General pathology · Inflammation
Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate !
- Mechanism
In the first minutes of inflammation small vessels widen and leak, so protein-rich fluid and cells flood the tissue and cause swelling.
Updated 2026-11-01
What it is
The first response to injury happens in the microcirculation. Arterioles dilate and bring more blood (redness and heat), and postcapillary venules become leaky, so plasma proteins and fluid escape into the tissue (swelling). The fluid that leaves is an exudate, rich in protein and cells, unlike the protein-poor transudate of heart failure or low albumin; telling them apart is a daily clinical skill.
Key facts
- Immediate transient response: endothelial contraction in venules starts within minutes and lasts about 15–30 minutes (histamine).
- Direct endothelial injury (burns, toxins, some bacteria) causes immediate, sustained leakage that can also involve capillaries and arterioles.
- Delayed prolonged leakage begins hours after a mild injury, as in sunburn.
- Leukocyte-mediated endothelial injury and increased transport across endothelial cells (VEGF) add to leakage; new vessels formed during repair stay leaky.
Step by step
- A brief arteriolar constriction may come first (seconds); then arterioles dilate under histamine and nitric oxide.
- More blood enters the capillary bed: the area becomes red and warm (rubor, calor).
- Endothelial cells of postcapillary venules contract and open gaps (histamine, bradykinin, leukotrienes).
- Protein-rich fluid leaves the vessel; tissue oncotic pressure rises and draws more water out: oedema (tumor).
- Fluid loss concentrates red cells in small vessels and slows the flow (stasis).
- With slow flow, leukocytes move to the vessel wall (margination) and start to stick to activated endothelium.
- Lymph flow rises to drain fluid, cells and debris; it can carry infection to nodes (lymphangitis, lymphadenitis).
Exudate vs transudate
| Feature | Exudate | Transudate |
|---|---|---|
| Mechanism | Increased vascular permeability (inflammation) | Altered hydrostatic or oncotic pressure; vessel wall intact |
| Protein | High | Low |
| Cells | Many (leukocytes, sometimes red cells) | Few |
| Specific gravity | High (above about 1.020) | Low (below about 1.012) |
| Pleural fluid (Light's criteria) | At least one: fluid/serum protein above 0.5, fluid/serum LDH above 0.6, or fluid LDH above two thirds of the upper normal serum value | None of the three |
| Typical causes | Pneumonia, cancer, tuberculosis, pancreatitis | Heart failure, cirrhosis, nephrotic syndrome |
Clinical notes
- Urticaria is a small, itchy wheal of superficial dermal oedema from histamine; angioedema is deeper swelling of the dermis and submucosa.
- Laryngeal oedema in anaphylaxis is the same venular leak, life-threatening because of where it happens.
- In ARDS, leaky alveolar capillaries fill the alveoli with protein-rich fluid that forms hyaline membranes.
In the lab
- Fluid obtained by thoracentesis, paracentesis or arthrocentesis is tested for protein, LDH, cell count, Gram stain and culture to classify it.
Test yourself
Think of the answer, then tap the question to see it.
Which vessel segment leaks most in acute inflammation, and by what mechanism?
Postcapillary venules, through contraction of endothelial cells that opens gaps between them, triggered by histamine, bradykinin and leukotrienes.
A pleural fluid has high protein and many neutrophils. Is it an exudate or a transudate?
An exudate: high protein and many cells point to increased vascular permeability, as in a parapneumonic effusion.
Why does blood flow slow down in inflamed tissue?
Fluid leaves the vessels, red cells concentrate and viscosity rises, producing stasis that favours leukocyte margination.
Related
- Inflammation: the cardinal signs and its five steps
- Histamine, serotonin, bradykinin and the plasma protein cascades
- Mediators of inflammation: the table to know
- Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxis
- Edema and effusions: the four mechanisms
- Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer
Related conditions
- Urticaria and angioedema
- Anaphylaxis
- Burns (thermal, chemical, electrical; inhalation injury)
- Pleural effusion
- Acute respiratory distress syndrome (ARDS)
- Acute pericarditis
- Cellulitis of the leg
Elsewhere in DurgiPedia
- Starling forces at the capillary
- How edema forms
- How the lymphatic system works
- Mast cell and basophil
- Nitric oxide (NO)
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: 17.5 Inflammation and Fever (OpenStax (Microbiology), 2016); Hives | Rash | Skin Rash | Itchy Skin | MedlinePlus (MedlinePlus, US National Library of Medicine, 2026); Hereditary angioedema: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026).
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Representative model, for educational purposes only.