Retinal arterial obstructions can manifest as central retinal artery obstruction (most common), branch retinal artery obstruction, or chorioretinal artery obstruction. The document discusses the history, etiology, clinical features, investigations, management, and prognosis of these conditions. Common causes include emboli (cholesterol, calcific), atherosclerosis, hypertension, and giant cell arteritis. Clinical features include sudden visual loss, afferent pupillary defect, and pale retina. Investigations include fluorescein angiography and ultrasound. Management involves ocular massage, oxygen, fibrinolytics, and treating underlying conditions. Prognosis depends on location and severity of obstruction.

1. Retinal Arterial ObstructionsRetinal Arterial Obstructions
DR.SHAH-NOOR HASSAN FCPS,FRCS
Assistant Professor
Vitreo-Retina Unit
Dept. of Ophthalmology
BSMMU

2. IntroductionIntroduction
Retinal arterial obstructive diseases can
manifest in different clinical forms.
Classification:
1. Central retinal artery obstruction (57%)
2. Branch retinal artery obstruction (38%)
3. Ciioretinal artery obstriction (5%)
4. Combined CRAO and CRVO
5. Cotton-wool spots

3. HistoryHistory
Von Graefe 1859: Embolic CRAO in
patients with endocarditis
Sweiger 1864: Histopathological
description
Mauthner 1868: Spasmodic contractions
could lead to retinal arterial obstruction
Loring 1874: Focal obstructive disease
within retinal vessels as the cause

4. AetiologyAetiology
Intramural
◦ Emboli
◦ Thrombus
Mural
◦ Luminal narrowing
Extra-mural
◦ External compression

5. Intra-mural- EmboliIntra-mural- Emboli
Most common cause of retinal arterial
occlusions
Visible in 20-40% of arterial occlusions
Systemic implications
◦ 9 year mortality-56% with emboli
27% without emboli
Types:
◦ EXOGENOUS
◦ ENDOGENOUS

6. Endogenous emboliEndogenous emboli
Cholesterol emboli
◦ Glistening yellow
◦ Small peripheral asymptomatic block
Fibrin-platelet emboli
◦ Dull, grey, elonagetd, multiple
◦ Fills the entire lumen
Calcific emboli
◦ Larger, more severe obstruction
◦ Single, white, near the disc

7. Endogenous emboliEndogenous emboli
 Fat emboli
 Long bones
 Amniotic fluid emboli
 Complications of pregnancy
 Tumor emboli
 Atrial myxoma
 Erythrocyte aggregation
 Sickle cell disease
 Leuko-emboli

8. Exogenous EmboliExogenous Emboli
Air emboli
◦ Trauma or surgery
Talc
◦ IV drug abuse impurities
Corticosteroid
◦ Intralesional Rx
Synthetic material
◦ Valves, catheters, prosthesis

9. Luminal narrowingLuminal narrowing
Atherosclerosis with thrombosis
◦ Commonly seen with CRAO
Haemorrhage into the atheromatous
plaque
Vasospasm
Vasculitis

10. Atherosclerosis-related thrombosis at
the level of the lamina cribrosa is by far
the most common underlying cause of
central retinal artery occlusion (CRAO),
accounting for about 80% of cases.
Atherosclerosis is characterized by focal
intimal thickening comprising cells of
smooth muscle origin, connective tissue
and lipid-containing foam cells .

11. Blood VesselBlood Vessel

13. External compressionExternal compression
Disc oedema
◦ Papillitis
◦ Papilledema
◦ AION
◦ CRVO
RB injection
Ocular Compression
◦ During surgery

14. Retinal HypoperfusionRetinal Hypoperfusion
Systemic hypotension
Ocular hypertension
Blood dyscrasias

15. Central retinal artery occlusionCentral retinal artery occlusion

16. IntroductionIntroduction
Blockage within the optic nerve
substance-CRAO
Blockage distal to lamina-BRAO

17. Incidence and DemographyIncidence and Demography
1:10,000 of outpatient visits
57% of the arterial occlusions
Older adults
Early sixties
M>F
1%-2% bilateral: consider cardiac valvular
disease, giant cell arteritis and other
vascular inflammations

18. Clinical featuresClinical features
Sudden onset painless visual loss
occurring over several seconds
Preceding history of amaurosis fugax
Afferent pupillary defect develops
seconds
Anterior segment:
◦ Initially normal

19. Cont…Cont…
Vision
◦ 90% cases: CF to PL
◦ No PL: choroidal or optic nerve damage
◦ 10% cilioretinal artery spares foveola
 VA>20/40 in 80% over 2 weeks
 Small island of central vision

