Fibrinous inflammation, purulent inflammation, and abscesses
THE CONTEXT
Acute inflammation can produce fibrin-rich exudates or pus. The composition and subsequent fate of these exudates determine their morphologic appearance and consequences.
Formation and appearance of fibrinous inflammation
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Fibrinous inflammation results from local activation of coagulation and deposition of fibrin.
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Large increases in vascular permeability allow high-molecular-weight proteins such as fibrinogen to accumulate in exudates. Fibrin forms when a procoagulant stimulus is present.
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Fibrinous exudates characteristically involve the linings of body cavities, including the meninges, pericardium, and pleura.
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Histologically, fibrin appears as an eosinophilic meshwork of threads or an amorphous coagulum.
Resolution and organization
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Fibrinous exudates may resolve through fibrinolysis and clearance by macrophages.
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Unresolved exudates may undergo organization: fibroblasts and blood vessels grow into the exudate, leading to scarring.
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Extensive organization within the pericardial cavity may obliterate the pericardial space and result in restrictive cardiomyopathy.
Purulent inflammation and abscess formation
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Purulent, or suppurative, inflammation produces pus consisting of neutrophils, liquefied necrotic cell debris, and edema fluid.
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The most frequent cause is infection by bacteria that cause liquefactive tissue necrosis, such as staphylococci. These organisms are called pyogenic, meaning pus-producing.
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Acute appendicitis is a common example of acute suppurative inflammation.
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An abscess is a localized collection of pus within a tissue, organ, or confined space, produced by seeding of pyogenic bacteria.
Mediators of inflammatory symptoms and injury
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IL-1, TNF, and prostaglandins mediate fever.
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Prostaglandins, bradykinin, and neuropeptides mediate pain.
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Leukocyte lysosomal enzymes and reactive oxygen species mediate tissue damage.