Retinal Artery and Vein Occlusions

Slide 1 · Retinal Artery and VeinOcclusions

Mechanisms • morphology • clinicopathologic interpretation

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes: Explain the vascular lesion

Distinguish arterial infarction from venous occlusive injury.

Relate arterial territory to the distribution of retinal opacity.

Explain how emboli and local atherosclerotic thrombosis arise.

Slide 3 · Learning outcomes: Interpret the visible fundus

Derive the cherry-red spot from retinal and foveal anatomy.

Explain why storage diseases can yield the same ophthalmoscopic sign.

Contrast ischemic and nonischemic retinal vein occlusion.

Slide 4 · Occlusion produces different forms of injury

Arterial obstruction deprives retinal tissue of its blood supply.

Venous obstruction is associated with hemorrhage, exudation, and/or ischemia.

Ischemia may induce a secondary angiogenic response.

Vessel occlusion

Altered perfusion

Tissue response

Visible pathology

Slide 5 · Two vascular backgrounds must be distinguished

Retinal tissue has a vascular supply vulnerable to arterial occlusion.

The choroid is richly vascular and normally supplies an orange-red fundus background.

Retinal opacity changes how much choroidal color is visible.

Retinal arteries

Retinal tissue

Inner retinal vascular supply

Choroidal vascular background

Conceptual orientation • two vascular compartments

Slide 6 · Central and branch vessels define lesion extent

Central-vessel obstruction threatens a broad retinal territory.

A branch-vessel lesion produces a more limited segmental distribution.

The topography of injury follows the supply of the occluded vessel.

Central artery

Diffuse retinal infarction

Widespread fundus opacity

Slide 7 · Anatomy explains the color of the normal fundus

The retina is relatively transparent under normal viewing conditions.

The choroidal circulation contributes the usual red-orange background.

Opaque retinal tissue can mask this underlying vascular color.

Simplified fundus schematic

Slide 8 · The fovea is anatomically distinct

Fovea and foveola are particularly thin.

The foveal center lacks ganglion cells.

This thin central area remains comparatively transparent when surrounding retina becomes opaque.

Perifoveal ganglion-cell layer

No ganglion cells

Thin fovea

Vascular choroid: Orange-red background

Foveal thinness permits a choroidal color window

Cross-sectional concept • schematic; Not histology

Slide 9 · Arterial versus venous obstruction: A framework

Feature

Retinal artery

Retinal vein

Primary event

Loss of arterial inflow

Venous occlusive injury

Dominant textbook lesion

Retinal infarction

Ischemic or nonischemic consequences

Visible tissue changes

Acute whitening/opacity

Hemorrhage, exudate, edema; Neovascularization if ischemic

Major complication

Severe visual loss/blindness

Neovascular glaucoma in ischemic disease

Slide 10 · Thromboembolism is the leading arterial mechanism

Thromboembolism as the most common cause of retinal artery occlusion.

The thrombus may form locally in a diseased central artery.

Alternatively, an embolus may originate upstream and lodge in the retinal circulation.

Slide 11 · Atherosclerosis predisposes to local thrombosis

Atherosclerotic plaque narrows the central retinal arterial lumen.

Luminal narrowing creates conditions that favor thrombosis.

The resulting obstruction interrupts distal retinal perfusion.

Plaque-related luminal narrowing

Narrowed lumen

Atherosclerotic narrowing

Local thrombosis risk

Simplified artery longitudinal section

Slide 12 · The carotid artery can supply an embolic source

An ulcerated carotid atheromatous plaque can release embolic material.

Embolization to the central retinal artery interrupts flow downstream.

The clinically observed retinal lesion is therefore potentially a consequence of proximal vascular disease.

Carotid atheroma

Embolus

Retinal artery occlusion

Retinal infarction

Slide 13 · Cardiac thrombi can also embolize

A thrombus within the heart is another source of retinal arterial emboli.

A cardiac-source embolus and a carotid-source embolus may converge on the same retinal end-organ lesion.

The retinal appearance reflects the vascular insult; It does not itself identify the embolic source.

Cardiac thrombus

Embolus

Retinal artery

Tissue ischemia

Slide 14 · Local thrombosis and embolization are distinct

Question

Local arterial thrombosis

Retinal arterial embolus

Origin

At a diseased arterial segment

Proximal heart or carotid artery

Predisposing process

Atherosclerotic luminal narrowing

Thrombus or ulcerated atheromatous plaque

Shared endpoint

Interruption of retinal arterial flow

Interruption of retinal arterial flow

Interpretive limit

Fundus infarction alone does not prove which mechanism occurred

Fundus infarction alone does not prove which source embolized

Slide 15 · Retinal arterial obstruction initiates infarction

Cessation of arterial supply causes abrupt deprivation of perfusion.