20. Clinical features: posterior segmentClinical features: posterior segment
Yellow-white opacified retina :
◦ Ischaemic necrosis affecting the inner half
of the retina
◦ Less in areas outside the macular area
Cloudy swelling
Cherry red spot at the foveola:
◦ Extremely thin foveal retina
◦ View of underlying RPE and choroid
◦ Nourished underlying choroid

21. Clinical featuresClinical features
Attenuated retinal arteries
Retinal veins: can be thin, dilated or even
normal in appearance
Segmentation or “boxcarring” of the
blood column: in severe obstruction

22. Later stagesLater stages
Opacification vanishes in
4-6 weeks
Pale disc
Narrowed retinal vessels
Visible absence of nerve fiber layer in the
region of optic disc
Pigmentary changes: choroidal circulation
is involved

23. Clinical featuresClinical features
Presence of emboli: poor prognosis
Emboli seen in 20%-40% of CRAO
◦ Hollenhorst plaque (Cholesterol emboli)
◦ Calcific emboli

24. Cholesterol emboliCholesterol emboli
 Hollenhorst plaque
 Most common variant
 Glistening, yellow coloured
 Small
 Usually do not obstruct the complete lumen
 Origin
 atherosclerotic deposits in the carotid arteries
 Aortic arch
 Ophthalmic artery
 Proximal central retinal artery

25. Calcific emboliCalcific emboli
Less common
Larger and cause more severe
obstruction
Originate from cardiac valves

26. NeovascularizationNeovascularization
20 % acute central retinal artery
obstruction
Mean time of 4-5 weeks (range 1 to 15
weeks)
NVD 2%-3%
If NVI and NVD already present at the
time of acute CRAO- suspect underlying
carotid artery obstruction

27. InvestigationsInvestigations

28. Fluorescein AngiographyFluorescein Angiography
Delay in the retinal arterial
filling (most specific)
Delay in the arterio-venous
transit time(most sensitive)
Late staining of the optic
disc
Complete lack of filling of
retinal arteries-2% cases

29. FAFA

30. FAFA
Choroidal filling is usually normal
◦ Prolongation of choroidal filling in presence of
cherry-red spot s/o ophthalmic or carotid
artery obstruction
FA reverts back to normal at later stages
as the circulation re-establishes

31. ERGERG
 Decrease in the amplitude of
b-wave
 a-wave is unaffected
 May be normal in some eyes
in spite of less vision because
of re-establishment of retinal
blood flow

32. Visual fieldsVisual fields
Remaining temporal island-choroid
nourishing corresponding temporal retina
Small island of central vision-patent cilio-
retinal artery

33. OCTOCT
Diffuse thickening of the neurosensory
retina. Increased reflectivity was noted
from the inner retinal layers
corresponding to retinal ischemia and
decreased backscattering was observed
from the retinal photoreceptors.

34. OCT SpectralisOCT Spectralis

35. PathologyPathology
 Site: Lamina cribrosa or its posterior aspect
 First week:
 Inner layer intracellular
oedema
 Pyknosis of the ganglion cell
nuclei
 Ischaemic necrosis
 Posterior pole:thick NFL and ganglion cells
 Chronic:
 Diffuse inner retinal atrophy
 Homogenous scar formation

36. Pathology Cont..Pathology Cont..

37. Systemic associationsSystemic associations
90% have systemic disease
2/3rd
of patients have HTN
1/4th
have DM
45% show Carotid atherosclerosis
Increased thrombogenecity
Cardiac valvular disease

38. List of systemic causes…..List of systemic causes…..
 Arterial hypertension
 Carotid atherosclerosis
 Cardiac valvular disease
 Rheumatic
 mitral valve prolapse
 Mural thrombus after MI
 Cardiac myxoma
 Tumours
 IV drug abuse
 Lipid emboli
 Pancreatitis
 Purscher’s retinopathy
 Loiasis
 Radiologic studies
 Carotid angiography
 Lymphangiography
 Hysterosalpingography
 Head & neck corticosteroid
inj
 Retrobulbar injections
 Trauma
 Orbital # repair
 Anaesthesia
 Drug or alcohol induced
stupor
 Coagulopathies
 Sickle cell disease

39. List continues…List continues…
 Homocystinuria
 Oral contraceptives
 Platelet and factor
abnormalities
 Pregnancy
 Prepapillary arterial
loops
 Optic disc drusen
 Increased IOP
 Collagen-vascular
diseases
 SLE
 PAN
 GCA
 Ventriculography
 Fabry’s disease
 Sydenham’s chorea
 Migraine
 Hypotension
 Fibromuscular
hyperplasia
 Optic neuritis
 Orbital mucormycosis

