Ref Robbins 8/e p46-47 9/e p74 ACUTE INFLAMMATION The vascular and cellular reactions that characterize acute inflammation are reflected in the morphologic appearance of the reaction. The severity of the inflammatory response, its specific cause, and the paicular tissue involved all can modify the basic morphology of acute inflammation, pro- ducing distinctive appearances. The impoance of recog- nizing these morphologic patterns is that they are often associated with different etiology and clinical situations. MORPHOLOGY * Serous inflammation is characterized by the outpour- ing of a watery, relatively protein-poor fluid that, depend- ing on the site of injury, derives either from the plasma or from the secretions of mesothelial cells lining the perito- neal, pleural, and pericardial cavities. The skin blister resulting from a burn or viral infection is a good example of the accumulation of a serous effusion either within or immediately beneath the epidermis of the skin (Fig. 2-11). Fluid in a serous cavity is called an effusion. * Fibrinous inflammation occurs as a consequence of more severe injuries, resulting in greater vascular perme- ability that allows large molecules (such as fibrinogen) to pass the endothelial barrier. Histologically, the accumu- lated extravascular fibrin appears as an eosinophilic mesh- work of threads or sometimes as an amorphous coagulum (Fig. 2-12). A fibrinous exudate is characteristic of inflam- mation in the lining of body cavities, such as the meninges, pericardium, and pleura. Such exudates may be degraded by fibrinolysis, and the accumulated debris may be removed by macrophages, resulting in restoration of the normal tissue structure (resolution). However, exten- sive fibrin-rich exudates may not be completely removed, and are replaced by an ingrowth of fibroblasts and blood vessels (organization), leading ultimately to scar- ring that may have significant clinical consequences. For example, organization of a fibrinous pericardial exudate forms dense fibrous scar tissue that bridges or obliterates the pericardial space and restricts myocardial function. * Suppurative (purulent) inflammation and abscess formation. These are manifested by the collection of large amounts of purulent exudate (pus) consisting of neutrophils, necrotic cells, and edema fluid. Ceain organ- isms (e.g., staphylococci) are more likely to induce such localized suppuration and are therefore referred to as pyogenic (pus-forming). Abscesses are focal collections of pus that may be caused by seeding of pyogenic organ- isms into a tissue or by secondary infections of necrotic foci. Abscesses typically have a central, largely necrotic region rimmed by a layer of preserved neutrophils (Fig. 2-13), with a surrounding zone of dilated vessels and fibroblast proliferation indicative of attempted repair. As time passes, the abscess may become completely walled off and eventually be replaced by connective tissue. Because of the underlying tissue destruction, the usual outcome with abscess formation is scarring.