Page 61 - Textbook of Pathology, 6th Edition

eosinophilic cytoplasm. Occasionally, it may show hydrolytic enzymes. The common examples are infarct brain 45
cytoplasmic vacuolation or dystrophic calcification. and abscess cavity.
ii) Denaturation of proteins. This process is morphologically Grossly, the affected area is soft with liquefied centre
seen as characteristic nuclear changes in necrotic cell. These containing necrotic debris. Later, a cyst wall is formed.
nuclear changes may include: condensation of nuclear
chromatin (pyknosis) which may either undergo dissolution Microscopically, the cystic space contains necrotic cell CHAPTER 3
(karyolysis) or fragmentation into many granular clumps debris and macrophages filled with phagocytosed
material. The cyst wall is formed by proliferating
(karyorrhexis) (see Fig. 3.7).
capillaries, inflammatory cells, and gliosis (proliferating
glial cells) in the case of brain and proliferating fibroblasts
Types of Necrosis
in the case of abscess cavity (Fig. 3.26).
Morphologically, there are five types of necrosis: coagulative,
liquefaction (colliquative), caseous, fat, and fibrinoid necrosis. 3. CASEOUS NECROSIS. Caseous necrosis is found in the
centre of foci of tuberculous infections. It combines features
1. COAGULATIVE NECROSIS. This is the most common of both coagulative and liquefactive necrosis.
type of necrosis caused by irreversible focal injury, mostly
from sudden cessation of blood flow (ischaemia), and less Grossly, foci of caseous necrosis, as the name implies,
often from bacterial and chemical agents. The organs resemble dry cheese and are soft, granular and yellowish.
commonly affected are the heart, kidney, and spleen. This appearance is partly attributed to the histotoxic
effects of lipopolysaccharides present in the capsule of the
Grossly, foci of coagulative necrosis in the early stage are tubercle bacilli, Mycobacterium tuberculosis. Cell Injury and Cellular Adaptations
pale, firm, and slightly swollen. With progression, they
become more yellowish, softer, and shrunken. Microscopically, the necrosed foci are structureless,
Microscopically, the hallmark of coagulative necrosis is eosinophilic, and contain granular debris (Fig. 3.27). The
the conversion of normal cells into their ‘tombstones’ i.e. surrounding tissue shows characteristic granulomatous
outlines of the cells are retained so that the cell type can inflammatory reaction consisting of epithelioid cells with
still be recognised but their cytoplasmic and nuclear interspersed giant cells of Langhans’ or foreign body type
details are lost. The necrosed cells are swollen and appear and peripheral mantle of lymphocytes.
more eosinophilic than the normal, along with nuclear
changes described above. But cell digestion and lique- 4. FAT NECROSIS. Fat necrosis is a special form of cell death
faction fail to occur (c.f. liquefaction necrosis). Eventually, occurring at two anatomically different locations but
the necrosed focus is infiltrated by inflammatory cells and morphologically similar lesions. These are: following acute
the dead cells are phagocytosed leaving granular debris pancreatic necrosis, and traumatic fat necrosis commonly in
and fragments of cells (Fig. 3.25). breasts.
In the case of pancreas, there is liberation of pancreatic
2. LIQUEFACTION (COLLIQUATIVE) NECROSIS. Lique- lipases from injured or inflamed tissue that results in necrosis
faction or colliquative necrosis occurs commonly due to of the pancreas as well as of the fat depots throughout the
ischaemic injury and bacterial or fungal infections. It occurs peritoneal cavity, and sometimes, even affecting the extra-
due to degradation of tissue by the action of powerful abdominal adipose tissue.

Figure 3.25 Coagulative necrosis in infarct kidney. The affected area on right shows cells with intensely eosinophilic cytoplasm of tubular cells
but the outlines of tubules are still maintained. The nuclei show granular debris. The interface between viable and non-viable area shows non-
specific chronic inflammation and proliferating vessels.