40. Differential diagnosisDifferential diagnosis
Bilateral
◦ Cardiac valvular disease
◦ Giant cell arteritis
◦ Vascular inflammations
Aminoglycoside toxicity
Purtscher’s retinopathy

41. ManagementManagement
 Ocular emergency
 Irreversible damage – 90 to 100 mins
 Aim: is to restore the circulation
 Recovery noted to occur till 3 days after the event
 Give ocular treatment if patient is seen within 24
hours
 Modalities:
 Ocular massage
 Carbogen
 Anterior chamber paracentesis
 Fibirinolytic agents
 Other modalities

42. Transluminal Nd:YAG laser
embolysis has been advocated for
BRAO or CRAO in which an occluding
embolus is visible; shots of 0.5–1.0 mJ or
higher are applied directly to the embolus
using a fundus contact lens. Embolectomy
has been said to occur if the embolus is
ejected into the vitreous via a hole in the
arteriole. The main complication is
vitreous haemorrhage

43. Ocular massageOcular massage
In and out movement with three-mirror
(Goldmann)contact lens or digital
massage
Can dislodge an obstructing embolus-
rare
Increase pressure for 10-15 secs
followed by sudden release
Produces arterial dilatation improving
retinal perfusion
86% increase in volume of flow

44. Oxygen and COOxygen and CO22 (Carbogen)(Carbogen)
95% O2 and 5 % CO2
CO2:
◦ Vasodilator
◦ Increases retinal blood flow
100% O2
◦ Vasoconstriction
◦ Normal pO2 through diffusion from choroid
◦ Improves visual function in CRAO
Rebreathing in the paper bag

45. AC paracentesisAC paracentesis
Causes sudden decrease in the IOP
Perfusion pressure behind the
obstruction pushes the obstructing
embolus

46. Fibrinolytic agentsFibrinolytic agents
Delivered via injection through
supraorbital artery
Reaches CRA in doses 100 times greater
than by systemic administration
Vision improvement noted in 50% of the
patients

47. Other treatment modalitiesOther treatment modalities
Retrobulbar or systemic vasodilators:
papaverine or tolazoline
Sublingual nitroglycerine
Systemic anticoagulants

48. Systemic EvaluationSystemic Evaluation
Many patients will have a history of
vascular disease.
Enquiry should be made about smoking.
Symptoms of GCA should be kept in
mind in older age group

49. Pulse particularly to detect atrial
fibrillation.
Blood pressure
Carotid examination.

50. ECG to detect arrhythmia and other
cardiac disease.
Erythrocyte sedimentation rate and
C-reactive protein to detect the
remote possibility of GCA.

51. Other blood tests include FBC,
random glucose, lipids, urea and
electrolytes.
Carotid duplex scanning is a non-
invasive screening test involving a
combination of high-resolution real-time
ultrasonography with Doppler flow
analysis. If significant stenosis is present,
surgical management may be considered.

52. Special testsSpecial tests
Echocardiography Usually performed
if there is a specific indication such as a
history of rheumatoid fever, known
cardiac valvular disease.
 Chest X-ray - Sarcoidosis,
tuberculosis, left ventricular hypertrophy
in hypertension

53. Additional blood testAdditional blood test
Fasting plasma homocysteine level
Thrombophilia screen
Plasma protein electrophoresis
Autoantibody
Blood cultures.

54. BRAOBRAO

55. PresentationPresentation
Seventh decade
Sudden, painless loss of vision
Corresponding visual field deficit
H/O amaurosis
H/O transient ischaemic attack or
strokes
1/3rd
have H/O carotid occlusive disease
or hypertension

56. FunduscopicallyFunduscopically
Localized region of
superficial retinal whitening
Prominent at the posterior pole, along
distribution of obstructed vessel
Intense whitening at the borders of
ischaemic areas: secondary to blockage of
axoplasmic flow
90% involve temporal retinal arteries

57. PrognosisPrognosis
Good if foveola is not surrounded by
retinal whitening
80% improve to 20/40 or better
Residual visual field remains
Posterior segment neovascularization
Iris neovascularization
Artery-artery collateral vessels –
pathognomic of BRAO

58. FFAFFA
Delayed or no filling of occluded branch
Hypofluorescence
◦ Lack of perfusion
◦ Blockage by edema
Retrograde filling of distal veins
Flow restored after dissolution of
obstruction

