Infarction

Slide 1 · Infarction

A clinicopathologic approach to ischemic tissue necrosis

Vascular causes, red versus white infarcts, evolution and modifying factors

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Define infarction and discriminate it from vascular obstruction without tissue death.

Predict red or white morphology from blood supply and tissue properties.

Describe necrosis, inflammation, repair and the four key outcome determinants.

Slide 3 · Definition: An area of ischemic necrosis

An infarct is a region of tissue death caused by loss of perfusion.

The obstructed pathway can be arterial supply or venous drainage.

Necrosis, not simply impaired blood flow, defines an infarct.

Vascular obstruction

Insufficient perfusion

Irreversible necrosis

Slide 4 · Occlusion does not invariably cause infarction

Some vascular obstructions produce little detectable tissue injury.

Other occlusions cause organ dysfunction or lethal necrosis.

The tissue outcome depends on perfusion alternatives, time and oxygen needs.

Residual perfusion

Speed of obstruction

Tissue vulnerability

Slide 5 · Arterial supply versus venous drainage

Arterial obstruction

Venous outflow obstruction

Reduces oxygenated inflow

Causes impaired drainage / congestion

Most common infarct cause

More often causes congestion alone

Often pale in solid organs

When infarction occurs, often hemorrhagic

Slide 6 · Why infarction is clinically important

Myocardial and cerebral infarction cause major morbidity and death.

Pulmonary infarction complicates some thromboembolic events.

Bowel infarction and extremity gangrene are further tissue-specific outcomes.

Heart

Brain

Lung / bowel

Extremity

Slide 7 · Most common proximate causes

Arterial thrombosis and arterial embolism underlie most infarctions.

The occlusion deprives a vascular territory of its usual supply.

Recognition of the vascular cause explains the territorial distribution of necrosis.

Arterial thrombus / embolus

Downstream obstruction

Tissue infarction

Slide 8 · Thrombosis: Local obstruction

Thrombosis forms within the vasculature at or near the obstructed site.

Local loss of arterial flow may result in downstream necrosis.

The effect depends on how much collateral perfusion is available.

Local thrombus

Reduced downstream flow

Variable ischemic injury

Slide 9 · Embolism: Distant obstruction

An embolus moves from a remote source and lodges in a smaller vessel.

Its arrival can abruptly interrupt regional arterial perfusion.

Sudden occlusion may leave little time for compensatory collateral flow.

Embolic source

Transport in blood

Distal vascular blockage

Slide 10 · Less-common cause: Vasospasm

Local vascular spasm can markedly reduce arterial inflow.

Severe or prolonged reduction can contribute to ischemic necrosis.

This mechanism differs from an obstructing thrombus or embolus.

Functional narrowing

Reduced flow

Potential necrosis

Slide 11 · Hemorrhage into an atheromatous plaque

Bleeding within a plaque may abruptly worsen arterial narrowing.

The resulting reduction in blood flow can produce an infarct.

The occlusion mechanism is local plaque change rather than a traveling embolus.

Atheromatous plaque

Hemorrhage / narrowing

Arterial flow compromise

Slide 12 · Extrinsic vascular compression

A mass such as a tumor may compress a supplying vessel.

Loss of perfusion arises from pressure exerted outside the lumen.

Both intraluminal and extraluminal causes must be considered.

External mass

Vessel compression

Reduced perfusion

Slide 13 · Vascular torsion

Torsion twists vascular channels and impairs tissue perfusion.

Examples include testicular torsion and bowel volvulus.

Venous drainage may be particularly vulnerable in twisted pedicles.

Torsion / volvulus

Vascular compromise

Ischemic tissue injury

Slide 14 · Traumatic vascular disruption

Traumatic rupture may abolish blood flow through an arterial segment.

Loss of downstream supply can lead to tissue ischemia.

Here tissue damage is caused by vascular disruption, not necessarily thrombosis.

Vessel injury

Perfusion failure

Possible infarction

Slide 15 · Edema and compartment pressure

Increased local tissue pressure can compromise vessel perfusion.

Anterior compartment syndrome of the leg as an example.

The surrounding tissue compartment becomes the obstructive factor.

Swelling / pressure

Vascular compromise

Ischemic necrosis risk

Slide 16 · Entrapment in a hernia sac

Entrapped bowel may suffer vascular compromise.

Both inflow and outflow can be affected in a constricted segment.

The pathologic endpoint can be bowel infarction.

Entrapment

Vascular obstruction

Bowel ischemic necrosis

Slide 17 · Venous thrombosis: Congestion is common

Venous thrombi more often produce congestion rather than infarction.

Alternative venous channels may open rapidly and decompress the tissue.

