Pathology chapters
Haemorrhage, hyperaemia, congestion and infarction
Active hyperaemia versus passive congestion, the classic congested organs (nutmeg liver, heart failure cells), types of haemorrhage, and infarction: red versus white infarcts, the factors that decide whether tissue dies, and how infarcts look in different organs.
- Hyperaemia is an active increase in blood flow from arteriolar dilation (red, warm: inflammation, exercise); congestion is a passive build-up of venous blood from poor outflow (blue-red: heart failure, venous block).
- Chronic congestion gives the nutmeg liver (congested centrilobular areas) and heart failure cells (haemosiderin-laden macrophages) in the lungs.
- An infarct is an area of ischaemic necrosis: white (anaemic) in solid organs with end arteries (heart, kidney, spleen) and red (haemorrhagic) in loose tissue, dual supply, venous occlusion or reperfusion (lung, intestine, testis in torsion); most infarcts show coagulative necrosis, the brain shows liquefactive necrosis.
On this page
Hyperaemia and congestion
Both mean more blood in a tissue, but they arise differently.
| Feature | Hyperaemia | Congestion |
|---|---|---|
| Process | Active: arteriolar dilation raises inflow | Passive: reduced venous outflow |
| Colour | Red (oxygenated blood), warm | Blue-red (cyanotic): deoxygenated blood |
| Examples | Inflammation, exercising muscle, blushing | Heart failure (systemic), venous obstruction (local, e.g. deep vein thrombosis) |
Congestion often comes with oedema because high venous pressure pushes fluid out of capillaries.
Chronic passive congestion of the lungs
Cause: left heart failure (or mitral stenosis).
- Acute: alveolar capillaries engorged; alveolar oedema.
- Chronic: alveolar walls thicken and fibrose; small haemorrhages are eaten by macrophages that fill with haemosiderin: "heart failure cells" (siderophages).
- Gross: firm and brown: "brown induration".
Chronic passive congestion of the liver
Cause: right heart failure (or constrictive pericarditis, hepatic vein thrombosis in Budd-Chiari syndrome).
- Centrilobular (zone 3, around the central vein) regions are congested and red-brown, and the hepatocytes there may undergo centrilobular necrosis (they are farthest from the blood supply).
- The periportal regions are paler and may show fatty change.
- Cut surface: dark red centres against paler surroundings: the "nutmeg liver".
- Long-standing severe cases may develop fibrosis (cardiac cirrhosis).
Nutmeg liver = chronic passive congestion from right heart failure; heart failure cells = haemosiderin-laden macrophages in the lungs in left heart failure.
Haemorrhage
Haemorrhage is the escape of blood from a vessel, usually from vessel injury; a bleeding tendency (haemorrhagic diathesis) arises with defects of vessels, platelets or clotting factors.
| Pattern | Size | Typical cause |
|---|---|---|
| Petechiae | 1–2 mm, skin and mucosa | Low platelets or platelet dysfunction, raised venous pressure |
| Purpura | 3 mm or more (up to about 1 cm) | Platelet disorders, vasculitis, vascular fragility |
| Ecchymoses (bruises) | Larger, more than 1 cm | Trauma; clotting disorders |
| Haematoma | A collection forming a mass | Trauma, aneurysm rupture, bleeding disorders |
Blood in body cavities: haemothorax, haemopericardium (can cause cardiac tamponade), haemoperitoneum, haemarthrosis (typical of haemophilia).
Significance
- Volume and rate: a sudden loss of about 20% or more of the blood volume can cause hypovolaemic shock; slow losses are tolerated better.
- Site: a small bleed in the brainstem or around the heart can be fatal.
- Chronic or repeated external loss (peptic ulcer, heavy periods) causes iron-deficiency anaemia; bleeding into tissues lets iron be reused.
Infarction
An infarct is an area of ischaemic necrosis caused by blocked arterial supply or venous drainage. Nearly all infarcts are due to arterial thrombosis or embolism. Other causes: vasospasm, compression by tumour, twisting of vessels (testicular or ovarian torsion, volvulus), trapping in a hernia.
Red vs white infarcts
| Feature | White (anaemic) infarct | Red (haemorrhagic) infarct |
|---|---|---|
| Where | Solid organs with end-arterial supply | Loose tissues, organs with dual blood supply, venous occlusion, reperfusion |
| Examples | Heart, kidney, spleen | Lung, small intestine, liver (rarely), testis or ovary in torsion, brain after reperfusion |
| Why | Solid tissue limits bleeding into the dead area | Blood from the second supply or from collaterals enters the dead area |
Septic infarcts arise when infected emboli (from vegetations in endocarditis) lodge; the infarct becomes an abscess.
White infarcts: heart, kidney, spleen (end arteries). Red infarcts: lung, intestine, testicular torsion (dual supply, loose tissue, venous block).
Morphology
- Usually wedge-shaped: the apex points to the blocked vessel and the base is at the organ surface (often with fibrinous exudate on the surface, for example pleuritis over a lung infarct).
- Margins become well defined with a rim of hyperaemia and inflammation.
- Microscopy: coagulative necrosis (outlines of dead cells preserved) in most organs. In the brain, infarcts show liquefactive necrosis.
- Healing: inflammation, then granulation tissue and a fibrous scar (or a fluid-filled cyst in the brain).
Factors that decide whether infarction happens
| Factor | Effect |
|---|---|
| Nature of the blood supply | Dual supply (lung: pulmonary and bronchial; liver: hepatic artery and portal vein; hand and forearm) resists infarction; end arteries (kidney, spleen) do not |
| Rate of occlusion | Slow blockage allows collaterals to develop (for example, coronary collaterals) |
| Vulnerability to hypoxia | Neurons die in 3–4 minutes; cardiac muscle in 20–30 minutes; fibroblasts survive much longer |
| Oxygen content of blood | Anaemia, hypoxaemia or heart failure make infarction more likely |
The lung rarely infarcts in a healthy person because of its dual blood supply; it does so when the bronchial circulation is poor, as in left heart failure.
Expect: hyperaemia vs congestion, nutmeg liver and centrilobular necrosis, heart failure cells and brown induration, the sizes of petechiae, purpura and ecchymoses, the significance of haemorrhage, red vs white infarcts with examples, wedge shape and coagulative necrosis, liquefactive necrosis in the brain, and the four factors that decide infarction.
Quick revision
- Hyperaemia: active, red. Congestion: passive, cyanotic.
- Lung congestion (left heart failure): heart failure cells, brown induration.
- Liver congestion (right heart failure): nutmeg liver, centrilobular necrosis.
- Petechiae 1–2 mm; purpura ≥3 mm; ecchymoses >1 cm.
- White infarct: heart, kidney, spleen. Red: lung, intestine, torsion.
- Wedge-shaped, coagulative necrosis; brain: liquefactive.
- Infarction depends on supply type, rate of occlusion, tissue vulnerability, blood oxygen.
Written by The House Job from standard pathology references (Robbins and Cotran Pathologic Basis of Disease is the book named in the UHS PGET syllabus).
FAQ
What is the difference between hyperaemia and congestion?
Hyperaemia is an active increase in arterial inflow from arteriolar dilation; congestion is a passive build-up of venous blood from impaired outflow.
What is a nutmeg liver?
The liver of chronic passive congestion (usually right heart failure), where congested centrilobular areas look dark red against paler periportal tissue.
Which organs get white infarcts?
Solid organs with end-arterial supply, such as the heart, kidney and spleen.
Why are lung infarcts usually red?
The lung has a dual blood supply and loose tissue, so blood from the bronchial circulation enters the dead area.