Thrombus, Embolism & Infarction
This flipped classroom covers three related processes: thrombus, embolism, and infarction.
Threading case
Maria Santos, 52
On the third day after a right total hip replacement, she becomes acutely short of breath with sharp right-sided pleuritic chest pain during her first physiotherapy session. Pain from the surgery had kept her in bed for the previous two days, and her right calf has been swollen and painful since the previous evening. She has chronic heart failure. Her temperature is 99.3°F, pulse 118/min, respiratory rate 24/min, blood pressure 118/74 mmHg, and SpO₂ is 88% on room air. On examination, the jugular venous pressure is elevated and the chest is clear. Her right calf is swollen, warm, and tender.
Before reading, note your initial thinking
Q1. What is the most likely diagnosis? How did her surgery lead to it?
Q2. If an infarct forms in her lung, how would the tissue look on autopsy?
Q3. What can happen to the thrombus in her calf vein? Which outcome is most dangerous?
How are the three processes connected?
A thrombus can break off as an embolus, and an embolus can lodge in a vessel and cause an infarct. This session follows that chain from where Virchow's Triad left off, and Maria's case runs through all three.
Do you remember?
Recall the three components of Virchow's Triad. Think of how each one relates to Maria's case before reading Section 1.
Learning objectives covered in this resource
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Thrombus
Distinguish a thrombus from a postmortem clot, and identify what becomes of it.
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Definition. A thrombus is a solid mass of blood components (platelets, fibrin, and trapped red cells) formed within the living circulation. It differs from a postmortem clot in that it is adherent to the vessel wall and shows Lines of Zahn.
Morphology
The cross-section below shows a vessel with an antemortem thrombus. Click each numbered marker to identify the structure.
Thrombus morphology
Click a numbered marker to identify each structure.
Now compare against the full table below.
Thrombus vs postmortem clot
| Feature | Postmortem clot | Thrombus (antemortem) |
|---|---|---|
| Platelets | Not involved | Central; initiates thrombus formation |
| Location | Inside postmortem vessels, or outside (hematoma, test tube) | Only inside a living vessel |
| Color | Uniformly dark red | Venous: red. Arterial: pale (platelet-rich) |
| Consistency | Gelatinous, slides freely | Firm and friable, adherent |
| Attachment | Not attached to vessel wall | Firmly adherent at point of formation |
| Microscopy | No Lines of Zahn. Uniform fibrin mesh | Lines of Zahn: alternating pale (platelets + fibrin) and dark (RBC) laminations |
Autopsy specimens
1
2
Thrombus in the left and right ventricular apices, overlying white fibrous scar
3
Laminated thrombus in a dilated abdominal aortic aneurysm
Fate of the thrombus
Once formed, a thrombus can follow four paths. Click each card for its mechanism and consequence.
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✓
Resolution
What is the mechanism?
Mechanism
Fibrinolysis
Plasmin dissolves the thrombus, fully restoring blood flow. Most likely with small, recent thrombi, and leaves no residual damage.
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↻
Organization & Recanalization
What replaces the thrombus?
Mechanism
Fibroblast invasion
Fibroblasts and endothelial cells invade the thrombus, replacing it with connective tissue. New capillary channels form (recanalization), partially restoring flow. The thrombus becomes incorporated into the vessel wall.
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↓
Propagation
Which direction? What risk?
Mechanism
Extends proximally
Further platelet and fibrin deposition extends the thrombus along the flow of blood, increasing occlusion and embolic risk.
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→
Embolization
Most dangerous fate
Mechanism
Fragment detaches
A fragment breaks off and travels in the bloodstream until it lodges where the vessel narrows, causing ischemia or infarction at that distant site. A venous DVT lodges in the pulmonary circulation; a left heart thrombus in any end artery.
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Maria's thrombus embolized: a fragment detached from her proximal leg DVT, traveled via the IVC to the right heart, and lodged in a pulmonary artery branch, causing her symptoms.
Arterial and venous thrombosis
Toggle between arterial and venous, then click any marker on the body to see where that type of thrombus forms and what it can cause.
