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PathologyInflammation and Repair

Inflammatory fluid leakage, edema, and stasis

THE CONTEXT
Increased microvascular permeability follows vasodilation and allows protein-rich fluid to enter extravascular tissues.

Exudate, transudate, edema, and pus

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Exudation is the escape of fluid, proteins, and blood cells from vessels into interstitial tissue or body cavities.
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An exudate is extravascular fluid with a high protein concentration and cellular debris. It indicates increased small-vessel permeability, typically during inflammation.
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A transudate has low protein content, predominantly albumin, little or no cellular material, and low specific gravity. It is an ultrafiltrate of plasma produced by osmotic or hydrostatic imbalance without increased vascular permeability and is usually unrelated to inflammation.
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Edema is excess fluid in interstitial tissue or serous cavities and may consist of either an exudate or a transudate.
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Pus is a purulent inflammatory exudate rich in leukocytes, mostly neutrophils, and dead cell debris; microbes are present in many cases.

Mechanisms of increased permeability

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The principal mechanism is endothelial cell contraction, which creates openings between endothelial cells.
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Histamine, bradykinin, leukotrienes, and other mediators elicit this response. It occurs within 15 to 30 minutes after mediator exposure and is usually short lived.
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Direct endothelial injury can cause increased permeability in unusual situations such as burns. Leakage begins immediately and persists for several hours until the damaged vessels become thrombosed or are repaired.

Development of stasis

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Fluid loss and increased vessel diameter slow blood flow and concentrate red cells in small vessels, increasing blood viscosity.
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Engorgement of small vessels with red cells is termed stasis. It appears histologically as vascular congestion and externally as localized redness.
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