The affected retina undergoes acute injury and swelling.

Sufficiently severe arterial occlusion produces an infarct.

Arterial occlusion

Cessation of blood supply

Retinal swelling

Infarction

Slide 16 · A branch-artery lesion has a segmental footprint

Total occlusion of one retinal arterial branch produces segmental infarction.

Opacity is confined to the affected vascular territory.

Fundus distribution therefore helps localize the arterial obstruction.

Segmental opacity

Simplified fundus schematic

Slide 17 · Central artery occlusion has a diffuse footprint

Total central retinal artery occlusion can produce diffuse retinal infarction.

Much of the retina becomes optically opaque.

The thin foveal region remains a conspicuous exception.

Foveal red spot

Simplified fundus schematic

Slide 18 · Vascular geography determines infarct geography

Characteristic

Branch artery occlusion

Central artery occlusion

Occluded level

Arterial branch

Central retinal artery

Infarct pattern

Segmental

Diffuse

Fundus opacity

Regional area of whitening

Widespread retinal whitening

Optical foveal contrast

Depends on distribution

Classically explains cherry-red appearance

Slide 19 · Acute retinal injury causes swelling

The acutely swollen retina with the brain, from which it is derived.

Swelling is an immediate structural consequence of sudden ischemia.

The altered tissue becomes optically opaque rather than transparent.

Slide 20 · Why retinal infarction looks white

The normal red-orange choroid lies beneath the retina.

The infarcted, swollen retina blocks that choroidal background.

The affected fundus appears white rather than the usual orange-red.

Ischemic swelling

Retinal opacity

Choroid obscured

White fundus

Slide 21 · The apparent whiteness is an optical effect

The color change does not require the retina itself to contain white pigment.

It results from opaque swollen retinal tissue over a red vascular bed.

Interpret tissue transparency and background color together.

Perifoveal ganglion-cell layer

No ganglion cells

Thin fovea

Vascular choroid: Orange-red background

Foveal thinness permits a choroidal color window

Cross-sectional concept • schematic; Not histology

Slide 22 · Diffuse whitening leaves a foveal color window

In central artery occlusion, surrounding retinal tissue becomes opaque.

Fovea and foveola are much thinner than neighboring retina.

The red-orange choroid remains visible centrally.

Foveal red spot

Simplified fundus schematic

Slide 23 · A cherry-red spot arises from contrast

The central red area is highlighted by pale, infarcted surrounding retina.

It represents choroidal color seen through thin foveal tissue.

The surrounding white retina creates the diagnostic visual contrast.

Diffuse retinal opacity

Thin foveal window

Choroidal red visible

Cherry-red spot

Slide 24 · Cherry-red does not mean central hemorrhage

The textbook mechanism is optical transmission of the choroidal background.

The spot is not defined by extravasated blood in the fovea.

The distinction matters because the same appearance occurs through different mechanisms.

Foveal red spot

Simplified fundus schematic

Slide 25 · The fundus links anatomy to pathology

Structure

Normal optical role

During central retinal artery occlusion

Choroid

Orange-red vascular background

Background persists

Nonfoveal retina

Relatively transparent

Swollen, white, opaque

Fovea / foveola

Thin window over choroid

Remains comparatively transparent

Composite appearance

Orange-red fundus

Pale retina with central red spot

Slide 26 · Arterial infarction may cause blindness

The central retinal artery supplies a large vulnerable retinal territory.

Total occlusion can lead to diffuse infarction.

Robbins explicitly identifies blindness as a possible consequence of arterial occlusion.

Slide 27 · Reason from distribution before naming a lesion

Diffuse whitening suggests a central supply interruption.

Sectoral whitening favors interruption of a branch territory.

Topographic reasoning is more informative than color alone.

Segmental opacity

Simplified fundus schematic

Slide 28 · Case 1: Distinguish level of occlusion

A fundus schematic shows a white sector rather than diffuse retinal opacity.

Which arterial territory is more likely to be occluded?

What tissue event explains the white sector?

Slide 29 · Case 1: Tissue and vessel correlate

A branch-vessel obstruction best explains a segmental infarct.

Acute ischemic swelling makes that segment optically opaque.

The opacity obscures the orange-red choroid only in the involved area.

