Acute inflammation: morphology and serous exudates
THE CONTEXT
Acute inflammatory reactions share vascular and cellular changes, while their specific morphologic patterns can help identify the underlying cause.
Mediator functions and robustness
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Substance P contributes to transmission of pain signals and increases vascular permeability.
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Redundancy and synergistic actions among inflammatory mediators help maintain a robust protective response.
General morphology of acute inflammation
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The morphologic hallmarks are dilation of small blood vessels and accumulation of leukocytes and fluid in extravascular tissue.
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The pattern varies with reaction severity, etiology, and the tissue and site involved. Gross and microscopic appearances can provide clues to the cause.
Serous inflammation
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Serous inflammation produces serumlike, protein-rich exudates in cavities lined by the peritoneum, pleura, or pericardium, or in spaces created by tissue injury.
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The fluid is typically sterile and lacks large numbers of leukocytes.
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Fluid in body cavities may come from plasma because of increased vascular permeability or from mesothelial secretions caused by local irritation.
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Fluid accumulation in a mesothelium-lined cavity is called an effusion.
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Skin blisters caused by burns or viral infections contain serous fluid within or immediately beneath the damaged epidermis.