60. Cilio-retinal arteryCilio-retinal artery
obstructionobstruction

61. Cilio-retinal arteryCilio-retinal artery
Clinically 20%; Angiographically 32%
Fill concurrently with choroidal
circulation 1-2 secs before retinal
circulation
Papillo-macular retinal circulation
Supplies foveola in 10% of cases

63. PresentationPresentation
Sudden onset visual loss
Area of superficial retinal whitening
3 clinical variants
◦ Isolated
◦ Associated with CRVO
◦ Aoosciated with AION

64. Isolated cilio-retinal artery obstruction (40%):
◦ Good visual prognosis
◦ 90 % 20/40 or better
◦ Intact superior and inferior NFL bundles
With CRVO (40%)
◦ Seen in 5% of CRVO (non-ischaemic)
◦ 70% >20/40
◦ Low hydrostatic pressure in cilio-retinal
artery as compared to CRA
◦ Swelling of the optic disc

65. Associated with AION (20%):
◦ Poor visual prognosis
◦ 20/400 to no PL
◦ Optic nerve damage
◦ Hyperaemic or pale disc along with retinal
whitening
 Acute pale swelling s/o GCA
◦ Posterior ciliary insufficiency

66. Carotid arteryCarotid artery
obstructionobstruction

67. PresentationPresentation
Visual loss (20/20 to No PL)
Severe pain due to ischaemia or NVG
Dot-blot haemorrhages, narrowed
arteries, dilated veins
FFA:
◦ Increase in the A-V transit time (95% cases)
◦ Prolonged patchy choroidal filling (60%)

69. CourseCourse
Visual improvement takes several weeks
◦ poor visual prognosis
Optic atrophy, arteriolar attenuation,
NVE
NVI in 2/3rd
cases (NVG in half)

70. InvestigationsInvestigations
 Digital ophthalmodynamometry
 Decreased ocular perfusion pressure
 Diminished or absent pulse of ipsilateral
cervical carotid artery
 Bruit if partial stenosis
 Absent if complete stenosis
 Digital subtraction angiography, MRI,
Intra-arterial angiography

71. ManagementManagement
To prevent permanent vision loss and
stroke
Screen for systemic illnesses
Antiplatelet therapy
Anticoagulants
Carotid end-arterectomy
◦ Stenosis greater than 70%

72. Combined retinal arteryCombined retinal artery
and vein occlusionand vein occlusion

73. PresentationPresentation
 Retrobulbar injections-1/4th
of cases
 Clinical features of CRVO & CRAO
 Sudden onset of painless loss of vision
 Fundus:
 Superficial retinal opacification
 Cherry red spot
 Dilated and tortuous retinal veins
 Retinal haemorrhages
 Swollen optic disc
Central retinal artery
obstruction
Central retinal vein
occlusion

74. Fluorescein Angiography
◦ Severe retinal capillary non-perfusion
◦ Sudden termination of mid-sized retinal vessels
◦ Minimal leakage-shutdown of retinal vessels
Visual prognosis
◦ Poor
◦ Within HM range
◦ 80% develop rubeosis and NVG (6 weeks)
◦ Aggressive PRP to prevent rubeosis (may fail)

75. Cotton-wool spotsCotton-wool spots

76. Cotton-Wool Spots (soft exudate)Cotton-Wool Spots (soft exudate)
Yellow white lesion in superficial retina
with feathery margins
Less than 1/4th
DD
Correspond to areas of retinal capillary
non-perfusion or bordered by
microaneurysmal abnormalities

77. CWSCWS
Develop secondary to obstruction of a
retinal arteriole and resultant ischaemia
Hypoxia ->blockage of axoplasmic
transport within NFL -> deposition of
intra-axonal organnels
Largely made of mitochondria and lipid
Light microscopy:
◦ Cytoid bodies
◦ Cellular appearing bodies with psedonucleus

78. CWSCWS
 Spots in the visual field may cause a small
scotoma
 Most resolve within 5-7 weeks
 May remain longer in diabetic pts.
 95% cases have some systemic disease
 Even one cotton-wool spot in non-diabetics
warrants evaluation
 Common causes:
 Diabetes Mellitus
 Systemic Arterial Hypertension

79. To conclude…..To conclude…..
Retinal artery occlusion is an ocular emergency
 Immediate intervention improves chances of
visual recovery, but even then, prognosis is poor.
Follow up for ocular neovascularization needed
Although restoration of vision is of immediate
concern, retinal artery occlusion is a harbinger
for other systemic diseases that must be
evaluated .

80. THANKYOUTHANKYOU