Segmental opacity

Simplified fundus schematic

Slide 30 · The cherry-red spot is not disease-specific

The sign in central retinal artery occlusion.

It may also occur in certain rare lysosomal storage diseases.

An identical visible sign can therefore arise from different retinal pathology.

Foveal red spot

Simplified fundus schematic

Slide 31 · Tay–Sachs and Niemann–Pick: Examples

Both are named in the Robbins passage as conditions with cherry-red spots.

Storage material accumulates in retinal ganglion cells.

Ganglion-cell-rich retinal tissue surrounding the fovea becomes relatively opaque.

Perifoveal ganglion-cell layer

No ganglion cells

Thin fovea

Vascular choroid: Orange-red background

Foveal thinness permits a choroidal color window

Cross-sectional concept • schematic; Not histology

Slide 32 · Storage material changes perifoveal transparency

The ganglion cell layer is comparatively thick around the fovea.

Intracellular storage material reduces transparency of those adjacent cells.

The foveal center lacks ganglion cells and is relatively spared by this mechanism.

Perifoveal ganglion-cell layer

No ganglion cells

Thin fovea

Vascular choroid: Orange-red background

Foveal thinness permits a choroidal color window

Cross-sectional concept • schematic; Not histology

Slide 33 · The foveal center remains visibly red in storage

No retinal ganglion cells occupy the center of the fovea.

The ganglion-cell storage process therefore spares this central optical window.

Choroidal orange-red remains visible through the central macula.

Foveal red spot

Simplified fundus schematic

Slide 34 · Same sign, different mechanisms

Element

Retinal artery occlusion

Lysosomal storage disease

Why surrounding retina is opaque

Acute ischemic swelling

Stored material in retinal ganglion cells

Why fovea remains red

Foveal thinness

Absent ganglion cells in the center

Source of red color

Underlying choroid

Underlying choroid

Interpretation

Acute vascular mechanism

Storage-related cellular mechanism

Slide 35 · A shared appearance is not shared pathogenesis

Both diseases increase contrast between the fovea and adjacent retina.

Arterial infarction changes tissue hydration and optical opacity.

Storage diseases change ganglion-cell content and transparency.

Different causes

Opaque perifoveal retina

Transparent foveal center

Red choroid visible

Slide 36 · Case 2: Avoid overcalling arterial occlusion

A fundus has a central red area surrounded by pale retina.

Is the red spot alone sufficient to establish thromboembolism?

Which alternative pathogenic category is?

Slide 37 · Case 2: The differential is mechanistic

No: The cherry-red sign is not unique to central retinal artery occlusion.

Ganglion-cell storage disorders are one mechanistically distinct explanation.

Use accompanying evidence rather than assigning etiology from this sign alone.

Perifoveal ganglion-cell layer

No ganglion cells

Thin fovea

Vascular choroid: Orange-red background

Foveal thinness permits a choroidal color window

Cross-sectional concept • schematic; Not histology

Slide 38 · Retinal vein occlusion has two broad patterns

The focused textbook passage divides retinal vein occlusion by the presence or absence of ischemia.

Ischemic disease may induce retinal angiogenic activity.

Nonischemic disease may be complicated by hemorrhage, exudates, and macular edema.

Retinal vein occlusion

Without ischemic designationHemorrhage • exudates • macular edema

With retinal ischemiaVEGF → neovascularization

Slide 39 · Arteriovenous crossings matter to branch veins

Retinal arterioles and veins share a common adventitial sheath at their crossings.

Pronounced arteriolosclerosis can compress an adjacent vein.

Distal venous stasis may precipitate branch retinal vein occlusion.

Arteriovenous crossing

Arteriole

Vein

Crossing-site compression

Conceptual schematic • not a vessel micrograph

Slide 40 · Retinal hypertension creates a venous mechanism

A thickened retinal arteriolar wall can produce crossing-site compression.

This mechanism differs from an arterial embolus lodging downstream.

Retinal vascular diseases may interact anatomically at shared vessel crossings.

Arteriolosclerosis

Vein compression

Distal venous stasis

Branch vein occlusion

Slide 41 · Ischemic vein occlusion is an angiogenic trigger

Retinal ischemia causes upregulation of VEGF and other proangiogenic factors.

The angiogenic response promotes formation of new vessels.

Their location determines complications involving the retina, optic disc, and iris.

Venous ischemia

VEGF upregulation

Neovascularization

Ocular complications

Slide 42 · VEGF links retinal hypoxia to vessel growth

Vascular endothelial growth factor is a molecular mediator of retinal angiogenesis.