Sites and consequences
Select a site
Arterial vs venous: appearance and signs
| Feature | Arterial thrombus | Venous thrombus |
|---|---|---|
| Color | Pale (platelet-rich) | Red (RBC-rich) |
| Shape | Eccentric; does not conform to vessel | Cylindrical cast of the vessel |
| Limb color | Pale and cold (ischemia) | Warm and red (congestion) |
| Limb signs | Pulseless, painful, cold | Swelling, pitting edema, tenderness, warmth |
| Embolizes to | End arteries: brain, bowel, lower limbs | Pulmonary circulation |
Gross
Dark gray friable mass. Arterial thrombi are pale; venous thrombi are red.
Microscopy
Lines of Zahn: alternating pale (platelets and fibrin) and dark (RBCs) layers.
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Trousseau's syndrome. Recurrent, migratory thrombophlebitis with no obvious precipitant should prompt screening for occult malignancy, especially pancreatic adenocarcinoma, whose procoagulant secretions drive a chronic hypercoagulable state.
Self-check
Attempt before revealing.
1
At autopsy, the femoral vein contains dark red gelatinous material that slides freely. Histology shows no Lines of Zahn. What is this, and what two gross features would distinguish a true antemortem DVT in the same vessel?
Answer · 3043
This is a postmortem clot, formed passively after death with no platelet involvement. Two gross features that would indicate an antemortem DVT: (1) firm adherence to the vessel wall, so it would not slide when the vessel is opened; and (2) firm, rubbery consistency rather than gelatinous. Histologically, Lines of Zahn would confirm it.
Before you move on
Decision point
Maria is 48 hours post right total hip replacement and has been immobile in bed since the operation. Which component of Virchow's Triad is the principal driver of her DVT risk at this moment?
Explanation
Learning objectives covered
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Embolism
Define embolism, sort the types, and follow what minor, major and massive emboli do.
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Definition. An embolus is a detached intravascular solid, liquid, or gaseous mass carried by blood to a distant site, causing tissue dysfunction or infarction. 99% are dislodged thrombus fragments (thromboembolism). The other types are far rarer and are classified below.
Types
Classification of embolism
| Type | Key context / trigger |
|---|---|
| Thromboembolism | 99% of all emboli; dislodged thrombus, usually from DVT or cardiac mural thrombus |
| Fat | Trauma to bone, subcutaneous tissue, or burns; marrow sinusoids rupture releasing fat globules |
| Air / gas | Neck wounds, central line placement; >150 mL can be fatal via right ventricular outflow obstruction |
| Nitrogen (Caisson disease) | Rapid decompression in divers; N₂ bubbles out of solution, causing bends, chokes, and bone necrosis |
| Amniotic fluid | Labor and delivery; fetal squames and hair enter maternal pulmonary vessels; frequently fatal from DIC |
| Tumor cells | Hematogenous spread; mechanism of distant metastasis |
| Atherosclerotic debris | Ulcerated plaque ruptures; cholesterol crystals and debris embolize distally |
| Bone marrow | Severe trauma or CPR; hematopoietic cells and fat enter pulmonary vasculature |
| Infective | Septic emboli from infective endocarditis or other infected thrombi. |
| Foreign body | Iatrogenic (catheter fragments, pacemaker leads) or injected material |
Pulmonary thromboembolism
Most PEs originate from deep leg veins and are clinically silent. PE is a major contributor to in-hospital death, often occurring on the patient's first mobilization.
Severity spectrum
| Feature | Massive | Major | Minor |
|---|---|---|---|
| Vessels occluded | ≥60% of pulmonary vasculature; saddle embolus at main bifurcation | Multiple medium-sized branches | Small peripheral branches |
| Consequence | Sudden death from obstructive shock; no time for infarction to develop | Dyspnea and pleuritic pain; infarction in ~10% where bronchial collateral supply is compromised (e.g. heart failure) | Usually asymptomatic; clot is lysed If recurrent: organized thrombi incorporated into vessel wall → pulmonary hypertension |
1
Embolus from a lower extremity deep venous thrombosis, lodged at a pulmonary artery branchpoint
Systemic thromboembolism
Arterial emboli block end arteries, causing infarction downstream. Most originate from the heart.
Sources and destinations
| Pulmonary | Systemic (arterial) | |
|---|---|---|
| Origin | Deep leg veins (90%) | Heart: mural thrombus (80%); aortic atherosclerotic plaque |
| Destination | Pulmonary arteries | Lower extremities (75%), brain (10%), bowel, kidney |
| Consequence | Hypoxia, hypotension, right heart strain; infarction only if collateral supply fails | End-artery occlusion → infarction of supplied tissue |
Paradoxical embolism
A venous embolus that crosses to the arterial circulation via a septal defect. Work through the pathway below.