Improved drainage can restore effective arterial inflow.

Venous blockage

Alternative drainage

Preserved tissue viability

Slide 18 · The single-efferent-vein exception

Organs with a single dominant venous exit have fewer outflow alternatives.

The testis and ovary are examples identified.

Venous blockage here is more likely to progress from congestion to infarction.

Limited outflow routes

Severe congestion

Hemorrhagic infarction

Slide 19 · Compare arterial and venous pathways

Arterial lesion

Venous lesion

Common infarct mechanism

Often congestion without infarction

May be pale in compact organs

Typically red when infarction occurs

Collateral arteries modify risk

Alternative draining veins modify risk

Slide 20 · Two axes of infarct classification

Color axis

Infection axis

Red / hemorrhagic

Septic / infected

White / anemic

Bland / noninfected

Slide 21 · Red infarction: The central principle

A red infarct contains extravasated blood within the necrotic territory.

Vascular anatomy and tissue looseness determine whether blood can accumulate.

Venous obstruction, dual supply, congestion and reperfusion are typical settings.

Hemorrhagic territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 22 · Red infarcts with venous occlusion

Venous outflow obstruction can produce blood-filled necrotic tissue.

Testicular torsion exemplifies a setting predisposed to hemorrhagic infarction.

The lesion is red because blood cannot drain normally.

Hemorrhagic territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 23 · Red infarcts in loose or spongy tissue

Lung parenchyma provides space in which blood can accumulate.

Consequently, pulmonary infarcts are typically hemorrhagic.

Tissue structure contributes to color, beyond the identity of the occluded vessel.

Hemorrhagic territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 24 · Red infarcts in dual circulation

Lung and small intestine are examples of tissues with parallel inflow routes.

An unobstructed supply may introduce blood into the necrotic region.

Thus residual inflow does not necessarily prevent a hemorrhagic appearance.

Hemorrhagic territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 25 · Red infarcts after prior congestion

Sluggish venous drainage can leave a tissue vascular bed congested.

If infarction supervenes, the lesion is predisposed to hemorrhage.

The pre-existing hemodynamic state modifies the gross appearance.

Venous congestion

Tissue ischemia

Hemorrhagic infarct

Slide 26 · Red infarcts after reperfusion

Flow can return to tissue already injured by arterial occlusion.

Reperfusion may permit blood entry into a necrotic zone.

Robbins gives angioplasty after arterial blockage as an example.

Arterial occlusion

Tissue necrosis

Reflow → hemorrhagic infarct

Slide 27 · Five conditions favoring red infarcts

Venous occlusion or preceding congestion.

Loose pulmonary-type architecture or dual vascular supply.

Reperfusion of a previously necrotic vascular territory.

Venous / congested

Spongy / dual supply

Reperfused

Slide 28 · White infarction: The central principle

White infarcts occur after arterial occlusion in compact solid organs.

End-arterial supply limits alternative perfusion.

Dense parenchyma restricts seepage of blood from adjacent capillaries.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 29 · End-arterial circulation

Kidney and spleen are examples with limited collateral alternatives.

Blocking the relevant artery typically kills its downstream territory.

The infarct is commonly pale because there is little hemorrhagic re-entry.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 30 · Tissue density limits hemorrhage

Loose lung parenchyma

Compact renal or splenic parenchyma

Blood can accumulate in necrotic spaces

Blood seepage is constrained

Often hemorrhagic infarct

Often pale infarct

Slide 31 · White infarction: Common sites

Heart, spleen and kidney as common solid-organ settings.

Arterial occlusion and limited collateral supply explain the tissue loss.

Color and shape are consequences of vascular arrangement and tissue density.

Myocardium

Spleen

Kidney

Slide 32 · Red versus white: Diagnostic comparison

Red / hemorrhagic

White / anemic

Often venous obstruction

Often arterial obstruction

Spongy or dual-supply tissue

Compact end-arterial tissue

Lung and intestine examples

Heart, kidney, spleen examples

Slide 33 · Wedge shape reflects vascular geography

Many infarcts are roughly wedge-shaped.

The occluded vessel corresponds to the narrow apex.

The organ periphery often forms the broad base.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 34 · Apex points toward the blocked vessel

A branching vascular territory expands from a proximal feeding vessel.

When that vessel is occluded, downstream necrosis follows its distribution.

The apex-to-base pattern therefore records the anatomy of blood supply.

Hemorrhagic territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 35 · Serosal surface may develop fibrin

If an infarct reaches a serosal surface, fibrinous exudate can overlie it.

Necrotic cells generate mediators that recruit acute inflammation.

Surface fibrin is a local reaction to the underlying tissue injury.

