coagulative necrosis
Summary
Coagulative necrosis is a form of cell death in which tissue architecture is preserved for several days despite loss of cellular nuclei, due to denaturation of proteins including enzymes that would otherwise degrade the cell. It is the hallmark of ischemic infarction in solid organs (except the brain) such as the heart, kidney, and spleen.
Detail
Coagulative necrosis occurs when there is denaturation of both structural proteins and enzymatic proteins, which blocks proteolysis of the dead cells, allowing the basic tissue architecture (cell outlines) to remain visible on histology for days to weeks. Nuclei disappear through pyknosis (shrinkage), karyorrhexis (fragmentation), and karyolysis (dissolution), but the eosinophilic, anucleate 'ghost' cell outlines persist. This is the typical morphologic pattern seen in hypoxic/ischemic death of cells in all solid organs except the brain (which undergoes liquefactive necrosis due to high lipid content and autolytic enzymes from microglia). Classic examples include myocardial infarction (pale infarcts), renal infarction, and splenic infarction. Grossly, an infarct due to coagulative necrosis appears as a wedge-shaped, pale area with the base at the organ surface. Over time, the necrotic tissue is removed by leukocyte infiltration and phagocytosis, followed by repair via granulation tissue and eventual scar formation. An important exception is caseous necrosis (a subtype of coagulative necrosis with a friable, cheese-like appearance), classically seen in tuberculosis and fungal infections, where necrotic tissue does not fully retain architecture but instead appears as amorphous granular debris surrounded by granulomatous inflammation. Coagulative necrosis is distinguished clinically and on exams from liquefactive necrosis (brain infarcts, abscesses), fat necrosis (pancreatitis, breast trauma), fibrinoid necrosis (immune-mediated vascular damage, e.g., malignant hypertension, vasculitis), and gangrenous necrosis (a clinical term describing coagulative necrosis with superimposed liquefactive changes from bacterial infection, seen in limb ischemia).
Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th ed.
- Goljan's Rapid Review Pathology
- First Aid for the USMLE Step 1
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