Hypoxic retina is the stimulus described.

A molecular response can create clinically important secondary pathology.

Hypoxic retina

VEGF expression

New vessel growth

Slide 43 · The retinal surface can develop new vessels

Ischemic retinal vein occlusion can cause neovascularization on the retina.

Surface neovascularization is distinct from a normal retinal vascular tree.

The pathologic vessels reflect a response to nonperfused retina.

Surface neovessels — schematic

Slide 44 · The optic nerve head is another site

Ischemia-driven neovascularization may develop on the optic nerve head.

Robbins also identifies retinal surface neovascularization.

The distribution of new vessels matters when interpreting ocular complications.

Surface neovessels — schematic

Slide 45 · Retinal ischemia can affect the anterior segment

Ischemic retinal vein occlusion may stimulate new vessels on the iris.

This is an anterior-segment consequence of posterior retinal ischemia.

The pathologic linkage is mediated by angiogenic factors.

Ischemic retina

Angiogenic factors

Iris neovascularization

Slide 46 · Iris neovascular membranes can contract

VEGF-associated iris neovascularization may produce a fibrovascular membrane.

Contraction can bring the iris toward the trabecular meshwork.

Peripheral anterior synechiae obstruct aqueous outflow.

Anterior-chamber outflow angle

Aqueous humor pathway

Trabecular meshwork

Iris surface membrane

Membrane contracts

Outflow obstructed

Mechanism schematic • not scaled anatomy

Slide 47 · Neovascular glaucoma is an outflow disorder

The trabecular meshwork is a principal route of aqueous humor drainage.

An iris fibrovascular membrane can close off this route.

Obstructed drainage raises intraocular pressure: Secondary angle-closure (neovascular) glaucoma.

Anterior-chamber outflow angle

Aqueous humor pathway

Trabecular meshwork

Iris surface membrane

Membrane contracts

Outflow obstructed

Mechanism schematic • not scaled anatomy

Slide 48 · The pathway from vein occlusion to glaucoma

Glaucoma is not simply caused by hemorrhage within the retina.

The source links ischemia to VEGF, then iris neovascularization and angle closure.

Every step explains a distinct tissue or functional change.

Vein occlusion with ischemia

VEGF increase

Iris new vessels

Angle-closure glaucoma

Slide 49 · Posterior ischemia has distant consequences

The primary nonperfusion occurs in the retina.

The angiogenic response may extend beyond the site of nonperfusion.

Iris pathology can become the immediate cause of impaired aqueous drainage.

Anterior-chamber outflow angle

Aqueous humor pathway

Trabecular meshwork

Iris surface membrane

Membrane contracts

Outflow obstructed

Mechanism schematic • not scaled anatomy

Slide 50 · Nonischemic vein occlusion can cause hemorrhage

Retinal hemorrhages as a complication of nonischemic vein occlusion.

Hemorrhage reflects vascular injury rather than an arterial white infarct.

Hemorrhage alone should not be equated with the ischemic neovascular pathway.

Hemorrhages — schematic

Slide 51 · Exudates reflect a second venous consequence

Exudates may complicate nonischemic retinal vein occlusion.

Material accumulating outside vessels changes the retinal appearance.

This differs mechanistically from the acute whitening of arterial infarction.

Venous occlusive disease

Vascular leakage/injury

Retinal exudates

Slide 52 · Macular edema threatens a critical retinal region

Macular edema is named as a complication of nonischemic vein occlusion.

The macula is central to the appearance being discussed in retinal vascular disease.

Edema is distinct from the diffuse infarct pattern of a central artery occlusion.

Hemorrhages — schematic

Slide 53 · Venous occlusion need not be ischemic

Aspect

Nonischemic RVO

Ischemic RVO

Perfusion descriptor

Without significant ischemic designation

With retinal ischemia

Textbook complications

Hemorrhage, exudates, macular edema

VEGF upregulation

Neovascular sites

Not specified in the focused passage

Retina, optic nerve head, iris

Additional complication

Macular edema

Neovascular angle-closure glaucoma

Slide 54 · Interpret retinal hemorrhage separately from ischemia

A venous occlusion may produce hemorrhage or edema without the neovascular sequence.

Ischemic venous disease has an additional angiogenic pathway.

Do not infer all complications of every case from a single visible abnormality.

Slide 55 · Retinal neovascularization has a defined location

Adjacent Robbins material distinguishes intraretinal changes from new surface vessels.

Surface new vessels breach the internal limiting membrane.