Necrosis near serosa

Inflammatory response

Fibrinous surface exudate

Slide 36 · Fresh infarcts are poorly demarcated

Early infarcts may be subtle and ill-defined grossly.

Slight hemorrhage may be present even in lesions that ultimately become pale.

Appearance evolves with necrosis and inflammation.

Early: Indistinct

Days: Clearer margins

Later: Repair / scar

Slide 37 · Inflammatory congestion defines the edge

Over several days the infarct boundary becomes more visible.

A narrow hyperemic rim corresponds to the inflammatory reaction.

The edge demarcates necrotic tissue from preserved parenchyma.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 38 · White infarcts become paler with time

In organs without dual supply, arterial infarcts tend to become progressively pale.

Their borders become more sharply demarcated.

The gross appearance therefore depends partly on lesion age.

Fresh lesion

Paler and distinct

Scar formation

Slide 39 · Red cell removal in hemorrhagic infarcts

Extravasated erythrocytes are removed by macrophages.

Heme iron is converted to hemosiderin.

Extensive old hemorrhage can leave a firm brown residuum.

Extravasated RBCs

Macrophage phagocytosis

Hemosiderin deposition

Slide 40 · Coagulative necrosis is the usual pattern

Most non-CNS infarcts show coagulative necrosis.

The dominant morphologic finding is ischemic death of cells.

The tissue reaction progresses through inflammation toward fibrosis.

Ischemia

Coagulative necrosis

Inflammation → scar

Slide 41 · Microscopic injury can lag occlusion

Immediately after a lethal occlusion, histologic necrosis may not yet be visible.

Characteristic microscopic changes require about 4–12 hours.

An apparently bland section cannot exclude very recent ischemic injury.

Minutes–hours: Injury

4–12 h: Visible necrosis

Later: Inflammation / repair

Slide 42 · Early inflammation at the infarct edge

Inflammatory cells begin accumulating near the margins within hours.

The preserved margins supply the substrate for a reparative response.

Spatial separation of dead center and inflamed border is important morphologically.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 43 · The 1–2-day inflammatory stage

The inflammatory margin as well defined within 1–2 days.

Inflammation helps demarcate the zone of necrosis.

This timing must be interpreted in relation to tissue and clinical context.

Occlusion

Acute inflammatory margin

Organization / repair

Slide 44 · Reparative response begins at viable margins

Repair develops from tissue surviving at the edge of an infarct.

The central necrotic zone cannot itself regenerate simply by restored blood flow.

Organization proceeds toward replacement by fibrous tissue.

Viable margin

Reparative reaction

Collagenous scar

Slide 45 · Most infarcts heal by fibrosis

Scar replacement is the usual end stage for many infarcts.

A remote renal infarct replaced by fibrotic scar.

The healed shape may retain evidence of the original vascular territory.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 46 · Brain infarction is the major exception

Most solid organs

Central nervous system

Coagulative necrosis

Liquefactive necrosis

Fibrous scar often remains

Different tissue removal / repair pattern

Slide 47 · Bland versus septic infarction

Bland infarct

Septic infarct

Ischemic necrosis without infection

Necrosis involving microbes

Sterile inflammatory repair

Often greater inflammatory response

Progression to scar

May progress through abscess formation

Slide 48 · Septic emboli may seed infarcts

Infected cardiac valve vegetations can embolize into arteries.

Microbes carried with embolic material can infect the ischemic territory.

Necrotic tissue can also become secondarily seeded by microorganisms.

Infected embolic material

Ischemic tissue

Septic infarct

Slide 49 · Septic infarction may become an abscess

Microbial infection changes the evolution of the necrotic focus.

Conversion of a septic infarct into an abscess.

The inflammatory response is greater than in a bland lesion.

Ischemic necrosis + microbes

Abscess formation

Organization / repair

Slide 50 · Four determinants of infarction risk

Collateral vascular anatomy is the most important determinant.

Rate of occlusion affects the opportunity for bypass perfusion.

Tissue sensitivity to hypoxia and the oxygen content of blood also matter.

Vascular anatomy

Rate of occlusion

Tissue vulnerability

Blood oxygenation

Slide 51 · Anatomy: Alternative perfusion protects

Protected by alternative flow

More end-arterial

Lung: pulmonary + bronchial arteries

Kidney: regional arterial supply

Liver: hepatic artery + portal vein

Spleen: limited collateral flow

Hand/forearm: radial + ulnar

Greater risk with occlusion

Slide 52 · Pulmonary dual supply

Pulmonary arterial flow and bronchial arterial flow provide alternative sources.

This helps explain why not every pulmonary embolus causes infarction.

If compensatory perfusion is inadequate, pulmonary infarction can occur.

