Necrosis

FIGURE 2-11 Coagulative necrosis.

A, A wedge-shaped kidney infarct (yellow). B, Microscopic view of the edge of the infarct, with normal kidney (N) and necrotic cells in the infarct (I) showing preserved cellular outlines with loss of nuclei and an inflammatory infiltrate (seen as nuclei of inflammatory cells in between necrotic tubules).

FIGURE 2-12 Liquefactive necrosis.

An infarct in the brain, showing dissolution of the tissue.

FIGURE 2-14 Fat necrosis.

The areas of white chalky deposits represent foci of fat necrosis with calcium soap formation (saponification) at sites of lipid breakdown in the mesentery.

FIGURE 2-13 Caseous necrosis.

Tuberculosis of the lung, with a large area of caseous necrosis containing yellow-white and cheesy debris.

FIGURE 2-15 Fibrinoid necrosis

in an artery. The wall of the artery shows a circumferential

Liquefactive necrosis,

in contrast to coagulative necrosis, is characterized by digestion of the dead cells, resulting in transformation of the tissue into a liquid viscous mass. It is seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of leukocytes and the liberation of enzymes from these cells. The necrotic material is frequently creamy yellow because of the presence of dead leukocytes and is called pus. For unknown reasons, hypoxic death of cells within the central nervous system often manifests as liquefactive necrosis (Fig. 2-12).

Coagulative necrosis

is a form of necrosis in which the architecture of dead tissues is preserved for a span of at least some days (Fig. 2-11). The affected tissues exhibit a firm texture. Presumably, the injury denatures not only structural proteins but also enzymes and so blocks the proteolysis of the dead cells; as a result, eosinophilic, anucleate cells may persist for days or weeks. Ultimately the necrotic cells are removed by phagocytosis of the cellular debris by infiltrating leukocytes and by digestion of the dead cells by the action of lysosomal enzymes of the leukocytes. Ischemia caused by obstruction in a vessel may lead to coagulative necrosis of the supplied tissue in all organs except the brain. A localized area of coagulative necrosis is called an infarct.

Fibrinoid necrosis:

is a special form of necrosis usually seen in immune reactions involving blood vessels. This pattern of necrosis typically occurs when complexes of antigens and antibodies are deposited in the walls of arteries. Deposits of these "immune complexes," together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called "fibrinoid" (fibrin-like) by pathologists (Fig. 2-15). The immunologically mediated vasculitis syndromes in which this type of necrosis is seen are described in Chapter 11.

Fat necrosis

is a term that is entrenched in medical parlance but does not in reality denote a specific pattern of necrosis. Rather, it refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. This occurs in the calamitous abdominal emergency known as acute pancreatitis (Chapter 19). In this disorder pancreatic enzymes leak out of acinar cells and liquefy the membranes of fat cells in the peritoneum. The released lipases split the triglyceride esters contained within fat cells. The fatty acids, so derived, combine with calcium to produce grossly visible chalky-white areas (fat saponification), which enable the surgeon and the pathologist to identify the lesions (Fig. 2-14). On histologic examination the necrosis takes the form of foci of shadowy outlines of necrotic fat cells, with basophilic calcium deposits, surrounded by an inflammatory reaction.

Caseous necrosis:

is encountered most often in foci of tuberculous infection (Chapter 8). The term "caseous" (cheeselike) is derived from the friable white appearance of the area of necrosis (Fig. 2-13). On microscopic examination, the necrotic area appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border; this appearance is characteristic of a focus of inflammation known as a granuloma (Chapter 3).

Gangrenous necrosis:

is not a specific pattern of cell death, but the term is commonly used in clinical practice. It is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone necrosis (typically coagulative necrosis) involving multiple tissue planes. When bacterial infection is superimposed there is more liquefactive necrosis because of the actions of degradative enzymes in the bacteria and the attracted leukocytes (giving rise to so-called wet gangrene).