDUS
• Tortuosity with dot/blot &
flame-shaped haemorrhages
• Cotton wool spots and
retinal oedema are present
• SUPEROTEMPORAL
quadrant
• Resolution over 6–12
months.
• Retinal neovascularization
8%

49. Superior branch vein occlusion

50.  Residual findings-
Venous sheathing and sclerosis, persistent /recurrent
haemorrhages.
Collaterals may form near areas of limited capillary
perfusion.
 FA shows peripheral and macular ischaemia, Venous
filling delayed
 OCT is useful in quantification of CMO

51. Management
 Systemic assessment
 Observation without intervention if VA is 6/9 or
better
 NVE/NVD: sector photocoagulation 400-500 µm
diameter for 0.05 sec duration and spaced one burn width
apart are applied to ischaemic area.
 NVI : Sector PRP
 Intravitreal anti-VEGF agents
 Intravitreal Dexamethasone implant

52.  Macular laser:
Eligibility criteria
Method
 Intravitreal Triamcinolone
 Review : After 3months and then 3-6 monthly
intervals for 2 years to detect neovascularization

53. HEMIRETINAL VEIN OCCLUSION
 Hemiretinal vein occlusion is generally
regarded as a variant of CRVO and may be
ischaemic or non-ischaemic.

54. DIAGNOSIS
 Sudden onset altitudinal visual field defect.
 VA reduction is variable.
 NVI more common than BRVO , but less than
CRVO
 FUNDUS shows the features of BRVO,
involving the superior or inferior hemisphere ,
NVD more common
 FA shows masking by haemorrhages , hyper
fluorescence due to leakage and variable
capillary non perfusion

55. Inferior hemiretinal vein
occlusion

56. TREATMENT
 Depends on the severity of retinal ischaemia
Extensive retinal ischaemia carries the risk of
neovascular glaucoma and should be
managed in the same way as ischaemic
CRVO.
 Macular oedema usually responds poorly to
grid laser due to extensive foveal capillary
shutdown

57. Systemic treatment in retinal vein
occlusion
 Control of systemic risk factors
 Antiplatelet therapy with aspirin or an
alternative agent should be considered

59. COMBINED RETINAL ARTERY AND VEIN
OCCLUION

61. References
 Ryan Retina
 American Academy of ophthalmology
 Kanski’s clinical ophthalmology
 Retinal vein occlusions by royal college of
ophthalmologists

62. THANK YOU