The source names new vessels on the optic disc or elsewhere on the retina.

Ischemic retina

New vessel growth

Retinal surface / optic disc

Slide 56 · VEGF-mediated vessels may cause further injury

In adjacent retinal-vascular disease sections, fragile neovascular membranes are associated with hemorrhage and traction.

These are mechanisms shared across ischemic retinal vasculopathies.

They provide context, not a claim that every vein occlusion has these sequelae.

Ischemia

Neovascular membrane

Hemorrhage / traction

Slide 57 · Retinal artery versus vein: Morphology

Morphologic clue

Arterial occlusion

Venous occlusion

Primary tissue event

Infarction

With or without ischemia

Retinal color change

Whitening/opacity

Hemorrhages and exudates may be present

Macular change

Foveal red contrast in central occlusion

Macular edema in nonischemic disease

Angiogenesis

Not the characteristic mechanism in the focused section

VEGF-driven in ischemic disease

Slide 58 · Retinal artery versus vein: Mechanism

Step

Arterial mechanism

Venous mechanism

Initiator

Thromboembolism; Possibly atherosclerotic thrombosis

Venous occlusion; Branch stasis may relate to AV compression

Direct consequence

Abrupt loss of arterial supply

Ischemic or nonischemic consequences

Structural change

Acute swelling and opacity

Hemorrhage/exudate/edema or neovascularization

Important outcome

Retinal infarction and blindness

Neovascular glaucoma if iris angiogenesis develops

Slide 59 · The same fundus feature can mislead

A cherry-red spot alone is not specific for thromboembolic occlusion.

Retinal whitening depends on optical masking of choroidal color.

Hemorrhage and exudate are not interchangeable with infarct opacity.

Slide 60 · Case 3: Ischemic retinal vein occlusion

After retinal venous occlusion, new vessels appear on the iris.

Which retinal signal links ischemia to the iris?

How can these new vessels eventually elevate intraocular pressure?

Slide 61 · Case 3: Derive the complete causal sequence

Ischemic retina upregulates VEGF and other proangiogenic mediators.

Iris fibrovascular membrane formation and contraction obstruct the drainage angle.

Reduced trabecular outflow produces secondary neovascular glaucoma.

Retinal ischemia

VEGF

Iris membrane

Angle obstruction

Slide 62 · Case 4: Nonischemic venous consequences

A venous occlusive process is associated with macular edema, exudates, and hemorrhage.

Which of the two textbook venous patterns emphasizes these lesions?

Does their presence alone prove iris neovascularization?

Slide 63 · Case 4: Avoid an unwarranted inference

The nonischemic pattern is explicitly associated with these retinal changes.

The ischemic form has the prominent VEGF-driven neovascular sequence.

A specific ischemic classification cannot be assigned from these findings alone.

Hemorrhages — schematic

Slide 64 · A mechanism-based approach to fundus signs

Visible clue

Immediate interpretation

Potential lesion to consider

White retinal territory

Swollen opaque retina masks choroid

Retinal artery infarction

Red fovea on pale retina

Relatively transparent foveal window

Central artery occlusion or storage condition

Hemorrhage, exudate, edema

Venous-associated retinal injury

Nonischemic vein occlusion

Retinal / disc / iris new vessels

Response to retinal ischemia

Ischemic vein occlusion

Slide 65 · Final integration: Four causal pathways

Atherosclerotic narrowing or emboli → arterial interruption → infarction.

Infarct swelling → retinal opacity; Spared thin fovea → red spot.

Venous ischemia → VEGF → retinal/iris neovascularization.

Iris membrane contraction → angle obstruction → neovascular glaucoma.

Slide 66 · Five high-yield distinctions

Branch-artery infarct is segmental; Central-artery infarct may be diffuse.

The red spot is transmitted choroidal color, not diagnostic of a unique etiology.

Storage disease and arterial occlusion cause different forms of perifoveal opacity.

Nonischemic RVO: Hemorrhage, exudates, macular edema.

Ischemic RVO: VEGF-driven angiogenesis and possible neovascular glaucoma.

Slide 67 · References and source boundaries

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th ed. (2026), Chapter 29, “The Eye,” pp. 1201–1205.

Primary topic: “Retinal Artery and Vein Occlusions,” p. 1204.

Context: “Retinal Vascular Disease,” “Diabetes Mellitus,” and “Glaucoma” sections in the same chapter.

Fundus, retinal-layer, vessel, and outflow visuals here are original editable schematics, not clinical photographs.