Necrosis

Necrosis is defined as a localised area of death of tissue followed later by degradation of tissue by hydrolytic enzymes liberated from dead cells.

• It is invariably accompanied by infl ammatory reaction.

• Necrosis can be caused by various agents such as hypoxia, chemical and physical agents, microbial agents, immunological injury, etc.

• Based on etiology and morphologic appearance, there are 5 types of necrosis:

1.Coagulative necrosis

2.Liquefaction (colliquative) necrosis

3.Caseous necrosis

4.Fat necrosis

5.Fibrinoid necrosis

1. COAGULATIVE NECROSIS :- This is the most common type of necrosis caused by irreversible focal injury, mostly from sudden cessation of blood flow (ischaemic necrosis), and less often from bacterial and chemical agents.

2. LIQUEFACTION (COLLIQUATIVE) NECROSIS :- Liquefaction or colliquative necrosis also occurs commonly due to ischaemic injury and bacterial or fungal infections but hydrolytic enzymes in tissue degradation have a dominant role in causing semi-fl uid material.

The common examples are infarct brain and abscess cavity.

3. CASEOUS NECROSIS :- Caseous (caseous= cheese-like) necrosis is found in the centre of foci of tuberculous infections. It combines features of both coagulative and liquefactive necrosis.

4. FAT NECROSIS :- Fat necrosis is a special form of cell death occurring at mainly fat-rich anatomic locations in the body.

Examples : traumatic fat necrosis of the breast, especially in heavy and pendulous breasts, and mesenteric fat necrosis due to acute pancreatitis.

5. FIBRINOID NECROSIS :- Fibrinoid necrosis is characterised by deposition of fibrin-like material which has the staining properties of fibrin such as phosphotungistic acid haematoxylin (PTAH) stain.

It is encountered in various examples of immuno logic tissue injury (e.g. in immune complex vasculitis, autoimmune diseases, Arthus reaction etc), arterioles in hypertension, peptic ulcer etc.