Pulmonary artery blocked

Bronchial flow persists

Potentially spared parenchyma

Slide 53 · Liver and limb arterial alternatives

The liver receives hepatic arterial and portal venous inflow.

The hand and forearm receive blood via radial and ulnar arteries.

These parallel circulations provide resilience against isolated obstruction.

Hepatic artery

Portal vein

Radial / ulnar arteries

Slide 54 · End-arterial vulnerability of kidney and spleen

Regional occlusion in kidney or spleen usually leaves little functional bypass.

These organs are prone to sharply demarcated pale infarction.

The morphology can therefore reveal the vascular architecture.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 55 · Speed of occlusion modifies tissue outcome

Slow occlusion

Abrupt occlusion

Collateral adaptation possible

Limited adaptation time

Infarction may be avoided

Higher ischemic risk

Example: gradual coronary plaque growth

Example: abrupt arterial embolism

Slide 56 · Coronary collateral example

Small anastomoses connect major coronary arterial distributions.

If obstruction progresses slowly, collateral flow can increase.

This can prevent infarction even when a major artery eventually closes.

Gradual coronary stenosis

Collateral recruitment

Myocardial perfusion maintained

Slide 57 · Neurons: Extremely ischemia-sensitive

Neurons may be irreversibly damaged after 3–4 minutes without blood supply.

This emphasizes the clinical impact of rapid loss of cerebral perfusion.

The number describes cellular vulnerability, not the visibility of later histology.

Flow stops

3–4 min: Neuronal injury

Later: Morphologic change

Slide 58 · Cardiomyocytes: Vulnerable but less rapid

Myocardial cells may die after 20–30 minutes of ischemia.

The cells are more resilient than neurons but still highly oxygen-dependent.

Microscopic visibility of necrosis still lags for approximately 4–12 hours.

Myocardial ischemia

20–30 min: Cell death

4–12 h: Histologic necrosis

Slide 59 · Fibroblasts: Relatively ischemia-tolerant

Myocardial fibroblasts remain viable for many hours of ischemia.

Different cell populations in the same organ can therefore survive differently.

This helps explain how repair may occur at margins of injured tissue.

Neurons: Minutes

Myocytes: Tens of minutes

Fibroblasts: Many hours

Slide 60 · Hypoxemia lowers the ischemic threshold

Low blood oxygen content worsens oxygen delivery through remaining vessels.

It increases both the likelihood and the extent of infarction.

Vascular patency and oxygen content must be considered together.

Reduced oxygen content

Poor tissue oxygenation

More extensive infarction

Slide 61 · Integrate cause, morphology and susceptibility

Identify the blocked inflow or outflow route.

Predict hemorrhagic versus pale morphology using tissue and collateral anatomy.

Estimate injury likelihood from rate of occlusion, tissue type and oxygenation.

Cause of obstruction

Vascular / tissue context

Necrosis + red / white type

Inflammation → repair

Slide 62 · Case: A wedge-shaped pale splenic lesion

Clinical reasoning

A splenic arterial branch is abruptly obstructed.

A peripheral wedge is pale and relatively sharply demarcated.

Which anatomic and histologic principles predict this appearance?

Slide 63 · Case reasoning: The splenic infarct

The spleen has a largely end-arterial circulation.

Dense splenic parenchyma limits blood seepage into the dead area.

The lesion is a white infarct whose apex points toward the obstructed vessel.

Pale territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 64 · Case: Torsion with a hemorrhagic lesion

Clinical reasoning

An organ with limited venous outflow develops sudden torsion.

Marked congestion is followed by tissue necrosis with extensive hemorrhage.

Which hemodynamic mechanism produces a red infarct?

Slide 65 · Case reasoning: Venous infarction

Torsion blocks venous drainage and can compromise further inflow.

Congested vessels allow blood to accumulate in necrotic tissue.

The result is a hemorrhagic infarct, as classically occurs in testicular torsion.

Hemorrhagic territory — schematic

Feeding vessel

Territorial necrosis

Schematic, not a specimen

Slide 66 · Synthesis: Four essential questions

Did arterial inflow or venous outflow fail?

Is the tissue solid/end-arterial or loose/dual-supply?

How long and how rapidly was perfusion impaired?

What is the tissue’s intrinsic susceptibility and oxygen delivery?

Cause

Vascular anatomy

Time course

Oxygen needs

Slide 67 · Source and interpretation

Primary teaching source: Robbins, Cotran & Kumar, Pathologic Basis of Disease, 11th ed., chapter on hemodynamic disorders.

The infarction topic extract had a misplaced thrombosis passage; this deck follows the verified full-text infarction section.

Diagrams are editable schematic representations, not photographs of clinical specimens.