Step 1 of 6
DVT forms in deep leg vein
A thrombus forms in the deep venous system, typically the popliteal, femoral, or iliac vein. Virchow's Triad: stasis, endothelial injury, and hypercoagulability. Entirely within the venous circulation at this stage.
Self-check
Identify the type of embolism and explain the mechanism.
1
Two days after a closed femoral shaft fracture, a 24-year-old develops sudden dyspnea, petechiae across his chest and axillae, and confusion. What is the diagnosis, and by what two mechanisms does it produce this clinical picture?
Answer
Fat embolism syndrome. First, mechanical obstruction: fat globules released from ruptured marrow sinusoids enlarge in the circulation, and platelets adhere to them forming secondary thrombi that obstruct pulmonary and systemic capillaries. Second, biochemical injury: free fatty acids released from circulating lipid are directly toxic to vascular endothelium, triggering DIC and diffuse capillary damage. The resulting triad of pulmonary insufficiency (dyspnea), neurological symptoms (confusion), and petechiae from thrombocytopenia typically appears 1 to 3 days after the injury.
Before you move on
Decision point
Maria's popliteal DVT has embolized to a medium-sized pulmonary artery branch. She has background heart failure. What is the most likely immediate consequence in her lung?
Explanation
Learning objectives covered
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Infarction
Identify the causes of infarction, and what decides whether an infarct is red or white.
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Definition. An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of a tissue. Both heal by organization to fibrous scar, except in the brain, where liquefactive necrosis leaves a cystic cavity instead.
Before you read
Maria developed pulmonary infarction where most patients with a medium PE do not. Without scrolling back, write down the single factor in her history that explains this. Then continue.
Red and white infarcts
Whether an infarct is red or white depends on a single question: can blood re-enter the necrotic territory? Click each card.
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Red (Hemorrhagic) Infarct
Hemorrhagic
Blood re-enters the necrotic zone in four settings: soft organs with tissue spaces (lung); dual blood supply where anastomosing vessels bleed into the zone (lung, small intestine); venous infarcts where congestion precedes infarction; and reperfusion after arterial occlusion.
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◯
White (Anemic) Infarct
Anemic
Little bleeding enters the affected tissue. Solid organs (kidney, spleen, heart) have dense parenchyma that prevents blood seeping back into the necrotic zone. Arterial occlusion is the usual mechanism. The territory becomes pale, firm, and dry.
Self-check
Attempt before revealing.
?
Is Maria's pulmonary infarct red (hemorrhagic) or white (anemic)? Explain why.
Answer
Red (hemorrhagic). The lung's soft tissue spaces and residual bronchial blood supply normally allow blood to seep into any necrotic zone. In Maria's case, compromised bronchial circulation removes the dual-supply protection the lung normally relies on, making hemorrhagic infarction inevitable once a medium PE occurs.
Morphology
Most infarcts are wedge-shaped. What is it about arterial supply that produces this shape? The diagram uses Maria's pulmonary infarct as an example. Click each marker for more.
Pulmonary infarct
Pulmonary infarcts are usually hemorrhagic and wedge-shaped, with the base at the pleural surface and the apex pointing toward the occluded vessel. PA = pulmonary artery.
Click a numbered marker to identify each feature.
Gross morphology
The appearance evolves in stages.
| Stage | Appearance |
|---|---|
| Early | Congested, ill-defined margins. Wedge-shaped: occluded vessel at the apex, organ periphery at the base. |
| Intermediate | Margins sharpen. A well-defined rim of hyperemia forms at the border with viable tissue. |
| Late | Brown discoloration from hemosiderin deposition as red cells are cleared. |
Microscopy
Ischemic coagulative necrosis throughout the wedge. The ghost outlines of cells are preserved but nuclei are lost. This pattern is common to most infarcts regardless of organ.
Septic infarct
When an infected embolus (e.g. from infective endocarditis) occludes a vessel, the infarct undergoes abscess formation rather than simple coagulative necrosis.
Factors that determine whether infarction occurs
Not every vascular occlusion causes an infarct. Four factors set the threshold. Click each card.
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Nature of blood supply
Factor 1
Dual blood supply reduces infarction risk. Examples: lungs (pulmonary + bronchial), liver (portal + hepatic artery), brain (Circle of Willis), hand (ulnar + radial arteries). Collateral circulation also protects: enlargement of coronary anastomoses can reduce infarction risk with gradual narrowing.
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Rate of occlusion
Factor 2
A sudden occlusion is more likely to cause infarction. A slowly developing occlusion is less likely to, because it gives the tissue time to grow collateral vessels that keep it perfused.
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Tissue vulnerability to hypoxia
Factor 3
Brain is the most vulnerable. Skeletal muscle and bone are relatively tolerant.
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Oxygen carrying capacity of blood
Factor 4
Anemia raises the risk of infarction. With less oxygen in the blood, even a partial blockage can cause an infarct.
Healing and evolution
Cell death, inflammation and repair
| Stage | Cellular events |
|---|---|
| Acute | Cell death. Polymorphs and macrophages are recruited to clear necrotic debris. |
| Subacute | Granulation tissue grows in from the viable margin, accompanied by lymphocytes and plasma cells. |
| Repair | Fibrous scar replaces the granulation tissue. The scar contracts over time. In the brain: microglia clear liquefied tissue, leaving a glial scar and cystic space rather than fibrous tissue. |
Other clinical examples
Cerebral infarction
Coming in NCRS
- Embolism is the most common cause: mostly from cardiac mural thrombi (myocardial infarction, atrial fibrillation), but emboli can originate in the carotids too (usually from atherosclerotic plaques).
- Thrombotic occlusions: superimposed on atherosclerotic plaques at the carotid, origin of the middle cerebral artery, and either end of the basilar artery.
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Acute
Up to 24 hours
What changes?
Up to 24 hours
Red neuron
The injured neuron looks pink and shrunken under the microscope (cytoplasmic eosinophilia, nuclear pyknosis and karyorrhexis). Earliest histological sign of irreversible neuronal injury.
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Subacute
24 hours to 2 weeks
What changes?
24 hours to 2 weeks
Inflammation moves in
Tissue necrosis triggers an early influx of neutrophils, then macrophages a few days later. By the end of this window, new blood vessels grow in and reactive glial cells appear.
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Repair
After 2 weeks
What is left?
After 2 weeks
Glial scar and cyst
Macrophages have cleared the dead tissue. What remains is a glial scar surrounding a cystic cavity (compare with the late-infarct image below).
Myocardial infarction
Coming in NCRS
The heart is supplied by end arteries with no effective collateral, so a coronary occlusion produces a white (anemic) infarct with coagulative necrosis, the pattern set out in Red and white infarcts above.
- Cause
- Coronary atherosclerosis with superimposed thrombosis.
- Site
- Left anterior descending is the most common vessel involved.
- Pathology
- Coagulative necrosis. Initially blotchy, later pale scar tissue (shown below).
- Clinical
- Severe chest pain; cardiac enzymes elevated in serum.
Decision point
A patient develops sudden left flank pain and hematuria. CT shows a peripheral wedge-shaped area of low density in the upper pole of the left kidney. An embolus from the heart has lodged in a branch of the renal artery. Is this a red or white infarct, and why?
Explanation
Learning objectives covered
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Summary
Work through Maria’s case and the three questions you set aside at the start.
Threading case
Maria Santos, 52
On the third day after a right total hip replacement, she becomes acutely short of breath with sharp right-sided pleuritic chest pain during her first physiotherapy session. Pain from the surgery had kept her in bed for the previous two days, and her right calf has been swollen and painful since the previous evening. She has chronic heart failure. Her temperature is 99.3°F, pulse 118/min, respiratory rate 24/min, blood pressure 118/74 mmHg, and SpO₂ is 88% on room air. On examination, the jugular venous pressure is elevated and the chest is clear. Her right calf is swollen, warm, and tender.
Return to the threading case
Now answer the questions from the Overview
Having read Sections 1 to 3, write down your answers before the lecture.
Now answer with what you have learned
Q1. What is the most likely diagnosis? Name each step from her surgery to her lung.
Q2. If an infarct forms in her lung, how would the tissue look on autopsy, and why?
Q3. What can happen to the thrombus in her calf vein? Which outcome is most dangerous?
Learning objective covered
PATH.3053
You are ready for the lecture
You have covered thrombus formation, embolism, and infarction: the three core processes in this class. Bring Maria with you. The lecture will build directly on what you have just read.
Thank you!
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Pathology images are reproduced from Robbins and Cotran, Pathologic Basis of Disease, and used with permission for classroom teaching at St. George’s University.